“Becoming a
USRN
Study guide
2019
Roadmap
to NCLEX”
100 m
NCLEX-RN study guide
Introduction
Welcome to RoadMap to NCLEX®. This book is based on the need of Filipino nurses
to pass their NCLEX-RN examination and other foreign licensure tests. NCLEX-RN in
the United States is a standardized test used to determine competencies for entry
level nurses in each state. It is regarded by many as one of the toughest
examinations to pass especially for foreign nurses like Filipinos. Working here in the
US, I see that one of the reasons behind is that, the exam is not as consistent as
what we learned in the Philippines even though we use American references.
Simply because we don’t see it in our hospital practice. But in here, it is mostly
consistent with what they learn and do. The percentage of passing rate for first time
takers, US educated for NCLEX-RN in 2019 is within 86-92% comparing to 47.1% for
internationally educated. Filipino nurses are on top of the list for NCLEX-RN takers.
Nevertheless, I am driven to bring the gap closer. There is no big difference
between me and my co-nurses in the Philippines or elsewhere in terms of passing
the NCLEX-RN and be able to practice here in the US, we all can do it. Learning
does not stop. It is not as difficult as what you think, just don’t doubt yourself. NCSBN
only need an entry level competency to get in.
In the Philippines, I am thankful to IPass who has been the instrument of success for
many nurses who passed including those who were unsuccessful, “believing” is the
key. IPass has been my enabler in making all this possible.
The resources from various top of the line review materials such as Saunders,
LaCharity, Uworld, online medical information access like Mayoclinic, Medscape,
American Heart Association, The Joint Commission, Center for Disease Control,
Osmosis and Khan academy videos and the likes, and images from various internet
sites. This book is basically a consolidation of these resources put as one, coherent
with the trending topics in the NCLEX-RN. In addition, past examinees contributed
by gathering information which came out from their exams themselves. These facts
are also seen in my workplace as a medical-surgical floor and in other acute
hospital settings in general which helped me align NCLEX knowledge into practice.
My family, who has been my inspiration all this time. We are family of nurses and
educators as well. We believe in the value of education. We survive with
persistence, as the saying goes “The river cuts through a rock not because of its
power, but its persistence” (James Watkins).
Lastly, I believe in blessings and not by luck. God gives us all this blessings, may be in
a form of hardships or prosperity. At the end of the day, his plans are greater and he
made it beautiful.
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7 routes of success
1. Know the NCLEX
7. Destination RN
2. Your Goal
4. Strategies
6. The Day
3. Your Abilities
5. Mastering the “Trends”
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1
Know the NCLEX
NCLEX is an adaptive testing system. As you answer a question,
the computer determines your competency based on the answer
you selected. If you selected a correct answer, the computer scans
the question bank and selects a more difficult question. If you
selected an incorrect answer, the computer scans the question
bank and selects an easier question until you meet the PASSING
standard or otherwise a failing mark. There are 75 – 265 number of
questions and as long as 6 hours to complete the exam. The
computer assesses at 75th item, it’s either satisfied or not. If not, then
it will continue until 6 hours or 265 whichever comes first. It may stop
at any time after 75th item as long as the computer already
determines your competency. If you completed the 265 items, last
item must be correct otherwise you fail the exam. On the other
hand, if you ran out of time, the average of the last 60 items will be
assumed as your competency level. It must be at least in line with
the minimum competency.
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The Test Plan
Type of questions
The NCSBN provides specific directions for you to follow with all question
types to guide you in your process of testing. Be sure to read these
directions as they appear on the computer screen
before you start answering the graded exam.
1. Multiple choice
2. Ordered Response (Place the sequence in order)
3. Select all that apply (SATA) – in SATA you can answer one up to all
choices as long as you think it’s the right answer(s)
4. Fill in the blank (usually computations)
5. Drag and drop
6. Hotspot (place the cursor over the area on the
diagram that does the selected action)
7. Chart/Exhibit – your answer is based on the chart or exhibit given
8. Graphic Option – showing you pictures or images where you can
base your answers
9. Audio – For example lung or heart sounds
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2
Your Goal
Remember:
Pass with 75 questions as much as possible. To pass with
75 questions you will most likely need to answer more
difficult and multiple response questions correctly like the
BEAST “Select All That Apply.” The key to slay this is to be
a master of the content! Don’t panic if you exceeded
the minimum 75 item. The goal is to pass the exam, so
take a break and relax before you answer the next
succeeding questions.
In 2012, the average number of items (questions) administered
per candidate was around 119 on the NCLEX-RN and 117 on the
NCLEX-PN.
3
Your abilities
Remember:
It’s important to know your strong and weak concepts
for you to focus on. It is not good to hope that your weak
points would not come out during exam, the secret is
focus on your weakness and maximize your strengths.
NCLEX® knows how to target weak points by throwing
more questions until you hit their standards.
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4
❖
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❖
❖
Strategies
Don’t start being anxious and especially don’t panic!
You don’t need to read extra meaning to the question.
Look for keywords and phrases to help you understand.
Interpret the question correctly first before reading into the
choices.
Read the stem correctly and notice, is it asking for the best
response or the initial response
Understand what the question is asking before considering the
distracter.
Rephrasing technique translates the question into your own
words.
Isolate choice that is relevant from what is not.
Judge all four alternative choices/options against the stem and
not against one another.
Use the process of elimination, cross out those variables that are
incorrect.
When you come across a difficult question and you cannot
immediately identify the answer, go back to your body of
knowledge and draw all the information that you do know
about the condition. Even though you do not know exactly
what to do, you might know what not to do
If one is the exact opposite of another (e.g. complete bed rest is
different from activity as tolerated; both cannot be correct
since they are of opposites), choose the one that seems to be
most logical.
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❖ If you cannot choose an alternative, use your intuition. Let
yourself feel which alternative might be right. Remember, it’s
better to choose one answer than none at all.
o Do we depend on this “hunch?”(Intuition). Current studies
support that hunches are often correct, for they are based
on rapid subconscious connections in the brain.
❖ So, if you have an initial hunch, go with it! Do not change the
answer if and only if, upon reflection, it just doesn’t seem right. (If
you are taking NCLEX®, you can take time as you want, but do
not dwell too much.)
❖ Remember, this is a nursing test and questions are designed to
test your nursing competency and safety.
❖ It is unlikely that a question would require a medical action for
the correct answer; it may, however offer these actions as
distracter.
❖ Beware of answers that contain specific qualifiers, such as
“always’ and “never,” they rarely fit within a logical framework.
❖ Content is King: “Select all that Apply” (SATA) format questions
are very much like a “T & F” quiz you may have taken during
nursing school. Unfortunately, there is no short cut to preparing
for the SATA questions, a candidate just has to have enough
content.
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5
Mastering the “Trends”
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1
Prioritization and
Delegation
Considerations in Prioritizing:
Remember: Registered Nurses
(RN) use “higher clinical
judgement skills”. Delegate
task that does not use much
of your clinical judgment. Do
not misuse prioritization
approaches for example,
CAB (Compression, Airway,
Breathing). This is used for
basic CPR guidelines.
1. ABCs
1. Airway/Breathing
2. Circulation/CV status
3. Infection/Sepsis
4. Pain/Injury
5. Nutrition/Elimination
6. Knowledge deficit/Anxiety & Fear
7. Other psychosocial prob
2. Acute patients before Chronic
❖ Acute patients will have unexpected symptoms,
chronic has expected manifestations and are
predictable.
3. Unstable patients before stable ones. Delegate task
4. Consider high vulnerable patients:
<2 YO, >65-70 YO, pregnant women, consciously
sedated patients.
5. Changing Condition/Deteriorating
Ex: Chronic can become acute at any time – Prioritize
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Question: An emergency department nurse is assigned to triage.
Which client should the nurse assess first?
1. Five-year-old with a superficial leg laceration
2. Lethargic 3-month-old with diarrhea for the past 12 hours
3. Seven-year-old with an elevated temperature of 101 F (38.3 C)
and hematuria
4. Seventeen-year-old with severe, acute abdominal pain
Answer: 2
Rationale:
1. Five-year-old with a superficial leg laceration
Bleeding/circulation problem but only superficial. Age is 5 YO
(non-vulnerable)
2. Lethargic 3-month-old with diarrhea for the past 12 hours
Vulnerable patient @ <2 YO, circulation problem, acute and
can deteriorate at any time, cannot be delegated, RNs
judgment is needed
3. Seven-year-old with an elevated temperature of 101 F (38.3 C)
and hematuria
Infection is not a priority, age is not vulnerable, stable and can
be delegated
4. Seventeen-year-old with severe, acute abdominal pain
2nd priority – could be appendicitis, or ectopic pregnancy that
can deteriorate at any time, however the age is not vulnerable.
Unless otherwise the patient develops sudden respiratory distress
– AIRWAY is a priority.
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Delegation:
General Tasks
RN
LPN/LVN
UAP
Assessment
Initial/admission
Acute/Unstable
Patient
Stable Patients
Follow-up
Assessment
Special
assessment:
Lung sounds,
Bowel sounds
etc.
Stable Patients
Monitor VS, I/O,
Height and
weight
Care Planning
Yes
Assist only
No
Evaluation
Yes
No
No
Education
Initial &
Discharge
Reinforce only
Reinforce only
Documentation
Yes
Yes
Yes
Medication
All
Except IV
No
Sterile Procedure
Yes
Yes – Routine
Only
No
Remember: 5 Rights of delegation
▪ right task
▪ right person
▪ right circumstances
▪ right communication/direction
▪ right supervision/evaluation
Blood Transfusion: Initial
assessment (15 mins) done by RN,
Then delegate to UAP.
Delegate positioning to UAP:
Unless with cervical injury in which
RNs must assess respiratory status.
Delegate feeding to UAP: CVA
patient: first 24-48° should be RN
(Risk for Aspiration)
PEG tube feeding: LPN/LVN
(stoma care is indicated)
Remember: RNs and LVNs have
professional license. Higher
accountability and responsibility is
implicated.
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2
Nursing Issues
Transcultural Nursing
Latino Americans
▪ May view illness as a sign of
weakness, punishment for evil
doing;
▪ May consult with a curandero or
voodoo priest
▪ Family members are typically
involved in all aspects of decision
making such as terminal illness
▪ May see no reason to submit to
mammograms or vaccinations.
•
African Americans
▪ May believe that illness is
caused by supernatural
causes and seek advice and
remedies from faith healers
▪ Family oriented;
▪ Higher incidence of HPN and
obesity;
▪ High incidence of lactose
intolerance
Arab Americans
Asian Americans
▪ May value ability to endure pain
and grief with silent stoicism;
▪ Typically family oriented;
extended family should be
involved in care of dying
patient;
▪ Believes in “hot-cold” yin/yang
often involved
▪ Sodium intake is generally high
because of salted and dried
foods;
▪ May believe prolonged eye
contact is rude and an invasion
of privacy;
▪ May prefer to maintain a
comfortable physical distance
between the patient and the
health care provider.
▪ May remain silent about health
problems such as STIs, substance
abuse, and mental illness
▪ A devout Muslim may interpret illness
as the will of Allah, a test of faith;
▪ May rely on ritual cures or alternative
therapies before seeking help from
health care provider
▪ After death, the family may want to
prepare the body by washing and
wrapping the body in unsewn white
cloth
▪ Postmortem examinations are
discouraged unless required by law.
▪ People suffering from chronic
illnesses, pregnant women, breastfeeding, or menstruating don’t fast.
▪ Females avoid eye contact with
males
▪ Use same-sex family members as
interpreters.
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Native Americans
▪ May turn to a medicine man
to determine the true cause
of an illness;
▪ May value the ability to
endure pain or grief with silent
stoicism;
▪ Diet may be deficient in
vitamin D and calcium
because many suffer from
lactose intolerance or don’t
drink milk;
▪ Obesity and diabetes are
major health concerns;
▪ May divert eyes to the floor
when they are praying or
paying attention.
Western Culture
▪ May value technology
almost exclusively in the
struggle to conquer
diseases;
▪ Health is understood to be
the absence, minimization,
or control of disease
process;
▪ Eating utensils usually
consists of knife, fork, and
spoon;
▪ Three daily meals is typical.
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What is HIPAA?
HIPAA is the acronym for the Health Insurance Portability and
Accountability Act that was passed by Congress in 1996.
HIPAA does the following:
1. Provides the ability to transfer and continue health
insurance coverage for workers and their families when
they change or lose their jobs;
2. Reduces health care fraud and abuse;
3. Mandates standards for health care information on
electronic billing and other processes; and
4. Requires the protection and confidential handling of
protected health information (PHI)
“Under HIPAA, a client's information regarding medical
treatment is private and cannot be released without
the client's permission. Nurses need to try to reasonably
limit use of, disclosure of, and requests for PHI in any
given situation.”
Remember:
Information should be provided only on a "need-to-know" basis.
The United States is serious about HIPAA and the citizens know
this law very much.
Ethical Principles:
Autonomy: Patient’s right to decide (consent/refuse)
Nonmaleficence: Do no harm to patients
Beneficence: To act in the best interest of patient
Justice: Fairness/equality of treatment regardless of status
Veracity: Truthfulness to patients
Fidelity: Loyalty to profession
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Informed Consent and Informed Refusal:
Must consist of the following:
1. The HCP MUST clearly explain to the patient
Diagnosis
Procedure/Surgery
Complications involved
Prognosis
Alternatives
2. The client has indicated understanding of the information.
3. The client is giving voluntary, legal consent for the procedure.
Question 1: The health care provider gives the preoperative nurse a
signed consent form and walks away rapidly. The client turns to
the nurse and states, "I don't know what is going on. Why do I
need surgery?" What is the most appropriate action?
1. Call the nursing supervisor
2. Call the operating room scheduler and cancel the surgery
3. Page the health care provider and request clarification on
behalf of the client
4. Report the incident to hospital administration
Answer: 3
Rationale: Informed consent requires that the health care provider
performing the procedure explain everything to the client's
satisfaction.
Remember:
Consent or refusal, patient must be INFORMED and aware.
Waiting until the client is awake to obtain consent for a
procedure already performed is illegal and would warrant
charges of assault and battery.
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Assault: An unlawful act that places another
person, without that person's consent, in fear of
immediate bodily harm. (Threatening the patient)
Battery: A completed assault is a battery
Slander: oral defamation
False imprisonment: Limiting patient to move
(illegal detention)
Emancipated Minor: "mature minor" who can give consent.
Criteria:
▪ Marriage
▪ In the armed forces,
▪ living apart from one's
parents
▪ Financial independence
▪ Pregnancy/parenthood
▪ A court decision
Question: The nurse is caring for a 4-year-old child in the emergency
department who has a 104 F (40 C) temperature, is obtunded,
and has a positive Kernig's sign. The parents are refusing
antibiotics and any treatment. The parents state that their
religious belief is to trust in just prayer and believe the child will
receive divine healing. What action does the nurse anticipate?
1. Assisting the parents in signing Against Medical Advice (AMA)
papers
2. Discharging the child if parents have power of attorney
papers
3. Notifying the hospital administration about the situation
4. Reassuring the parents that their decision will be respected
under the principle of autonomy.
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Answer: 3
Rationale: Hospital administration will obtain legal protective custody
of a minor child if the parents are deciding against life-saving
measures for their child or when there is child abuse/neglect.
Paternalism - A type of
medical decision making in
which health care
professionals assume over
an incapacitated parent of
a child with life threatening
condition
Ethical Dilemma
Occurs when there is a
conflict between 2 or more
ethical principles.
Negligence: Is a failure to exercise the care that a reasonably
prudent person would exercise.
Malpractice: Is a type of negligence, also known as “Professional
Negligence” unbecoming of a Professional Nurse.
Negligence can be:
Commission is care
rendered but wrong
Omission is never
rendered at all
Ordinary Negligence:
unintentional
Gross Negligence:
Intentional
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Patient Abandonment
The American Nurse’s Association’s definition of patient
abandonment is “a unilateral severance of the established
nurse-patient relationship without giving reasonable notice to
the appropriate person so that arrangements can be made for
continuation of nursing care by others”
Criteria:
1. Have first ACCEPTED the client assignment,
establishing a nurse client relationship;
2. DISENGAGED the nurse client relationship without
giving reasonable notice to the qualified person
(supervisor, colleague, etc.)
What is Self – Determination Act?
A law that indicates clients must be provided with information about
their rights to identify written directions about the care that they wish
to receive in the event that they become incapacitated and are
unable to make health care decisions.
Advance Directives
Include a living will, which states the medical care that you do and
do not want at the end of life, and a health care power of attorney
(by proxy), which designates a health care agent to make decisions
on your behalf if you are incapacitated.
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Five Wishes
Combining a living will and health
care power of attorney in addition
to addressing matters of comfort
care and spirituality.
Wishes 1 and 2: are both legal
documents. Once signed, they
meet the legal requirements for an
advance directive
Signed:
POA for Proxy: By lawyer(Notary)
Living Will: By patient only
Lateral Violence
Lateral violence (also known as horizontal violence) can be defined
as acts of aggression carried out by a co-worker against another coworker and designed to control, diminish, or devalue a colleague.
These behaviors usually take the form of verbal abuse such as namecalling, unwarranted criticism, intimidation, and blaming.
Remember:
Refusing to help someone,
sabotage, exclusion, and
unfair assignments, also fall
under the category of lateral
violence.
Actions to Take:
1. Confront the bully
2. Validate/Support the
colleague
3. Report
4. Document
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Good Samaritan Act
Good Samaritan laws protect caregivers from prosecution for medical
mistakes, as long as the caregivers are acting in a voluntary manner
without any expectation of reward.
Remember: Being a rescuer means accountability
Most states DO NOT cover acts of “gross negligence” or “willful
misconduct”. Gross negligence is generally taken to mean a reckless
action that is taken without regard for the safety of others while willfull
misconduct is generally considered to be an action that is reasonably
likely to cause an injury to another person. For instance, you are rescuing
the severely bleeding patient from an injury to his/her hand and you did
not apply a direct pressure from a near artery. This is an obvious
negligence on the part of the rescuer.
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3
Patient Safety
Patient Safety Goals
The purpose of the National Patient Safety Goals is to improve patient
safety. The goals focus on problems in health care safety and how to
solve them.
1
Identify patients correctly
Use at least two ways to identify patients.
Ex: Identifiers
▪ Patient’s Full Name,
▪ Date of Birth
▪ Medical Record Number (most distinct)
2
Improve Effective Communication
A. SBAR
S:
B:
A:
R:
Situation
Background
Assessment
Recommendation/read-back
An established reporting format used to communicate with the
health care provider (HCP). Use of SBAR ensures that the HCP
receives the necessary information to make a clinical
judgment regarding treatment or need for immediate
assessment.
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Ex: Place the following report information in the correct order
according to the SBAR format.
1. “He is restless and anxious: temperature is 100.3° F (38° C); pulse
is 110 beats/min; respiratory rate is 24 breaths/min; blood
pressure is 140/90 mm Hg. Abdomen is rigid and tender to
touch with hypoactive bowel sounds.”
2. “He had abdominal surgery yesterday. He is on PCA morphine,
but he says the pain is getting progressively worse.”
3. “I have tried to make him comfortable and he is willing to wait
until the next scheduled dose of pain medication, but I think his
pain warrants evaluation.”
4. “Would you like to give me an order for any laboratory tests or
additional therapies at this time?”
5. “Dr. S, this is Nurse J. I’m calling about Mr. D, who is reporting
severe abdominal pain.”
Answer: : 5, 2, 1, 3, 4
5. “Dr. S, this is Nurse J. I’m calling about Mr. D, who is reporting
severe abdominal pain.”
2. “He had abdominal surgery yesterday. He is on PCA morphine,
but he says the pain is getting progressively worse.”
1. “He is restless and anxious: temperature is 100.3° F (38° C); pulse
is 110 beats/min; respiratory rate is 24 breaths/min; blood
pressure is 140/90 mm Hg. Abdomen is rigid and tender to
touch with hypoactive bowel sounds.”
3. “I have tried to make him comfortable and he is willing to wait
until the next scheduled dose of pain medication, but I think his
pain warrants evaluation.”
4. “Would you like to give me an order for any laboratory tests or
additional therapies at this time?”
B. Verbal & Telephone Orders
Verbal Order is order received through face to face interaction
during emergency situation.
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Telephone Order is taken when physician is not present &
communication is over the telephone.
Remember:
The nurse “writes down and reads back “ the information to confirm
the telephone order. Verbal order must be “repeated/read back” to
the ordering physician before proceeding.
C. Approved and Unapproved Abbreviation
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Question: Which medication order for a client with a pulmonary
embolism is most important to clarify with the prescribing
physician before administration?
1. Warfarin (Coumadin) 1.0 mg by mouth (PO)
2. Morphine sulfate 2 to 4 mg IV
3. Cephalexin (Keflex) 250 mg PO
4. Heparin infusion at 900 units/hr
Answer: : 1
Remember:
Use of “Trailing Zero” e.g. 1.0 mg might be misinterpreted as 10 mg.
Use of “Preceding Zero” is allowed, e.g. 0.1 mg. Whereas writing .1
can be interpreted as 1 or 11.
D. Report critical results of tests and diagnostic procedures
on a timely basis.
Critical results of any tests and diagnostic procedures fall
significantly outside the normal range and may indicate a life
threatening situation. The objective is to provide the responsible
licensed caregiver these results within an established time frame so
that the patient can be promptly treated.
Remember:
Most institution requires 30 minute timeline from communicating until
treatment.
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3
2
Use Medicines Safely
A. High Alert Medications (HAM)
Drugs that bear a heightened risk of causing significant
patient harm when they are used in error.
How to reduce errors:
▪
▪
▪
▪
▪
▪
▪
▪
Standardizing the ordering
Storage
Preparation and administration
Improving access to information about these drugs
Limiting access to high alert medications;
Using auxiliary labels
Employing clinical decision support and automated alerts
Using redundancies such as automated or independent
double checks when necessary. Example in drug
calculations, “I check, you check separately, then
compare answers”.
Memorize at least this mnemonic! PINCH
P: Potassium Chloride
I: Insulin
N: Narcotics, Neuromuscular blocking agents (muscle
relaxants)
C: Concentrated electrolytes (>0.9% NaCl)
H: Heparin and other anticoagulants, thrombolytics
Remember:
All forms of insulin, subcutaneous and IV, are considered a class of
high-alert medications. Insulin U-500 has been singled out for
special emphasis to bring attention to the need for distinct
strategies to prevent the types of errors that occur with this
concentrated form of insulin.
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4
2
Use Alarms Safely
Remember:
Make improvements to ensure that alarms on medical equipment
are heard and responded to on time.
5
2
Prevent Infection
A. STANDARD PRECAUTION
Standard Precautions include a group of infection
prevention practices that apply to all patients, regardless
of suspected or confirmed infection status, in any setting in
which healthcare is delivered.
1. Hand hygiene
2. Use of personal protective equipment (e.g., gloves,
masks, eyewear)
3. Respiratory hygiene / cough etiquette
4. Sharps safety
5. Safe injection practices
6. Ensure appropriate patient placement
7. Handle textiles and laundry carefully
8. Clean and disinfected, instruments, devices and
environmental surfaces
Hand Hygiene
Remember:
Handwashing: When hands are visibly soiled, use soap and water
for 40-60 seconds
Hand rubbing: When hands are not visibly soiled, use alcohol
based hand rub for 20-30 seconds
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Moments of Hand Hygiene
Personal Protective Equipment PPE: Gloves, masks,
eyewear/goggles, gown
PPE Donning
1.
2.
3.
4.
Hand hygiene
Gown
Mask or respirator
Goggles/face
shield
5. Gloves
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PPE Removal
1.
2.
3.
4.
5.
Gloves
Goggles/face shield
Gown
Mask or respirator
Hand hygiene
Respiratory hygiene/cough etiquette
Measures to contain respiratory secretions: Recommended for all
individuals with signs and symptoms of a respiratory infection.
1. Cover your mouth and nose with a tissue when coughing or
sneezing;
2. Use in the nearest waste receptacle to dispose of the tissue
after use;
3. Perform hand hygiene
Healthcare facilities should ensure the availability of materials for
adhering to Respiratory Hygiene/Cough Etiquette in waiting areas for
patients and visitors.
1. Provide tissues and no-touch receptacles for used tissue
disposal.
2. Provide conveniently located dispensers of alcohol-based
hand rub; where sinks are available, ensure that supplies for
hand washing (e.g. soap, disposable towels) are consistently
available.
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Sharps safety
Remember:
▪ Fish hook technique
▪ No bending of needles
▪ Dispose container at ½
or 2/3 full
Needlestick injury: Things to do
1. Remove gloves
2. Wash area with soap and
water
3. Notify the nurse's supervisor
4. Go to employee health
clinic
5. Take post-exposure
prophylaxis
Disinfection
Hospital-approved
antiseptics:
▪ ≥ 0.5% chlorhexidine with
alcohol (most effective)
▪ 70% alcohol pads
▪ ≥10% povidone-iodine
Catheter Ports:
The nurse should scrub the
Foley collection port with
alcohol or chlorhexidine
solution for 15 seconds
before withdrawing a
specimen
Invasive Lines:
The nurse should "scrub the
hub" with alcohol or
chlorhexidine/alcohol for 1015 seconds. This should be
done before flushing,
drawing blood, or
administering medication.
Chlorhexidine is preferred
over povidone-iodine:
It achieves an antimicrobial
effect within 30 seconds
whereas povidone-iodine
takes ≥2 minutes.
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B. TRANSMISSION BASED PRECAUTION
Transmission-Based Precautions are the second tier of basic
infection control and are to be used in addition to Standard
Precautions for patients who may be infected or colonized
with certain infectious agents for which additional
precautions are needed to prevent infection transmission.
Contact Precautions
for patients with known
or suspected infections
that represent an
increased risk for
contact transmission
Droplet Precautions
for patients known or
suspected to be infected
with pathogens
transmitted by respiratory
droplets that are
generated by a patient
who is coughing,
sneezing, or talking
Airborne Precautions
for patients known or
suspected to be infected
with pathogens
transmitted by the
airborne route (e.g.,
tuberculosis, measles,
chickenpox, disseminated
herpes zoster)
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CONTACT precaution guidelines:
Ensure appropriate patient placement. Acute care hospitals - single
patient room if available
Use personal protective equipment (PPE) appropriately
Gloves and Gown - Wear a gown and gloves for all interactions that
may involve contact with the patient or the patient’s environment.
Limit transport and movement of patients. When transport or
movement is necessary, cover or contain the infected or colonized
areas of the patient’s body.
Use disposable or dedicated patient-care equipment
(e.g., blood pressure cuffs). If common use of equipment for
multiple patients is unavoidable, clean and disinfect such
equipment before use on another patient.
Prioritize cleaning and disinfection of the rooms
at least daily or prior to use by another patient if outpatient setting
focusing on frequently-touched surfaces and equipment in the
immediate vicinity of the patient.
Remember: Mnemonic is Mrs. Wee
M – Multi drug Resistant Organisms:
▪ MRSA (Methicillin resistant staph. aureus)
▪ VRSA (Vancomycin resistant staph. aureus)
▪ VRE (Vancomycin resistant enterococcus)
▪ ESBL (Extended spectrum beta lactamase)
▪ KPC (Klebsiella Pneumoniae Carbapenemase)
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R – Respiratory Infections:
▪ RSV (Respiratory syncytial virus – Viral Croup in children or
bronchiolitis) Contact and droplet
S – Skin Infections:
▪ Skin diphtheria
▪ Herpes simplex disseminated type
▪ Herpes zoster (shingles) disseminated type & Chicken Pox
(varicella zoster) Contact and airborne
▪ Impetigo
▪ Lice/Pediculosis (Head only)
▪ Scabies
▪ Small Pox (Variola) Contact and airborne
W – Wound Infections:
▪ Major Staphylococcal disease (S. aureus) Skin, wound, or
burn Major Draining abscess
E – Enteric Infections:
▪ Clostridium difficile
▪ Norovirus
▪ Rota Virus
▪ Hepatitis A (Diapered or incontinent patients)
E – Eye Infections:
▪ Conjunctivitis Acute viral (acute hemorrhagic)
DROPLET precaution guidelines:
Source control: put a mask on the patient.
Ensure appropriate patient placement
Acute care hospitals: in a single room if possible.
Use personal protective equipment (PPE) appropriately.
Don mask upon entry into the patient room or patient space.
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Limit transport and movement of patients outside of the room to
medically-necessary purposes. If transport or movement outside of
the room is necessary, instruct patient to wear a mask and follow
Respiratory Hygiene/Cough Etiquette.
Droplets are large and travel less distance (3 feet and then fall)
Keep a distance of 3 – 6 feet when possible (3 – 6 ft rule)
Patient’s door can stay open.
No special ventilation is required.
Remember: Mnemonic is SPIDERMAN
S - Scarlet Fever/Streptococcal pharyngitis, Streptococcal
Pneumonia
P - Parvovirus B19 (5th Disease/Erythema Infectiosum), Pertussis,
Pneumonic Plague (Yersinia pestis)
I - Influenza
D- Diphtheria (pharyngeal)
E - Epiglottitis (Hemophilus Influenza Type B – HIB/Bacterial Croup)
R - Rubella (German Measles), Rhinovirus, RSV (Respiratory
syncytial virus aka Viral Croup in children or bronchiolitis
Contact and droplet
M - Mumps, Meningitis (Bacterial), Mycoplasmal Pneumonia
An - Adenovirus Pneumonia Contact & droplet
AIRBORNE precaution guidelines:
Source control: put a mask on the patient.
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Ensure appropriate patient placement in an airborne infection
isolation room (AIIR)
Restrict susceptible healthcare personnel from entering the room of
patients known or suspected to have measles, chickenpox,
disseminated zoster, or smallpox if other immune healthcare
personnel are available.
Use personal protective equipment (PPE) appropriately: fit-tested
NIOSH-approved N95 or higher level respirator for healthcare
personnel.
Limit transport and movement of patients outside of the room to
medically-necessary purposes. If transport or movement outside an
AIIR is necessary, instruct patients to wear a surgical mask, if
possible, and observe Respiratory Hygiene/Cough Etiquette.
Healthcare personnel transporting patients who are on Airborne
Precautions “do not need to wear a mask or respirator during
transport” if the patient is wearing a mask and infectious skin lesions
are covered.
Single room (negative pressure room), with suction effect.
The room will have 6-12 air changes an hour to decrease infectious
particles in the room. Keep room door closed at ALL TIMES!
Remember: Mnemonic is MTV
M - Measles (Rubeola)
T - Tuberculosis
V- Varicella Zoster (Chicken Pox), Herpes Zoster
(Shingles - disseminated type) Airborne and Contact
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Others:
Severe acute respiratory syndrome (SARS): Airborne, Droplet
and Contact
Smallpox (variola): Airborne, Droplet and Contact
Middle east respiratory syndrome -Corona Virus (MERS-COV):
Airborne, Droplet and Contact
Healthcare Associated Infections (HCAIs): Bundles of Care
Ventilator associated pneumonia (VAP)
▪ Keep the head of the patient’s bed raised between
30 and 45 degrees unless other medical conditions
do not allow this to occur.
▪ Assessment of readiness to extubate
▪ Hand hygiene before and after touching the
patient or the ventilator.
▪ Oral care - chlorhexidine (minimizes
microaspiration)
▪ Peptic ulcer prophylaxis - PPIs (minimizes
complications and length of stay)
▪ Venous Thromboembolism (VTE) prevention (minimizes complications and length of stay)
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Central line associated blood stream infections(CLABSI)
• Comply hand hygiene religiously
• Avoid femoral site in obese adult patients.
• Prepare the insertion site with >0.5% chlorhexidine
with alcohol.
• Immediately replace dressings that are wet, soiled,
or dislodged – NO WET DRESSING
• If blood or blood products or fat emulsions are
administered change tubing every 24 hours.
• Promptly remove unnecessary central lines
• Perform daily audits to assess whether each central
line is still needed
Catheter associated urinary tract infections(CAUTI)
• CATHETERIZE patient only when necessary
• Perform daily assessment of the need for
catheter
• Secure catheter properly
• Ensure that urine bag is below bladder, not
touching the floor
• Perform catheter care daily
• Empty drainage regularly
6
2
Identify patient safety risks
Find out which patients are most likely to try to commit suicide.
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Suicide Assessment
SAD PERSONS
(1 point for each positive answer on the above)
S
A
D
P
E
R
S
O
N
S
Sex. Men are more likely to commit suicide
Age. 15-24 YO / >40 YO
Depression
Prior History of suicide
Ethanol/alcohol and drug abuse.
Rational thinking loss, Psychosis
Separated divorced or widowed
Organized Plan. Having a method in mind
No Significant Other
Sickness. Terminal illness
Score Risk
0-2: No real problems, keep watch
3-4 : Send home, but check frequently
5-6: Consider hospitalization involuntary or voluntary,
depending on your level of assurance patient with
return for another therapy
7-10: Definitely hospitalize involuntarily or voluntarily
7
2
Prevent mistakes in surgery
Remember:
▪ Make sure that the correct surgery is done on the correct
patient and at the correct site on the patient’s body.
▪ “Surgical Site Marking”: Mark the correct place on the
patient’s body where the surgery is to be done
▪ “Team Time-out”: Pause before the surgery to make sure that
a mistake is not being made
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Facility Safety
Fire
When a fire occurs in a health care agency, the nurse should use the
mnemonic RACE to remember the priority steps. The mnemonic PASS
is often used to help people remember the steps used in operating a
fire extinguisher:
R: Rescue any clients in danger and move them to safety
A: Alarm-sound the alarm and activate the agency's fire response
C: Confine the fire by closing all doors to all rooms
E: Extinguish the fire, if possible, with a fire extinguisher
P: Pull the pin on the handle to release the extinguisher's lock
A: Aim the spray at the base of the fire
S: Squeeze the handle to release the contents
S: Sweep the spray from side to side until the fire is extinguished
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Child Safety
▪ The safest place for all children to ride, regardless of age, is
in the back seat of the car.
▪ Lock the car doors; 4-door cars should be equipped with
child safety locks on the back doors.
▪ Do not leave the infant unattended in the bath. Check for
water temperature.
▪ Do not hold the infant near hot liquids or items.
▪ Use cool vaporizers instead of steam should if needed, to
prevent burn injuries.
▪ Prevent choking by avoiding round shaped food or similar
to the size of the airway.
▪ Toys must have no small parts.
▪ Toys hanging over the crib should be out of reach, to
prevent strangulation.
▪ Avoid placing large toys in the crib because an older infant
may use them as steps to climb.
▪ Cribs should be positioned away from curtains
▪ Cover electrical outlets.
▪ Remove chemicals such as cleaning or other household
products, medications, poisons, and plants from the infant’s
reach.
▪ Toddlers need to be supervised at play to ensure safety.
▪ Keep all medicines, poisons, household plants, and toxic
products in high areas and locked out of reach.
▪ Teach a preschooler and school-age child to leave an area
immediately if a gun is visible and to tell an adult.
▪ Children should always wear a helmet when riding a bike or
using in-line skates or skateboards.
▪ Teach the child water safety rules.
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Remember: CDC recommendation
Up to age 2 YO: Rear facing seat or per state requirement
>2 – 5 YO: Forward facing seat or per state requirement
>5 up: Booster seat until seat belt fits properly (no booster seats)
≥12 YO: Can seat on a front or per state requirement
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4
Nursing
Fundamentals
Common Drag and Drop:
Fall Incident
1. Assess for presence of adequate
pulse
2. Inspect the client for injuries
3. Get help and move the client to
the bed
4. Notify the client's health care
provider (HCP)
5. Complete an incident report
Fire Incident: RACE protocol
1. Rescue/remove any clients in
immediate danger
2. Pull the fire alarm / activate Code
system
3. Close the door to the area of fire
4. Attempt to put out the fire with a
fire extinguisher – evacuate as
needed
5. Discourage visitors from using the
elevators
Volume Oriented Incentive
Spirometer
1. Exhale normally and place the
mouthpiece in the mouth
2. Seal lips tightly on mouthpiece
3. Inhale deeply, until piston is
elevated to predetermined level
4. Hold breath for at least 2-3
seconds
5. Exhale slowly around the
mouthpiece
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Measuring peak expiratory flow: peak flow
meter
1. Slide the indicator to the 0 or lowest level and
instruct the client to sit upright
2. Instruct the client to inhale deeply, place the
mouthpiece in the mouth, and tightly seal
using the lips
3. Instruct the client to exhale as quickly and
forcibly as possible, note the reading on the
numbered scale
4. Repeat the procedure 2 more times with a 5–
10-second rest period between exhalations
5. Record the highest reading (personal best)
Metered Dose Inhaler (MDI)
1. Shake canister well for 3-5 seconds
2. Tilt head back and exhale slowly for 3-5
seconds
3. Place mouthpiece between teeth and
wrap lips around mouthpiece
4. Compress canister while inhaling slowly
through the mouth for 3-5 seconds
5. Hold breath for 10 seconds before
exhaling
6. Wait at least 1-2 minutes before taking a
second puff as prescribed
Metered Dose Inhaler (MDI)
With Spacer
1. Shake the medicine
2. Insert the mouthpiece of the inhaler to the end
of the spacer
3. Exhale all air out of your lungs. Then put the
spacer into mouth between teeth. Make a tight
seal around the mouth piece with your lips.
4. Press the metered dose inhaler down the
medicine. The medicine will be trapped in the
spacer. Breathe in slowly and deeply.
5. Hold your breath for at least 5-10 seconds.
Breathe out slowly.
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Huff Coughing: to decrease lung secretion
1. Position upright
2. Inhale through the nose using abdominal
breathing and through pursed lips for 3
breaths (prolong exhalation)
3. Hold breath for 2–3 seconds following an
inhalation while keeping the throat open,
then exhale
4. Deeply inhale and, while leaning forward,
force the breath out gently using the
abdominal muscles while making a "ha"
sound (huff cough); repeat 2x
Tracheostomy Care / Dressing:
1. Gather supplies and position client
2. Don mask, goggles, and clean
gloves
3. Remove soiled dressing
4. Don sterile gloves; remove dispose
old cannula and replace with a
new one
5. Clean around stoma with sterile
water or saline; dry and replace
sterile gauze pad
Lumbar Puncture (Prep):
1. Check consent
2. Gather the lumbar puncture tray
and supplies
3. Have the patient empty the
bladder
4. Assist the patient into the side-lying
position with the knees drawn up
5. Label specimen vials as they are
collected
6. Place a bandage on the insertion
site
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Central line tubing change (client
suddenly begins gasping for air and
writhing):
1. Clamp the catheter tubing
2. Place the client in Trendelenburg
position on the left side
3. Administer oxygen as needed
4. Notify the health care provider
(HCP)
5. Stay with the client and provide
reassurance
Z-Track technique: IM Injection:
1. Pull the skin 1-1 ½" (2.5-3.5 cm) laterally and
away from the injection site
2. Hold the skin taut with non-dominant hand
and insert needle at a 90-degree angle
3. Inject medication slowly with dominant hand
while maintaining traction
4. Wait 10 seconds after injecting the
medication and withdraw the needle
5. Release the hold on the skin, allowing the
layers to slide back to their original position
6. Apply gentle pressure at the injection site but
do not massage
Administration of nasal sprays:
1. Assume a high Fowler's position with
head tilted forward
2. Insert the nasal spray nozzle into
nostril, occluding the other nostril
with a finger
3. Point the nasal spray tip toward the
side and away from the center
(septum)
4. Spray the medication while inhaling
deeply
5. Remove the nozzle and breathe
through the mouth
6. Repeat the above steps for the
other nostril
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Ear Irrigation (Adult):
1. Assess the patient for ear infection,
or tympanic membrane injury
2. Place the client in a sitting position
with the head tilted toward the
affected ear
3. Place a towel and an emesis basin
under the ear
4. Straighten the ear canal by pulling
the pinna up and back (down &
back - ≤ 3YO)
5. Gently irrigate the ear canal with a
slow, steady flow of solution
Administration of suppositories:
1. Apply clean gloves and position the
client (infant: supine with raised legs,
Adult: left side lying with knees flexed)
2. Lubricate the tip of the suppository
with water-soluble jelly.
3. Insert the suppository past the internal
sphincter using the fifth finger (<3 YO).
4. Hold the buttocks together for several
minutes, or until the urge to defecate
has passed, to prevent immediate
expulsion
Inserting NGT
1. Assess and select nares
2. Measure, mark, and lubricate tube
3. Instruct client to extend neck back
slightly
4. Gently insert tube just past
nasopharynx
5. Ask client to flex head forward and
swallow
6. Advance tube to the marked point
7. Verify tube placement and anchor
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Inserting Urinary Catheter:
1. Perform hand hygiene
2. Apply sterile gloves
3. Use non-dominant hand to spread
the labia
4. Cleanse labial fold with antiseptic
swab
5. Wipe meatus with antiseptic swab
6. Insert catheter until urine is seen
Bowel Irrigation:
1. Fill the irrigation container with 500-1000 mL
of lukewarm water, flush irrigation tubing,
and re-clamp and hung.
2. Instruct the client to sit on the toilet, place
the irrigation sleeve over the stoma,
extend the sleeve into the toilet.
3. Place the irrigation container
approximately 18-24 inches above the
stoma
4. Lubricate cone-tipped irrigator, insert cone
and attached catheter gently into the
stoma.
5. Slowly open the roller clamp, allowing
irrigation solution to flow for 5-10 minutes.
Clamp the tubing if cramping occurs, until
it subsides
6. Once the desired amount of solution is
instilled allow feces is allowed to drain
through the toilet
Guaiac Fecal Occult blood test:
1. Obtain supplies, wash hands, and
apply nonsterile gloves.
2. Open the slide's flap and apply 2
separate stool samples to the boxes
on the slide.
3. Open the back of the slide and
apply 2 drops of developing solution
to each box.
4. Wait 30-60 seconds.
5. Document the results
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BSE: Breast Self-examination
1. Place arm behind the head and lie
down
2. Use the left hand to palpate the right
breast and right hand for the left breast.
3. Palpate the breast with the use of finger
pads of the three middle fingers
4. Using circular motion, palpate the
breast tissue progressing from light,
medium and firm pressure
5. Palpate each breast from top to bottom
and then by going across the breast
from side to side
Anaphylactic shock due to IV
medications (e.g. Antibiotics)
1. Stop the infusion and call for help
2. Assess airway and place client on
oxygen supplement
3. Give IM epinephrine and start IV
normal saline
4. Administer diphenhydramine IV
5. Monitor vital signs for changes
Blood Transfusion Administration
1. Always verify blood products, type and
crossmatch results, and client identifiers
with another nurse prior to transfusion.
2. Obtain vital signs before, during, and
after blood administration.
3. Use Y tubing primed with NS and an IV
pump for administration.
4. Watch for transfusion reaction
5. Stop the transfusion immediately if a
reaction occurs.
Blood Transfusion Reaction
1. Stop the blood transfusion
2. Using new tubing, infuse normal
saline into the vein
3. Administer prescribed
vasopressor
4. Collect urine specimen
5. Document the incident
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5
Pain Management
Pain Assessment:
Severity: Mild (1-3) Moderate (4-6) Severe (7-10)
1.
2.
3.
4.
Verbal Scale (Conscious/Awake ≥9 YO)
Faces (Wong-Baker) (Conscious/Awake <9 YO)
“Can also be used for conscious/awake ≥9 YO, to support
verbal scale”
FRAAC Scale (unconscious, confused, demented ≥9 YO)
Faces, Respiration, Activity, Audibility, Consolability
FLACC Scale (unconscious <9 YO)
Face, Legs, Activity, Cry, Consolability
Pain Ladder: WHO
Pain ladder (aka analgesic ladder): By World Health Organization (WHO)
Is a guideline for the use of drugs in the management of pain. Originally
published in 1986 for the management of cancer pain, it is now widely
used in all types of pain. The principle is to start with first step drugs, and
then to climb the ladder if pain is still present. One of the purpose is to limit
tolerance and dependence to opioid analgesics
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Mild Pain (1-3)
NSAIDS/Non Opioid:
Acetaminophen, Aspirin,
Ibuprofen, Ketorolac
Adjuvant: Steroids,
antidepressants (amitriptyline,
nortriptyline, venlafaxine,
duloxetine) Antiseizures
(pregabalin, gabapentin),
anticholinergics (Oxybutynin)
Moderate Pain (4-6)
Weak Opioids:
Tramadol, Codeine
Hydrocodone, Oxycodone
+/- NSAIDS/Non Opioid
+/- Adjuvant
Severe Pain (7-10)
Strong Opioids:
Morphine, Hydromorphone,
Fentanyl
+/- NSAIDS/Non Opioid
+/- Adjuvant
Facts:
▪ Meperidine – High risk for seizure due to neurotoxic effects
▪ Hydromorphone (Dilaudid) – Fast acting opioid, potent
narcotic that has 5-10 times the strength of morphine, typical
maximum dose is 2 mg
▪ Hydromorphone IV push, given undiluted or diluted with 5 mL
of sterile water or normal saline, should be administered
slowly over 2-3 minutes; rapid infusion increases the risk of
opioid-induced adverse reactions (e.g. nausea, itching).
▪ Undiluted morphine IV push should be administered slowly
over 4-5 minutes; rapid infusion increases the risk of opioidinduced adverse reactions (e.g., hypotension, flushing).
▪ Most commonly abused narcotics in the US: heroin,
morphine, codeine
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▪ Morphine can be used for pancreatitis; worsening
pancreatitis due to increase in sphincter of Oddi pressure
“has not been proven in studies”.
▪ Fentanyl (IV): Strongest narcotic 100x stronger than morphine
Patch: Less potent (not given in post-op pain) due to slower
effect (17 hours to achieve full effect) The patch provides
continuous analgesia for up to 72 hours.
Remember: There is still some drug remaining on the patch
when it is removed after the 72 hours. This can be harmful if
children, pets, or caregivers are exposed. The patch must be
contained and immediately disposed of (flushed down the
toilet, discarded deep into the trash).
▪ Common side effects of opioid analgesics: Short term:
Pruritus, nausea and vomiting (vomiting 3X or more is
reportable), urine incontinence. Long term: constipation
▪ A neonate born to an opioid-dependent mother: is at high risk
for neonatal abstinence syndrome, an opioid withdrawal
typically within 24-48 hours after birth. Clinical manifestations:
irritability, jitteriness, high pitched cry, sneezing, diarrhea,
vomiting, poor feeding
▪ Naloxone: Drug of choice for opioid intoxication
▪ Methadone: Drug of choice for opioid withdrawal (longer
half-life of up to 60 hours)
Stages of drug addiction:
1. Experimentation (controlled) – use without legal consequence “for
fun only”
2. Regular Use (controlled) – use with legal consequence
“driving under influence”
3. Risky use/abuse (uncontrolled) – craving , depression, anxiety
4. Dependence (uncontrolled) – withdrawal, compulsion, psychiatric
implications
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Question 1: Client with cancer pain is prescribed oxycodone. Which teaching is
most essential to help prevent long-term complications?
1. Teach the client how to assess blood pressure daily
2. Teach the client how to prevent constipation
3. Teach the client how to prevent itching
4. Teach the client how to prevent nausea
Answer: 2
Rationale: Constipation is an expected long-term side effect of opioid use; clients
will not develop tolerance to this side effect. It is important to teach
aggressive preventive measures (e.g. defecate when the urge is felt, drink 23 L of fluid/day, high-fiber diet, exercise) and simultaneous use of a stool
softener and a stimulant.
Question 2: A post-surgical client is unresponsive to painful stimuli and is given
naloxone. Within 5 minutes, the client is arousable and responds to verbal
commands. One hour later, the client is again difficult to arouse, with
minimal response to physical stimuli. Which actions should the nurse take?
Select all that apply.
1. Administer oxygen
2. Assess respiratory rate
3. Initiate rapid response or code team
4. Notify the health care provider
5. Prepare a second dose of naloxone
Answer: 1,2,4,5
Rationale: Naloxone (Narcan) is usually prescribed as needed for post-surgical
clients for over-sedation related to opioid use. The nurse should continue to
monitor clients who are given naloxone with the understanding that the
opioid antagonist has a shorter half-life (1-2hours) than most of the opioids it is
meant to counteract. As a result, a second dose of naloxone may be
necessary
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6
Cardiovascular
Anatomy
4 chambers:
▪ Atria (2)
▪ Ventricle (2)
4 Valves:
▪ Semilunar: Aortic, pulmonic
▪ Atrioventricular: Tricuspid,
Bicuspid/Mitral
Remember:
Stenosis – is a narrowing of
valves
Regurgitation – is the process
(backflow of blood)
Murmur – is the symptom
(assessment)
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Coverings (epicardium):
Pericardium
▪ Fibrous
▪ Serous (parietal,
pericardial cavity,
visceral)
Myocardium
Endocardium
Major Veins
▪ Inferior & Superior Vena
Cava (unoxygenated)
▪ 4 Pulmonary Veins
(oxygenated)
Major Arteries
▪ Pulmonary arteries
(unoxygenated)
▪ Aorta (oxygenated)
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Physiology
Action - Potential: the potential of a tissue to produce an effect
(ex: contraction)
Resting - Potential: the potential of a tissue not to cause an effect
(ex: relaxation)
Electrolytes: determine action potential in the cell membrane
Sodium (Na+) Extracellular
Potassium (K+) Intracellular
Calcium (Ca++) Extracellular
Remember:
Action – Potential: occurs in 3
types of tissues
1. Heart
2. Nerve
3. Muscles (smooth and
skeletal)
Heart Action-Potential: 2 types
1. Electrolytes:
Ca++, Na+: Contract
K+: Relax
2. Conduction System
SA, AV nodes, Bundle of His,
Purkinje Fibers (propagation
of heart rate)
Phase 0: Na+ in beginning of action-potential (contraction)
Remember: Na+ is extracellular, if it goes inside the cell it causes
contraction together with Ca++
Phase 1: K+ out after rapid influx of Na+ inside the cell
Remember: Active Na+ K+ pump is ongoing
Phase 2: Ca++ in, K+ out
Phase 3: K+ out
Phase 4: beginning of resting – potential (relaxation)
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Conduction System: Propagation of heart rate
Remember: Action potential
vs Conduction system
▪ Action potential is for
contraction and relaxation
▪ Conduction system is for
heart rate propagation
Remember:
Autonomic Nervous System
influences conduction system
through
▪ Sympathetic/Adrenergic
Nerves: Increase heart rate
▪ Vagus Nerve/Cholinergic:
decrease heart rate
How?
Sympathetic Nerves: Binding of catecholamines (e.g. epinephrine, epinephrine)
to adrenergic receptors in the heart (Beta 1, alpha 1)
Vagus Nerve: Binding of acetylcholine to muscarinic/cholinergic receptors in
the heart (M2)
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Conduction system
Remember:
EKG is the reflection of Conduction System
(See in EKG interpretation)
Cardiac Output
Cardiac output (CO) is the amount of blood the heart pumps in
1 minute, and it is dependent on the heart rate, contractility,
preload, and afterload.
Normal CO: 4-8 liters per minute, depending on the persons size.
Basically, total blood volume circulates to heart in 1 full minute
as a cardiac output (CO)
Remember: Cardiac output
Cardiac Output is just simply what you want from heart to produce
in order to nourish nutrients and O2 in each body system.
Persistent decrease CO means abnormal heart and subsequent
problem to brain, kidneys, heart, liver tissues, etc.
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Cardiac CO: Heart Rate (HR) x Stroke Volume
Heart Rate (HR): Heart rate is the speed of the heartbeat measured
by the number of contractions (beats) of the heart per minute
(bpm) propagated by conduction system.
Stroke Volume (SV): Volume of blood pumped by the ventricles
with each heartbeat. Approximately 70 ml.
Preload: aka “Filling Pressure”. Is the pressure that stretches the right
or left ventricle during relaxation or before it contracts to
produce cardiac output.
Afterload: is a pressure against which the heart must overcome to
eject blood during contraction. Ex: aortic pressure
Summary:
As mentioned cardiac output is simply the most important
component of cardiac physiology. In a normal circumstance, body
systems received sufficient CO to perform their functions including the
heart itself via patent coronary arteries. Decrease CO means
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decrease volume and decrease blood pressure. Hence, in every
heart conditions, it is very important to check the patient’s BP to
determine severity.
Cardiac output explained:
Ex: Cardiac Tamponade (sudden accumulation of fluid in the
pericardial sac leading to compression). Increase HR results from
compensatory mechanisms. However, increase HR does not
necessarily mean increase in CO. For this instance, the ability of
the heart to produce a sufficient CO is also determined by the
volume of blood during the process of contraction/relaxation.
Compression of the heart decreases stroke volume.
Becks Triad:
Hypotension/narrowed pulse pressure
Narrowed PP (difference between SBP and DBP – normal is 40–
60 mmhg) Hypotension causes narrowed PP. This is caused by
alterations in CO due to compression.
Jugular venous distention
Limits the ability of the heart to expand due to pressure build up
affecting preload and afterload, subsequently the CO.
Muffled heart sounds/Distant heart sounds
Inaudible heart sounds due to fluid build-up in the pericardium
Inotropic is a cardiac drug that affects cardiac contraction.
Chronotropic is a cardiac drug that affects heart rate.
Dromotropic is a cardiac drug that affects conducting tissues of the heart.
Sample medication:
DIGOXIN: (+) Inotropic (-) Chronotropic, (-) Dromotropic
DOPAMINE, EPI, NE: (+) Inotropic (+) Chronotropic, (+) Dromotropic
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Question: A client has developed atrial fibrillation, with a ventricular rate of 150
beats/minute. The nurse should assess the client for which associated
signs/symptoms?
1. Flat neck veins
2. Nausea and vomiting
3. Hypotension and dizziness
4. Hypertension and headache
Answer: 3
Rationale: The client with uncontrolled atrial fibrillation with a ventricular rate
more than 100 beats/minute is at risk for low cardiac output because of loss
of atrial kick. The nurse assesses the client for palpitations, chest pain or
discomfort, hypotension, pulse deficit, fatigue, weakness, dizziness, syncope,
shortness of breath, and distended neck veins. Test strategy, most likely the
answer is between the two opposing answers (3. Hypotension, 4.
Hypertension)
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EKG interpretation: Steps
1. Identify PQRST
Must know what are PQRST represents. Don’t mind the gridlines
initially. Remember EKG takes an analysis, step by step process is
applied.
P wave: Atrial contraction/depolarization
PR Interval: Atrial relaxation/repolarization
QRS complexes: Ventricular contraction/depolarization
T wave: Ventricular relaxation/repolarization
Remember: Isoelectric line
An imaginary line to determine
ST segment deviation. (dotted
lines on the image)
Depression: ischemia
Elevation: infarction
Remember: Possible implications to abnormalities in PQRST
P wave – Atrial arrhythmias (missing, aberrant)
PR Interval – AV Block (prolonged)
QRS complexes – Ventricular arrhythmias (widened, bizarre)
T wave – Hypo/hyperkalemia, Pulmonary embolism, Digoxin,
AMI (inversion, peaked)
ST segment – AMI (elevation, depression)
QT Interval – Hypomagnesemia (prolonged)
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2. Determine PR Interval, QRS Complex (time)
Since you identified PQRST. This time, EKG gridlines are
considered to measure PR interval and QRS complex. Measuring PR
interval is basically determining the relationship of atria and
ventricles. Deviation from this interval (prolonged) simply means an
atrioventricular concern (ex: AV Block). In addition, measuring QRS
complex is identifying ventricular activity (contraction) which is the
most important component of heart electrophysiological activity in
relation to producing sufficient CO. This means that a ventricular
arrhythmia is more life threatening if not treated promptly. In fact,
the most common cause of death among AMI patients.
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Normal values:
PR Interval: 0.12-0.20 secs
Abnormal: ≥ 0.24 secs
QRS comp: 0.6-0.12 secs
Abnormal: > 0.12 secs
3. Check rhythm.
What is a regular rhythm? A regular rhythm means the same
distance between PRQST complexes by measuring R-R intervals.
What is irregular rhythm? An irregular rhythm simply means
abnormal distances between R-R intervals.
Remember:
Checking rhythms is important in counting the heart rate. One cycle of
PQRST represents the other in a regular rhythm. In contrast, one cycle
may not represent the other in an irregular rhythm.
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Regular rhythm: Same distances between R – R
Irregular rhythm: Different distances between R - R
Common regular rhythm
(R-R Intervals):
▪ Sinus Rhythm
▪ Sinus Tachycardia
▪ Sinus Bradycardia
▪ Supraventricular
Tachycardia(SVT)
▪ Atrial Flutter (variable)
▪ 3rd degree AV block (CHB)
Common irregular rhythm
(R-R Intervals):
▪ Premature Atrial Contractions
▪ (PACs)
▪ Premature Ventricular
Contractions (PVCs)
▪ Atrial Fibrillation
▪ 2nd degree AV block (Type 1)
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4. Determine the heart rate.
A normal resting heart rate is 60 to 100 beats per minute per EKG
reading. In a normally paced heart, SA node (pacemaker)
produce 60-100 bpm enough to influence a sufficient cardiac
output with a normal preload and afterload physiology. On the
other hand, a non-pacemaker such as AV node may not produce
enough rate at 40-60 bpm. If you have arrhythmias such as
ventricular ectopy (PVCs), as the word says ectopy which means
“out of place”, the conduction must not be coming from the SA
node. This causes alteration in a normal rate and rhythm which
subsequently affects normal cardiac output.
Six (6) seconds strip method:
Applicable for both regular and irregular rhythm. Count the number of QRS
complexes over a 6 second interval. Multiply by 10 to determine heart rate.
10 R waves or QRS complexes in a 6 second strip in a regular rhythm
multiply by 10 is 100 bpm. 10 QRS X 10 = 100 bpm
5 R waves or QRS complexes in a 6 second strip in an irregular rhythm
multiply by 10 is 50 bpm. 5 QRS X 10 = 50 bpm
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1,500 method: Applicable ONLY for regular rhythm. Since R-R intervals are all the
same or constant in all cycles, one R-R represents the other. Determine the
heart rate by counting the number of smallest boxes between R-R. (Most
accurate in calculating HR)
Smallest boxes: 1500 mm/min ÷ 15 = 100 bpm
Note:
1mm = 1 smallest box
1 sec = 25 smallest boxes
60 sec (1 min) = 1,500 smallest boxes (1,500 mm)
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Application:
1. Identify PQRST
Notable Question:
Is there distinct P wave? Yes, P wave is positively deflected (upward)
Is there QRS? Yes, QRS complex is present, (Q: negative deflection,
R: positive deflection, S: negative deflection)
Is there T? Yes, T wave present with positive deflection and is slightly
higher than the P wave.
Is there ST depression or elevation? No
Is there peaked or inverted T wave? No
Findings: This is a normal morphology of a PQRST.
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2. Determine PR Interval, QRS Complex (time)
Notable Question:
Since there distinct P wave and a QRS complex, what is the PR
interval? 0.16 secs (4 smallest squares x 0.04 secs)
Is it within normal limits? Yes
What is the QRS complex? 0.06 secs (1½ smallest squares x 0.4 sec)
Is it within normal limits? Yes
Findings: This is a normal morphology of a PQRST with normal PR
(normal relationship between atria and ventricles) and normal QRS
(normal ventricular contraction)
Remember:
QRS complex identifies
ventricular activity
(contraction), the most
important component of
heart electrophysiological
activity to produce sufficient
CO.
Ventricular arrhythmia such
as PVC is significant.
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68
3. Check rhythm.
Notable Question:
Is the rhythm regular or irregular? Regular (same distances on R-R)
Findings: Normal morphology of a PQRST with normal PR and QRS
time limits on a regular rhythm
4. Determine the heart rate.
Notable Question:
Which method will be used to get the HR? Either six (6) second strip
or 1,500 method (more accurate).
Six (6) seconds strip method: 8 R or QRS comp x 10 = 80 bpm
1
2
3
4
5
6
7
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1,500 method: 1,500 ÷ 19 smallest boxes = 79 bpm
Findings: Normal morphology of a PQRST with normal PR and QRS
time limits on a regular rhythm and heart rate within 60-100 bpm.
Interpretation: Normal Sinus Rhythm
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Common Arrhythmias
I. Sinus Bradycardia
PQRST
P wave: Normal
PR Interval: Normal
QRS complex: Normal
Rhythm: Regular
Rate: <60 bpm
Remember: The only abnormality in this rhythm is the heart rate
which is below 60 bpm. In determining the HR, you can use
either 1,500 or 6 second strip method. In this example, the
HR is 40 bpm using six second strip (4 QRS x 10 = 40 bpm). If
bradycardia doesn't cause symptoms, it usually isn't
treated.
Management: (follow ACLS bradycardia algorithm)
It takes 1 question to decide which type of management is
necessary. Is the bradycardia causing symptoms?
Hypotension, altered mental status, ischemic chest
discomfort, signs of acute heart failure (short of breath)
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If not: Monitor and observe
If symptomatic: Emergency management
1. Consider administering atropine 0.5 mg IV if IV access is
available. This may be repeated every 3 to 5 minutes up
to 3 mg or 6 doses.
2. Prepare for transcutaneous pacing. If no IV is present
pacing can be first.
Note:
If the atropine is ineffective, begin transcutaneous
pacing.
Consider epinephrine or dopamine while waiting for
the pacer or if pacing is ineffective.
Epinephrine 2 to 10 µg/min
Dopamine 2 to 20 µg/kg per minute
Consider expert consultation for Transvenous Pacing
if efforts are ineffective.
Transcutaneous Pacing (TCP) is a temporary means of pacing a
patient’s heart during an emergency and stabilizing the patient
until a more permanent means of pacing is achieved.
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Transvenous pacing is also a temporary means of treating
symptomatic bradycardias that do not respond to transcutaneous
pacing or to drug therapy. Transvenous pacing is achieved by
threading a pacing electrode through a vein into the right atrium,
right ventricle, or both.
II. Sinus Tachycardia
PQRST
P wave: Normal
PR Interval: Normal
QRS complex: Normal
Rhythm: Regular
Rate: >100 bpm
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Remember: The only abnormality in this rhythm is the heart rate
which is above 100 bpm. In determining the HR, you can
use either 1,500 or 6 second strip method. In this example,
the HR is 130 bpm using six second strip (13 QRS x 10 = 130
bpm). If tachycardia doesn't cause symptoms, it usually
isn't treated.
Management:
Is the tachycardia ≥ 150 bpm?
If not: Monitor and observe. Underlying causes are treated
if present.
Causes: Pain, Fever, Anxiety, Dehydration, Anemia
Hyperthyroidism, Sepsis, Pulmonary embolism
Intake of stimulants such as caffeine, theophylline,
nicotine, cocaine, or amphetamines
If ≥ 150 bpm: Evaluate the rhythm. This might be one of the
several tachycardia rhythms
Supraventricular tachycardia (SVT)
Atrial fibrillation
Atrial flutter
Ventricular tachycardia
Note: Management discussed in specific tachycardias
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III. Atrial arrhythmias
Remember that this abnormal rhythm originates from the atria
which is reflected on the P waves (Atrial contraction) in the EKG. P
wave abnormality is expected.
1. Atrial Fibrillation
PQRST
P wave: Absent, Fibrillatory
PR Interval: Non existent
QRS complex: Normal
Rhythm: Irregular
Rate: Slow - rapid
Remember: The two (2) main characteristics of Atrial fibrillation
are absence of P waves and irregular rhythm. It is classified
according to its HR as follows:
Atrial fibrillation with slow ventricular response (SVR): HR
below 60 bpm.
Atrial fibrillation with moderate ventricular response (MVR):
HR within 60 – 100 bpm.
Atrial fibrillation with rapid ventricular response (RVR): HR
above 100 bpm. Ventricular rate control is a priority in
clients with atrial fibrillation
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Management: Acronym is ABCD
A: Anticoagulants (warfarin, dabigatran, rivaroxaban,
apixaban) Patients with A-fib greater risk for forming
clots due to abnormal atrial activity. Blood stasis in atria
influences clot formation.
B: Beta Blockers (metoprolol) blocks beta adrenergic cells
stimulation.
C: Calcium Blockers (diltiazem, verapamil)
Catheter Ablation – Heating or freezing the area to
destroy tissues that causes fibrillatory waves
D: Digitalis (Digoxin)
E: Electrocardioversion
2. Atrial Flutter
PQRST
P wave: Flutter waves (sawtooth)
PR Interval: Not applicable
QRS complex: Normal
Rhythm: Regular/irregular
Rate: Rapid (atrial/P Waves)
Remember: Less common than atrial fibrillation. The main
characteristic of atrial flutter is “sawtooth” formation of P
waves.
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Management: (same with A-fib) Acronym is ABCD
A: Anticoagulants (warfarin, dabigatran, rivaroxaban,
apixaban) Patients with A-fib greater risk for forming
clots due to abnormal atrial activity. Blood stasis in atria
influences clot formation.
B: Beta Blockers (metoprolol) Blocks beta adrenergic cells
stimulation.
C: Calcium Blockers (diltiazem, verapamil)
Catheter Ablation – Heating or freezing the area to
destroy tissues that causes fibrillatory waves
D: Digitalis (Digoxin)
E: Electrocardioversion
3. Premature Atrial Contraction/Complex (PAC)
PAC
PQRST
P wave: Present (if not: Premature Junctional Comp./PJC)
PR Interval: Normal
QRS complex: Normal
Rhythm: Irregular (the premature complex makes it irregular)
Rate: Variable
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Remember: The above is an example of a single, isolated PAC.
The heart rate in this example is 80 bpm using the six
second method (8 QRS x 10 = 80) as the rhythm is irregular.
The first five cycles are normal, but the sixth beat occurs
prematurely that are not generated by the SA node. You
can see the P wave right after the T wave of the previous
beat. PACs generally have very little medical significance.
However, in some cases PACs are triggers of life
threatening arrhythmias such as A-fib.
Management:
PACs are often benign, requiring no treatment. However, it
is important to monitor patients with co-morbidities such as
hypertension, hyperlipidemia as it leads to more serious
arrhythmias.
4. Supraventricular Tachycardia (SVT)
PQRST
P wave: Frequently buried on preceding T waves
PR Interval: N/A
QRS complex: Normal (usually narrow complex, rarely
wide)
Rhythm: Regular
Rate: 150 – 250 bpm
Remember: SVT is one of the most common tachycardias that
originates form the atria (above the ventricles). Between
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SVT and ST, the former has a higher HR at 150 or higher. On
the other hand, ST has a visible P-waves. As for SVT, Pwaves will be entirely buried making it impossible to
describe their morphology and measure the PR interval. It
is also important to determine A-Fib with rapid ventricular
response, though both SVT and rapid A-fib has narrow QRS
complexes and no visible P-waves, SVT has a regular R-R
interval (regular rhythm) contrary to A-fib. The distinction
between regular and irregular rhythm (SVT vs. Rapid A-fib)
is fundamental since they are treated differently. For
instance, adenosine (drug of choice for SVT) cannot be
given to a patient with A-fib because it causes further fatal
arrhythmias.
Management:
Remember, the key to managing a patient with any
tachycardia is to check if pulses are present, decide if the
patient is stable or unstable and then manage. Low SBP
(<90 mmhg) is an implication of a low cardiac output.
Measuring BP is a primary assessment.
Is the patient stable or unstable?
If stable: Vagal Maneuvers
The act of "bearing down" as if having a bowel
movement (valsalva) is an example of these
maneuvers and may need to be attempted more
than once. (increases intra-thoracic pressure and
stimulates vagus nerve)
Other: Coughing, gagging, carotid massage (may be
performed by physician)
If not effective: Give medication
Adenosine is the first-line drug of choice for SVT.
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The half-life is <5 seconds, so adenosine should be
administered rapidly as a 6-mg bolus IV over 1-2
seconds followed by a 20-mL saline flush. Repeat
boluses of 12 mg may be given twice if the SVT persists.
(6mg – 12 mg – 12mg).
Remember: Brief period of asystole is due to adenosine
slowing impulse conduction through AV node. In
addition, monitor for flushing, dizziness, chest pain, or
palpitations during and after administration
If Adenosine not effective: Consider other medications
P: Procainamide
Decreases myocardial excitability by blocking
myocardial Na+ channels. It also depresses
myocardial excitability and conductivity
A: Amiodarone (anti-arrhythmic)
Prolongs Phase 3 of cardiac action-potential
(repolarization) by preventing potassium to leave the
cells.
B: Beta Blockers (metoprolol, sotalol) Blocks beta
adrenergic cells stimulation.
C: Calcium Blockers (diltiazem, verapamil)
Catheter Ablation – Heating or freezing the area to
destroy tissues that causes the arrhythmia
If unstable or medications are not effective:
Synchronized Cardioversion
Remember: Cardioversion rules for SVT
QRS narrow and regular (SVT, Atrial flutter):
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50 - 100 joules
QRS narrow and irregular (A-fib with RVR):
100 - 200 joules
Cardioversion
Defibrillation
Synchronized to R wave/QRS
Unsynchronized
Elective
Emergent
Conscious/Awake
Unconscious
Needs sedation
No sedation
Low energy/joules
High energy/Joules
Question: The telemetry nurse reports the cardiac monitor rhythms of 4 clients to
the medical unit nurse assigned to care for them. The nurse should assess
the client with which rhythm first?
1. Atrial fibrillation with a pulse of 76/min in a client prescribed rivaroxaban
2. Bradycardia in a client with a demand pacemaker set at 70/min
3. First-degree atrioventricular block in a client prescribed atenolol
4. Sinus tachycardia in a client with gastroenteritis and dehydration
Answer: 2. Bradycardia in a client with a demand pacemaker set at 70/min
Rationale: A demand electronic pacemaker should deliver an impulse when it
senses an intrinsic pacemaker drop below a predetermined rate.
Bradycardia with failure to capture (pacer spike with no QRS complex)
indicates malfunction and requires immediate notification of the health care
provider. On the other hand, Clients with atrial fibrillation are USUALLY
prescribed an anticoagulant, such as rivaroxaban (Xarelto), due to
increased risk for blood clots that can lead to stroke. This client's ventricular
response is moderate (A-fib in MVR), so there is no urgency. Unless otherwise
rapid ventricular response which requires immediate intervention. First-degree
atrioventricular (AV) block can be associated with beta adrenergic blockers.
Tachycardia is an expected mechanism to increase the cardiac output
associated with hypotension.
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Test strategy: prioritization. Obviously there are no airway problems in the
given choices. Do not also choose expected findings that does not require
immediate intervention.
IV. Ventricular arrhythmias
Remember that this abnormal rhythm originates from the
ventricles which is reflected on the QRS complex (ventricular
contraction) in the EKG. QRS abnormality is expected. More
importantly, ventricular arrhythmias are associated with increase
mortalities.
1. Premature Ventricular Contraction/Complex (PVC)
PVC
PQRST
P wave: Absent: associated with premature beat
PR Interval: N/A
QRS complex: Widened, Bizarre “weird”
Rhythm: Irregular (the premature complex makes it irregular)
Rate: Variable
Remember: The above is an example of a single, isolated PVC.
The heart rate in this example is 90 bpm using the six
second method (9 QRS x 10 = 90) as the rhythm is irregular.
The first six cycles are normal, but the seventh beat occurs
prematurely that are not generated by the SA node. This
abnormal rhythm is life threatening as it involves the
ventricles. An isolated PVC can lead into a more serious
ventricular arrhythmias such as ventricular tachycardia
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and ventricular fibrillation if not treated promptly. In
addition, an isolated PVC can lead into the following
patterns presented as follows:
PVCs in QUADRIgeminy: (1 single PVC and 3 normal cycles)
1
3
2
1
2
3
4. PVC
4. PVC
PVCs in TRIgeminy: (1 single PVC and 2 normal cycles)
1
2
1
1
2
3. PVC
2
3. PVC
3. PVC
PVCs in BIgeminy: (1 single PVC and 1 normal cycle)
1
1
2. PVC
1
1
2. PVC
2. PVC
2. PVC
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VCs in Couplets: (2 consecutive PVCs)
Note: 3 consecutive PVCs or PVCs in triplets is considered
ventricular tachycardia
Couplets
PVCs according to morphology:
Unifocal/Monomorphic PVC: (PVCs in identical forms )
Multifocal/Polymorphic PVC: (PVCs in non-identical forms )
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Management:
For patients with occasional PVCs with no other symptoms and
no underlying heart disease or structural problems, no treatment
is necessary. For persistent and recurrent ventricular
arrhythmias such as PVCs, management are as follows:
Acronym: ABC - PALS
A: Amiodarone (anti-arrhythmic)
Prolongs Phase 3 of cardiac action-potential
(repolarization) by preventing potassium to leave the
cells.
B: Beta Blockers (metoprolol, sotalol) blocks beta
adrenergic cells stimulation.
C: Calcium Blockers (diltiazem, verapamil)
Catheter Ablation – Heating or freezing the area to
destroy tissues that causes the arrhythmia
OR
P: Procainamide
Decreases myocardial excitability by blocking
myocardial Na+ channels. It also depresses
myocardial excitability and conductivity
A: Amiodarone
L: Lidocaine Shortens cardiac-action potential by
blocking myocardial Na+ channels
S: Sotalol (beta-blocker)
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2. Ventricular Tachycardia
Note: Ventricular tachycardia can be non-sustained (NSVT) or
sustained. Non-sustained is referred as 3 or more consecutive
v-tach that stops by itself within 30 seconds. On the other
hand, the patient can be pulseless (unstable) or with pulse
(stable), which will be the basis of management.
PQRST
P wave: Absent
PR Interval: N/A
QRS complex: Widened, Bizarre “weird”
Rhythm: Variable
Rate: Rapid (Ventricular)
Remember: Ventricular tachycardia is simply untreated PVCs
Monomorphic Ventricular Tachycardia: (identical QRS forms)
Polymorphic Ventricular Tachycardia: (non-identical QRS forms)
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Torsades de Pointes (TdP):
Is a specific form of polymorphic ventricular tachycardia
occurring in a patient with QT prolongation (normal: 0.36 to
0.44 sec/9-11 boxes) , these may combine to produce TdP. QT
prolongation may occur secondary to hypokalemia or
hypomagnesemia. It has a characteristic morphology in
which the QRS complexes “twist” around the isoelectric line.
Management:
Aims to either terminating an episode of the abnormal heart
rhythm or to reduce the risk of another V-tach episode.
Treatment also depends on the patient’s stability
Pulseless/Unstable or With Pulse/Stable) as well as the underlying
cause (e.g. Torsades de Pointes – Mg, Potassium replacement).
Remember, the key to managing a patient with any
tachycardia is to check if pulses are present, decide if the
patient is stable or unstable and then manage. Low SBP (<90
mmhg) is an implication of a low cardiac output. Measuring BP
is a primary assessment.
A. With Pulse/Stable
Synchronized Cardioversion - If the waveform is monomorphic
synchronize to QRS to avoid ventricular fibrillation or worst
asystole. An initial energy of 100J is recommended. If the
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waveform is polymorphic, then higher energies and an
unsynchronized shock should be provided (aka. Defibrillation)
Cardioversion
Defibrillation
Synchronized to R wave/QRS
Unsynchronized
Elective
Emergent
Conscious/Awake
Unconscious
Needs sedation
No sedation
Low energy/joules
High energy/Joules
Acronym: ABC - PALS
A: Amiodarone (anti-arrhythmic)
Prolongs Phase 3 of cardiac action-potential
(repolarization) by preventing potassium to leave the
cells.
B: Beta Blockers (metoprolol, sotalol) Blocks beta
adrenergic cells stimulation.
C: Calcium Blockers (diltiazem, verapamil)
Catheter Ablation – Heating or freezing the area to
destroy tissues that causes the arrhythmia
Cardioversion
Cardioverter/Defibrillator (Implantable) or Implantable
Cardioverter Defibrillator) Implanted to chest wall and
more effective than drug therapy in recurrent V-tach.
OR
P: Procainamide
Decreases myocardial excitability by blocking
myocardial Na+ channels. It also depresses myocardial
excitability and conductivity
A: Amiodarone
L: Lidocaine Shortens cardiac-action potential by blocking
myocardial Na+ channels
S: Sotalol (beta-blocker)
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Implantable Cardioverter Defibrillator (ICD): Is an automated
device implantable inside the body, that detects abnormal
impulses and if necessary, perform cardioversion, defibrillation,
and pacing of the heart.
B. Pulseless/Unstable
When dealing with pulseless ventricular tachycardia is the same
way with ventricular fibrillation. The primary management
includes cycles of CPR, defibrillation and medication. Using
advanced algorithm is the best method of restoring
spontaneous circulation. (ACLS algorithm as discussed in the
next succeeding topics)
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Emergency management in ORDER: Acronym CDEA
C: Cardiopulmonary Resuscitation (CPR)
Provide supplemental oxygen. If bag-mask ventilation is
adequate, providers may defer insertion of an advanced airway.
Begin 5 cycles of CPR (approximately 2 minutes). Each cycle
contains 30 chest compressions followed by 2 breaths.
Interrupt chest compressions only for ventilation, rhythm checks,
and actual shock delivery. CPR should never be interrupted for
more than 10 seconds. Push hard (> 2 inches) & fast (100-120/min)
D: Defibrillation
▪ Attach defibrillator pads,
▪ Continue CPR while the defibrillator is charging.
▪ Clear the patient for shock .
▪ Deliver the shock.
▪ Resume CPR immediately after shock, 5 cycles.
E: Epinephrine
If IV is available, administer epinephrine 1mg IV during the CPR
cycle. Lidocaine or amiodarone can also be given.
A: Advanced airway
The value of securing the airway must be balanced against the
need to minimize the interruption in perfusion in the early steps of
resuscitation (CPR). Includes LMA (Laryngeal mask airway),
laryngeal tube, and ET tube (endotracheal tube)
Note: In a WITNESSED arrest with V-tach or V-Fib In the context of a
witnessed arrest by a trained first responder or bystander who has an
AED or manual defibrillator, the importance of early defibrillation is
irrefutable. Remember: DCEA (Defibrillation, CPR, Epinephrine,
Advanced airway)
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Medications
Note: These are medications that are given generally for
Ventricular Arrhythmias
A: Amiodarone (anti-arrhythmic)
Prolongs Phase 3 of cardiac action-potential
(repolarization) by preventing potassium to leave the
cells.
B: Beta Blockers (metoprolol, sotalol) Blocks beta
adrenergic cells stimulation.
C: Calcium Blockers (diltiazem, verapamil)
OR
P: Procainamide
Decreases myocardial excitability by blocking
myocardial Na+ channels. It also depresses
myocardial excitability and conductivity
A: Amiodarone
L: Lidocaine Shortens cardiac-action potential by
blocking myocardial Na+ channels
S: Sotalol (beta-blocker)
3. Ventricular Fibrillation
Note: V-fib is a lethal dysrhythmia characterized by varying shapes
and amplitude on the EKG. Mechanically, the ventricle is just
"quivering" with no effective contraction or cardiac output.
V-fib results in a pulseless, unresponsive, apneic state.
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PQRST
P wave: Absent
PR Interval: N/A
QRS complex: Fibrillatory, Bizarre “weird”
Rhythm: Extremely irregular
Rate: Extremely rapid (ventricular)
Remember: Ventricular Fibrillation is simply untreated ventricular
arrhythmias. However, patient might have V-tach or
V-fib with no preceding PVCs that requires
immediate management. Patient is absolutely
unconscious and unstable.
Course Ventricular Fibrillation
Fine Ventricular Fibrillation
Management: Same management with ventricular tachycardia
(pulseless/unstable)
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Question: The nurse is preparing to defibrillate a client who suddenly went into
ventricular fibrillation. Which steps are essential prior to delivering a shock?
Select all that apply.
1. Apply defibrillator pads
2. Call out and look around to ensure that everyone is "all clear"
3. Continue chest compressions until ready to deliver shock
4. Ensure adequate IV sedation has been given
5. Ensure that the synchronization button is turned on
Answer: 1,2, 3
Rationale: Defibrillation is indicated in clients with ventricular fibrillation (V-fib) and
pulseless ventricular tachycardia. Cardiopulmonary resuscitation (CPR)
should be initiated and compressions continued until the shock is ready to be
delivered Certain pulseless rhythms (asystole and pulseless electrical activity)
do not need defibrillation.
Steps to perform defibrillation are as follows:
1. Turn on the defibrillator
2. Place defibrillator pads on the client's chest
3. Charge defibrillator. Chest compressions should continue until defibrillator
has charged and is ready to deliver the shock.
4. Before delivering the shock, ensure that the area is "all clear." Confirm that
no personnel are touching the client, bed, or any equipment attached to
the client
5. Deliver the shock
6. Immediately resume chest compressions
IV sedation is not necessary for defibrillation as the client is already unconscious.
It is often given prior to elective synchronized cardioversion to ease anxiety and
decrease pain.
Synchronized cardioversion delivers a shock on the R wave of the QRS complex
and would not be appropriate for a client in V-fib (no identifiable QRS
complexes). Rhythms that are ideal for synchronized cardioversion are
supraventricular tachycardia, ventricular tachycardia with a pulse, and atrial
fibrillation with rapid ventricular response. If the defibrillator is not synchronized
with the R wave in a client with a pulse, the shock may be delivered on the T
wave and can cause V-fib or asystole.
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V. Atrioventricular Blocks
Atrioventricular block (AV block) is an impaired conduction
between the atria and ventricles. Remember that Sinoatrial node
(SA node) is the Pacemaker, and impulses travel down to the
ventricles. In an AV block, this impulses are impaired. Hence, it is
imperative to determine PR interval which represents relationship
between atria and ventricles. Abnormal PR ≥ 0.24 secs is AV Block.
1. First degree AV block (1° AV Block)
0.48
secs
0.48
secs
0.48
secs
0.48
secs
0.48
secs
PQRST
P wave: Present (1P:1QRS)
PR Interval: ≥ 0.24 (consistent/same with each cycles)
QRS complex: Usually normal
Rhythm: Regular
Rate: Variable (slow-fast)
Remember:
1. All types of AVB are with PR ≥ 0.24 secs
2. PR intervals are consistent or the same with each cycles
3. Ratio: 1 P-wave is to 1 QRS complex
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2. Second degree AV block/2° AVB (Type 1)/Mobitz 1/Wenckebach
Irregular rhythm (R-R)
0.24
secs
0.32
secs
0.40
secs
P-wave:
No QRS
0.24
secs
0.32
secs
PQRST
P wave: Present (some P-waves are not followed by QRS)
PR Interval: ≥ 0.24 (inconsistent/different with each cycles)
QRS complex: Usually normal
Rhythm: Irregular
Rate: Variable (slow-normal)
Remember:
1. All types of AVB are with PR ≥ 0.24 secs
2. PR intervals are inconsistent or different with each cycles
(increasingly prolonged). Can have normal PR intervals.
3. Rhythm: Irregular
3. Second degree AV block/2° AVB (Type 2)/Mobitz 2
P-wave:
No QRS
0.24
secs
0.24
secs
0.24
secs
P-wave:
No QRS
0.24
secs
PQRST
P wave: Present (≥2P:1QRS)
PR Interval: ≥ 0.24 (consistent/same with each cycles)
QRS complex: Usually normal
Rhythm: Regular/irregular
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Rate: Variable (slow-normal)
Remember:
1. All types of AVB are with PR ≥ 0.24 secs
2. PR intervals are consistent or the same with each cycles
3. Ratio: ≥2 P-waves is to 1 QRS complex
4. Third degree AV block/3° AVB/Complete heart block (CHB)
Regular rhythm (R-R)
0.40
secs
0.52
secs
0.60
secs
P-wave:
No QRS
0.20
secs
P-wave:
No QRS
PQRST
P wave: Present (predominantly not associated with QRS)
PR Interval: ≥ 0.24 (inconsistent/different with each cycles)
P-waves not associated with QRS
QRS complex: Normal/wide
Rhythm: Regular
Rate: Usually slow
Remember:
1. All types of AVB are with PR ≥ 0.24 secs
2. PR intervals are inconsistent or different with each cycles
Atria is completely independent from ventricles. There
are P-waves with no QRS
3. Rhythm: Regular
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How to distinguish types of AVB?
PR ≥ 0.24 secs
Consistent PR
Inconsistent PR
1° AVB
2° AVB (II)
2° AVB (I)
3° AVB
1P:1QRS
≥2P:1QRS
Irregular
Rhythm
Regular
Rhythm
Management: See ACLS bradycardia algorithm
Chronic heart blocks are treated with permanent pacemakers:
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Question: Which client should the nurse assess first?
1. Client with atrial fibrillation with a new prescription for warfarin
2. Client with chronic obstructive pulmonary disease with an oxygen
saturation of 91%
3. Client with postoperative pain rated 8 out of 10
4. Client with third-degree heart block with a pulse of 42/min
Answer: 4
Rationale: Clients with third-degree atrioventricular (AV) block should be
assessed immediately due to the potential for life-threatening consequences
(e.g. shock, syncope, asystole) caused by decreased cardiac output and
severe bradycardia. The client with third-degree AV block requires a
permanent pacemaker.
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Common Cardiovascular Disorders
Acute Coronary Syndrome (ACS)
Acute coronary syndrome (ACS) encompasses a range of
cardiac events, including unstable angina & acute myocardial
infarction (with or without ST segment elevation). Clients with ACS
require immediate treatment.
ACS
Stable Angina
▪ Relieved by rest
▪ Monitor
Unstable Angina
AMI (NSTEMI)
AMI (STEMI)
(-) EKG
(-) Cardiac Markers
Pain Mgt:
▪ Nitrates
▪ Morphine
(-) ST Elevation, can
have ST depression,
T-wave inversion
(+) Cardiac Markers
Pain Mgt:
▪ Nitrates
▪ Morphine
(+) ST Elevation
(+) Cardiac Markers
Pain Mgt:
▪ Nitrates
▪ Morphine
Goal: Prevent
further clot
formation
▪ Antiplatelet
▪ Anticoagulant
Goal: Prevent further
clot formation and
break down clots
▪ Antiplatelet
▪ Anticoagulant
▪ Fibrinolytics/
Thrombolytics/
TPA (window
period: 30 mins-1
hr. from the start of
S/S)
(Proceed with PCI if
>1 hour has past)
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Cardiac Markers In order rising:
Myoglobin:
0 - 85 ng/ml
Troponin:
< 0.6 ng/ml (most specific and most sensitive)
CPK:
12 - 70 U/ML (m)
10 - 55 U/ml (f)
AST:
10 - 50 IU/L
LDH:
100 - 190 U/L
EKG Changes:
Common Anticoagulants and Antiplatelet:
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Anticoagulation Therapy:
Heparin: antidote is Protamine sulfate
aPTT:
30-40 sec (more sensitive)
(1.5 – 2X is therapeutic)
Risk for Bleeding: > 80 secs
PTT:
25 – 35 sec (less sensitive)
(1.5 – 2X is therapeutic)
Risk for Bleeding: > 70 secs
Warfarin (Coumadin): antidote is Vitamin K
PT:
10—12 sec
(1.5 – 2X is therapeutic)
Risk for Bleeding: > 24 secs
INR:
0.9—1.18
(up to 3X is therapeutic)
Risk for Bleeding: > 3.5 secs
Thrombolytics/Fibrinolytic/Tissue Plasminogen Activator (TPA):
Thrombolytic therapy is aimed at stopping the infarction
process, dissolving the thrombus in the coronary artery, and
reperfusion of the myocardium. This treatment is used in
facilities without an interventional cardiac catheterization
laboratory or when one is too far away to transfer the client
safely.
Window period: (30 mins-1 hr. from start of s/s)
Example: Alteplase, Tenecteplase, Reteplase, Streptokinase
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Contraindications:
▪ Prior intracranial
hemorrhage
▪ Arteriovenous malformation
(AVM): aneurysms
▪ Ischemic CVA within 3 mos.
▪ Suspected aortic dissection
▪ Active bleeding
▪ Significant head trauma
within 3 mos.
Percutaneous Coronary Intervention (PCI)/ Balloon angioplasty:
Inflation of a balloon within the coronary artery to crush the
plaque into the walls of the artery. Angioplasty is often
combined with the permanent placement of a small wire mesh
tube called a stent to help prop the artery open and decrease
its chance of narrowing again.
Preparation:
▪ Check dye allergy
▪ Check for intake of Metformin
▪ Check for intake of
antiplatelets
▪ Check BUN, creatinine
▪ NPO 6-8 hours
Risk:
▪ Re-narrowing of artery
▪ Blood clots
▪ Bleeding
▪ Heart attack
▪ Coronary artery damage.
▪ Acute Kidney Disease
▪ Stroke
▪ Arrhythmias
Remember:
Antiplatelet agents should
be stopped at least 5-7
days prior to the surgery to
reduce the chance of
intraoperative and
postoperative bleeding.
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Remember:
Check BUN, creatinine and
intake of metformin (anti
diabetic) to patients
receiving contrast dye.
Kidney primarily excretes this
materials
Metformin:
(withheld until 48 hrs. after
procedure). Induces toxic
accumulation of lactic
acid. Aggravates renal
failure
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Question: The client is scheduled to have a cardiac catheterization. Which
findings will cause the nurse to question the safety of the test proceeding? Select
all that apply.
1. Allergy to shellfish
2. Elevated C-reactive protein
3. Prolonged PR interval on electrocardiogram
4. Serum creatinine of 2.5 mg/dL (221 µmol/L)
5. Took metformin today for type 2 diabetes
Answer: 1, 4, 5
Rationale: Cardiac catheterization uses iodinated contrast to assess for artery
obstruction. Contrast should be avoided in clients who have allergies to
iodine or shellfish, have taken metformin within 24 hours of the procedure, or
have kidney disease.
Complications of IV contrast use include the following:
Contrast nephropathy: Contrast that contains iodine can cause kidney injury,
although this risk can be reduced with adequate hydration. However, clients
with existing renal impairment (e.g. elevated serum creatinine >1.3 mg/dL
[115 µmol/L]) should not receive IV contrast unless necessary for a life-saving
procedure Lactic acidosis: Metformin (Glucophage) given with large-dose IV
iodine contrast can increase the risk for lactic acidosis. As a result, most
clinicians discontinue metformin 24-48 hours prior to IV iodine contrast
exposure (regardless of baseline creatinine) and restart the drug at least 48
hours later.
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Common disorders: Infective Endocarditis
Risk: Preexistent disorders
▪
▪
▪
▪
Prosthetic valves
Cong. heart defects
Rheumatic heart disease
Intravenous drug use
Remember:
Inflammatory type of
Endocarditis is called Libman
Sacks Endocarditis: related to
SLE.
Causative Agents:
▪ Streptococcus viridans
(most common but not
virulent)
▪ Staph aureus (common
and virulent)
▪ Staph epidermidis
Remember:
High risk groups with
prosthetic valves for example
should have antibiotics
before dental procedures.
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Splinter hemorrhages: Thin,
red to reddish-brown lines of
blood under the nails due to
product of Ag-Ab complexes
forming emboli. It runs in the
direction of nail growth.
Janeway lesion: non-tender,
small erythematous or
hemorrhagic macular lesions
indicative of infective
endocarditis also due to AgAb complexes.
Osler’s nodes: Painful, red,
raised lesions on the hands
and feet caused by immune
deposition from Ag-Ab
complexes.
Roth spots: Retinal
hemorrhages with white or
pale centers due dysfunction
of the retinal capillaries from
Ag-Ab complexes or
inflammatory reactions.
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Common disorders: Myocarditis
Causative Agents:
▪ Coxackie virus
▪ Parasitic/protozoal
(Trypanoma cruzi):
Severe case “Chagas
disease” needs heart
transplant
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Common disorders: Pericarditis
Remember: Anatomy
Pericardial cavity:
< 50 ml fluid: normal
> 50 ml fluid: abnormal
(pericardial effusion)
> 150 ml fluid: cardiac
tamponade
Causes:
▪ Idiopathic
▪ Coxackie virus
▪ Dressler’s syndrome
(Post AMI)
▪ Uremia (Urea irritates
pericardium)
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Classic sign:
▪ Chest pain on lying
(relieved by sitting up)
▪ Pericardial friction rub
Treatment of choice:
▪ Pericardiocentesis
Complication:
Cardiac Tamponade
Beck’s Triad
▪ Narrowed pulse
pressure (Hypotension)
▪ Muffled/distant heart
sound
▪ Distended neck veins
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Common disorders: Rheumatic Heart Disease (RHD)
Rheumatic fever:
An inflammatory disease (autoimmune) that can involve the heart, joints,
skin or brain. These diseases are closely associated with one another. (e.g.
Rheumatoid arthritis, rheumatic heart disease, scarlet fever, impetigo,
pharyngitis) and are usually triggered by Streptococcal infections (group A
beta-hemolytic streptococcus, aka GABHS)
Remember: Diagnostic criteria
▪ Acronym JONES (major criteria) CAFÉ PAL (minor criteria)
▪ Throat cultures for (+) GABHS, elevate Anti- streptolysin titer
Remember:
Autoimmune diseases
are chronic condition that
are triggered by infections
and environmental factors
causing over-activation of
immune cells. Symptoms
arise from this mechanism.
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Erythema marginatum:
is a type of erythema
(redness of the skin or
mucous membranes)
involving pink rings on the
torso and inner surfaces of
the limbs which come and
go for as long as several
months.
Sydenham chorea:
Characterized especially
by involuntary movements
of the face, arms, legs,
and trunk
(dance like movements)
Root word:
“Choreography”
Subcutaneous nodules:
Painless, small (0.5-2 cm),
mobile lumps seen
beneath the skin overlying
the bony prominences,
particularly of the hands,
feet, elbows and occiput.
It is a delayed
manifestation of RF.
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Common disorders: Kawasaki disease (Mucocutaneous
lymph node syndrome)
Kawasaki disease (KD):
Is a systemic vasculitis of
childhood that presents
with ≥5 days of fever,
nonexudative
conjunctivitis,
lymphadenopathy,
mucositis, hand and foot
swelling, and a rash.
Treatment:
IV Immunoglobulin along
with aspirin is the
recommended initial
treatment for Kawasaki
disease, with the primary
goal of coronary disease
prevention.
Diagnosis: CRASH & Burn
4/5 of the given criteria
+ Fever ≥5 days
Remember:
Aspirin is given to prevent
coronary complication. It
outweighs the risk of
having Reye syndrome in
children having KD.
Remember:
IVIG creates high plasma
oncotic pressure, and
signs of fluid overload and
pulmonary edema
develop if it is given in
large quantities.
Therefore, the child should
be monitored for
symptoms of CHF
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Review of cardiopulmonary circulation
Right Side of the Heart 1. Un-oxygenated blood enters the heart through the
SUPERIOR & INFERIOR VENA CAVA. 2. RIGHT ATRIUM 3. Then it is squeezed through
the TRICUSPID VALVE 4. RIGHT VENTRICLE 5. Then it is squeezed into the
PULMONIC VALVE then to 6. PULMONARY ARTERY and enters into the lungs for
oxygenation
Left Side of the Heart 7. Oxygenated blood to PULMONARY VEIN 8. LEFT ATRIUM 9.
Down through the BICUSPID VALVE (mitral valve)
10. Then blood is squeezed into the LEFT VENTRICLE 11. Up through the AORTIC
VALVE 12. Lastly the AORTA for multi system distribution.
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Common disorders: Congenital heart defects (CHD)
Acyanotic: Left-Right shunt
Pressure on the left side of
the heart is normally
greater than right. It just
simply means left – right
shunt (acyanotic type)
directs blood towards
pulmonary artery and
towards lungs for
oxygenation.
Cyanotic: Right-Left shunt
Right – left shunt forces
blood towards the aorta.
Less chances of blood
going to pulmonary artery
for oxygenation due to
defect.
Left-Right shunt: Acyanotic
An atrial septal defect
(ASD) is a hole in the wall
between the two upper
chambers of your heart
(atria). Blood goes back to
right side because of the
pressure and goes into
lungs for oxygenation
A ventricular septal defect
(VSD) is a defect in the
septum between the right
and left ventricle. Blood
goes back to right side
because of the pressure
and goes into lungs for
oxygenation
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Remember: Ductus arteriosus
Connects the pulmonary
artery with the aorta in fetal
life. Closes when the
newborn infant starts to
breath. Prostaglandin keep
the DA open.
Aorta (left-higher pressure)
pushes blood to pulmonary
artery for oxygenation.
DOC for PDA:
Indomethacin
(Prostaglandin
inhibitor)
Classic sign: continuous
machinery-like murmur
Coarctation of Aorta:
"Coarctation" means
narrowing of the aorta
Classic sign: Hypertension
in the arms with low blood
pressure and weak pulses
in the lower extremities.
This due to deficient blood
flow prior to coarctation.
This directs more blood
flow to subclavian,
brachiocephalic, carotid
arteries.
Acyanotic type general S/S:
▪ Shortness of breath
▪ Tachycardia
▪ Tachypnea
▪ Diaphoresis
▪ Fatigue
▪ Frequent respiratory infections
May not have symptoms
depending on the size of
the defect.
Remember:
Heart failure is a complication of any
congenital heart defects
The early signs of HF include
tachycardia, tachypnea, profuse
scalp or eyebrow sweating, fatigue
and irritability, sudden weight gain,
and respiratory distress.
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Right-Left shunt: Cyanotic
Tetralogy of Fallot (TOF):
TOF is made up of 4 main
defects. Narrowing of the
pulmonary valve (pulmonic
stenosis) prevents blood
from flowing to lungs for
oxygenation causing the
cyanosis. Multiple defect
favors R-L shunting as blood
backflows to right side of the
heart such as overriding of
aorta, VSD and right
ventricular hypertrophy.
Transposition of the great
arteries:
The two main arteries
(Aorta and pulmonary
artery) leaving the heart is
reversed or transposed.
Unoxygenated blood
coming from the right side
goes directly to the aorta
without a chance of
oxygenation
Tricuspid Atresia:
Complete absence of the
tricuspid valve. Associated
with other defects such as:
ASD, PDA, VSD. Classic sign
is holosystolic murmur d/t
the VSD.
DOC for TA:
Prostaglandin
(To maintain PDA). Directs
blood from aorta to lungs
for oxygenation
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Truncus arteriosus:
Occurs when the 2 major
vessels (Pulmonary artery &
Aorta) fails to separate
completely during
development, leaving a
connection between them.
Usually associated with
VSD.
Question: A nurse is assisting a new mother as she is breastfeeding her infant. The
infant has been diagnosed with tetralogy of Fallot (TOF). During feeding, the
infant becomes cyanotic and is having difficulty breathing. What should be
the nurse's first action?
1. Administer morphine to the infant
2. Administer oxygen via mask
3. Assess infant's vital signs and pulse oximetry
4. Place the infant in the knee-chest position
Answer: 4
Rationale: This infant is experiencing a hyper-cyanotic episode, or
"TET SPELL," which is an exacerbation of tetralogy of Fallot that can happen
when a child cries, becomes upset, or is feeding. The child should first be
placed in a knee-to-chest position. Flexion of the legs provides relief of
dyspnea by increasing the abdominal pressure forcing the blood back to
aorta for left-right shunting via VSD.
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Common disorders: Congestive Heart Failure (CHF)
Remember: Anatomy and
physiology is the key
Right sided: Resistance to right
side d/t failure causes backflow
to both large veins (vena
cavas). Excess fluids pool in GI
tract, liver, extremities (U/L)
Left sided: Resistance to left side
d/t failure causes backflow to
lungs through pulmonary veins.
Excess fluids causes pulmonary
edema.
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Question: A client seen in the clinic with shortness of breath and fatigue is being
evaluated for a possible diagnosis of heart failure. Which laboratory result
will be most useful to monitor?
1. Serum potassium
2. B-type natriuretic peptide (BNP)
3. Blood urea nitrogen
4. Hematocrit
Answer: 2
Rationale: B-type natriuretic peptide levels increase in clients with poor left
ventricular function and symptomatic heart failure and can be used to
differentiate heart failure from other causes of dyspnea and fatigue such as
pneumonia. BNP is widely used in the acute care settings nowadays. The
other values should also be monitored, but do not indicate whether the client
has heart failure.
Remember: Diuretics
Potassium Sparing (SEAT):
▪ Spironolactone
▪ Eplerenone
▪ Amiloride
▪ Triamterene
Potassium Wasting (BF):
▪ Bumetanide
▪ Furosemide
Low Na diet:
DASH (Diet Approach to Stop HTN)
▪ All foods high in sodium (>400
mg/serving) should be avoided.
▪ Do not add salt or seasonings containing
sodium when preparing meals
▪ Do not use table salt
▪ Avoid high-sodium foods (e.g. canned
soups, processed meats, cheese, frozen
meals)
▪ Limit milk products to 2 cups daily
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Common disorders: Aortic Aneurysms
Aortic Aneurysm:
Enlargement of the aorta
to greater than 1.5 times
normal size. It will cause no
symptoms except when
ruptured.
Aortic aneurysm increases
your risk of developing an
aortic dissection (tearing).
Aneurysm: Occurs when part of an artery wall
weakens, allowing it to balloon out or widen
abnormally. Abdominal aneurysm is more
common than thoracic aneurysms (both are
aortic aneurysms)
Remember: Dysphagia is a
sign of enlarging thoracic
aneurysm including dull
chest, collarbone and back
pain
Pulsatile lump with
abdominal pain are signs of
enlarging abdominal aortic
aneurysm (AAA).
S/S of shock (hypotension,
tachycardia tachypnea) are
signs of rupture.
AAA Management:
Surgically repaired when
they measure about 6 cm
or are causing symptoms.
▪ Femoral percutaneous
placement of a stent
graft (endovascular
aneurysm repair)
▪ Open surgical incision of
the aneurysm with
synthetic graft
placement.
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Remember:
Following repair of an
abdominal aortic
aneurysm, hemodynamic
stability is a priority.
Prolonged hypotension can
lead to graft thrombosis. A
falling blood pressure and
rising pulse rate can also
signify graft leakage.
Signs of graft leakage:
▪ pain in back, pelvis, or
groin
▪ ecchymosis of the groin
scrotum, or penis
▪ tachycardia
▪ weak or absent
peripheral pulses
▪ decreasing hematocrit
and hemoglobin
▪ increased abdominal
girth
▪ decreased urinary output
Open vs endovascular:
Open repair – A large incision
in the abdomen is made to
expose the aorta. Once the
abdomen is opened, a graft
can be used to repair the
aneurysm
Endovascular repair: A
minimally invasive procedure
via incision in the femoral
artery to the aneurysm. A
stent and/or graft is placed to
repair the aneurysms.
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Common disorders: Aortic Dissection
Aortic dissection: Occurs when the arterial wall intimal layer tears and
allows blood between the inner (intima) and middle (media) layers.
Results from high blood pressure that puts stress on weakened areas of
the aortic wall causing tearing.
Remember:
An aortic dissection,
which classically has
moving, "ripping" back
pain, is a medical
emergency.
Hypertension is the most
important contributing
factor.
Remember:
Extending dissection from
uncontrolled HTN can cause
cardiac tamponade or
arterial rupture, which is
rapidly fatal. Emergency
treatment includes surgery
(open or endovascular)
and/or lowering the blood
pressure.
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Common disorders: Venous thromboembolism (VTE)
Deep vein thrombosis vs
Pulmonary embolism
DVT occurs when a blood clot
(thrombus) forms in one or
more of the deep veins in
your body, usually in your
legs. Pulmonary embolism
(PE) is a DVT that breaks loose
and travels through the
bloodstream to the lung
vasculature. Death from PE is
often attributed to a missed
diagnosis. Early identification
of risk factors can have a
positive effect on client
outcome.
Risk Factors:
Trauma, surgery (especially
orthopedic, knee, hip),
prolonged
immobility/inactivity, oral
contraceptives, pregnancy,
varicose veins, obesity,
smoking, and advanced age.
Remember: Virchow’s Triad
1. Venous stasis
2. Vein trauma/Endothelial
injury
3. Hypercoagulability
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Duplex ultrasonography
is the standard imaging
test to diagnose DVT.
D-dimer blood test:
Measures a substance in the
blood that is released when
a clot breaks up. Indicated
for suspicion of DVT, PE or
coagulopathies such as
disseminated intravascular
coagulation (DIC).
Computed tomographic
pulmonary angiography
(CTPA): A special type of Xray test that includes injection
of contrast material (dye) into
a vein. This test can provide
images of the blood vessels in
the lungs. Standard imaging
test to diagnose PE.
The areas of the tip of the arrowhead
are slightly darker than the normal
indicating decreased ability for contrast
dye to enter pulmonary artery and its
branches. This is indicative of PE.
Remember: Procedure with
contrast dye
▪ Check BUN, Creatinine
▪ Check intake of metformin
▪ Check for allergies to dye
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Ventilation-perfusion (V/Q)
scan: A specialized test that
uses a radioactive substance
to show the parts of the lungs
that are getting 02 (ventilation
scan) and getting blood flow
(perfusion scan). Used when
CTPA is not available or when
contraindicated.
Pulmonary angiography:
Special type of X-ray test that
requires insertion of a large
catheter to femoral vein &
into the pulmonary arteries,
followed by injection of
contrast dye through the
catheter. Most accurate test to
diagnose PE but invasive.
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VTE PROPHYLAXIS/
TREATMENT
Pharmacologic
Mechanical
Unfractionated
Heparin (IV)
Graduated compression
stocking/ted hose
Low molecular weight
heparin (LMWH): given SQ
Intermittent pneumatic
compression device
Vitamin K
Antagonist (PO)
IVC filter
Thrombolytics
Thrombectomy/
Embolectomy
Unfractionated
Heparin
Heparin Induced
Thrombocytopenia (HIT)
HIT occurs over several days.
Report a decrease of ≥50% from
baseline or a drop below
150,000/mm3. If the client has
HIT, all heparin products must
be stopped immediately, and a
different anticoagulant should
be started to prevent
thrombosis risk.
Remember: High Alert
Medication (HAM)
Most central lines require IV
heparin flushes to maintain
patency and prevent clotting
by using single-dose vials of 2–3
mL of 10 units/mL or 100
units/ml. A dose of 1000–10,000
units is given for cases of
thromboembolism.
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LMWH
Heparin
Monitoring: Anticoagulants
LMWH (Enoxaparin): Requires
monitoring of CBC,
(thrombocytopenia) but not
coagulation studies.
Unfractionated heparin:
Requires monitoring with PTT
Warfarin: requires PT/INR
monitoring.
Remember: LMWH (Enoxaparin)
Comes in a prefilled syringe. To
ensure complete medication
delivery, the air bubble should
not be expelled prior to injection.
▪ Right or left side of abdomen, 2
inches from umbilicus
▪ Insert the needle at a 90degree angle into a pinchedup area of skin.
▪ Discourage the client from
rubbing the site.
Vit K antagonist
Warfarin (coumadin)
Warfarin:
Must be taken at the same time
daily to reach a therapeutic INR
level. A diet high in Vitamin K
(e.g. green leafy vegetables)
may decrease warfarin's
anticoagulant effect, (eat
consistent amount). In addition,
most antibiotics will increase INR
by causing vitamin K deficiency.
Intestinal bacteria produce
Vitamin K.
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Heparin
Warfarin (Coumadin)
aPTT: 30-40 sec (normal range)
(1.5-2X therapeutic: 45-80 sec)
Risk for Bleeding: > 80 sec
PTT: 25-35 sec (normal range)
(1.5-2X therapeutic: 45-70 sec)
Risk for Bleeding: > 70 sec
PT: 10-12 sec (normal range)
(1.5-2X therapeutic: 18-24 sec)
Risk for Bleeding: > 24 sec
Antidote: Protamine Sulfate
INR: 0.9-1.18 sec (normal range)
(up to 3X therapeutic: <3.5 sec)
Risk for Bleeding: ≥ 3.5 sec
Antidote: Vitamin K
Remember: Normal vs. Therapeutic range
Therapeutic range is expectedly higher than the normal range if the
patient is taking anticoagulants but with certain limits. Exceeding
therapeutic range increases risk for bleeding. For patients not taking
anticoagulants, exceeding the normal range is ruling out liver
conditions, blood dyscrasias, etc.
Thrombolytics
Thrombolytic agents:
Indicated to resolve acute
thrombotic events (e.g.,
ischemic stroke, myocardial
infarction, massive pulmonary
embolism). They are
recombinant plasminogen
activators (RTPA) that activate
the blood fibrinolytic system
and dissolve thrombi (e.g.
alteplase, tenecteplase,
reteplase)
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Graduated
compression stocking
Anti-embolism stockings:
Anti-embolism stockings improve
blood circulation in the leg veins
by applying graduated
compression. When fitted
properly and worn consistently,
the stockings decrease VTE risk.
The stockings should not be rolled
down, folded down, cut, or
altered in any way. If stockings
are not fitted and worn correctly,
venous return can actually be
impeded.
Intermittent pneumatic
compression device
Intermittent pneumatic
compression device or
sequential compression device
(SCD):
A mechanical prophylactic
treatment to reduce the
incidence of VTE by enhancing
the blood flow in the deep veins
of the legs, thereby reducing
venous stasis. SCD utilize sleeves
with separated areas or pockets
of inflation, which works to
squeeze on the appendage in a
“milking action.” The most distal
areas will initially inflate, and the
subsequent pockets will follow in
the same manner.
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IVC filter
An inferior vena cava filter:
A device that is inserted
percutaneously, via the femoral
vein. The filter traps blood clots
(embolus from DVT) from lower
extremity and prevents them
from causing PE. Prescribed
when clients have recurrent
emboli or anticoagulation is
contraindicated. Clients should
report any metallic implants (e.g.
vascular filters/coils) to the health
care team prior to radiologic
imaging.
Thrombectomy/
Embolectomy
Surgical or catheter
embolectomy:
Performed in patients with
massive pulmonary embolism.
Embolectomy is used for patients
with persisting shock despite
supportive care and who have
an absolute contraindication for
thrombolytics
Thrombectomy:
Involves removal of the clot in a
patient with DVT.
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Question 1: A client with obesity is diagnosed with pulmonary embolism (PE).
Which assessment data would the nurse expect to find? Select all that
apply.
1. Bradycardia
2. Chest pain
3. Chills and fever
4. Hypoxemia
5. Tachypnea
6. Tracheal deviation
Answer: 2,4,5
Rationale: A pulmonary embolus usually originates from the deep veins of the
legs (>90%), travels to the pulmonary circulation, and obstructs a pulmonary
artery or one of its branches, resulting in decreased perfusion in relation to
ventilation and impaired gas exchange (hypoxemia).
Clients are at risk for formation of venous thromboembolism (VTE) when the
conditions detailed in Virchow's Triad are present (e.g. hypercoagulability,
venous stasis, and endothelial damage). Clients at risk for PE include those
with prolonged immobilization (e.g. during hospitalization if not ambulatory),
obesity, recent surgery, varicose veins, smoking, heart failure, advanced age,
or history of VTE.
Characteristic of PE include:
▪ Dyspnea (85%)
▪ Pleuritic chest pain (60%)
▪ Tachycardia
▪ Tachypnea
▪ Hypoxemia
▪ Apprehension and anxiety
A more atypical presentation can be associated with a larger sized PE, and
may include manifestations of cardiopulmonary compromise and
hemodynamic instability (e.g. right ventricular dysfunction, pulmonary
hypertension, systemic hypotension, syncope, loss of consciousness,
distended neck veins).
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Question 2: A client with a diagnosis of atrial fibrillation has just been placed on
warfarin therapy. The registered nurse (RN) overhears a student nurse
teaching the client about potential food-drug interactions. Which
statement made by the student nurse requires an intervention by the RN?
1. "Do you take any nutritional supplements?"
2. "You will need to monitor your intake of foods containing vitamin K."
3. "You will not be able to eat green, leafy vegetables while taking this
medication."
4. "Your blood will be tested at regular intervals."
Answer: 3
Rationale: Warfarin (Coumadin) works by blocking the availability of vitamin K,
which is essential for blood clotting. As a result, the clotting mechanism is
disrupted, reducing the risk of a stroke, venous thrombosis, or pulmonary
embolism.
Sudden increases or decreases in the consumption of vitamin K-rich foods
could inversely alter the effectiveness of warfarin. An increase in vitamin K
could decrease the effectiveness of warfarin, placing the client at increased
risk of blood clot formation; a decrease could increase the effectiveness of
warfarin, placing the client at increased risk for bleeding. Keep vitamin K
intake consistent from day to day to keep INR/PT stable and within the
recommended therapeutic range.
Many medications can interfere with warfarin metabolism. Nutritional
supplements may contain vitamin K, and so any new medication or
nutritional supplement should be approved by the health care provider.
Cranberry juice, grapefruit, green tea, and alcohol may also interfere with
the effectiveness of warfarin.
Rather than avoid vitamin K-rich foods, the client needs to keep vitamin K
intake consistent from day to day to keep INR/PT stable and within the
recommended therapeutic range. If the client enjoys vitamin K-rich foods
(e.g., kale, broccoli, spinach, Brussels sprouts, cabbage, green leafy
vegetables), these may be consumed in the same amounts, consistently on
a daily basis. There is some evidence that a very low intake of vitamin K
could decrease the overall effectiveness of warfarin.
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Common disorders: Arterial insufficiency vs Venous insufficiency
Signs/Symptoms
Arterial insufficiency
Cause
Arteriosclerosis,
Atherosclerosis
Incompetent valves
Pain
Intermittent claudication:
Bilateral legs
(pain relieved by rest)
Pain may signify DVT;
Unilateral
(not relieved by rest)
Color
Cold
Warm
Swelling
No
Yes
Hair loss
Yes
No
Temperature
Cold
Warm
Ulcers
Circular, small and deep
Location: Toes
Irregular, large, superficial
Location: Ankle
Peripheral artery disease (PAD):
Previously called peripheral
vascular disease refers to arteries
that have thickened, have lost
elasticity due to calcification of
the artery walls, and are
narrowed by atherosclerotic
plaques (made up of fat and
fibrin). Pain (intermittent
claudication) d/t decreased
blood flow is the most common
symptom of PAD.
Venous insufficiency
Chronic venous insufficiency
(CVI): Refers to inadequate
venous blood return to the heart.
Too much venous blood remains
in the lower legs, and venous
pressure increases. This increased
venous pressure inhibits arterial
blood flow to the area, resulting
in inadequate supply of oxygen
and nutrients to area. DVT
resulted from a clot from
Virchow’s triad mechanism
whereas CVI is caused by more
specifically to incompetent
valves
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7
Anatomy and Physiology
Respiratory
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Remember: Lung coverings
The volume of fluid is small,
at around 15-20 ml and
normally reabsorbed by
lymphatic vessels. Excess
fluids lead to pleural
effusion.
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Normal:
Bronchial/Tracheal: High
pitch an loud
Bronchovesicular: Moderate
pitch, moderate loudness
Vesicular: Low pitch and soft
Adventitious: Abnormal
Wheeze/rhonchi:
whistling/sibilant, musical
Stridor:
whistling/sibilant, musical
Crackles/Rales:
cracking/clicking/rattling
Common respiratory findings:
Mediastinal
shift
Condition
Lung sounds
Vibration
(tactile fremitus)
Normal
Bronchial,
Bronchovesicu
lar, vesicular
Normal
Resonance
No
Pneumonia
Crackles
Normal
Dull
None
Percussion
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Pleural
effusion
Decreased or
absent
Decreased
Dullness
Yes if large
Pneumothorax
Decreased or
absent
Decreased
Hyper
resonant
Yes
COPD
Wheezing
Decreased
Hyper
resonant
No
Remember:
The lung is filled with 99% air. Hence, percussion gives a resonant sound. This step
helps identify areas of lung with fluid which causes dullness and air trapping
causes hyperresonance. Percussion sounds in general are composed of dullness
(flat organ such as liver), resonance (filled with air such as lung), tympany (filled
with fluid and air like stomach).
Oxygen administration:
Device
Flow rate
Percentage of O2 (FIO2)
Nasal cannula
1-4 liters
Up to 40%
Simple face mask
4-6 liters
40-60%
Non-rebreather
10-15 liters
80-100%
Venturi
(venti) mask
Depending on the
color code
Up to 60%
(depending on the
color code)
Remember: Drying effect
When the O2 flow rate is higher than 4 L/min, the mucous membranes can be
dried out. The best treatment is to add humidification to the O2 delivery system.
Applying water-soluble jelly to the nares can also help decrease mucosal
irritation.
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Nasal Cannula
Simple face mask
Nonrebreather mask
Remember: COPD
Clients with COPD breathe in
response to low arterial O2 levels
(hypoxemia). If they receive more
oxygen than they need to
maintain an arterial saturation, the
increased level can decrease the
drive to breathe. Therefore,
supplemental oxygen should be
administered in the lowest
concentration possible to
maintain a pulse oxygen
saturation of 90%-93% or PaO2 of
60-70 mm Hg.
Non rebreather mask: Nursing
care
▪ Monitoring the reservoir bag to
assure continual inflation during
inhalation
▪ Monitoring the 2 exhalation
(flutter) valves that cover the
ports on each side of the mask
(valves close on inhalation to
prevent entry of room air and
open on exhalation to prevent
re-inhalation of exhaled air. The
ports should be occluded when
initiating the device to fill the
reservoir with oxygen)
▪ Keeping the mask secured to
the face by adjusting the
tightness of the head strap to
minimize leaks
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Venturi mask
Remember:
The Venturi mask is best for
COPD patients because it
provides all the oxygen required
in the exact amount because
the device controls the mixture
of room air. The fraction of
inspired oxygen is therefore
"guaranteed" and does not vary
with changes in the client's
respiratory rate, depth, or tidal
volume.
Positive pressure ventilation: Invasive vs non-invasive
Invasive
Remember: Positive pressure
Positive pressure compresses the
vena cavas and increases
intrathoracic pressure during
inspiration. This leads to less
venous return, ventricular
preload, and cardiac output,
which results in hypotension.
The hypotensive effect of PPV is
greater in the presence of
hypovolemia (e.g. hypovolemic
shock) and decreased venous
tone (e.g. septic shock,
neurogenic shock).
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Modes
Mechanism
Mandatory/Assist control
(AC mode)
▪ Previously known as Continuous Mandatory
ventilation (CMV)
▪ Triggered either by the patient or mechanically by
the ventilator. The ventilator is set to deliver a
breath according to parameters.
▪ Can ASSIST OR CONTROL ventilation regardless of
spontaneous breathing
Intermittent Mandatory
Ventilation (IMV):
Synchronized IMV (SIMV)
Spontaneous Ventilation:
Pressure Support
Ventilation (PSV)
▪ Regular series of breaths are scheduled but the
ventilator senses patient effort and reschedules
mandatory breaths based on the calculated
need of the patient.
▪ Improve weaning from ventilator
▪ Any mode of mechanical ventilation where every
breath is spontaneous or triggered by patient.
▪ Ventilator controls O2 amount and pressure
▪ Delivers flow and volume as needed to SUPPORT
the patient breathe
▪ e.g. CPAP, BIPAP
Settings
Function
Parameters
Respiratory rate
Breaths delivered per minute
4-20/minute
Tidal volume (VT)
Volume of air delivered
during ear ventilator breath
5-15 ml/kg
FIO2
Amount of O2 delivered
20-100%
(to keep PO2 >60% and
Saturation >90%)
Inspiratory and
expiratory ratio (I:E)
Positive end
expiratory pressure
(PEEP)
Length of inspiration vs
expiration
1:2 or 1:1.5
Amount of pressure during
end of expiration to prevent
collapse
10-20 cmH20
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High
Low
Alarms
Non-invasive
CPAP vs BIPAP
Continuous positive airway
pressure (CPAP): Applying
continuous pressure to the
airways. Same on both inhalation
and expiration
Bi-level Positive Airway Pressure
(BiPAP): Two different pressures,
reduce the pressure when
exhaled and increases pressure
when inhaled. It helps to get more
air in and out without much effort.
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Question: A client has chronic obstructive pulmonary disease (COPD)
exacerbation. The pulse oximeter shows a saturation of 86% on room air. The
nurse assesses diminished lung sounds and low-pitched wheezing posteriorly,
shallow respirations, respiratory rate of 32/min, and use of accessory
muscles. What is the most appropriate oxygen delivery device for this
client?
1. Nasal cannula
2. Non-rebreathing mask
3. Oxymizer
4. Venturi mask
Answer: 4
Rationale: The Venturi mask is a high-flow device that delivers a guaranteed
oxygen concentration regardless of the client's respiratory rate, depth, or
tidal volume (TV). The adaptor or barrel can be set to deliver 24%–60% (varies
with manufacturer) oxygen concentration. In the presence of tachypnea,
shallow breathing with decreased TV, hypercarbia, and hypoxemia, it is the
most appropriate oxygen delivery device for this client as rapid changes in
inspired oxygen concentration can blunt the hypoxemic drive to breathe in
clients with COPD.
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Arterial blood gas analysis (ABG)
Normal Values
1. Determine if the deviation/problem is Acidosis or Alkalosis
Note: Use 7.40 (mean) instead of the range (7.35-7.45)
<7.40 – Acidosis
>7.40 - Alkalosis
2. Identify which is responsible for the deviation.
PCO2: Respiratory (Respiratory System)
<35 – Alkalosis
>45 - Acidosis
HCO3: Metabolic (Renal System)
<22 – Acidosis
>26 – Alkalosis
3. After identifying, you need to know if there is compensation.
Remember, ABG is about buffer system. If there is deviation
then the other one must compensate.
How do you know if it is COMPENSATED?
If the other value opposes and attempts to
neutralize (buffer): Compensated
If not: Uncompensated
4. If compensated, determine if full or partial.
Note: This time, refer to the range (7.35-7.45)
If within 7.35 – 7.45: FULL
If not within 7.35 – 7.45: PARTIAL
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Application
Example: pH 7.39
PCO2 49 mmHg
HCO3 28 meqs/L
1. Determine if the deviation/problem is Acidosis or
Alkalosis
Note: Use 7.40 (mean) instead of the range (7.35-7.45)
<7.40 – Acidosis
>7.40 - Alkalosis
Ex: pH 7.39: ACIDOSIS (<7.40 – Acidosis)
2. Identify which is responsible for the deviation.
PCO2 – Respiratory (Respiratory System)
<35: Alkalosis
>45: Acidosis
HCO3 – Metabolic (Renal System)
<22: Acidosis
>26: Alkalosis
PCO2 49 mmHg (ACIDOSIS): RESPIRATORY
HCO3 28 meqs/L (ALKALOSIS): METABOLIC
Problem: RESPIRATORY ACIDOSIS
3. After identifying, you need to know if there is
compensation. Remember, ABG is about buffer
system. If there is deviation then the other one must
compensate.
How do you know if it is COMPENSATED?
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▪ If the other value opposes and attempts to
neutralize (buffer): Compensated
▪ If not: Uncompensated
HCO3 28 meqs/L (ALKALOSIS)
OPPOSES? YES: COMPENSATED
Problem: RESPIRATORY ACIDOSIS COMPENSATED
4. If compensated, determine if full or partial.
Note: This time, refer to the range (7.35-7.45)
If within 7.35 – 7.45: FULL
If not within 7.35 – 7.45: PARTIAL
pH 7.39
Within normal range? Yes
Problem:
RESPIRATORY ACIDOSIS (FULLY COMPENSATED)
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Chest tube
Remember: 3 aspects of chest tube drainage system
Collection chamber: measures the collected fluid and also allows passage of
air to the water seal.
Water seal: prevents any entry of air into the thorax and measures any air
exiting the system in the air leak portion of the water seal.
Suction chamber: The amount of negative pressure it exert to promote suction
effect (-10 to -20 cmH20)
Water Seal
Fluctuation is normal, continuous
bubbling is air leak, absence of
fluctuation can be a sign of a lung
fully inflated.
Suction Chamber
Continuous bubbling is normal,
Intermittent bubbling (check
gauge), no bubbling (check
connection)
Remember:
Chest tube drainage (50-500 mL
for the first 24 hours) is expected to
be sanguineous (bright red) for
several hours and then change to
serosanguineous (pink) followed
by serous (yellow) over a period of
a few days.
Notify HCP: >100 mL/hour
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Remember: “Milking”
Is generally contraindicated as it
can cause tissue damage from
highly increased pressure changes
in the pleural space. It is only
done if ordered and a
clot/obstruction is suspected.
Emergency bedside equipment:
▪ 2 chest tube clamps,
▪ 250 mL bottle of sterile H2O or
NS and antiseptic wipes
Remember: Clamping
Chest tubes should not be
clamped during transport of a
client. A clamped chest tube
may cause a tension
pneumothorax. The chest tube is
clamped only a few hours prior to
removal to check for an air leak,
or if the drainage system needs to
be changed.
Remember: Disconnection
If a chest tube disconnects from
the chest drainage system and
cannot be reattached quickly, or
if a chest drainage unit cracks or
malfunctions, submerge the distal
end of the chest tube 1-2 in (2-4
cm) below the surface of a 250
mL bottle of sterile H2O or saline
solution.
Question: The client has a chest tube for a pneumothorax. While repositioning
the client for an x-ray, the technician steps on the tubing and accidently
pulls the chest tube out. The client's oxygen saturation drops and the pulse is
132/min; the nurse hears air leaking from the insertion site. What is the nurse's
immediate action?
1. Apply an occlusive sterile dressing secured on 3 sides
2. Apply an occlusive sterile dressing secured on 4 sides
3. Assess lung sounds
4. Notify the health care provider (HCP)
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Answer: 1
Rationale: If a chest tube is dislodged from the client and the nurse hears air
leaking from the site, the immediate action should be to apply an occlusive
sterile dressing taped on 3 sides. This action decreases the risk for a tension
pneumothorax by inhibiting air intake on inspiration and allowing air to
escape on expiration
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148
Common Respiratory Disorders
Obstructive lung diseases: Asthma
Asthma:
Characterized by airway hyperreactivity and chronic
inflammation, resulting in
bronchial muscle spasm,
mucosal edema, and
hypersecretion of mucus. The
airways narrow, resulting in
increased airway resistance,
air trapping, and lung
hyperinflation.
Remember:
Asthma is a chronic disorder. It is
not the most priority unless it
becomes acute/ exacerbated.
Expiratory wheezing is
expected. However, if it says
inspiratory wheezing and/or
diminished lungs sounds, it’s a
sign of worsening condition.
Common characteristic:
▪ Use of accessory muscle
▪ Chest tightness related to air
trapping
▪ Diminished breath sounds
related to hyperinflation
▪ High-pitched, sibilant
wheezing on expiration
▪ Tachypnea (alkalosis initially)
▪ Cough from inflamed
airways
▪ Increased secretions
Common asthma triggers:
Allergens: Dander (e.g., cat,
dog), dust mites, pollen
Drugs: Beta blockers; NSAIDS
(Ibuprofen, ASA)
Environmental: Chemicals,
sawdust, soaps/detergents
Infectious: Upper RTI
Intrinsic: Emotional stress, GERD
Irritants: Aerosols/perfumes,
cigarette smoke (including
secondhand smoke),
dry/polluted air.
Acute exacerbation management
1. Oxygen to maintain saturation >90%
2. High-dose inhaled short-acting beta agonist (SABA)
Albuterol (Ventolin) & anticholinergic agent
ipratropium (Atrovent) nebulizer treatments every 20
minutes
3. Systemic corticosteroids
Methylprednisolone (Solu-Medrol)
Preventive management: leukotriene receptor blocker
(bronchodilator, anti-inflammatory)
Montelukast (Singulair)
Zafirlukast (Accolate)
Long-term mgt: Long acting beta-agonist (LABA)
Salmeterol (Serevent)
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Diagnosis: PEF measures
severity of asthma
The peak flow meter is used to
measure PEFR and is most
helpful for clients with moderate
to severe asthma. A reading is
obtained by exhaling as quickly
and forcibly as possible through
the mouthpiece of the device.
Measuring peak expiratory flow: peak
flow meter
1. Slide the indicator to the 0 or lowest
level and instruct the client to sit as
upright
2. Instruct the client to breathe in
deeply, place the mouthpiece in
the mouth, and tightly seal using
the lips
3. Instruct the client to exhale as
quickly and forcibly as possible,
note the reading on the numbered
scale
4. Repeat the procedure 2 more times
with a 5–10-second rest period
between exhalations
5. Record the highest reading or
personal best
Green Zone:
80 to 100 % of your usual or "normal" peak
flow rate signals all clear. A reading in this
zone means that your asthma is under
reasonably good control.
▪ Continue management
Yellow Zone:
50 to 80% of your usual or "normal" peak
flow rate signals caution.
▪ May require extra treatment.
▪ Your symptoms can get better or
worse. Contact HCP for changes in
medications or management plan.
Red Zone:
<50 % of your usual or "normal" peak flow
rate signals a Medical Alert. Severe
airway narrowing may be occurring.
▪ Take your rescue medications
immediately
▪ Contact HCP immediately and
follow the plan they have given
you for red zone readings.
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Obstructive lung diseases:
Chronic Obstructive Pulmonary Disease (COPD)
Emphysema
Chronic bronchitis
Causes
▪ Smoking (active or
passive)
▪ Chemical exposure (CO,
fuel, coal)
▪ Air pollution
▪ Genetics (alpha 1
antitrypsin deficiency
Diagnosis
Pathological: Permanent
enlargement and damage
to air spaces. Hyperinflated
lungs with flattened
diaphragm (X-ray)
Clinical: Chronic productive
cough that lasts for ≥ 3
months out of the year
(usually winter months) and
occurs in 2 consecutive
years.
Mechanism
Damages the alveoli. These
air sacs lose their elasticity,
swell and some even burst.
Damages the airways.
Typically produces cough
d/t to its effects on the
mucus producing cells in the
linings of the airways.
Classic
appearance
▪ Pink puffers (no cyanosis
and does pursed lip
breathing)
▪ Barrel chest (air trapping)
Lung sounds
Usually quiet
▪ Smoking (active or
passive)
▪ Chemical exposure (CO,
fuel, coal)
▪ Air pollution
Blue bloaters (blue and
obese)
Rhonchi and wheezing
Chronic obstructive pulmonary disease (COPD):
Generally refers to 2 conditions, emphysema and chronic bronchitis. A
combination of the 2 is common. It is the 3rd leading cause of death in the US. It
occurs commonly in the age 70s. COPD is categorized by slowly progressive,
persistent airflow obstruction that is closely associated with chronic airway
inflammation.
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Emphysema
Typically called PINK PUFFERS
because the normal
compensatory mechanism of
the patient to support
breathing is to expire air in a
longer period by “pursed lip”.
Prolonged expiration helps
expire “trapped air”
Air-trapping is hallmark of
airway diseases which causes
build-up of CO2
Barrel Chest: d/t air trapping
Normal chest A/P diameter:
2:1 (Posterior is half the dm of
anterior). Emphysema 1:1
(same dm). Barrel chest, and
assumption of a sitting position
leaning over the nightstand
are common in patients with
chronic emphysema.
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Chronic Bronchitis
Typically called BLUE BLOATERS
because patients tend to be
obese and cyanotic. The
chronic complication is
pulmonary HTN d/t reactive
vasoconstriction from
hypoxemia leading to right
sided CHF (fluid retention).
Other complication:
Polycythemia (elevated RBC)
d/t chronic hypoxemia
(compensatory)
Chronic bronchitis vs. Acute bronchitis
Chronic Bronchitis: Chronic productive cough that lasts for ≥ 3 months out of
the year (usually winter months) and occurs in 2 consecutive years.
Acute Bronchitis: AKA “chest cold”, is short-term bronchitis. 90% of cases are
caused by viral infection, some cases are by air pollution or bacteria.
Recurrence lead to chronic bronchitis
COPD: Management
▪ Reduce risk factors, prevent & treat
acute exacerbations, manage
associated illnesses.
▪ SMOKING CESSATION
▪ Prevent infection: Influenza,
pneumococcal vaccines
▪ Bronchodilators: SABA, LABA
▪ Systemic corticosteroids:
Methylprednisolone
▪ Antibiotics: Macrolides (“mycins”)
▪ Mucolytics: Acetylcysteine
▪ Oxygen therapy: Noninvasive (BIPAP,
CPAP)
▪ Pulmonary rehabilitation: Exercise,
pursed lip breathing, “huff cough”
▪ Comfort: Morphine (improves SOB)
Remember: Contraindication
Codeine is a narcotic
analgesic used for acute pain
or as a cough suppressant.
Depressing the cough reflex
can cause an accumulation of
secretions in COPD, leading to
respiratory difficulty.
Remember: Theophylline
Generally cause more harm
than benefit and thus are
usually not recommended. But
can be used as second line of
treatment. Theophylline has
narrow therapeutic index
causing seizures and SVT.
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Remember: Use of Incentive
spirometry (IS) vs “huff” cough
In COPD, the pathophysiology
involves structural changes and
permanent airflow limitations,
“AIR TRAPPING” The client
needs help to expel the air, not
get more air into the lungs. IS is
not generally used for COPD.
The low-pressure "huff" cough,
which uses a series of minicoughs, is more effective in
mobilizing and expectorating
secretions in clients with COPD.
Ladder of
management:
COPD
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Obstructive lung diseases:
Cystic Fibrosis (CF)/Mucoviscidosis
Cystic Fibrosis (CF):
Autosomal recessive disorder that results in a mutation of a gene that
impairs chloride transport and sodium absorption, resulting in thickened
secretions (dehydrated secretions) that blocks major ducts in the body.
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Salty Skin: Diagnosed through sweat
chloride test (SC) in the skin. > 60
mEq/L is CF. (Remember SC
“senior citizen” is 60)
Persistent Cough: d/t recurrent sinus &
pulmonary infections-the
thickened mucus inhibits normal
ciliary action and cough
clearance. The resulting airway
obstruction can lead to frequent
infections and eventual
bronchiectasis. Respiratory failure
is the leading cause of mortality.
Bronchiectasis – recurrent infection
related to CF characterized by
thick secretions “layered sputum”.
Most commonly associated with
pseudomonas infection.
Normal:
moist mucus
with healthy cilia
CF: Thick dry mucus
Bronchiectasis:
layered sputum
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Foul smelling fatty (steatorrhea): d/t
pancreatic insufficiency-mucus plugs in the
pancreas obstruct the release of
pancreatic enzymes, leading to
malabsorption of nutrients (CHO, protein,
fats) and fat-soluble vitamins (A,D,E, K).
Bowel obstruction (meconium ileus): Often
the first sign of CF in NB (inability to pass
stool in 24 hrs.) d/t tenacious mucus
preventing passage in the colon.
Failure to thrive (FTT): d/t malabsorption and
an increased metabolic rate associated
with frequent infection, children with CF
have difficulty maintaining adequate
weight & growth
Infertility: -d/t conngenital absence of vas
deferens in male clients, resulting in low
sperm levels and infertility. Female clients
have thick cervical secretions that can
obstruct sperm entry.
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Management:
▪ Antibiotics: Aminoglycoside
(tobramycin)
▪ Pancreatic enzyme supp.
▪ Diet: High in calories, fat, and
protein.
▪ Chest physiotherapy
▪ Genetic testing/counseling
Remember: Pancreatic enzyme
Are supplements used to aid
the absorption of nutrients in a
child with CF. They are taken
with or just before every meal
(not as needed); should be
swallowed whole or sprinkled on
an acidic food; and should not
be crushed or chewed. They
should not be taken with milk.
Remember:
When addressing the
multiple needs of a client
with cystic fibrosis, airway is
the priority.
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Obstructive lung diseases:
Obstructive sleep apnea (OSA)
Obstructive sleep apnea (OSA): Characterized by partial or complete airway
obstruction during sleep that occurs from relaxation of the pharyngeal
muscles. The result is repeated episodes of apnea (≥10 seconds) and
hypopnea (≤50% normal ventilation), which cause hypoxemia and
hypercarbia.
S/S:
▪ loud snoring
▪ witnessed apnea episodes
(waking with gasping or a
choking sensation)
▪ morning headaches irritability
▪ excessive sleepiness
Management:
▪ CPAP/BIPAP at night to keep
the structures of the pharynx
and tongue from collapsing
backward
▪ Limiting alcohol intake at
bedtime as it can cause
muscles of the oral airway to
relax and lead to airway
obstruction
▪ Lifestyle changes: Weight loss
because obesity contributes to
the development of OSA, and
exercise can reduce snoring.
Smoking cessation
▪ Avoiding sedatives(eg,
benzodiazepines,
antidepressants, antihistamines,
opiates) as they may
exacerbate OSA and worsen
daytime sleepiness
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Restrictive lung diseases: Pleural effusion
Pleural Effusion:
Abnormal collection of fluid
(>15-20 mL) in the pleural
space between the
parietal and visceral pleura
that prevents the lung from
expanding fully. This results
in decreased lung volume,
atelectasis, and ineffective
gas exchange.
Common s/s:
▪ Pain (pleurisy)
▪ SOB on exertion
▪ non-productive cough
▪ diminished breath sounds
▪ dullness to percussion
▪ decreased tactile fremitus
▪ trachea (mediastinum)
deviation
Common causes:
▪ Infection - Pneumonia
▪ Trauma
▪ Malignancy
Management:
▪ Diuretics
▪ Chest tube thoracotomy
▪ Thoracentesis
Mechanism: Fluid or air outside the lung interrupts the transmission of sound,
resulting in decreased fremitus in pleural effusion and pneumothorax. Breath
sounds are diminished or absent over a pleural effusion or pneumothorax.
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A thoracentesis involves
the insertion of a largebore needle through an
intercostal space to
remove excess fluid.
Thoracentesis
Complications:
Iatrogenic pneumothorax,
hemothorax, pulmonary
edema, and infection.
If any abnormalities are
noted, a post-procedure
chest x-ray is obtained.
Indications:
▪ Diagnostic: analysis of
fluid including cytology,
and culture to diagnose
infection, malignancy,
heart failure
▪ Therapeutic: removal of
excess fluid (>1 L)
improves dyspnea and
client comfort
Pulmonary edema
Involved mechanisms
Pulmonary edema
▪ Oncotic pressure
▪ Hydrostatic pressure
▪ Capillary permeability
Cardiogenic
Non-cardiogenic
AKA: ARDS
Acute
Respiratory
Distress
Syndrome
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Capillary permeability:
Capacity of a blood
vessel wall to allow for
the flow of small
molecules (drugs,
nutrients, water, ion,
leukocytes in and out of
the vessel. In an event of
an inflammation, blood
vessels become leaky.
PUSHING PRESSURE
PULLING PRESSURE
Capillary hydrostatic
pressure:
PUSHING force that is
exerted by a fluid against
the capillary wall. It helps
in the movement of fluid
between capillaries and
the interstitial fluid.
Oncotic pressure:
(AKA colloidal osmotic
pressure)
A form of osmotic pressure
exerted by albumin, in a
blood vessel's plasma
(blood/liquid) that PULL
water into the circulatory
system.
Hydrostatic pressure exerts more pushing force in arterial end at 35mm. Osmotic
pressure at 25mm (net pressure 10mm) on the left side. Contrary to venous end (right
side), osmotic pressure exerts more pulling force with constant net pressure at 10mm.
The movement of fluids are controlled within the capillaries by this pressure gradients
necessary to nourish tissues. In an event of conditions eg. hypoalbuminemia
(albumin-maintaining gradient to oncotic pressure), pressure changes in the
capillaries. The capillaries become leaky and promotes movement of fluid to
interstitium (edema). In addition, arterial HTN pushes more fluid to interstitium causing
the same effect.
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Cardiogenic Type
Causes:
▪ Left sided CHF: promotes
backflow of blood back to
the lungs
▪ Hypertension
▪ Valvular disease
▪ AMI
▪ Cardiomyopathy
S/S:
▪ Acute-onset DOB
▪ Tachypnea
▪ Pink, frothy sputum
▪ Diffused crackles
▪ Anxiety, restlessness
Non-Cardiogenic/ARDS
Causes:
▪ Sepsis: most commonly
from pneumonia
▪ Acute pancreatitis
▪ Aspiration, near drowning
▪ Chest injuries
▪ Nephrotic syndrome
(Hypoalbuminemia)
S/S:
Refractory hypoxemia:
Hallmark of acute ARDS, a
progressive form of acute
respiratory failure that has
a high mortality rate.
ARDS: Massive inflammatory
response that causes the lung
tissue to release inflammatory
mediators (leukotrienes,
proteases) that cause damage
to the alveolar-capillary (A-C)
membrane. As a result of the
damage, the A-C membrane
becomes more permeable,
and intravascular fluid then
leaks into the alveolar space,
resulting in a noncardiogenic
pulmonary edema.
Management: Treat the cause and relieve symptoms
The priority of care is to improve oxygenation (Mechanical ventilation,
O2 supplementation) or by reducing pulmonary pressure and
congestion. IV Diuretics (e.g. furosemide) are prescribed to remove
excess fluids. Antibiotics for sepsis are given.
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Acute respiratory failure (ARF)
ARF
Type I
Type II
Oxygenation
Example:
▪ ARDS
▪ Pulmonary
edema
▪ Pulmonary
emboli
▪ Pneumonia
▪ Shock
Ventilatory
Example:
▪ COPD
▪ MG, GBS, ALS
▪ flail chest
▪ OSA
▪ Drug overdose
Impaired O2
transfer
Impaired CO2
elimination
Impaired gas
exchange (ABG)
Respiratory failure:
Occurs when oxygenation is inadequate (hypoxemic failure)
and/or when ventilation is inadequate (hypercapnic failure).
Arterial blood gas (ABG) analysis provides objective data about
the efficiency of gas exchange in the lungs.
Management:
▪ Treat underlying cause
▪ Mechanical ventilation
▪ Antidotes (naloxone, flumazenil)
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Other diseases:
Superior vena cava syndrome:
An obstruction of blood flow
through the superior vena cava
(SVC). SVC is a medical
emergency and most often
manifests in patients with a
malignant disease process
within the thorax compressing
SVC. Blockage of blood flow to
the venous system of the head
resulting in facial edema is a
classic sign of SVC syndrome.
Remember:
Carbon monoxide (CO) has a
much stronger bond to Hgb
than oxygen does.
Consequently, CO displaces
oxygen from Hgb. The priority is
to administer 100% oxygen
using a nonrebreather mask to
treat or reverse hypoxia and
help eliminate CO.
Levels:
10 to 20% (Headache)
> 20 % (Generalized weakness)
> 30% (Chest Pain)
> 40% (Seizure, unconsciousness)
> 60% (Coma - Death)
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Other diseases: Respiratory infections in children
Condition
Classic signs
Nasopharyngitis
“common colds”
Nasal congestion with
discharges, cough, sore
throat, sneezing
Rhinovirus, corona virus,
influenza virus
Epiglottitis
(bacterial croup)
4 Ds: dysphonia (muffled
voice), dysphagia (difficulty
swallowing), drooling, and
distressed respiration.
Hemophilus influenzae
Laryngotracheitis
(viral croup)
URTI symptoms, hoarseness,
barking cough, stridor,
respiratory distress
Parainfluenza virus
Bronchiolitis
(viral croup)
URTI symptoms, wheezing,
cough, respiratory distress
Respiratory syncytial virus
Tripod position and epiglottitis
Causative agent
Remember: Epiglottitis
An inflammation by bacteria of
the tissues surrounding the
epiglottis, a long, narrow
structure that closes off the glottis
during swallowing. Edema can
develop rapidly (as quickly as a
few minutes) and obstruct the
airway by occluding the trachea.
There has been a 10-fold
decrease in its incidence due to
the widespread use of the Hib (H.
influenzae type B) vaccine.
The classic symptoms:
▪ High-grade fever, severe sore
throat, and the 4 Ds-dysphonia
(muffled voice), dysphagia
(difficulty swallowing), drooling,
and distressed respiration.
▪ Tripod position opens the
airway. The child should be
allowed to assume a position of
comfort in response to PROTECT
AIRWAY.
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8
Neurology
Anatomy and Physiology
CNS: Brain and Spinal cord
Remember:
Knowing the anatomical site
and its function is vital in ruling
out s/s related to certain
disorders.
Decussation: crossing of the
corticospinal tract
Describes the point where the
nerves cross from one side of
the brain to the other. If the
tract is interrupted in the
cerebrum or at any level
above the pyramids of the
medulla, the manifestation is
contralateral side of the body
(e.g. hemiplegia).
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Broca’s vs Wernicke’s
Illustration: language processing
If a person is asking your name.
1. Wernicke’s area RECEIVES and
UNDERSTANDS the information
thru auditory function.
(Receptive/Sensory)
2. Broca’s area generates the
language so that the person can
SPEAK fluently.
(Expressive/Motor)
3. Motor cortex initiates the
complex muscle MOVEMENTS
necessary for speech.
4. Verbal output
Aphasia: language deficit
▪ Receptive/sensory aphasia
Unable to receive or
understand the information.
Lesion to Wernicke’s
▪ Expressive/motor aphasia
Unable to speak fluently. Lesion
to Broca’s.
▪ Global/mixed aphasia
Lesion to both Wernicke’s and
Broca’s
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Meninges
Blood-brain barrier
(BBB)
Remember: Brain tissues are unique from the rest.
It is made up of glial type of cells (glial-“glue”)
that protects the integrity of neurons from
having harmful substances. BBB is one protective
mechanism which has HIGHLY SELECTIVE
semipermeable border that separates the
circulating blood from the brain and
extracellular fluid in the CNS.
Significance: The brain tissues are very sensitive to any toxic substances. If a there is a
sudden change in mental status in a certain condition, there must be a break in the BBB.
Remember, brain tissues are very dependent to glucose and O2 to function adequately. It
is a major challenge in terms of giving medications to treat most brain disorders due to BBBs
neuroprotective role. In addition, BBB functions to hinder the delivery of many potentially
important diagnostic and therapeutic agents to the brain. Therapeutic molecules and
antibodies that might otherwise be effective in diagnosis and therapy do not cross the BBB
in adequate amounts such as treating multiple sclerosis.
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Cranial nerves
Bell's palsy: is peripheral, unilateral
facial paralysis characterized by
inflammation of the facial nerve
(CN VII) in the absence of a stroke
or other causative agent/disease.
Paralysis of the motor fibers
innervating the facial muscles
results in flaccidity on the affected
side.
Trigeminal neuralgia (Tic
douloureux): is sudden, sharp pain
along the distribution of the
trigeminal nerve (CN VII). The
symptoms are usually unilateral
and primarily in the maxillary and
mandibular branches. Clients
may experience chronic pain with
periods of less severe pain, or
"cluster attacks" of pain between
long periods without pain.
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Bell’s palsy vs Trigeminal neuralgia
Bell’s palsy:
S/S (sensory and motor function)
▪ Inability to completely close the
eye on the affected side
▪ Flattening of the nasolabial fold
on the side of the paralysis
▪ Inability to smile or frown
symmetrically.
▪ Decreased tearing with
extreme dryness/excessive
tearing due to lower eyelid
muscle weakness
▪ loss of taste on the anterior 2/3
of the tongue.
Eye care: Use glasses during the
day; wear a patch (or tape the
eyelids) at night to protect the
exposed eye. Use artificial tears
during the day as needed to
prevent excess drying of the
cornea
Oral care: Chew on the
unaffected side to prevent food
trapping; a soft diet is
recommended. Maintain good
oral hygiene after every meal to
prevent problems from
accumulated residual food (eg,
parotitis, dental caries)
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Trigeminal neuralgia
S/S (sensory and motor function):
▪ Severe, intense, burning, or
electric shock-like pain
depending on the zones
affected
Triggers:
▪ Washing the face
▪ Chewing food
▪ Brushing teeth
▪ Yawning
▪ Talking
DOC: Carbamazepine (seizure
medication but is highly
effective for neuropathic pain).
Report fever or sore throat
(agranulocytosis)
Care: Use a small, soft-bristled
toothbrush or a warm mouth
wash Use lukewarm water;
avoid beverages or food that
are too hot or cold. Room
should be kept at an even and
moderate temperature Avoid
rubbing or facial massage. Use
cotton pads to wash the face if
necessary. High calorie soft
diet; avoid foods that are
difficult to chew. Chew on the
unaffected side of the mouth.
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PNS: Autonomic nervous system
Sympathetic NS (SNS) vs. Parasympathetic NS (PNS)
ANS
SNS
PNS
Adrenergic/dopaminergic
fiber: from the prefix itself
“adreno” “dopamine”, it is
where adrenalines and
dopamine function is involved.
Sympathetic fibers are
structures that transmit
information to a target organ
Cholinergic fiber: from the
prefix itself “choline” , it is
where acetylcholine is
involved. Parasympathetic
fibers are structures that
transmit information to a target
organ
Catecholamines; Adrenalines
(epi, norepinephrine)
Dopamine:
Are group of excitatory
chemicals that bind to specific
receptor sites in a target
organ.
Acetylcholine (ACH):
A neurotransmitter (chemical
message) released by nerve
cells to send signals to target
organs by binding to specific
receptors sites.
Adrenergic receptors:
Are sites where adrenalines
bind to produce a certain
effect or reaction.
Alpha receptors
Beta receptors
Cholinergic receptor:
Are sites where ACH bind to
produce a certain effect or
reaction.
Nicotinic receptors
Muscarinic receptors
Example:
Alpha 1 & 2- smooth muscle
contraction, mydriasis (pupil
dilation)
Beta 1 – heart muscle
contraction (inotropic);
increased HR (chronotropic);
Increased conductivity
(dromotropic)
Beta 2 – smooth muscle
relaxation, bronchodilation in
the lungs
Example:
Nicotinic receptors (N) –
excitation on skeletal muscle
by opening Na+ channel and
Na+ ions flow into the cell
membrane (contraction)
Muscarinic receptors (M) smooth muscle contraction
(increased peristalsis)
bronchoconstriction in the
lungs, bradycardia, miosis
(pupil constriction)
FIGHT or FLIGHT
(generally increased activity
in response
to stress)
REST and REPAIR/DIGEST
(generally decreased
activity in response
to stress)
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Organ system
Eyes
Salivary gland
Heart
Blood vessels
SNS
Dilation
(mydriasis)
Decrease
production
PNS
Significance
Constriction
(Miosis)
Tear production
(lacrimation)
Beta-adrenergic antagonists
(miotic): This helps reducing the
production of aqueous humor in
glaucoma, e.g. TimOLOL
Increase
production
(salivation)
Pyridostigmine (Mestinon): DOC
for myasthenia crisis. An
anticholinesterase medication to
increase ACH production.
Common s/e in increase
salivation. Atropine is the
opposite, given to patient with
cholinergic crisis (inhibit PNS
effect/anticholinergic)
▪ Increase force
(Inotropic)
▪ Decrease force
(-) Inotropic
▪ Increase HR
(chronotropic)
▪ Decrease HR
(-) chronotropic
▪ Increase
conductivity
(dromotropic)
▪ Decrease
conductivity
(-) dromotropic
▪ Peripheral
vasoconstriction
(Increase BP)
▪ Coronary
vasodilation
▪ Vasodilation to
vessels of
skeletal muscles
(muscle
contraction)
▪ Vasodilation to
blood vessel in GI
tract: Increase
peristalsis
(digestion)
▪ Vasodilation to
blood vessel in
penis, clitoris
(erection and
arousal)
Anticholinergic: Atropine DOC for
symptomatic bradycardia to
inhibit PNS effect.
Adrenergic agonist: Epinephrine,
Norepinephrine, dopamine to
increase SNS activity in cardiac
arrest. Increase CO, HR
Beta-adrenergic blocker:
Decreases cardiac workload,
HR, BP, conductivity
Selective: antagonizes only
beta 1(does not cause
bronchoconstriction) e.g.
metoprOLOL
Non-selective: antagonizes both
beta 1 & 2 (causes
bronchoconstriction) e.g.
propranOLOL:
contraindicated in asthma
Adrenergic agonist: Epinephrine,
Norepinephrine, dopamine to
increase SNS activity in cardiac
arrest. Increase CO, HR
Beta-adrenergic blocker:
Decreases cardiac workload,
HR, BP, conductivity
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Respiratory
GI tract
Genitourinary
Bronchodilation
(improve O2)
Bronchoconstriction
(decrease O2)
Anticholinergic: Ipratropium
(Atrovent) is a short-acting
anticholinergic used as a rescue
medication for COPD and
asthma
Short-acting beta agonist (SABA):
Albuterol (Ventolin),
Adrenergic agonist: Epinephrine,
Norepinephrine, used to relax
bronchial muscles
(bronchodilation)
▪ Decrease
peristalsis, HCL
acid
(constipation)
▪ Decrease
pancreatic
secretions
(digestive
enzymes)
▪ Decrease bile
secretions
▪ Glucose
production
(hyperglycemia)
▪ Increase
peristalsis, HCL
acid (diarrhea)
▪ Increase
pancreatic
secretions
(digestive
enzymes)
▪ Increase bile
secretions
(digestion)
Dopamine antagonist/Antiemetic:
Metoclopramide (Reglan): A
serious adverse effect r/t long
term use of metoclopramide is
tardive dyskinesia (TD) which can
cause unusual uncontrollable
movements.
▪ Bladder
relaxation
(urinary
retention)
▪ Stimulates
orgasm
(ejaculation)
▪ Bladder
contraction
(urination)
▪ Vasodilation of
vessels causes
erection and
clitoris arousal
Anticholinergic: antispasmodic
Oxybutynin (Ditropan): used for
bladder spasms, an expected
complication of the TURP
procedure. They also decrease
urinary urgency and frequency.
The most common
anticholinergic s/e are (e.g. dry
mouth, constipation)
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PNS: Somatic nervous system
Muscle contraction:
Calcium triggers release of ACH
(action-potential). ACH binds to
nicotinic receptors (cholinergic
receptors) in the muscle cells to
cause contraction.
Equilibrium/balance:
Acetylcholinesterase is an enzyme
that degrades (breaking down)
ACH to promote balance.
Remember: In myasthenia gravis,
ACH is unable to bind with its
receptors d/t auto immune
antibodies (autoimmunity) present.
Increase ACH causes more
acetylcholinesterase which
promotes more degradation to
ACH.
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Injury related disorders:
Traumatic brain injury (TBI), Spinal cord injury (SCI)
Traumatic
brain injury (TBI)
Extra-axial
Intra-axial
Diffuse axonal
injury
Meninges
Brain tissues
Brain tissues
Epidural
Arterial bleed
Subdural
Venous bleed
Subarachnoid
Arterial bleed
Intracerebral
Microhemorrhage
Intracerebral
Shearing of
axons &
dendrites (white
matter tract)
Remember: Lucid interval
The client may regain
consciousness quickly and
feels well for some time after
the injury. This transient
period of well being is called
a “lucid interval”,
particularly in epidural
hematoma. It is followed by
a quick decline in mental
function that can progress
into coma and death
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Remember: Basilar fracture
An NGT must not be inserted
when a basilar skull fracture is
suspected. CSF leakage is an
indication of this and can be
evidenced by a positive
halo/ring test of the blood-tinged
nasal drainage (coagulated
blood surrounded by CSF).
Other s/s:
Otorrhea, racoon’s eye, postauricular ecchymosis (battle’s
sign)
Remember: Clients in a
coma (GCS score≤7) or
with aphasia may need
an advance directive to
make treatment
decisions because they
cannot directly express
their wishes.
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Autonomic dysreflexia vs spinal shock vs neurogenic shock
Autonomic
dysreflexia
Spinal shock
Neurogenic shock
Mechanism
Hyperreflexia:
Overreaction of
SNS where PNS
cannot overcome.
CNS is unable to
control resulting to
incoordination
PNS: above level of
injury (e.g.
bradycardia)
SNS: below level of
injury (e.g. HTN)
Hypo/Hyperreflexia
(Variable):
Peripheral neurons
become
unresponsive to
stimuli. AKA “False
shock” because it
does not lose its
sympathetic tone or
to cause circulatory
collapse.
Loss of vasomotor
tone (blood vessel
tone): Loses its ability
to activate the SNS
and cannot trigger
compensatory
mechanisms. Only
parasympathetic
tone remains. “True
shock” because it
causes circulatory
collapse.
Level of injury
T6 or above
Variable
T6 or above
Trigger
Bladder distention
bowel impaction
pressure ulcer
Injury itself
Injury itself
Time
Within 24 hours after
injury
Within 24 hours after
injury
Within 24 hours after
injury
Urgency
Emergent
Urgent/self-limiting
Emergent
BP
Hypertension
(≥ SBP 300 mmhg)
Hyper/hypotension
Hypotension
HR
Bradycardia
Tachy/bradycardia
Bradycardia
RR
Tachypnea
Tachypnea
Tachypnea
Temperature
Hyperthermia
Hypothermia
Hypothermia
Other S/S
▪
▪
▪
▪
▪
▪
▪ Loss of reflexes
below level of
injury
▪ Paralysis
▪ Loss of sensation
▪ Bladder/bowel
problems
S/S Circulatory
collapse:
▪ Decreased LOC
▪ Cold clammy skin
▪ Diaphoresis
▪ Low urine output
▪ Generalized
weakness
Flushing
Restlessness
Headache (initial)
Diaphoresis
Piloerection
“Feeling of doom”
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Goal of
treatment
NCLEX-RN study guide
▪ Prevent trigger
Treat the spinal cord
▪ Treat HTN (may
injury (SCI)
lead to AMI, CVA)
▪ Prevent organ
failure (inotropes,
IV fluids,
▪ Respiratory support
Summary:
Spinal shock is the temporary reduction or loss of reflexes following a spinal cord
injury (SCI). Keep in mind that spinal shock is to SCI like fever are to infections. It
means, spinal shock is merely a symptom of an underlying problem, not a disease
itself. Furthermore, If the injury is T6 or above it may lead to a severe form called
Neurogenic shock or Autonomic dysreflexia. To distinguish both of these severe
forms, Neurogenic shock involves circulatory collapse and massive vasodilation
while Autonomic dysreflexia involves massive dysfunction to ANS.
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Common neurologic disorders:
Cerebrovascular accident (CVA/Stroke)
CVA
Etiology: Ischemic
HTN, Hyperlipidemia
Heart disease
(CAD, Atrial fibrillation)
Diabetes
Sickle cell disease (SCD)
(common cause of CVA in
children)
Etiology: Hemorrhagic
HTN
Ruptured aneurysm
Arteriovenous malformation
(AVM)/Ruptured aneurysm
(Subarachnoid hemorrhages)
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Ischemic CVA
Ischemic penumbra:
A zone of reversible
ischemia around core of
irreversible infarction.
Salvageable in first few
hours after onset of
ischemic CVA.
Window period : Saving
the penumbra
▪ Give thrombolytics
(tissue plasminogen
activator TPA) as long
as within the time frame
or window period
IV: <3-4.5 hours
Intraarterial: 6 hours
Contraindications to
thrombolytics:
▪ Prior intracranial
hemorrhage
▪ A/V malformation (AVM)
aneurysms
▪ Ischemic CVA within 3
mos.
▪ Suspected aortic
dissection
▪ Active bleeding
▪ Significant head trauma
within 3 mos.
Remember: Permissive hypertension
Maintain SBP ≥170 mmHg to ensure adequate
cerebral perfusion. Usually autocorrects within
24-48 hours and does not require treatment
unless the HTN is extreme (SBP >220 mm Hg or
DBP >120 mm Hg) or contraindicated d/t the
presence of another illness requiring strict
blood pressure control (e.g., active ischemic
coronary disease, heart failure, aortic
dissection)
Remember: Time is brain
in ischemic CVA
“Save the PENUMBRA”
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Hemorrhagic
CVA
Increase ICP in hemorrhagic
CVA:
An increase in intracranial
pressure is considered to be a
serious and life-threatening
medical emergency. Primarily
caused by an intracranial or
subarachnoid hemorrhage
(ruptured aneurysm)
Normal ICP: 0 - 10 mmHg
Remember: Monro-Kellie
hypothesis
Because of limited space in
the skull, an increase in any of
the component, brain tissue,
blood & CSF will cause a
change in the volume of the
others. With disease or injury,
ICP may increase. Increase
ICP eventually causes
decreases cerebral perfusion
causes ischemia and cell
death, and further cerebral
edema.
Early signs/symptoms:
▪ Decrease LOC
(restlessness, agitation,
irritability, confusion)
▪ Headache
▪ Projectile vomiting without
nausea
▪ Slowed speech
▪ Pupillary changes (sluggish
reaction)
▪ Temperature changes
Late signs/symptoms: Deteriorating VS
Cushing’s triad
▪ Irregular respiration
▪ Bradycardia
▪ Widened pulse pressure (systolic
HTN) e.g.: 200/80 mmhg
Rationale: The heart increases its force
during contractions in response to
decreased O2 in the brain. In this
response, longer relaxation is needed
resulting to low DBP.
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Manage ICP:
Other management:
▪ Pharmacologic: Mannitol and
▪ Frequent neuro assessments
corticosteroids (decrease inflammation)
▪ Keep the client NPO
▪ Reduce stimulation (structured care)
▪ Seizure precautions
▪ Maintain a quiet and dimly lit environment
▪ Prevent further bleeding
▪ Limit visitors
▪ (eg. Anticoagulants,
▪ Administer stool softeners
thrombolytics)
▪ Reduce exertion
▪ Ensure adequate O2
▪ Maintain strict bed rest
▪ Assist with ADLs
▪ Maintain head in midline position
Mannitol:
▪ (improve jugular venous return to the
Mannitol is an osmotic diuretic
heart)
that can help reduce cerebral
▪ Hyperventilate and preoxygenate the
edema and ICP through use of
client for brief periods such as before
a hyperosmolar solution to
suctioning to help reduce ICP
draw water from the brain
▪ Manage pain well without sedating the
tissues and extracellular fluid,
client too much
▪ Treat fever aggressively (cool sponges) but allowing excretion in a form of
diuresis.
avoid having the client shiver or shake
Neuromuscular disorders:
Myasthenia gravis (MG)
Muscle contraction:
Calcium triggers release of ACH
(action-potential). ACH binds to
nicotinic receptors (cholinergic
receptors) in the muscle cells to
cause contraction.
Equilibrium/balance:
Acetylcholinesterase is an enzyme
that degrades (breaking down) ACH
to promote balance.
Remember: In myasthenia gravis,
ACH is unable to bind with its
receptors d/t auto immune
antibodies (autoimmunity) present.
Increase ACH causes more
acetylcholinesterase which
promotes more degradation to ACH.
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Myasthenia gravis:
An autoimmune disease involving a decreased number
of acetylcholine (ACH) receptors at the neuromuscular
junction. As a result, there is fluctuating weakness of
skeletal muscles, most often presented as:
▪ Ptosis/diplopia
▪ Bulbar signs (difficulty speaking or swallowing)
▪ Difficulty breathing.
Muscles are stronger in the morning and become
weaker with the day's activity as the supply of available
acetylcholine is depleted.
Remember: Airway and
breathing are the priority in
neuromuscular disorders. It is
also important to know the
anatomy and physiology of
neurologic system to
determine the symptoms
related to the condition.
(e.g. GBS affects Autonomic
NS, MG affects Somatic NS)
Remember: Bulbar muscles
Are muscles involving
speaking and swallowing.
These are the main problems
in MG and ALS occurring
with the mouth, tongue and
swallowing muscles. In a
descending manner, it
affects the respiratory
muscles.
Remember:
Dysphagia (difficulty
swallowing) and Dysarthria
(difficulty of speaking) are
signs of impending
respiratory failure
DOC: Pyridostigmine
(Mestinon) given before
meals so that the client's
ability to swallow is strongest
during the meal.
Tensilon test: Edrophonium
HCL
Done by injecting the drug
Tensilon into a vein and
observing for rapid
improvement of strength,
usually of eye muscles.
Improvement in strength of
speech may also be
considered a positive test.
Primarily because Tensilon is
an anticholinesterase.
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Myasthenic crisis
Cause/mechanism
Signs/symptoms
Drug of choice
Cholinergic crisis
▪ Undermedication
▪ Disease exacerbation
Disease process:
↑ acetylcholinesterase
↓ acetylcholine
▪ Overmedication
▪ ↓ acetylcholinesterase
▪ ↑ acetylcholine
▪ Severe muscle
weakness
▪ Dysarthria
▪ Dysphagia
▪ Tachycardia
Respiratory failure
▪
▪
▪
▪
▪
▪
▪
Pyridostigmine (Mestinon):
anticholinesterase
Intubation
Atropine sulfate:
anticholinergic
Intubation
Muscle weakness
Bradycardia
Hypotension
Constricted pupils
Sweating
Abdominal pain
Respiratory failure
Amyotrophic lateral sclerosis (ALS)/ Lou Gehrig disease
Amyotrophic lateral sclerosis
(ALS)/ Lou Gehrig disease:
Is a debilitating, progressive
neurodegenerative disease with
no cure and death usually occurs
within 5 years of diagnosis..
Characterized by the progressive
loss of motor neurons in the
brainstem and SC. Clients have
spasticity, muscle weakness, and
atrophy. Neurons involved in
swallowing and respiratory
function are eventually impaired,
leading to aspiration, respiratory
failure, and death. Care of
clients with ALS focuses on
maintaining respiratory function,
adequate nutrition, and quality of
life.
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Symptoms :
▪ Fatigue
▪ Progressive muscle weakness
▪ Twitching and muscle spasms
▪ Bulbar signs
▪ (Dysphagia, dysarthria)
Respiratory failure
DOC: Riluzole (Rilutek) slows the
progression of ALS by slowing
glutamate production. The only
medication approved for ALS
treatment. Thought to slow neuron
degeneration by decreasing the
production and activity of the
neurotransmitter glutamate in the
brain and SC.
Management:
▪ Respiratory support with noninvasive
positive pressure BiPAP or CPAP or
invasive mechanical ventilation (eg. via
tracheostomy)
▪ Feeding tube for enteral nutrition
▪ Medications to decrease symptoms
(eg. spasms, uncontrolled secretions,
dyspnea)
▪ Mobility assistive devices (eg. walker,
wheelchair)
▪ Communication assistive devices (eg.
alphabet boards, specialized
computers)
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Multiple Sclerosis (MS)
Symptoms:
▪ Diplopia, Optic neuritis, Muscle
weakness, Spasticity, Paresthesia,
Incoordination, Loss of balance, Fatigue,
Impaired mobility
▪ Lhermitte’s sign
▪ Respiratory failure
Charcot’s Triad:
▪ Intentional tremors
▪ Nystagmus
▪ Scanning speech (staccato speech)
Management:
▪ Steroids (Immune suppression)
▪ Plasmapheresis
▪ Prevent exacerbation
Multiple sclerosis (MS):
Is a chronic relapsing and remitting
nerve disorder caused by patchy
demyelination of nerve fibers in the
brain and spinal cord causing a
variety of symptoms. MS is thought
by many medical researchers to be
an autoimmune disease. In MS,
attacks are against the fatty myelin
coating that surrounds and
insulates nerve cells (a process
called demyelination), resulting in
lesions. The immune response can
be triggered by infection to Epstein
barr virus.
Remember: MS affects the entire
nervous system, which means the
manifestations is a variety.
Lhermitte’s sign:
Is a physical exam maneuver
that is considered to have a
positive result when a patient
experiences an electric-like
shooting pain that radiates
from the back of the neck
down the back when the
neck is bent forward.
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Guillain-Barre Syndrome (GBS)
Management:
Measurement of forced vital
capacity (FVC) is the gold
standard for assessing
ventilation; a decline in FVC
indicates impending
respiratory arrest requiring
endotracheal intubation.
Others: Plasmapheresis, IV
immunoglobulins
Guillain-Barre Syndrome (GBS):
Is an acute, immune-mediated
polyneuropathy (autoimmune) that is
most often accompanied by
ascending muscle paralysis and
absence of reflexes. Lower-extremity
weakness progresses over hours to
days to involve the thorax, arms, and
cranial nerves (CNs). Neuromuscular
respiratory failure is the most life
threatening complication. In its most
severe form GBS is a medical
emergency. The exact cause is
unknown. But it is often preceded by
an infectious illness such as a
respiratory or stomach infection
(Campylobacter jejuni)
Remember: GBS affects the
peripheral nervous system (PNS),
which distinguishes the condition
from MS, which affects the entire
nervous system. However, both can
cause demyelination.
Symptoms:
▪ Prickling, pins and needles
sensations in your fingers, toes,
ankles or wrists
▪ Weakness, Unsteady gait
▪ Difficulty with eye or facial
movements, Dysarthria,
Dysphagia, Severe pain (cramp
like and may be worse at night)
▪ Impaired bladder/bowel control
▪ Tachycardia
▪ Hypo/hypertension
▪ Respiratory failure
Early signs of impending respiratory
failure include:
▪ Inability to cough
▪ Shallow respirations
▪ Dyspnea and hypoxia
▪ Inability to lift the head or eye
brows
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Myasthenia
Gravis (MG)
Amyotrophic Lateral
Sclerosis (ALS)
Multiple
Sclerosis (MS)
Guillain-Barre
Syndrome (GBS)
Autoimmune
Triggers:
GI infections
(C. jejuni)
Respiratory
Infections
Autoimmune
Thymoma
Genetic
(active T-cells)
Unknown
↑ A-cholinesterase ↑ Glutamate
↓ ACH
Autoimmune
Triggers:
Somatic NS
Voluntary muscles
Somatic NS
Voluntary muscles
Entire nervous
system
▪ Muscle
weakness
▪ Ptosis/diplopia
▪ Bulbar signs:
dysarthria,
dysphagia
▪ Muscle
weakness
▪ Diplopia, Optic
neuritis, Muscle
weakness,
Spasticity,
▪ Muscle
Paresthesia,
weakness with
Incoordination,
atrophy Fatigue
▪ Progressive
Loss of balance,
muscle
Fatigue,
weakness
Impaired
▪ Twitching &
mobility
muscle spasms
▪ Mental deficit
▪ Bulbar signs:
▪ Depression
dysarthria,
Lhermitte’s sign
dysphagia
Respiratory failure
Charcot’s Triad:
▪ Intent. tremors
▪ Nystagmus
▪ Scanning speech
Complication
Respiratory failure
Myasthenic &
Cholinergic crisis
Respiratory failure
Respiratory failure
Respiratory failure
Tests
Tensilon test:
Edrophonium HCL
Electromyography
MRI, CSF studies
Electromyography
Etiology/
Mechanism
NS affected
Signs/symptoms
Epstein Barr
Demyelination
Demyelination
(ascending)
Peripheral NS
(ANS, Somatic NS)
▪ Muscle
weakness
▪ Severe pain
Prickling
sensation
▪ Unsteady gait
▪ Difficulty with
eye or facial
movements
▪ Bulbar signs:
dysarthria,
dysphagia
▪ Impaired
bladder/bowel
control
▪ Tachycardia
▪ Hypo/HTN
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Management
▪ Pyridostigmine
(Mestinon)
▪ O2 Support for
exacerbation
▪ Supportive
management
▪ Riluzole (Rilutek)
▪ Respiratory
support
▪ Supportive
management
▪ Steroids (Immune
▪ Measurement of
suppression)
FVC
▪ Plasmapheresis
▪ Plasmapheresis
(removing
(removing
autoimmune
autoimmune
cells)
cells) IVIG
▪ Prevent
▪ Prevent
exacerbation
infections
▪ Stress mgt
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9
ACLS algorithms:
1. Bradycardia
Remember: H’s and T’s
▪ Hypovolemia
▪ Hypoxia or Hypoxemia
▪ Hydrogen Ion (Acidosis)
▪ Hypo/Hyperkalemia
▪ Hypothermia
▪
▪
▪
▪
▪
Tamponade (Cardiac)
Toxins (overdose)
Tension Pneumothorax
Thrombosis (Pulmonary)
Thrombosis (Coronary)
Transvenous
Pacing
Critical care
Remember: H’s and T’s
The H’s and T’s of ACLS is a
mnemonic used to help recall
the major contributing factors
to pulseless arrest including
PEA, Asystole, Ventricular
Fibrillation, and Ventricular
Tachycardia. Most
commonly associated with
PEA, but they will help direct
your search for underlying
potentially reversible causes
to any of arrhythmias
associated with ACLS.
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2. Tachycardia
Remember:
This algorithm is for HR ≥
150 bpm. This might be
one of the several
tachycardia rhythms:
SVT, Atrial fibrillation,
Atrial flutter, V-tach (with
pulse).
Remember:
The distinction between
regular and irregular
rhythm (SVT vs. Rapid A-fib)
is fundamental since they
are treated differently. For
instance, adenosine (drug
of choice for SVT) cannot
be given to a patient with
A-fib because it causes
further fatal arrhythmias.
Atrial Flutter
SVT
Atrial Fibrillation
V-tach (with pulse)
Torsades da pointes
V-fib
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3. Ventricular tachycardia (pulseless)
Ventricular fibrillation
Remember:
Basic airway
management involves
head tilt, chin lift
technique. On the other
hand, advanced airway
involves invasiveness using
LMA, laryngeal tube, and
ET tube with special
techniques and training.
D
C
Remember: CPR & defibrillation are
highest priority over advanced airway
The value of securing the advanced
airway (LMA, laryngeal tube, and ET
tube), must be balanced against the
need to minimize the interruption in
perfusion in the early steps of
resuscitation.
E
A
ROSC is resumption cardiac
perfusion with significant
respiratory effort after
cardiac arrest. Signs of ROSC
include breathing, coughing,
or movement and a
palpable pulse or a
measurable BP
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Remember: CDEA vs DCEA
CDEA: UNWITNESSED arrest
DCEA: The importance of
early defibrillation is
irrefutable in a WITNESSED
arrest (sudden change in
patients status to pulseless
v-tach and v-fib).
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4. Pulseless electrical activity (PEA)
Asystole
Remember: PEA
PEA occurs when you see a
rhythm on the monitor that
would normally be
associated with a pulse,
however the patient is
pulseless. The rhythm can
be anything, at any heart
rate
Remember: PEA is most
commonly associated
with H’s and T’s
▪ Hypovolemia
▪ Hypoxia or Hypoxemia
▪ Hydrogen Ion (Acidosis)
▪ Hypo/Hyperkalemia
▪ Hypothermia
▪
▪
▪
▪
▪
Tamponade (Cardiac)
Toxins (overdose)
Tension Pneumothorax
Thrombosis (Pulmonary)
Thrombosis (Coronary)
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Sepsis: A leading cause of mortality in critical care
Mild
1. SIRS (at least 2/4 criteria)
T: ≥100.4 F [38 C]) or ≤96.8 F [36 C])
HR: ≥90/min
RR: ≥20/min or alkalosis (PaCO2
≤32 mm Hg
WBC: ≥12,000/mm3 or ≤4,000/mm3
or ≥10% immature neutrophils
(bands cells) normal is 3.5%
2. Sepsis
SIRS + Identified causative agent
(eg. Pneumonia, UTI)
3. Septic shock
SIRS + Sepsis + Hypotension
(SBP ≤ 90 mmhg)
4. MODS
SIRS + Sepsis + Septic shock +
Multi organ system dysfunction
Severe
Sepsis continuum
SIRS: Systemic inflammatory response syndrome
(SIRS) occurs when the body undergoes a
major insult (eg. trauma, infection, burns,
hemorrhage, multiple transfusions). Stimulation
of the immune response leads to activation of
WBCs, release of inflammatory mediators,
increased capillary permeability, and
inflammation of organs.
Sepsis: Sepsis is an exaggerated systemic
inflammatory response associated with a
documented or suspected infection.
Septic shock: Sepsis-induced hypotension
despite fluid resuscitation (30 mL/kg) or 2L bolus
is defined as "septic shock." In addition,
inadequate tissue perfusion (ie. ↑serum lactate)
despite fluid resuscitation and decreased CVP
and pulmonary artery wedge pressure also
indicate the presence of septic shock.
Stages of septic shock:
1: Reversible (aerobic to anaerobic)
2: Compensatory (homeostasis)
sympathetic response
3: Failed compensation
4: Irreversible (beginning organ damage)
MODS: Multi Organ Dysfunction Syndrome is the
failure of 2 or more body organs (e.g. acute
kidney injury, ARDS). MODS occurs in related to
decreased perfusion is the end point of the
sepsis continuum. It is important for the nurse to
recognize manifestations of SIRS to promote
early recognition, prevention, & treatment of
infection and to limit its progression to MODS.
Sepsis continuum
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Central lines:
Central venous catheter CVC vs. Arterial line (A-line)
Central lines
Central venous lines
Common sites:
Subclavian (SC)
Intrajugular (IJ)
Purpose:
▪ Medications
▪ Parenteral nutrition,
▪ Chemotherapy
▪ Plasmapheresis
▪ Dialysis
▪ Blood draws
▪ Need for IV therapy
when peripheral
venous access is
impossible
▪ Blood transfusion
▪ CVP monitoring
Arterial lines
Common sites:
Radial arteries
Femoral arteries
Purpose:
▪ Monitor BP directly
in real-time
▪ Obtain ABG sample
Arterial lines are generally
not used to administer
medication, since many
injectable drugs may lead
to serious tissue damage.
Golden rule (Allen’s Test):
there has to be collateral
circulation to the area
affected by the chosen
artery, so that peripheral
circulation is maintained.
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Nursing care for CVC:
▪ A 10 mL syringe is generally preferred for
administering medications through a
CVC.
▪ CVCs require IV heparin flushes to
maintain patency and prevent clotting.
(Single-dose vials of 2–3 mL of 10
units/mL or 100 units/mL) Remember: A
dose of 1000–10,000 units is given for
cases of VTE.
▪ Prime tubing before insertion to prevent
air embolism
▪ Dressing changes (7 days) using
tegaderm transparent dressing and PRN
▪ Use mask when dressing changes
Preventing air embolism when
discontinuing a CVC:
▪ Instruct the client to lie in a supine
position. This will increase the CVP and
decrease the possibility of air getting
into the vessel
▪ Instruct the client to bear down or
exhale. The client should never inhale
during removal of the line; inhalation will
suck more air into the blood vessel via
negative suction pressure
▪ Apply an air-occlusive dressing (usually
gauze with a Tegaderm dressing) to help
prevent a delayed air embolism. If
possible, the nurse should attempt to
cover the site with the occlusive dressing
while pulling out the line (Option 1).
▪ Pull the line cautiously and never pull
harder if there is resistance. Doing so
could cause the catheter to break or
become dislodged in the client's vessel
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Nursing care for central lines: Preventing
CLABSI
▪ Comply hand hygiene religiously
▪ Avoid femoral site in obese adult
patients.
▪ Prepare the insertion site with >0.5%
chlorhexidine with alcohol.
▪ Immediately replace dressings that are
wet, soiled, or dislodged – NO WET
DRESSING
▪ If blood or blood products or fat
emulsions are administered change
tubing every 24 hours.
▪ Promptly remove unnecessary central
lines
▪ Perform daily audits to assess whether
each central line is still needed
Allen’s Test before arterial line insertion:
The patency of the ulnar artery must be
confirmed by performing a modified
Allen's test to assure adequate circulation
to the hand before proceeding with the
radial arterial insertion
1. Instruct the client to make a tight fist (if
possible)
2. Occlude the radial and ulnar arteries
using firm pressure
3. Instruct the client to open the fist; the
palm will be white if both arteries are
sufficiently occluded
4. Release the pressure on the ulnar artery;
the palm should turn pink within 15 secs
as circulation is restored to the hand,
indicating patency of the ulnar artery
(positive Allen's test)
If the Allen's test is positive, the arterial
insertion can be done; if negative and
the palm does not return to a pink color,
an alternate site (eg. brachial artery,
femoral artery) must be used.
Summary:
It is important to distinguish central lines in critical care. Central venous catheter
(CVC) uses the venous system to provide direct access to the heart with the
indications mentioned above. On the other hand, arterial line provides access to
the heart through arteries using shorter catheter contrary to CVC. Arterial lines are
short to prevent unnecessary obstruction to arterial circulation. In terms of
monitoring hemodynamics, both of these central lines use the same set-up.
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Hemodynamic monitoring:
Set-up for CVC and Arterial line
Monitor: Shows
the pressure
reading
Fast-flush (aka) Square wave
test: Perform a dynamic
response test (square wave
test) using the fast flush valve
every 8-12 hours, when the
system is opened to air or
when accuracy of
measurements is questioned.
This test helps to verify if the
arterial line is functioning
correctly. Square wave
because when flushing the
line, the wave forms turn into
square in the monitor.
Pressure bag: Inflating
the pressure bag to 300
mm Hg regularly helps
prevent backflow of
blood to transducer
Saline: Fluid inside the
pressure bag which
maintains patency of
the line
Transducer: Reads
fluctuations of
pressure from the
heart.
Zeroing: Leveling
or positioning the
transducer to
baseline or to
phlebostatic axis.
Phlebostatic axis:
At the 4th ICS, at the midway
point of the AP diameter (½
AP)of the chest wall. Zeroing
stopcock of the transducer
system must be placed at the
phlebostatic axis
If the transducer is placed
too low, the reading will be
falsely high; if placed too
high, the reading will be
falsely low. This concept is
similar to the positioning of
the arm in relation to the
level of the heart when
measuring blood pressure
indirectly using a
sphygmomanometer or
noninvasive blood pressure
monitoring device. The
upper arm should be at the
level of the phlebostatic axis
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Hemodynamic monitoring:
Pulmonary artery catheter (Swan-Ganz)
Pulmonary artery catheterization
(Swan-Ganz):
AKA right heart catheterization, is
the insertion of a catheter into a
pulmonary artery. Its purpose is
diagnostic; detects CHF etc. The
PAC allows direct, simultaneous
measurement of pressures in the
right atrium, right ventricle,
pulmonary artery, and the filling
pressure ("wedge" pressure) of the
left atrium.
Remember:
Right heart catheterization is PAC
(venous approach). Whereas, left
heart catheterization (arterial
approach) refers to conventional
cardiac catheterization used to
diagnose and treat blockages
(e.g. AMI, CAD)
Technique: The catheter is introduced through a large vein (IJ, SC, femoral). The passage of the
catheter is monitored by dynamic pressure readings from the catheter tip. Readings will show in
the monitor depending on the site of the catheter tip as it advances to right atrium, the right
ventricle, and subsequently into the pulmonary artery. The balloon, when inflated causes the
catheter to "wedge" (force into a narrow space) in a small pulmonary blood vessel. Ideally, this
measures CHF by measuring left ventricular function and ventricular preload.
CVP/RAP:
2–8 mmHg
RVP: 15–25
mmHg
(systolic)
PCWP: 8-13
mmHg
PAP: 20-30
mmHg
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Pulmonary artery catheter
Balloon: Should be inflated
for only 10-15 seconds and
then allowed to deflate
passively. A balloon that is
inflated for a long period
may cause PA rupture.
Locking the balloon port of
the PA catheter will prevent
the balloon from being
accidentally inflated.
Thermistor port: Connected
to the cardiac output
computer. Measures core
blood temperature.
Balloon port: Cannot be
connected to a pressure
monitoring system. Used to
inflate the balloon at the tip of
the PA catheter, allowing for
the measurement of PA
wedge pressures. Special
syringe is used (1-3 ml). Always
lock the balloon port.
Proximal port: Connected to
a pressure monitoring
system to measure CVP
because its lumen exits into
the right atrium.
Distal port: Connected to a
pressure monitoring system
to measure PA pressure
because its lumen exits into
the PA.
Remember: PA catheterization
Conventionally, PAC is utilized 3-5 days. Its usage is limited due to its controversy in the
recent times due to risk of injury (eg. PA rupture). There is growing evidence the use of
PAC does not necessarily lead to improved outcome in ICU because there are
available test measuring heart function. Hospital based catheter infections clearly
limits the usage of this type of invasive ICU procedure.
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Peripherally inserted central line
(PICC):
Commonly used for long term
antibiotic administration,
chemotherapy, and total
parenteral nutrition (TPN). PICC
lines can be left in for weeks or
months. Complications related to
the PICC are occlusion of the
catheter, phlebitis, air embolism,
and infection due to bacterial
contamination. Care approach is
similar to central lines.
PICC vs Midline Catheter:
Midline catheter are not central
lines. It is considered as a
peripheral line. However, both has
lower incidences of infections
Chest Ports: Port-a-cath or Mediport:
Consists of a reservoir compartment
(portal) that has a silicone bubble
for needle insertion (septum), with
an attached plastic tube (catheter).
Surgically inserted under the skin in
the upper chest or in the arm and
appears as a bump under the skin.
Ideally, the catheter terminates in
the superior vena cava or the right
atrium. Most commonly used for
chemotherapy, antibiotics, BT,
blood draws.
Permacath: Double lumen dialysis
catheter placed in the jugular vein.
It is tunneled under the skin along
the upper chest under collar bone
and the end of the catheter will
come out about 4 inches (10cms).
Permacath is temporarily used for
hemodialysis until a permanent
access has time to "mature" AV graft
or AV fistula. Although it can last up
to 12 months.
Trialysis catheter has its 3rd lumen
used for CVP monitoring, blood
draws ,medication & contrast
administration
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Question: The nurse working in an intensive care unit receives a prescription from
the primary health care provider to discontinue a triple-lumen subclavian
central venous catheter. Which interventions will help prevent air embolism
on removal? Select all that apply.
1. Applying an air-occlusive dressing
2. Instructing the client to bear down
3. Instructing the client to lie in a supine position
4. Pulling the line harder if there is resistance
5. Pulling the line out when the client is inhaling
Answer: 1, 2, 3
Rationale: To prevent air embolism when discontinuing a central venous
catheter, it is important for the nurse to pull the line cautiously, have the client
in a supine position to increase the CVP and decrease the possibility of air
getting into the vessel, have the client bear down or exhale (inhalation will
suck more air into the blood vessel via negative suction pressure), and apply
an air-occlusive dressing while pulling out the line.
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10
Renal
Anatomy and Physiology
Cardiac output: Renal system
The renal system receives
blood about 20-25% (1L) of the
total CO. About 10% (100 ml) is
subject for filtration and
cleared in a form of urine AKA
glomerular filtration rate (GFR).
Creatinine clearance is
basically GFR. The main
function of kidneys is to excrete
waste which is more specific to
creatinine. This means that
elevated creatinine is a
specific sign of a failing renal
system.
Ureter: Is a tube that carries urine
from the kidney to the urinary
bladder.
Bladder: A hollow and elastic organ
which stores the urine produced by
the kidneys. Residual amounts >100
mL should be reported (urinary
retention)
Urethra: A duct that transmits urine
from the bladder to the exterior of
the body during urination.
Creatinine clearance: GFR
Normal is approximately 100
ml/min. There is 1 ml of creatine
cleared in 1 ml of blood filtered
(1:1). In kidney injury, there is
decreasing creatinine
clearance (e.g. 50 ml/min). If
the kidneys are expected to
clear 100 ml/min of creatinine,
where is the other 50 ml/min? It
went back to serum which
subsequently increases the
serum or blood creatinine
levels. <GFR is <creatine
clearance = kidney injury
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Functions:
1. Acid – base balance
2. Fluid and electrolyte balance
(Regulation of osmolality)
3. Hormones & enzyme secretions
Erythropoietin (RBC production)
Calcitriol (Calcium absorption)
Renin (BP regulation)
4. Excretion of waste
Formation of urine
Acid-base balance:
The lungs contribute to acid-base
homeostasis by regulating carbon
dioxide (CO2) concentration.
Mixed with H20 to form carbonic
acid (H2CO3). It dissociates to
form Hydrogen ions (H+) and
bicarbonate (HCO3). Kidneys
reabsorb and regenerate HCO3
from urine to neutralize blood,
and to excrete H+ ions to prevent
blood from become acidic.
Osmolality: Concentration
An increase in osmolality causes the
posterior pituitary gland to secrete
antidiuretic hormone (ADH), resulting
in water reabsorption by the kidney
and an increase in urine
concentration.
Remember:
Water is a diluent. The two factors
work together to return the plasma
osmolality to its normal levels.
Implications: In a presence of
disease, the kidneys are not able to
excrete H+ ions making the blood
acidic. H+ ions are powerful acidifying
agents (power of hydrogens: pH).
Acidosis is hyperkalemia: To reduce
the acidity of your blood, H+ ions
move from your circulation into your
cells in exchange for K+. Movement of
K+ from cells causes hyperkalemia.
Remember: Human cells are irritated
with acids. Hyperkalemia causes
serious arrhythmias. Dialysis is
indicated.
Implications:
In a presence of disease, the kidneys are
not able regulate blood osmolality. Fluid
volume overload is the subsequent
symptom that may eventually cause
pulmonary edema. Fluid volume overload
contributes to elevated BP found in
chronic kidney disease (CKD).
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Secretion of hormones:
Erythropoietin: Stimulates
erythropoiesis (production of RBC)
in the bone marrow.
Calcitriol: Activated form of
vitamin D, promotes intestinal
absorption of calcium and renal
phosphate reabsorption.
Renin: An enzyme which regulates
angiotensin and aldosterone
levels (RAA System) which
regulates blood pressure.
Implications:
In CKD, erythropoietin synthesis is
decreased causing anemia.
Hypocalcemia is due to decrease
secretion of calcitriol. In addition,
elevated BP is due to abnormal
regulation of ADH and abnormal
renin-angiotensin-aldosterone
mechanism causing retention or
reabsorption of sodium and water.
Patient is at risk for developing CHF.
Renin – angiotensin – aldosterone system: Elevating blood pressure
in response to dehydration, renin is produced by kidneys.
Angiotensin 1 is not a potent vasoconstrictor so angiotensin
converting enzyme (ACE) is needed to convert angiotensin 1 to
angiotensin 2 (potent vasoconstrictor) causing BP elevation.
Aldosterone promotes H20 and Na+ retention (close relationship of
Na+ and H20) causing hypernatremia and elevated BP. K+ and H+
are excreted by kidneys causing hypokalemia and alkalosis. This
also explains the inverse proportion of sodium and potassium.
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Urine formation: Excretion of waste through the nephrons
(functional units of kidneys)
1. Filtration: The process by which
cells and LARGE PROTEINS are
retained while small materials pass
through glomerulus and eventually
becomes urine. Waste products
must be excreted to urine.
Hydrostatic pressure pushes fluids
and materials through the capillary
networks of the glomerulus.
Remember: Damaged glomerulus
are not able to filter waste products
well and retains them to the
circulation (↑Crea, BUN etc.) Large
proteins are excreted in the urine
causing proteinuria and
hypoalbuminemia consequently.
which causes interstitial edema, a
common manifestation in kidney
disorder (albumin maintains fluid in
the serum).
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2. Reabsorption: The transport of
molecules that passed through
glomerular membrane back into the
peritubular capillary. H2O is 55%
reabsorbed in the proximal tubule.
Glucose and amino acids are
reabsorbed in the proximal tubule.
Reabsorption happens in proximal
tubule, descending & ascending loop
of Henle, distal convoluted tubule,
collecting tubules.
Remember: Loop diuretics
(Furosemide, Bumetanide, Torsemide)
act in the loop of Henle to inhibit Na+,
Ch- and K+ reabsorption thereby
causing diuresis/excretion (wasting
K+). However, K+ sparing diuretics
(Spironolactone) antagonizes
aldosterone effects, preventing Na+
reabsorption and preventing K+
excretion.
3. Secretion: The reverse of
reabsorption in which molecules are
transported from the peritubular
capillary through the interstitial fluid.
This is the process of cleaning the
blood by moving the harmful
molecules (ammonium, some K+, H+
ions) back to tubules to for excretion
making urine acidic.
4. Excretion: The last step in forming
the urine is excretion. Waste is
excreted in the form of a clear pale
yellowish-colored urine.
Remember: All waste products are
acidic. Retention of these products
due to abnormal regulation of the
kidneys results to metabolic acidosis.
Hence, it causes harm to most human
cells. Any form of acidosis is way
more harmful than alkalosis.
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Common renal disorders: Acute kidney injury (AKI)
Acute kidney injury (AKI): Previously known as Acute renal failure (ARF)
Is sudden damage to the kidneys (< 3 months) characterized by rapid reduction in
kidney function, based on serum BUN, creatinine, or based on a rapid reduction in urine
output, oliguria (less than 400 ml/24 hours). It can range from minor loss of kidney
function to complete kidney failure.
The cause is before the
kidneys: ↓ blood flow
↓ blood filtered
Absolute fluid loss:
Hypovolemic shock
▪ Major hemorrhage
▪ Dehydration (diarrhea,
persistent n/v)
▪ Burns
Relative fluid loss:
Distributive shock
▪ Septic shock
▪ Neurogenic shock
▪ Anaphylactic shock
CHF
Renal artery stenosis,
embolus
The cause is within the kidneys:
damage the kidney itself
Acute tubular necrosis:
Nephrotoxins
Aminoglycosides “mycins”
Myoglobin (Rhabdomyolysis)
Contrast dye
Uric acid
Glomerulonephritis
Nephrotic, nephritic syndrome
Acute interstitial nephritis
NSAIDs, penicillins, diuretics
Pyelonephritis
The cause is after the kidneys:
Obstruction to outflow
Compression:
Abdominal tumors
Benign prostatic hyperplasia
Blockage:
Kidney stones (ureter,
urinary bladder)
Manifestations: Associated with the underlying cause.
The symptoms of AKI are related to the various kidney functions. Accumulation of BUN
and creatinine (azotemia) lead to fatigue, loss of appetite, headache, nausea and
vomiting etc. Metabolic acidosis for instance is a life threatening condition that can lead
to CNS depression. Hyperkalemia can also lead to fatal arrhythmias. Furthermore, fluid
balance affects blood pressure regulation which leads to heart failure and pulmonary
edema.
Management:
The management of AKI is the treatment of the underlying cause and preventing
complications such as metabolic acidosis, hyperkalemia and pulmonary edema.
Remember, AKI is reversible because the underlying causes are treatable. However,
serious complications may occur if not treated promptly. Dialysis maybe indicated.
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Common renal disorders: Chronic kidney disease (CKD)
Chronic kidney disease (CKD): Characterized by gradual loss of kidney function over a
period of months or years (>3 months + GFR < 60 ml/min). Remember that chronic diseases
are irreversible. Such causes of CKD includes, hypertension and DM which makes CKD as an
irreversible condition contrary to AKI. Both HTN and DM cause sclerosis of glomerulus
overtime.
Causes:
Hypertension
Causes:
Diabetes Mellitus
The sticking of glucose
to proteins in the vessel
walls
Other Causes:
▪ SLE
▪ Rheumatoid
arthritis
▪ HIV
▪ NSAIDs (chronic
use)
▪ Tobacco
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Azotemia: Abnormally high
levels of nitrogencontaining compounds
(BUN, creatinine).
Azotemia leads to uremia
(urine in blood).
Remember: Brain cells are
very sensitive to waste
products (waste products
are acids). Monitor
alteration in level on
consciousness. Patient
safety is a priority.
Hypocalcemia: Due to low
production of calcitriol
which causes less
absorption of calcium.
Inversely, it can cause
↓Phosphorus
Hyperkalemia and
metabolic acidosis: Results
from retention of K+ and
less excretion in the urine.
This is also in response to H+
ion acidosis (body’s
response is to eliminate H+
ions) in exchange of K+
thereby causing ↑K+.
Remember: ↑K+ is acidosis.
A very important indicator
to initiate dialysis
Hypertension: Low cardiac
output to kidney is the
effect of HTN. This causes
activation of RAA system
increasing risk of HTN and
CHF. This creates a cycle
since HTN is a significant
cause of CKD.
Remember: ACE inhibitor
“prils” or angiotensin II
receptor blocker “sartans”
are commonly given to
treat CKD with HTN.
Hyperkalemia is a
common adverse effects.
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Anemia: Due to abnormal
synthesis of erythropoietin
causing anemia.
Remember: Anemia in
CKD is treated with
recombinant human
erythropoietin (Epogen,
epoetin). Target HgB is
10-11.5 g/dL (100-115 g/L)
Epogen: to ↑ RBC
Neupogen: to ↑ WBC
Oprelvekin: to ↑ platelet
Stage
Severity
GFR
Stage 1
Diminished function/compensatory
≥90 ml/min
Stage 2
Mild CKI
60–89 ml/min
Stage 3
Moderate CKI
30–59 ml/min
Stage 4
Severe CKI
15–29 ml/min
Stage 5
End-stage kidney disease (ESRD)
<15 ml/min
AKI vs. CKD
AKI
CKD
Definition
▪ Sudden damage to kidneys
< 3 months
▪ ↑BUN, creatinine
▪ oliguria (<400 ml/24 hours)
▪ Gradual loss of kidney
function over a period of
months or years (>3 months +
GFR < 60 ml/min
Causes
Prerenal, Intrinsic, Post-renal
HTN, DM
SLE, RA, HIV, NSAIDs (chronic
use), Tobacco
S/S
▪ Depending on the underlying ▪ Depending on the
cause
underlying cause: HTN, DM
▪ Related to ↑BUN, creatinine:
▪ Azotemia, uremia
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Diagnosis
Management
Hypocalcemia
Hyperphosphatemia
Hyperkalemia
Metabolic acidosis
Hypertension
Anemia
fatigue, loss of appetite,
headache, n/v, acute
confusion, seizures, coma
▪ Hyperkalemia
▪ Metabolic acidosis
▪ CHF, pulmonary edema
▪
▪
▪
▪
▪
▪
Clinical exam, GFR, BUN,
Creatinine (sudden ↑ within
several days -weeks)
Clinical exam, GFR, BUN,
Creatinine (over several
months or years)
Supportive/ Treat symptoms:
Anemia: Erythropoietin
Hyperkalemia:
1. IV 50% dextrose + regular
insulin (glucose transports K+
out from serum)
2. Calcium gluconate (if +
arrhythmia)
3. Sodium polystyrene
sulfonate (Kayexalate)
administered PO or enema
(removes K+ from the body
by exchanging Na+ for K+
ions in GIT; K+ excreted in
feces) Last priority d/t
delayed onset.
4. Dialysis – last resort
Hypocalcemia/Hyperphosphat
emia: Calcium supplements
Metabolic acidosis: NaHCO3
Hypertension: ACEIs “prils” or
ARBs “sartans”
Renal replacement therapy:
Hemodialysis, Peritoneal
dialysis, Kidney transplant
Treat underlying cause
Prevent complications by
treating the symptoms:
Hyperkalemia
CHF, pulmonary edema
Metabolic acidosis
Renal replacement therapy
Hemodialysis
Peritoneal dialysis
Avoid nephrotoxins:
NSAIDs, contrast dye,
aminoglycosides
Diet: Low protein, low sodium
and potassium, low
phosphate, fluid-restricted
Diet: Low protein, low sodium
and potassium, low
phosphate, fluid-restricted
Prognosis
Reversible but can lead to
CKD if not treated promptly
Irreversible
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Question: A client with advanced kidney disease has serum potassium of 7.1
mEq/L (7.1 mmol/L) and creatinine of 4.5 mg/dL. What is the priority
prescribed intervention?
1. Administer IV 50% dextrose and regular insulin
2. Administer IV furosemide
3. Administer oral sodium polystyrene sulfonate
4. Prepare the client for hemodialysis catheter placement
Answer: 1
Rationale: Severe hyperkalemia (potassium >7.0 mEq/L [7.0 mmol/L]) requires
urgent treatment because cardiac muscle cannot tolerate very high
potassium levels. Severe hyperkalemia increases the risk ventricular
tachycardia and fibrillation, asystole.
50 mL 50% dextrose + 10 units of regular insulin is the priority intervention as
it is most effective in reducing the potassium level quickly. Glucose is a
transporter of potassium from the extracellular fluid back into the
intracellular fluid. Insulin is added in the presence of concentrated dextrose
(50%) .
If the client has ECG changes (e.g. tall peaked T waves), calcium
gluconate should be given before insulin/dextrose. This will stabilize the
cardiac muscle until the potassium level can be reduced with
insulin/dextrose.
Furosemide (Lasix) increases the renal excretion of potassium and is usually
prescribed for clients with fluid overload. However, administration of
furosemide would take time to be effective and is not the priority.
Sodium polystyrene sulfonate (Kayexalate) is administered by mouth or
enema to remove potassium from the body by exchanging sodium for
potassium ions in the intestines; these are then excreted in feces. This is not
the priority due to the delayed onset of potassium removal.
Placement of hemodialysis catheter will delay treatment.
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Dialysis: Hemodialysis
Arteriovenous
Access (A/V)
Internal A/V shunt
External A/V
shunt
A/V Fistula
Matures 6-8
weeks
Permacath
(2 lumen-tunneled)
Last up to 12 mos.
A/V Graft
Matures
2 weeks
External A/V shunts
can be used
immediately while
waiting for internal
shunts to mature
Trialysis
(3 lumen)
3rd lumen used for
CVP monitoring,
blood draws
,medication &
contrast
administration
Hemodialysis is used as a
temporary measure in
either AKI or in CKD - ESRD
as a permanent measure
where transplant is not
possible. The principle is the
same as other methods of
dialysis (e.g. peritoneal
dialysis); it involves diffusion
of solutes across a
semipermeable membrane
(dialyzer)
HD is usually done 3X/week
for about 3-4 hours/therapy.
The dialyzer is composed of
bundles of hollow fibers,
whose walls are made of
semipermeable membrane.
Pressure gradients are applied
into the dialyzer to move fluid.
Remember to monitor
patient’s BP during this
process.
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Dialysis disequilibrium
syndrome (DDS):
A rare but potentially lifethreatening complication
during the initial stages HD;
related rapid rate of HD
Rationale: During HD, solutes
are removed more quickly
from the blood than the
brain and CSF due to blood
and brain barrier (BBB)
mechanism, creating a
concentration gradient that
can lead to excess fluid in
the brain.
Manifestations are r/t ↑ICP
(cerebral edema): n/v,
headache, restlessness,
confusion and seizure
Thrill : Palpable vibration at the
A/V site caused by arterial
pressure through the walls of the
vessels.
Bruit: A blowing or swooshing
sound caused by turbulent
blood flow assessed through
auscultation.
Remember: Absence of the thrill
or bruit can indicate potential
clot formation in the A/V site.
Other complications:
Hypotension: hold BNP meds
before HD
Muscle cramps: electrolyte
replacement
A/V access occlusion:
▪ check bruit and thrill
(AVF)
▪ check thrill (AV graft)
Bleeding d/t heparin:
monitor coagulation
studies
A/V access infection
(CLABSI): Strict bundle of
care implementation
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Dialysis: Peritoneal dialysis
Peritoneal dialysis (PD):
Uses the peritoneum as a
semipermeable membrane to
dialyze a blood. A catheter is
placed into the peritoneal
cavity, and dialysate solution
(hypertonic) is infused. The
tubing is clamped to allow the
fluid to remain in the cavity
(dwelling). Finally, the fluid is
drained.
Remember:
There are 2 basic
compartments in the human
body, intravascular
(serum/blood) and
extravascular (interstitial,
intracellular). PD solution is a
hypertonic solution which
attracts fluid from low
concentration of solutes to
higher concentration. Waste
products are drawn to
peritoneum.
Remember:
Peritonitis is a major
complication. Signs of
peritonitis are low to high
grade fever, tachycardia
and cloudy outflow
Insufficient outflow:
▪ Monitor bowel movements
Administer stool softeners
▪ Check tubing for kinks or
clots
▪ Keep drainage bag below
the abdomen;
▪ Place patient on a side-lying
position or assist with
ambulation.
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Common renal disorders: Alport syndrome vs Glomerulonephritis
(nephrotic & nephritic syndrome)
Alport syndrome
Etiology
Mechanism
Genetic mutation
Mutation to the collagen
containing membrane in
eyes, cochlea & kidneys
This genetic changes
lead to abnormal
structure of glomerular
basement membrane
(kidneys) promoting
leakage of large
molecules to urine
(protein, RBC).
Manifestations are also
associated with eyes and
ear disorders.
Classic sign
▪ Hematuria (Tea
colored)
▪ Proteinuria
▪ ↓ serum albumin
▪
▪
▪
▪
▪
Other S/S
Periorbital edema
Peripheral edema
Anasarca
Hypertension
Eye changes: thinning
of cornea, Hearing loss
Remember: Albumin
controls fluid in the serum.
↓ serum albumin
promotes leakage of
fluids to extravascular
compartment (edema)
Glomerulonephritis
Nephrotic syndrome
Idiopathic (unknown)
Nephritic syndrome
Post streptococcal:
glomerulonephritis
Inflammation as well as
Immune-complexformation of a crystalline mediated mechanism
material within
(delayed hypersensitivity)
glomerular cells allows
that is develop after
large molecule proteins
Group A beta hemolytic
such as albumin,
streptococcus (GABHS)
antithrombin or the
infection GBM is damage
immunoglobulins to pass d/t inflammation
through the glomerular
Impetigo (post 6 weeks)
basement membrane
Pharyngitis (1-2 weeks).
(GBM) towards urine.
Noninflammatory
Inflammatory
▪ Proteinuria
▪ ↓ serum albumin
▪ ↑ serum lipids
▪ ↓ anti-thrombin
▪ Hematuria (Tea
colored)
▪ Proteinuria
▪ ↓ serum albumin
▪ Periorbital edema
▪ Peripheral edema
▪ Anasarca
▪ Hypertension
Complication:
▪ Infection (d/t ↓Ig)
▪ DVT/PE (d/t ↓antithrombin)
▪ Hyperlipidemia (d/t
compensatory
response to ↓ serum
albumin)
▪
▪
▪
▪
Periorbital edema
Peripheral edema
Anasarca
Hypertension
Infection:
Fever, tachycardia,
headache, malaise,
anorexia, nausea
Diagnosis
Physical exam, biopsy
Genetic testing
Physical exam, biopsy
Physical exam, Culture &
sensitivity
Treatment
Goal: ↓ BP (ACE inhibitor)
Dialysis (kidney failure)
Goal: ↓ BP (ACE inhibitor)
↓ edema (diuretics),
Prevent infection
Goal: Treat infection
(Penicillin)↓ BP (ACE
inhibitor), diuretics
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Common renal disorders: Kidney stones (urolithiasis)
Calcium stones
Ca oxalate:
Acidic
Ca Phosphate:
Alkaline
Uric stones
Acidic
Remember:
Kidney stones can be
elsewhere in the
Kidneys: nephrolithiasis
Ureter: ureterolithiasis
Bladder: cystolithiasis/
vesicolithiasis
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Struvite stones
Alkaline
Cystine stones
Acidic
Classic sign:
▪ Flank pain (mid-lower
back)
▪ Renal colic (constant
sharp pain)
Diagnosis:
History and physical exam
X-ray, CT scan, USD
Urinalysis - Hematuria
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Treatment:
Hydration – to reverse stone
precipitation
Medication:
Pain – NSAIDS
Reduce stone – K+ citrate
Pass stone – Alpha
adrenergic blocker,
Calcium channel blocker
(reduce spasms)
Shockwave lithotripsy
Stent placement
Nephrectomy/nephrolithotom
y
Remember: Extracorporeal
shock wave
(large stones)
lithotripsy (ESWL)
A noninvasive procedure used to break up
kidney stones. It is typically done on an
outpatient, although the client will require
local or general anesthesia. The shock
waves break up the stone(s) into a fine
sand that can then be excreted in the
urine. Bruising on the back or abdomen
after the procedure is normal.
Hematuria is concerning if the urine
remains bright red over a prolonged
period (>24 hr.).
Ureteral stents: Often placed after the
procedure to help with the passage of the
broken stone and prevent buildup within
the ureter. The stents are removed within
1-2 weeks.
Nursing care:
▪ Encourage fluid intake
▪ Prevent infection
▪ Administer analgesics (pain can be
severe)
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Alkaline ash diet: Indicated for acidic
stones
Acidic stones: Uric acid, Calcium
oxalate, cystine
Consisting mainly of fruits, vegetables,
and milk when catabolized leaves an
alkaline residue to be excreted in the
urine.
Acid ash diet: Indicated for alkaline
stones
Alkaline stones: Struvite (infection
stones), Calcium phosphate
VS
Remember: patient can still have
meat, fish, eggs (acid) but in minimal
amount
Consisting mainly of eggs, meat, fish
when catabolized leaves an acidic
residue to be excreted in the urine.
Remember: patient can still have fruits,
vegetables, and milk (alkaline) but in
minimal amount.
Common renal disorders: Urinary tract infection (UTI)
Lower UTI
Upper UTI
Definition
Infection to bladder (cystitis)
and urethra (urethritis)
Infection to ureter (ureteritis) is
rare. It usually affects kidneys
(pyelonephritis)
Causes
E. coli (most common)
Klebsiella, Enterobacter,
Proteus, Staphylococcus (2nd
most common)
Same
Risk factors
▪ Sexual intercourse “honeymoon
cystitis”
▪ Female – short urethra
▪ Post-menopausal - ↓estrogen
(loss of protective vaginal flora
▪ Urinary catheter – CAUTI
▪ Diabetes - ↑ blood sugar inhibits
phagocytosis
▪ Foreskin (boys) -uncircumcised
▪ Impaired bladder emptying
Mechanism
Bacteria colonizes the bladder
mucosa
Remember: Urine is sterile,
bacteria cannot thrive in high
urea and low pH environment.
Bacteria in urinalysis is a
significant finding.
Same with lower UTI
+
Vesicoureteral reflux (congenital
disorder) which promotes
ascending infections
Bacteria adheres to renal
interstitium. Typically spares blood
and glomerulus
Ascending infection: recurrent
lower UTI
Descending infection (rare): from
blood stream, consequence of
septicemia
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S/S
Diagnosis
▪ Suprapubic pain
▪ Dysuria
▪ Frequent urination
▪ Urgency
Infants: poor feeding, fussy,
fever
Elderly: fatigue, incontinence,
DELIRIUM (safety is the
priority – risk for fall)
Symptoms not usually present:
Fever, nausea and vomiting
Flank pain (costovertebral
angle tenderness)
Suggests upper UTI if present
Urinalysis:
▪ Abnormally ↑ WBC (>5/HPF)
▪ Cloudy urine appearance
▪ (+) cast: WBCs in clamps
Dipstick test:
Leukoesterase (+) – WBCs
Nitrites (+) – E. Coli converts
nitrates in urine to nitrites
Urine culture:
>100,000 CFU (colony forming
units) (+)
<100,000 CFU may still indicate
infection
▪ Suprapubic pain
▪ Dysuria
▪ Frequent urination
▪ Urgency
Infants: poor feeding, fussy, fever
Elderly: fatigue, incontinence,
DELIRIUM (safety is the
priority – risk for fall)
Fever, chills, nausea and vomiting
Flank pain (costovertebral angle
tenderness)
Same with lower UTI
+
Leukocytosis (↑WBCs) in the blood
and systemic symptoms such as
fever, n/v, chills helps distinguish
upper UTI
(+) pyuria (WBC in urine)
(-) urine culture: Suggests
urethritis (possible
chlamydia or gonorrhea –
sexually transmitted)
Treatment
Antibiotics: Penicillin’s,
cephalosporins,
sulfonamides fluroquinolones
Pain medication: NSAIDs
Prevention:
Hydration (flush out bacteria)
Good hygiene
Avoid bubble bath in young
children (girls)
Same with lower UTI
+
Preventing complications:
Chronic pyelonephritis (scarring)
Renal abscess (sepsis)
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Others: Circulatory shock
Shock: Is circulatory shock
Characterized by widespread
insufficient blood flow to the
tissues of the body. Contrary to
ischemia which pertains to
specific organ system.
HYPOTENSION:
Is a determinant of circulatory
shock. Consequently, circulatory
shock results to cellular damage.
Blood Pressure
Resistance to flow
Factors:
Diameter
Length
Example:
HTN, Peripheral
vascular disease
(PVD)
All forms of shock causes
low BP. It is a priority
condition because it
may cause immediate
multi organ failure.
Remember: All body
tissues are dependent
on the CO supplying
their O2 and nutrients
to sustain life
Cardiac output
Factors:
Heart rate x stroke
volume
Example:
Shock, CHF, Acute
coronary syndrome
(ACS)
1. Hypovolemic shock: Low volume
2. Cardiogenic shock: Pump failure
affects the CO
Non hemorrhagic – Dehydration, N/V
Hemorrhagic - Bleeding
Remember: 20-25% (approx. 1L) of blood
loss causes significant hypotension.
S/S: “hypo,tachy,tachy”
Hypotension, restlessness
Rapid, weak and thready pulse
(tachycardia)
Cold clammy skin, Diaphoresis,
Rapid shallow breathing (tachypnea),
polydipsia. Other s/s apart from
hypotension are compensatory
(autonomic response) d/t low tissue
perfusion
affects CO
AMI, Arrhythmias, Cardiomyopathies,
Valvular defects, cardiac tamponade
S/S: “hypo,tachy,tachy”
Hypotension, restlessness
Rapid, weak and thready pulse
(tachycardia)
Cold clammy skin, Diaphoresis,
Rapid shallow breathing (tachypnea)
Associated S/S: d/t underlying heart
condition
Arrhythmias
Jugular vein distention
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3. Distributive shock: Widespread vasodilation
affects resistance to flow and CO
Remember:
It is called distributive shock because there is
an abnormal distribution of fluid within the
involved compartments (intravascular &
extravascular). This is due to massive
vasodilation. Vasodilation tends to make
blood vessels more “leaky” (permeable).
However, in this form of shock there is no
absolute loss of fluid unlike hypovolemic
shock.
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Types of distributive shock:
Septic shock – vasodilation due to
widespread inflammatory process
Neurogenic shock – vasodilation
due to loss of sympathetic tone
from spinal cord injury
Anaphylactic shock – vasodilation
due to inflammatory process
(histamine)
Septic shock: S/S
“hypo,tachy,tachy”
Hypotension, restlessness
Rapid, weak and thready
pulse (tachycardia)
Warm skin, Rapid shallow
breathing (tachypnea)
+
SIRS criteria and Sepsis:
Temperature, HR, respiration,
WBCs, identified causative
agent
Neurogenic shock: S/S
“hypo,brady,tachy”
Hypotension, Warm, flushed
skin due to vasodilation and
inability to constrict blood
vessels, Bradycardia due to
loss of sympathetic tone,
Rapid shallow breathing
(tachypnea)
+
Priapism (constant painful
erection) due to vasodilation
Respiratory arrest – if above
C4 is affected
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Anaphylactic shock: S/S
“hypo,tachy,tachy”
Hypotension, restlessness
Itchiness, warm flushing, or
swelling (angioedema).
Shortness of breath,
wheezes, or stridor,
Tachypnea (due to
bronchoconstriction) ,
Tachycardia (Sympathetic
response), Abdominal pain,
N/V (due to gastric acid
secretion)
Type of shock
1. Hypovolemic:
Absolute loss of fluid
2. Cardiogenic:
Pump failure
Signs/symptoms
“hypo, tachy, tachy”
▪ Hypotension
▪ Rapid, weak and thready pulse
(tachycardia)
▪ Rapid shallow breathing
(tachypnea)
▪ Cold clammy skin
▪ Diaphoresis, polydipsia,
restlessness
“hypo, tachy, tachy”
▪ Hypotension
▪ Rapid, weak and thready pulse
(tachycardia)
▪ Rapid shallow breathing
(tachypnea)
▪ Cold clammy skin
▪ Diaphoresis, restlessness
arrhythmias, jugular vein
distention
Treatment
Stabilize blood pressure:
▪ Fluids (Normal saline, LR)
▪ Medications (inotropes)
Supplemental oxygen
Treat the cause:
▪ Blood transfusion
▪ Fluids (Normal saline, LR)
Stabilize blood pressure:
▪ Fluids (Normal saline, LR)
▪ Medications (inotropes)
Supplemental oxygen
Treat the cause:
▪ Antiarrhythmics
3. Distributive:
Widespread
vasodilation
Septic: widespread
infection
“hypo, tachy, tachy”
▪ Hypotension, restlessness
▪ Rapid, weak and thready pulse
(tachycardia)
▪ Rapid shallow breathing
Stabilize blood pressure:
▪ Fluids (Normal saline, LR)
▪ Medications (inotropes)
Supplemental oxygen
Treat the cause:
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Neurogenic: Spinal
cord injury
Anaphylactic:
Severe allergic
reaction
Others: Fluids
(tachypnea)
▪ Warm skin
▪ SIRS criteria and Sepsis:
Temperature, HR, respiration,
WBCs, identified causative
agent
“hypo, brady, tachy”
▪ Hypotension
▪ Bradycardia due to loss of
sympathetic tone,
▪ Rapid shallow breathing
(tachypnea)
▪ Warm flushed skin
▪ Priapism (constant painful
erection) due to vasodilation
▪ Respiratory arrest: if above C4
spine injury is affected
“hypo, tachy, tachy”
▪ Hypotension, restlessness
▪ Tachycardia, Abdominal pain,
N/V (due to gastric acid
secretion)
▪ Tachypnea (due to
bronchoconstriction)
▪ Warm flushed skin
▪ Itchiness, , or swelling
(angioedema). Shortness of
breath, wheezes, or stridor,
▪ Antibiotics (empiric/broad
spectrum)
Stabilize blood pressure: return of
sympathetic tone
▪ Medications (inotropes)
▪ Fluids (Normal saline, LR)
Supplemental oxygen
Airway protection (above C4 spine
injury)
Stabilize blood pressure:
▪ Fluids (Normal saline, LR)
▪ Medications (inotropes)
Airway management:
▪ Epinephrine (bronchodilation
and ↑BP)
▪ Anti-histamines
▪ Immune suppressants (steroids)
Osmotic vs Hydrostatic pressures:
Hydrostatic pressure is a PUSHING
force that is exerted by a fluid
against the capillary wall.
Osmotic pressure is a PULLING
force that attracts water and
solute from lower to higher
concentration and is dominant in
the venous end. Osmotic
pressure helps in the movement
of fluid between capillaries and
the interstitial fluid.
Remember: IV fluids are
administered intravenously.
Tonicity of fluid is consistent with
osmotic pressure involved.
Normal osmolality of blood :
approximately 300 mosmol/L
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Hypotonic Solution:
low solute, high solvent (low
osmolality)
As it is given intravenously
(intravascular), it causes
movement of fluids from
intravascular to
extravascular (interstitial,
intracellular) compartment
leading to cell swelling.
Given to patients with
cellular dehydration
(shrunken cell) such as DKA.
Remember: Elevated
glucose in the blood
(hypertonicity) attracts fluid
from extravascular to
intravascular causing
cellular dehydration.
Example:
0.45% Normal Saline (aka
Half Normal Saline,
0.45NaCl)
Remember:
Less than 0.9% NaCl is
considered hypotonic. It is
always avoided in patients
with burns, trauma, or liver
disease because of its
tendency to deplete
intravascular fluids.
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Isotonic Solution:
equal solute and solvent
As it is given intravenously
(intravascular), it causes no
movement of fluids within
both the compartments
Given to patients with any
types CIRCULATORY SHOCK
as a fluid replacement.
Hypertonic Solution:
high solute, low solvent
(high osmolality)
5% Dextrose in Water (aka
D5 or D5W) – becomes
hypotonic once given as
the dextrose is metabolized.
As it is given intravenously
(intravascular), it causes
movement of fluids from
extravascular (interstitial,
intracellular) to
intravascular compartment
leading to cell shrinkage.
Given to patients with cell
swelling such as cerebral
edema.
Remember: Cerebral
edema is swelling of brain
tissues. Giving a hypertonic
solution promotes
movement of fluids from the
brain tissues to the
intravascular compartment.
In lieu of homeostasis,
kidneys compensate to
cause diuresis removing
fluids from a hypertonic
intravascular space.
Remember:
LR contains NaCl, potassium
chloride, calcium chloride,
& sodium lactate in sterile
water. It is the most similar
to the body’s plasma and
serum concentration, and is
especially used for burns or
hypovolemia due to fluid
shifts. It is avoided in
patients with liver disease
because the liver may not
be able to efficiently
process the lactate (lactic
acidosis)
NS is the most common IV
fluids for hydration needs
due to vomiting, diarrhea,
hemorrhage, or shock. The
only fluid used in
conjunction with blood
product administration.
Example:
D10 W
3% NaCl
D5 0.45% NaCl (D5 half
saline)
D5 0.9% NaCl (D5NS)
Remember:
More than 0.9% NaCl is
hypertonic such as 3%
NaCl. 5% or more Dextrose
is hypertonic. However in
the case of D5W, the 5%
dextrose is diluted by water
(solvent)making it
hypotonic. In contrast,
0.45% and 0.9% NaCl gives
more tonicity to Dextrose
5%. D10W, 3% NaCl are high
alert medications.
Example:
Lactated Ringers (aka LR,
Ringers Lactate, or RL, or
Hartmann's solution )
9% Normal Saline (aka NS,
0.9NaCl, or NSS)
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Question: The nurse is caring for a 78-year-old client with a urinary tract infection
(UTI). Which assessment finding would be most concerning and require
immediate follow-up by the nurse?
1. Confusion
2. Presbyopia
3. Temperature 100.2 F (37.8 C)
4. White blood cell (WBC) count 12,000/mm3
Answer: 1
Rationale: Confusion is a common clinical manifestation of UTI in the elderly but
still should be cause for concern and requires follow-up to rule out other
possible causes. Confusion is not a normal finding in the elderly adult client
and compromises patient’s safety. Some causes of confusion in the elderly
include dehydration, lack of blood flow to the brain (stroke), decreased
ability to metabolize medications (polypharmacy: ≥ 4 medications) and
concurrent infections.
Presbyopia is the decrease in ability to see objects close up. This is common
in clients over age 40.
The elderly tend to have a lower body temperature, so 100.2 F (37.8 C) is
considered febrile. This elevation is an expected finding.
An elevated WBC count would be expected in the presence of a current
infection.
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11
Endocrine
Anatomy and Physiology
Hypothalamus:
Has a central neuroendocrine
function, by its control of the
anterior pituitary, which in turn
regulates various endocrine glands
and organs. Releasing hormones
are produced in hypothalamus
then transported, stored and
released as needed.
Hormones released:
▪ Thyrotropin-releasing hormone
(TRH)
▪ Corticotropin-releasing
hormone (CRH)
▪ Gonadotropin-releasing
hormone (GnRH)
▪ Growth hormone–releasing
hormone (GHRH)
Pituitary gland:
Referred to as the 'master gland'
because it controls the activity of
most other hormone-secreting
glands except pancreas, adrenal
medulla, and parathyroid.
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Anterior pituitary
Remember: Acronym
GTPAL-F (anterior
pituitary function)
1. Growth hormone
(GH)/ Somatotropin
2. Thyroid-stimulating
hormone (TSH)
3. Prolactin (PRL)
Hormones
Influenced by GHRH by
hypothalamus. Stimulates
musculoskeletal growth
▪ Influenced by TRH by
hypothalamus. Stimulates
release of thyroid hormones.
Thyroxine (T4)
Triiodothyronine (T3)
▪ Increase the body's sensitivity to
catecholamines necessary for
metabolism.
Remember: Epinephrine and
norepinephrine are
catecholamines that causes
stimulation of the sympathetic
nervous system (SNS) “fight/flight
response” which means
manifestations of overproduction
of thyroid hormones
(hyperthyroidism) correlates with
SNS effects.
Stimulates mammary gland to
PROduce milk (lactose)
▪ Released under the influence
of hypothalamic corticotropinreleasing hormone (CRH).
Stimulates release of hormones
in adrenal cortex.
4. Adrenocorticotropic
hormone (ACTH)
Remember: Acronym SSS
Sugar, Salt & Water, Sex
hormones
Glucocorticoids (cortisol):
Steroid hormone that activates
anti-inflammatory and anti-stress
effect by promoting glucose
production for energy
Related condition
Overproduction:
Gigantism (pediatrics),
Acromegaly (adults).
Remember: Acro means “tip
end” which means the enlarged
portion d/t ↑ GH is at the distal
end of the extremities.
Underproduction: Dwarfism
Overproduction:
Hyperthyroidism
Underproduction:
Hypothyroidism
Remember: Negative feedback
mechanism causes opposite
effects to level of TSH. Elevated
T3, T4 causes decrease TSH, vice
versa.
Overproduction:
Hyperprolactinemia
Underproduction:
Hypoprolactinemia
Overproduction:
▪ Cushing’s disease
(endogenous, d/t tumor)
▪ Cushing’s syndrome
(exogenous, d/t chronic use
of steroids)
▪ Conn's syndrome (primary
hyperaldosteronism) – only
involving excess production
of aldosterone.
Underproduction:
▪ Addison's disease (primary
adrenal insufficiency)
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consumption. It’s called
Hydrocortisone if used as a
medication.
Mineralocorticoids (aldosterone):
A steroid hormone that causes
reabsorption of sodium and
excretion of potassium by the
kidney (hypernatremia,
hypokalemia), thereby indirectly
influencing water retention or
loss, blood pressure and blood
volume as part of the RAS
system.
Androgens: A steroid hormone
that regulates the development
and maintenance of male
characteristics. Remember that
females also have them, but at
lower levels: they function in
libido and sexual arousal.
Androgens are also the
precursors to estrogens in both
men and women.
Remember: Adrenal medulla
hormones (epinephrine,
norepinephrine ) are not
controlled by pituitary gland just
as pancreas and parathyroid
gland.
5. Luteinizing hormone
(LH) and Folliclestimulating hormone
(FSH)
▪ Both released under the
influence of GonadotropinReleasing Hormone (GnRH)
In females: ovulation,
maintaining of corpus luteum
and secretion of progesterone.
In males: Testosterone secretion
Females:
Turner’s syndrome: A genetic
condition in which a female is
partly or completely missing an
X chromosome (X0 instead of
XX) associated with other
congenital disorders. Classic
sign, “webbed neck, low set
ears, small body structure”
Males:
Klinefelter syndrome: A
genetic condition in which
there are 2 or more X
chromosomes in males (XXY
instead of XY) Classic sign,
“testicular atrophy, tall and
lanky structure”
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Posterior pituitary
Remember: Acronym
OA
1. Oxytocin
2. Antidiuretic
Hormone
(ADH)/Vasopressin
Hormones
Related condition
Overproduction: Pitocin as a
Most of which is released from
synthetic oxytocin cause
the hypothalamus. Uterine
maternal hypotension, and
contractions stimulate the
fetal distress
release of oxytocin (positive
Underproduction: Depression,
feedback) from the posterior
anxiety, social phobia,
pituitary, which, in turn,
autism, schizophrenia, PTSD
increases uterine contractions.
anorexia nervosa,
This positive feedback
borderline personality
continues throughout labor.
disorder
Released in response to
intravascular fluid
hypertonicity
(hyperosmolarity) by
reabsorbing water back into
the circulation in the kidneys.
Remember: Water is a
universal solvent that causes
low tonicity or osmolarity
It also constricts arterioles,
which increases peripheral
vascular resistance and raises
arterial blood pressure.
Overproduction: Syndrome of
Inappropriate Antidiuretic
Hormone secretion (SIADH)
Underproduction: Diabetes
insipidus (DI)
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Other endocrine organs: Pancreas, Parathyroid gland
Function:
"endocrine" role (1%), relating to
the secretion of insulin and other
substances within pancreatic
islets and helping control blood
sugar levels
"exocrine" role (99%), relating to
the secretion of enzymes
involved in digestion.
Endocrine Function:
Alpha cells: producing glucagon
Beta cells: producing insulin
Delta cells: producing somatostatin
(suppresses both the exocrine and
endocrine function of pancreas)
Parathyroid gland:
The major function of the parathyroid
glands secretes parathyroid hormone
(PTH)s to maintain the body's calcium
and phosphate levels so that the
nervous and muscular systems can
function properly.
Remember:
Calcium level is inversely proportional
with phosphate level. It means, s/s of
hypercalcemia are the same with
hypophosphatemia vice versa.
PTH: increases serum calcium level
Calcitonin (released by thyroid gland):
decreases serum calcium level
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Common endocrine disorder affecting ADH: Syndrome of
inappropriate ADH (SIADH) vs. Diabetes insipidus (DI)
Remember:
Physiology of ADH is important in understanding DI and SIADH. ADH works in
response to intravascular fluid hypertonicity (hyperosmolarity) by reabsorbing water
back into the circulation in the kidneys. Water is a universal solvent that causes low
tonicity/concentration/osmolarity. In relation to kidney physiology, there are only 2
main areas where water goes, in the urine which affects urine concentration
(specific gravity) and in the blood which affects concentration (blood osmolarity).
SIADH
Diabetes insipidus
Acronym: “Use Increased
instead of inappropriate” to
easily remember
Mechanism
Etiology
Increased ADH causes NO
DIURESIS which means water is
in the blood/serum and less
water in the urine. The result is
concentrated urine and
diluted blood. Sodium as a
solute is diluted causing
“dilutional hyponatremia” as a
classic mechanism causing
manifestations. Elevated ADH
means less aldosterone as a
compensatory mechanism d/t
retained water. Less
aldosterone means less ability
to excrete potassium into
urine, causing hyperkalemia.
In summary it causes
↓Na, ↑K.
Conditions that dysregulate
ADH secretion in the CNS:
Tumors that secrete ADH
(lung CA), CNS infections
(meningitis), drugs that
increase ADH secretion
(morphine, amitriptyline,
carbamazepine)
Acronym: DD
Decreased ADH: DI
Decreased ADH causes
DIURESIS. More water to urine
makes the blood more
concentrated. Diuresis means
more waste of potassium in
urine. In response, aldosterone
is released to retain sodium
and H2O. This causes ↑Na, ↓K
Nephrogenic: Acquired DI
usually caused by lithium
toxicity and high blood
calcium. Remember: Calcium
has a diuretic effect
Neurogenic: post cranial
surgery, CVA, Tumor
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Classic S/S
Dilutional hyponatremia/
Water intoxication: Causes
brain tissue swelling,
(cerebral edema)
hallucination, confusion,
delirium, seizure tremors,
headache
Diagnostics
▪ High urine specific gravity:
High urine concentration
▪ Decreased hematocrit
▪ Hyponatremia
▪ Hyperkalemia
Complications Cerebral edema: Increased
ICP
▪ Fluid restrictions 500 ml/day
Treatment
Treatment of choice:
Hypertonic saline (3%)
Polyuria (2-3L/H)
Polydipsia
S/S of dehydration: Dry skin
and mucus membrane,
tachycardia, weak pulses,
weakness
▪ Low urine specific gravity:
Low urine concentration
▪ Increased hematocrit
▪ Hypernatremia
▪ Hypokalemia
Dehydration: Hypovolemia
▪ Increase fluid intake, prevent
dehydration
Treatment of choice:
Synthetic vasopressin:
Desmopressin (DDAVP)
(Intranasally, IV, IM, SQ)
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Common endocrine disorder affecting ACTH: Cushing’s vs.
Addison’s disease
Remember:
ACTH has a complex effects to adrenal cortex causing release of involved hormones
(cortisol, aldosterone, androgens: The “SSS” hormones). Note that hormones travels to
circulation with a systemic effects to many organs. It is also important to know that
negative feedback plays a role in the release of these hormones. For instance
increase levels of cortisol halts release of cortisol releasing hormones by hypothalamus
(CRH), and ACTH in anterior pituitary. This is mechanism is necessary in the diagnosing
between cushing ‘s syndrome and cushing’s disease.
Cushing’s
Mechanism
Elevated levels of ACTH, CRH,
Adrenal cortex hormones
particularly cortisol, aldosterone
and androgens
Etiology
Endogenous: Cushing’s disease
(pituitary or adrenal tumor)
Exogenous: Cushing’s syndrome
(steroids medications)
Classic S/S
Due to:
Glucocorticoids (cortisol)
S – Sugar
▪ Hyperglycemia
▪ Truncal obesity: Hyperglycemia
increases insulin levels and
targets adipose tissues in the
center of the body (activates
lipid build-up)
▪ Buffalo hump, moon shaped
face: cortisol disturbs lipid
metabolism (lipodystrophy)
▪ Sleeplessness/irritability
(Cortisol plays a role in
circadian rhythm)
▪ Mental disturbances: cortisol
disturbs brain function (unclear
reason)
▪ Risk for infection: cortisol
dampens immune response
Addison’s disease
(primary adrenal insufficiency)
Destruction of adrenal gland
resulting to low levels particularly
of cortisol and aldosterone, and
some androgens. It affects the
adrenal gland itself the reason
why it is called primary
insufficiency
Autoimmune
Due to:
Glucocorticoids (cortisol)
S – Sugar
▪ Hypoglycemia (weakness,
disorientation, lethargy)
▪ Bronze skin
(hyperpigmentation): low levels
of cortisol stimulates production
of ACTH and melanocyte
stimulating hormone (negative
feedback), high levels of ACTH
and MSH stimulates production
of melanin.
Mineralocorticoids
(aldosterone)
S – Salt
▪ Hyponatremia (salt craving,
seizure, confusion, syncope)
▪ Hyperkalemia (cardiac
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▪ Amenorrhea/infertility
/impotence: cortisol inhibits
gonadotropin releasing
hormone in both male and
female
▪ Muscle, bone (osteoporosis,
hypocalcemia), tissue
breakdown, easy bruising,
abdominal striae: d/t direct
effect of cortisol to tissues
Mineralocorticoids
(aldosterone)
S – Salt
▪ Hypernatremia, hypokalemia
▪ Hypertension: d/t retained
sodium and water
▪ Weight gain
Androgens
S – Sex hormones
▪ Hirsutism, acne, gynecomastia
in males
arrhythmias, metabolic acidosis)
Remember: Hyperkalemia = H+
ion acidosis
▪ Hypercalcemia: enhanced
absorption of calcium in GI d/t
low hemoconcentration (low
levels of water in the blood)
▪ Hypovolemia, Hypotension: d/t
inability to reabsorb sodium and
water
▪ Weight loss
Androgens
S – Sex hormones
Men: not affected (major source
of androgens in men is testes)
Women: Loss of pubic, armpit hair,
decrease sex drive
▪ 24 hour urine – cortisol level
(normal: 80-120 mcg/24hr)
▪ Dexamethasone suppression
test: Low dose of
dexamethasone is given
(exogenous)
Diagnostics
“Normally if cortisol level is high
by giving the exogenous
cortisol, ACTH is low d/t
negative feedback
mechanism”
If ACTH remains unchanged:
(+) endogenous type – tumor in
the pituitary
▪ MRI/CT scan
ACTH stimulation test: Low dose of
synthetic ACTH is given to
stimulate adrenal glands to
produce cortisol and aldosterone.
Positive (+) if no increase in
cortisol and aldosterone.
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"Addisonian crisis" or "adrenal
crisis": Abdominal, back, leg pain,
vomiting, diarrhea, severe
dehydration, hypovolemia, loss of
consciousness
Complications
▪ Diabetes
▪ Hypertension
▪ CHF
DOC: Lysodren (Mitotane)
Treatment
▪ Treat underlying cause:
remove tumor
▪ Prevent complications
Remember: Addison’s disease is
an autoimmune disorder.
Generally triggered by stressors
(infection, stress, injury). More
importantly, as a disorder
characterized by low cortisol
levels the patient does not
respond effectively to stressors.
This requires immediate care.
DOC: Hydrocortisone
▪ Prevent complications by
preventing stress
Remember: Stopping medications
can lead to Addisonian crisis. In
addition, endocrine disorders in
general requires lifetime
maintenance of medications.
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Common endocrine disorder affecting thyroid hormones:
Hyperthyroidism vs. hypothyroidism
Remember:
Thyroid hormones T4 once released in the blood is converted to T3 to exert its effect.
It increases the body's sensitivity to catecholamines (epinephrine and norepinephrine.
Catecholamines binds to sympathetic receptors to cause stimulation of the
sympathetic nervous system (SNS) “fight/flight response. It also speeds up cell
metabolism to burn more energy (fats and carbohydrates). Overall, increase levels of
thyroid hormones indicates increase body activity in hyperthyroidism. Hypothyroidism
is the exact opposite.
Hyperthyroidism
Hypothyroidism
Too much thyroid hormones
causing hypermetabolic state
due to an autoimmune response,
genetic mutation, injury or
infection
Thyroid gland does not produce
enough thyroid hormone.
Etiology
Autoimmune: Grave’s disease
(most common cause). B-cells
produce thyroid stimulating
antibodies that mimics TSH and
bind to thyroid receptor sites to
stimulate thyroid gland to
secrete thyroid hormones
Toxic nodular goiter: mutated
TSH receptor keeps thyroid
gland active
Thyroid adenoma: benign tumor
producing excessive thyroid
hormone
Iodine deficiency: most common
cause of hypothyroidism and
goiter worldwide d/t low supply
of iodine
Hashimoto's thyroiditis:
autoimmune disease
characterized by infiltration of
the thyroid gland with T-cells
and autoantibodies causing low
production of thyroid hormones
Pituitary tumor (central
hypothyroidism): causing low
levels of TSH
Congenital hypothyroidism in
children (cretinism): can be d/t
maternal hypothyroidism
Classic S/S
Exophthalmia (proptosis): d/t
sympathetic activity
overstimulating eye muscles to
contract, d/t immunemediated inflammation by
hypermetabolic state causing
fat deposit in the retro-orbital
(eye socket) pushing the eye
ball
Weight loss, (in spite of increase
appetite), diarrhea, fever, heat
intolerance, sweating, moist
warm skin, amenorrhea, hirsutism
Mechanism
Weight gain (in spite of poor
appetite), constipation,
hypothermia, cold intolerance,
dry course skin, menorrhagia
(abnormal heavy menstruation),
hair loss: d/t low metabolic rate
Bradycardia, hypotension,
bradypnea, lethargy, fatigue,
poor memory and concentration,
hypersomnia: d/t less sympathetic
activity
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: d/t body producing more heat,
increase metabolic rate
Tachycardia, hypertension,
palpitations, tachypnea, anxiety,
tremors, hyperactivity, insomnia,
fatigue, depression: d/t
sympathetic activity
Increased T3 T4
Decreased TSH: d/t negative
feedback mechanism
Diagnostics
Complications
Remember: If TSH is high, it is
caused by a pituitary tumor
(central hyperthyroidism). If low
then it is primary (caused by
thyroid condition itself)
Radioactive Iodine uptake test
and thyroid scan: remember
that thyroid is the only organ
that synthesizes iodine to
produce its hormones. In thyroid
tumor for example, it can be
visualized easily via scan d/t
increase absorption of iodine.
Thyroid Storm or thyroid crisis
(severe hypermetabolism):
triggered by stressors (infection,
injury, surgery, stopping
treatment)
Remember: Thyroid storm is
characterized by exaggerated
normal s/s of hyperthyroidism
(e.g. High fever, SVT) In addition,
it is most commonly caused by
Grave’s disease in which it can
be triggered by any stressors as
an autoimmune disorder.
Congestive heart failure: d/t
overactivity of SNS
Decreased T4
Increased TSH: d/t negative
feedback mechanism
T3: rarely helpful since there is
inadequate T4 (Normally T4 is
converted to T3 to exert its
metabolic effect)
Myxedema coma: developed
when there is another illness
characterized by severe
hypothermia without shivering,
bradycardia and
hypoventilation, mental
sluggishness and coma
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Treat cause: remove tumor
DOC:
▪ Tapazole (Methimazole)
▪ Propylthiouracil (PTU)
Treatment
Remember: Anti thyroid drugs
cause agranulocytosis,
thrombocytopenia
Symptomatic:
▪ Beta blockers “olols” –
regulates heart rate and
rhythm
HYPOTHYROIDSM
Prevent complication: prevent
triggers
Prevention: Iodine supplement to
common foods (e.g. iodized
salt) in developing countries
DOC:
▪ Levothyroxine (L-thyroxine,
Synthroid): synthetic longacting form of thyroxine.
Remember: Taken 30–60 minutes
before breakfast, or 4 hours after
food because food and calcium
can inhibit the absorption of
levothyroxine. Taken at HS
because it can cause insomnia.
Do not stop giving the medication
to pregnant women, stopping the
medication may cause
HYPERTHYROIDSM
congenital hypothyroidism
(cretinism). Growing fetus is
dependent on thyroid hormones
from the mother.
Prevent complication: do not stop
medications
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Common endocrine disorders: Diabetes mellitus
Remember:
To understand diabetes mellitus further, it is important to know the metabolism of nutrients
particularly glucose in causing effect to body tissues. Glucose apart from O2 is the primary
source of ATP (cell energy) of any living cells to function effectively. For instance, the brain
needs approximately 70% of glucose to maintain its function. It simply means,
abnormalities to glucose metabolism has an obvious neurologic manifestations. Acidosis,
as a complication of DM1 is a life threatening acute condition that is not compatible to
cell function. Remember, any form of acidosis (metabolic/respiratory) causes CNS
depression and subsequent effects to other organs.
Diabetes mellitus 1
Mechanism
Etiology
Absolute lack of insulin: d/t
failure of the pancreas (β-cells)
to secrete insulin. Insulin is
necessary to facilitate transfer or
diffusion of glucose to the cells
necessary to form ATP. Since
there is absolute lack of insulin,
the patient needs insulin
administration.
▪ Genetic
▪ Autoimmune: Unknown
▪ Epstein barr virus (EBV): triggers
autoimmune response,
inflammation to Islets of
Langerhans in the pancreas.
Diabetes mellitus II
Insulin resistance: pancreas
produces enough insulin but the
cells are just simply resistant to
insulin (insulin cannot bind to
insulin receptors) thereby leaving
the glucose outside the cell
(hyperglycemia). Overtime,
pancreas produces insulin
effectively as a compensation.
However, it cannot sustain this
mechanism leading to
hypoplasia and thereby
produces less insulin. Normally,
the patient does not need insulin.
Insulin resistance syndrome (aka
metabolic syndrome): Presence
of 3 or more of the following
criteria:
Increased waist circumference:
Men: ≥40 in (102 cm)
Women: ≥35 in (89 cm)
Blood pressure: (M/F)
≥130 mm Hg systolic or ≥85 mm Hg
diastolic or drug treatment for
hypertension
Triglyceride level: (M/F)
>150 mg/dL (1.7 mmol/L) or drug
treatment for elevated triglycerides
High-density lipoprotein (HDL:
Men: <40 mg/dL (1.04 mmol/L)
Women: <50 mg/dL (1.3 mmol/L) in
women or drug treatment for low HDL
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Fasting glucose levels: (M/F)
≥100 mg/dL (5.6 mmol/L) or drug
treatment for elevated blood
glucose
Acronym: "We Better Think High
Glucose"
Classic S/S
Polyphagia: d/t cellular
starvation (glucose is the
primary food for the cell)
Polyuria: d/t increase blood
concentration
(hemoconcentration), normal
body’s response is diuresis to
lessen blood osmolality caused
by hemoconcentration
Polydipsia: d/t excessive
urination (polyuria)
Glucosuria: d/t excessive
amounts of glucose in blood
(hyperglycemia)
Muscle wasting/weight loss: d/t
body’s response in the
absence of glucose. It uses
other sources of nutrients
through proteins stored in
muscles and fats (lipolysis)
stored in adipose tissues.
Acute:
Diabetic ketoacidosis: d/t
lipolysis, breaking down free
fatty acids. The liver then
converts fatty acids into ketone
bodies (acetoacetic, βhydroxybutyric acids)
Blood acidity by ketones: S/S
Complications
▪ Acetone breath: fruity odor d/t
accumulation of ketones
▪ Kussmaul’s respiration: deep
labored breathing as an
attempt of the body to reduce
acidity.
▪ Hyperkalemia: remember
acidosis is hyperkalemia. Body’s
response to acidosis is to
eliminate H+ ions in the blood
in exchange of K+ coming from
Polyphagia
Polyuria
Polydipsia
Glucosuria
(no weight loss due to the fact
that the there is no absolute lack
of insulin. It does not use other
sources such as lipids and protein
to cause lipolysis)
Acute:
Hyperosmolar hyperglycemia
state (HHS) – non ketosis:
hyperglycemia results in
excessive loss of water by
polyuria leaving the blood
concentrated (hyperosmolarity).
Remember, osmolarity works by
drawing solutes from lower
concentration to higher
concentration (cells-serum). This
results in severe cellular
dehydration as the cycle goes
on.
Cellular dehydration: S/S
▪ Mental status changes:
(Hallucination, confusion,
seizure, coma) – d/t loss of
circulating fluids to the brain
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the cells. However, due to
excessive diuresis, potassium
loss is anticipated
(hypokalemia)
▪ Arrhythmias: d/t potassium
imbalance.
▪ Mental status changes: d/t
severe ketoacidosis (acids
causes CNS depression)
Chronic:
▪ Neuropathy
▪ Retinopathy
▪ Gastropathy
▪ Nephropathy
▪ Peripheral vascular disease
▪ Erectile dysfunction
▪ Coronary artery diseases/AMI
▪ CVA
Diagnostics
▪ Weakness, nausea/vomiting,
dry mouth
▪ Hypokalemia: d/t excessive
urination
▪ Hypovolemia (Hypotension,
tachycardia, tachypnea)
Remember: HHS manifestations
also happen in type 1 since there
is the same hyperglycemic and
hyperosmolar mechanism.
However, there is only minimal
chance of developing acidosis
because there is no absolute lack
of insulin. Unless if not treated
promptly or hyperglycemia is not
controlled. Uncontrolled type 2
can also lead to chronic
complications in type 1.
▪ Fasting blood glucose
<200 mg/dl: normal
>100-125 mg/dl: pre-diabetes
>125 mg/dl: diabetes
▪ Glucose tolerance test
1. NPO (8hrs)
2. Take 100 g (40z) glucose
3. Take CBG after 2 hrs.
4. If >200 mg/dl: Diabetes
Remember: Blood glucose level is
stabilized in 2 hours.
▪ HBA1C (glycosylated HgB):
Measures 3 month average
blood sugar & can be used as
Same with type 1
a test for glycemic control in
patients with diabetes.
Remember: HgB is exposed to
glucose in the blood, and they
are bound together through the
glycation process.
Parameters:
Patients with diabetes:
< 7% Good control
> 9% Poor Control
> 12% Very Poor Control
With no diabetes:
4 - 5.6% normal level
5.7 - 6.4% high chance
≥6.5% Diabetes
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▪ Lifestyle modification
▪ Prevent DKA
▪ Insulin administration
Treatment
DKA Management:
▪ Fluids for dehydration
▪ Aggressive Insulin
▪ Electrolyte replacement
▪ Lifestyle modification (screening
for insulin resistance syndrome)
▪ Prevent HHS
▪ Insulin administration (if
needed)
HHS Management:
▪ Fluids for dehydration
▪ Electrolyte replacement
▪ Insulin (non-aggressive)
DKA
Blood sugar
S/S
Blood pH
Ketones
Management
>300 mg/dl (enough to cause
an acute complication)
Less pronounced altered
mentation, more rapid onset
of hyperglycemia symptoms,
hyperventilation, abdominal
pain (d/t acid accumulation)
common
<7.25 (acid)
HCO3 10-18 meqs/l
HHS
>600 mg/dl
More pronounced altered
mentation, gradual onset of
hyperglycemia symptoms,
hyperventilation, abdominal
pain (d/t acid accumulation)
less common
≥ 7.30 (usually normal)
>18 meqs/l HCO3
Positive
Minimal
Aggressive insulin and
dehydration management
Aggressive dehydration and
non-aggressive insulin
administration.
Insulin administration:
Remember:
▪ Glargine (Lantus) and
Detemir (Levemir)
cannot be mixed with
short acting insulins.
▪ Rapid acting insulins
such as Lispro are “see
food” insulins. Make
sure the patient eat
prior to administration.
RI insulins are the only
insulin that can be
given IV.
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1
2
3
4
Aspirating insulins:
1. Inject air to NPH (cloudy) insulin 2. Inject air to Regular (clear) insulin 3. Do not
remove needle from Regular insulin, aspirate desired amount 4. Aspirate desired
amount from NPH.
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Oral hypoglycemics (OHA):
OHA
Example
Mechanism
Common effects
↑ insulin sensitivity
↑ glucose uptake
↓ Glycogenolysis
(glycogenolysis:
breaking down
glycogen to form
glucose)
GI upset: Weight loss
Lactic acidosis
Remember: Cannot be given
to patient undergoing
procedures given with iodine
contrast or ↑BUN, ↑creatinine. It
may compromise kidney
function because kidney’s
normal response is to excrete
iodine and excessive waste
such as lactic acid.
Glimepiride,
Glipizide,
Glyburide
Stimulates β-cells
to secrete insulin
Hypoglycemia
Weight gain
Pioglitazone
↑ insulin sensitivity
Weight gain, edema
May cause liver damage,
CHF, fracture
Nateglinide
Repaglinide
Stimulates β-cells
to secrete insulin
Hypoglycemia
Weight gain
Sodium – glucose
transporter
inhibitor
Canagliflozin
Dapagliflozin
Prevents
reabsorption of
glucose in kidneys,
promotes excretion
of glucose
Diuresis, glucosuria
Hypotension
Weight loss
Alpha
glucosidase
inhibitors
Acarbose
Miglitol
Slows the digestion
of carbohydrates
and delay glucose
absorption
GI upset, bloating, diarrhea
Weight loss
Biguanide “first line
Metformin
drug”
Sulfonylureas
“ 3Gs”
Thiazolidinediones
/Glitazones
“TZDs”
Glinides
Weight loss:
Biguanide
Sodium–glucose transporter inhibitor
Alpha glucosidase inhibitors
Weight gain:
Sulfonylureas
Thiazolidinediones/Glitazones
Glinides
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Acute management: DKA and HHS
1
Fluid management:
(24-48 hours: 6-8 L/day)
Isotonic (0.9% NaCl): Replaces
loss fluids
Hypotonic (0.45% NaCl): to
reverse cellular dehydration by
forcing fluids from intravascular
to intracellular space.
Insulin management:
2
3
Can be concurrent with fluid
management (higher priority).
More aggressive in DKA than HHS
Potassium management:
(Preventing cardiac arrhythmias)
The administration of sodium
bicarbonate solution to correct
acidosis is controversial. There is
little evidence that it improves
outcomes beyond standard
therapy. It may actually lead in
certain complications.
1. Fluid bolus
2. If CBG ≤ 250 mg/dl
D5W for 8 hours (dextrose
containing to prevent sudden
hypoglycemia and a hypotonic
solution to maintain cellular
hydration)
3. If s/s of dehydration are still (+)
D5W + NaCl for 12 hours
1. Insulin bolus
(0.1 units/kg)
2. Insulin infusion
(0.1 units/kg/hr.)
If CBG not decreased by 10%:
Repeat loading dose
(0.1 units/kg)
If no response:
Double dose (0.2 units/kg)
2. If CBG ≤ 250 mg/dl
D5W for 8 hours (dextrose
containing to prevent sudden
1. <3.5
meqs/L (mmol/L):
hypoglycemia
and a hypotonic
20-30
meqs/L
solution
to maintain cellular
hydration)
2.
3.5
5.5dehydration
meqs/L (mmol/L):
3. If
s/s– of
are still (+)
20-30
meqs/L
D5W + NaCl for 12 hours
3. ≥5.5 meqs/L (mmol/L):
Discontinue potassium
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Other endocrine disorders: Turner vs. Klinefelter syndrome
Question: The nurse is caring for an adolescent client diagnosed with type 1
diabetes. The client exhibits hot, dry skin and a glucose level of 350 mg/dL
(19.4 mmol/L). Arterial blood gases show a pH of 7.27. STAT serum chemistry
labs have been drawn. Cardiac monitoring shows a sinus rhythm with
peaked T waves, and the client has minimal urine output. What is the nurse's
next priority action?
1. Administer IV regular insulin
2. Administer normal saline infusion
3. Obtain urine for urinalysis
4. Request prescription for potassium infusion
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Answer: 2
Rationale: This client has diabetic ketoacidosis (DKA). All clients with DKA
experience dehydration due to osmotic diuresis. Clients with DKA and
hyperosmolar hyperglycemic state require IV normal saline as a priority due
to severe dehydration. Once fluids are given as a bolus, insulin is initiated.
Potassium should never be given until the serum potassium level is known.
Peaked T waves indicate hyperkalemia in this client. Potassium repletion is
started once the serum potassium levels are normalized or trending low (from
elevated levels).
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12
Anatomy and Physiology
Gastrointestinal
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Common disorders affecting GI tract: Peptic ulcer disease
(PUD) (Gastric vs Duodenal ulcers)
Parts of the stomach:
Cardia: secretes mucus (water &
glycoproteins) by Foveolar cells
Fundus and body: contains parietal cells
that secretes HCl acid and chief cell’s
pepsinogen (digests protein)
Antrum: secretes gastrin (also found in
duodenum and pancreas) stimulates
parietal cells to secrete HCl acid.
Remember: With all this acids in the
stomach, it can digest the whole of its
tissues an duodenum. However, Brunner
gland in duodenum secretes mucus that
contain bicarbonate to neutralize this acids.
Stomach also has a thicker layers than
duodenum which is momentarily exposed to
acids. Finally, prostaglandin in stomach and
duodenum continuously stimulates mucus &
bicarbonate secretion, which inhibits acid
secretion and stimulates epithelial growth
by promoting vasodilation.
Gastric ulcer
Mechanism
Etiology
Duodenal ulcer
Loss of protective mechanism
causing break in the inner lining of
the stomach
Loss of protective mechanism
causing break in the inner lining of
the duodenum (first part of the small
bowel/intestines)
Helicobacter Pylori bacteria (most
common cause: Common in low
income settings. It releases
enzymes (adhesins, proteases) that
cause adhesion and damage to
mucosal and Foveolar cells
(secrets mucus & glycoproteins)
NSAIDs: Inhibits prostaglandin
synthesis causing less mucus and
bicarbonate secretions.
Zollinger Ellison syndrome (Gastric
tumor): Parietal cells secrete
excess HCl acid
H. Pylori: causes both gastric and
duodenal ulcers
NSAIDS: causes both ulcers but
mostly gastric
Zollinger Ellison: mostly causes
gastric ulcer but it can also extend
up to the distal end of duodenum.
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Common site
of ulcer
Classic S/S
Complications
Diagnostics
Lesser curvature of the antrum
▪ Epigastric pain: aching and
burning
PAIN WHILE EATING: Relieved by
vomiting
▪ Bloating, belching, vomiting
▪ Weight loss: d/t vomiting and less
desire to food because of pain
upon eating
Hemorrhage: d/t untreated deep
ulcer that affects the nearby artery
Perforation: This allows gastric
content into peritoneum. This leads
to peritonitis.
Remember: Peritoneal space is
usually sterile. Peritonitis is a serious
condition to any GI disorders that
can lead to septic shock.
Upper endoscopy with biopsy:
biopsy is done to see if there is
malignancy or H. Pylori infection
Proximal part of duodenum (right
after pyloric sphincter)
▪ Epigastric pain: aching and
burning.
PAIN IF NOT EATING: Relieved by
food (eating)
▪ Bloating, belching, vomiting
▪ Weight gain as food intake relieves
pain
Same
Same
H. Pylori test: blood, breath, stool
Treatment
Prevent substances that triggers
ulcer: smoking, alcohol, caffeine,
NSAIDs
Same
Triple Therapy (for H. Pylori infection):
Amoxicillin + Clarithromycin + PPIs
Acronym: ABCP
Anti-ulcers
A: Antacids
(Aluminum, Magnesium)
B: Blockers (H2 blockers) “dine”
(Ranitidine, Cimetidine)
C: Cytoprotective “fate”
(Sucralfate)
P: Proton pump inhibitors “zole”
(Pantoprazole, Omeprazole)
Remember:
Antiulcer medications cause diarrhea except Aluminum which causes
constipation.
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Gastric surgeries: Treatment for stomach cancer, severe PUD
Billroth I: (Gastroduodenostomy) - removal of the distal two-thirds of the
stomach; the remaining stomach is anastomosed to the duodenum.
Billroth II: (Gastrojejunostomy) - removes the distal two-thirds of the stomach,
the remaining is anastomosed to jejunum.
Roux operations (Roux-en-Ys): Gastric bypass surgeries for many indications
such as gastric cancer, treatment of morbid obesity, reconstruction of
previous surgeries, etc.
Roux-en-Y distal gastrectomy: An end-to-side surgical anastomosis of bowel
used to reconstruct the GIT. Typically, it is between stomach and small bowel
that is distal (or further down the gastrointestinal tract) from the cut end.
Roux-en-Y Gastric bypass: (RYGB) procedure uses a small proximal portion of
the stomach to create a gastric pouch that is anastomosed to the Roux limb
(the food recipient portion) of the small intestine, bypassing most of the
stomach and a portion of the duodenum.
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Common complication (gastric surgery): Dumping syndrome
Dumping syndrome: Rapid emptying of hypertonic gastric contents into the
duodenum and small intestine. This process leads to fluid shift from the
intravascular space to the small intestine. Remember that hypertonic solution
attracts fluid from an area of lower concentration to higher concentration. This
mechanism leads to hypotension and activation of the sympathetic nervous
system. Symptoms include abdominal pain, diarrhea, nausea and vomiting,
dizziness, generalized sweating, palpitations and tachycardia. Imagine the
feeling after periods of starvation, eating rapidly and dumping volume of food
to your stomach and eventually to duodenum for absorption. How much
would it feel more for a patient with smaller stomach capacity?
Nursing Care:
▪ Delay gastric emptying
▪ Small, frequent meals - reduces
the amount of food
▪ High in protein and fat - take
longer to digest and will remain
in the stomach longer than
carbohydrates
▪ Drink fluids between meals (at
least 30-60 mins before or after
meals) - fluids with meals would
promote passage of stomach
contents into the jejunum easily
and worsen symptoms
▪ Low carbohydrates carbohydrates are broken
down into simple sugars easily
▪ High in fiber – delay the
emptying of the stomach and
prevent rapid absorption of
simple sugars
▪ Eat slowly, Low fowler’s (while
eating) Avoid sitting up, low
fowler’s to flat position (after
eating) - gravity increases
gastric emptying. Lying down
after meals would slow down
gastric emptying.
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Post-operative diet progression: Clear vs. Full liquid vs. Soft
Common disorders affecting GI tract:
Celiac disease (Gluten enteropathy)
Gluten:
A group of various proteins found in
wheat and in other grains such as
barley and rye. Moderate quantities
are found in oat (depending on the
variety). Contains gliadin that triggers
immune response.
Celiac disease (Gluten enteropathy):
An autoimmune disorder in which chronic
inflammation caused by gluten damages the
small intestines. The inflammation is mediated by
T cells, leads to disruption of the structure and
function of the small bowel's mucosal lining and
causes malabsorption as it impairs the body's
ability to absorb nutrients, minerals, and fatsoluble vitamins A, D, E, and K from food.
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S/S:
Malabsorption to:
▪ Water: causes diarrhea
▪ Fat: causes Steatorrhea
(malodorous fat in the stool)
▪ Iron: causes microcytic
anemia
▪ Vitamin B12: causes
macrocytic anemia
Other S/S:
▪ Failure to thrive in children
▪ Weight loss
Diagnostics:
Biopsy, serum antibodies
Remember: Inflammatory
response usually happens to
duodenum because it is the first
to get exposed to gluten.
Ironically, this is where majority
of the absorption process takes
place. In fact, celiac disease is
one of the most common cause
of malabsorption syndrome.
Can have: 3 C’s
Corn, Cassava, Coconut
Cannot have: 4 C’s
Cakes, Cereals, Cookies,
Crackers
Cannot have: 4 P’s
Pasta, Pretzel, Pizza, Pastries
In general: Avoid BROW
B: Barley (high amounts)
R: Rye (high amounts)
O: Oat (depending on
variety)
W: Wheat (high amounts)
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Common disorders affecting GI tract: Inflammatory bowel
disease (IBS): Crohn's disease vs. Ulcerative colitis
Crohn's disease
(Regional enteritis)
Mechanism
Etiology
Classic S/S
Complications
An inflammatory response that
affects anywhere of the GI tract. It is
immune related, which means it is
triggered by a foreign pathogen in
the GI (e.g. Pseudomonas). The
inflammatory response is
uncontrolled and unregulated that
leads to destruction of the cells in
the GIT.
Characteristics:
▪ It affects all layers (transmural)
▪ Can affect any (mouth-anus)
▪ Most common site is ileum ((RLQ)
▪ Scattered or in patches “patchy”
Genetics - familial
▪ Abdominal pain: crampy, RLQ
pain associated with ileum site
▪ Diarrhea: d/t malabsorption of
water in the colon (3-4 /day)
▪ Bloody stool (porridge like): d/t
damaged intestinal tissues
▪ Fever: d/t inflammatory response
▪ Malabsorption: d/t affectation of
the small intestine (most
commonly ileum)
▪ Weight loss: d/t malabsorption
▪ Abscess to sepsis
▪ Fistula: d/t perforating ulcer
▪ Peritonitis
Ulcerative colitis
More common than Crohn’s
disease. An inflammatory response
that affects the colon (large
intestines including the rectum).
Autoimmune related, which means
the body’s own immune cells
promotes inflammatory response. It
characterized by remission (healing)
and flares (exacerbation/new
damage).
Characteristics:
▪ Affects mucosa and submucosa
only
▪ Affects colon only
▪ Most common site is
recto/sigmoid (LLQ)
▪ Continuous (from area to another)
▪ Autoimmune
▪ Genetics - familial
▪ Diet and stress
▪ Abdominal pain: crampy, LLQ pain
associated with recto/sigmoid
▪ Diarrhea (More severe and
painful): d/t malabsorption of
water in the colon (10 or more x
/day). More severe since it mainly
affects colon where water is
absorbed.
▪ Bloody stool (mucoid like with pus)
▪ Fever: indicates flares
▪ Malabsorption and weight loss
(seldom): because it does not
affect small intestines
▪ Dehydration: d/t severe diarrhea
▪ Toxic megacolon: rare but serious
d/t severe inflammation causing
air trapping in the colon. This leads
to enlargement and rupture.
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Diagnostics
Treatment
▪ Upper GI series (barium swallow)
▪ Lower GI series (barium enema)
▪ Colonoscopy with biopsy
▪ ↑ESR, ↑C-reactive protein (CRP):
indicates chronic inflammation
▪ CBC: Anemia d/t malabsorption
▪ Colonoscopy with biopsy
▪ Lower GI series (barium enema)
▪ CT scan/MRI
▪ Anti-inflammatory - Prednisone,
Infliximab (Remicade)
▪ Antibiotics – Ciprofloxacin,
Metronidazole
▪ Prevent flares (healthy lifestyle)
▪ Depends on the severity:
Anti-inflammatory: Sulfasalazine,
Mesalamine, Prednisone,
Cyclosporine, Azathioprine
For severe forms: Infliximab
Antibiotics: generally not useful
Surgery: Colectomy
Remember: IBD vs. IBS
Inflammatory bowel disorder (IBD) is different from irritable bowel syndrome (IBS).
IBD is a chronic incurable inflammatory GI disease whereas IBS is a functional
disorder that does not cause permanent damage. IBD is characterized by severe
diarrhea while IBS is alternating constipation and diarrhea
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Colostomies:
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Remember:
Clients with a descending or
sigmoid colostomy drain stool
that is more formed and similar
to a normal bowel movement
that requires irrigation. Although
less common, irrigating this
colostomies create a bowel
regimen that allows patient to
wear a smaller pouch or a
dressing over the stoma.
Remember:
The colostomy stoma should be
beefy red in the immediate
postoperative period. Any
discoloration to the stoma could
indicate decreased blood
supply to the area; the nurse
should notify the HCP.
Colostomies can be permanent
or temporary by performing
colostomy reversal procedure.
Stool characteristics: Possible etiologies
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Common disorders affecting GI tract: Diverticular disease
Diverticular disease:
▪ Diverticular disease of the colon
occurs when saclike protrusions
form in the large intestine (can also
happen in small intestine).
▪ When diverticula become infected
and inflamed, the client has
diverticulitis.
▪ Usually asymptomatic unless
inflamed.
▪ Most common site is sigmoid colon
(LLQ) (d/t smaller space or
diameter=higher pressure “La
Place’s law”).
▪ Exaggerated or abnormal smooth
muscle contractions d/t chronic
constipation mainly causes
formation of diverticula.
Diagnostics:
▪ CT scan
▪ Colonoscopy and barium enema :
contraindicated during acute
stage d/t risk of perforation
Management:
▪ Prevent constipation: High fiber diet
to prevent constipation causing
inflammation of the diverticula
(diverticulitis)
During diverticulitis: Rest bowel
▪ NPO status: severe case
▪ Low-fiber/clear liquid diet: if not
severe
▪ IV fluids (when NPO)
▪ IV Pain relief and antibiotics
▪ Preventing increased
intraabdominal pressure (avoid
straining): to avoid perforation
▪ Avoid laxatives and enemas:
prevent perforation
Etiology: forming the diverticula
▪ Increase colonic pressure: d/t
chronic constipation, low fiber diet
▪ Fatty and red meat intake
Cause: Diverticulitis (inflammation)
▪ Lodged fecalith (e.g. seeds as small
or smaller than “pencil eraser”)
▪ Erosion from high pressure
Classic S/S: Diverticulitis
▪ Painless rectal bleeding: Blood in
the stool (hematochezia) d/t
rupture of the blood vessels that
traverses the muscle layer of the
colon (can be both present in
diverticulitis and diverticulosis itself)
▪ Pain in the LLQ: associated with
sigmoid affectation
Remember: Pain that is not in LLQ
may be a sign of perforation
affecting other portion of the colon
Complication:
Fistula: connects nearby organ
Perforation: leading to peritonitis
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Common disorders affecting accessory organs of GIT:
Liver cirrhosis
Liver cirrhosis: Characterized by chronic scarring and damage of liver tissues. This is due
to constant processing of alcohol (Laennec’s cirrhosis), exposure to Hepatitis B virus, or
any long term or chronic state of hepatocyte destruction such as drugs (hepatotoxicity).
At any point, this can cause fibrotic tissues to build up and eventually becomes
irreversible. This process is called liver cirrhosis (end stage liver damage)
Estrogen
metabolism:
Inactivates harmful
estrogen metabolites
Detoxification:
Converts
ammonia to urea
Liver cirrhosis:
Gynecomastia,
Palmar erythema,
Spider nevi,
Caput medusae
(estrogen promotes
vasodilation, and
capillary fragility
Clotting factors
production: Ability to
coagulate blood
Liver cirrhosis:
Easy bruising
Bleeding
Liver cirrhosis:
Encephalopathy
Asterixis – flappy
tremors
Fetor hepaticus –
musty breath
Bile production:
Breaks down fats
in the duodenum
Albumin :
Maintains oncotic
pressure
Liver cirrhosis:
Ascites
Edema
Liver cirrhosis:
Jaundice, pruritus
(d/t build-up of bile
salts in skin)
Clay colored stool
and dark urine
(d/t bile in the
circulation instead
of draining to GIT)
Glucose metabolism,
iron storage: Source
of energy, HgB
processing
Liver cirrhosis:
Weakness,
Fatigue
Weight loss
Complication
Mechanism
Hepatic encephalopathy
Ammonia that is not converted to urea travels to
circulation and eventually to the CNS. Remember that
any form of acids, practically all waste products can
cause CNS depression. Other symptoms associated with
encephalopathy: Altered mental status (confusion,
agitation, lethargy, somnolence), seizure and coma.
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Portal hypertension
Constant fibrosis and scarring leads to increase pressure
in the portal circulation affecting the “portal triad”
(hepatic artery, hepatic vein, bile duct). Increase
pressure causes cascade of manifestations such as
ascites when fluid is pushed out of the blood vessels. In
addition, portosystemic shunt happens where fluid
channels thru a lower pressure towards systemic
circulation (inferior vena cava – heart). This abnormal
build-up of fluids results into vasoconstriction of the
vessels involving kidneys resulting into renal failure aka
hepatorenal syndrome.
Other manifestations: Splenomegaly, hepatomegaly
Congestive heart failure
(CHF)
Results when the heart compensates due to fluid build-up
which resulted from portal hypertension
Esophageal varices
Results from collateral portal blood flow through vessels in
the stomach and esophagus. When these blood vessels
become enlarged, they are called varices and are more
likely to rupture. Rupture often leads to severe bleeding.
Diagnostics:
▪ Gold standard: Liver biopsy
▪ Laboratory findings: Liver enzymes
(elevated AST, ALT, alkaline
phosphatase) elevated bilirubin, low
albumin, Elevated PT/INR, Elevated
ammonia, low platelet
Treatment: generally irreversible
▪ Prevent liver damage: identify the cause
(e.g. stop alcohol, treat hepatitis)
▪ Liver transplant
▪ Supportive treatment:
Antipruritic: Cholestyramine (Questran)
promotes excretion of bile salts
Albumin replacement: to prevent
ascites
Prevent encephalopathy or elevated
ammonia levels:
Lactulose - promotes excretion of
colonic bacteria (thru feces) as it plays
a role in ammonia production.
Remember: 3x bowel movement is the
goal of lactulose treatment.
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Spider angioma
(spider nevi,
telangiectasia)
Capput medusae
(“medusa” snake
hair, jellyfish)
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Tubes and drains:
Remember:
Keep scissors at the
bedside at all times;
monitor for respiratory
distress, and if it occurs,
cut the tubes to deflate
balloons.
Double port
Linton–Nachlas tube
1. gastric balloon
2. gastric suction
Lumen
Triple port
Sengstaken Blakemore
1. gastric balloon
2. gastric suction
3. esophageal balloon
Quadruple port
Minnesota Tube
1. gastric balloon
2. gastric suction
3. esophageal balloon
4. esophageal suction
Nasogastric
Nasointestinal
Single Lumen
Levine
Cantor
Double lumen
Salem Sump
Miller Abbott
Remember: Acronym single lumen “single word” Levine and Cantor tubes,
double lumen “double word” Salem Sump and Miller Abbott
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Remember:
Continuous suction can be
applied to decompress the
stomach if a double lumen
Salem-sump tube is in place. The
larger lumen is attached to
suction and the smaller lumen
(within the larger one) is open to
air as an air vent. The air vent
(blue pigtail) must remain open
as it provides a continuous flow
of atmospheric air through the
drainage tube at its distal end (to
prevent excessive suction force).
This prevents damage to the
gastric mucosa. If gastric
content refluxes, 10-20 mL of air
can be injected into the air vent.
However, the air vent is kept
above the level of the client's
stomach to prevent reflux.
Common disorders affecting accessory organs of GIT:
Acute pancreatitis, Acute cholecystitis
Protecting the pancreas from
being auto digested:
Pancreas itself continuously
produces ZYMOGEN (inactive
enzyme) to prevent the
enzymes from digesting
proteins in the cells in which
they are made of or
synthesized.
Pancreatitis: A condition
characterized by inflammation
of the pancreas.
Functions:
▪ Endocrine (islets of
Langerhans): 1%
▪ Exocrine (acinar cells): 99%
(production of digestive
enzymes for metabolism)
Trypsin: protein
Amylase: carbohydrates
Lipase: Lipid
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Cullen’s Sign
Grey Turner’s
Sign
Hypocalcemia
Chvostek’s Sign: facial
spasm when touched
Trousseau Sign: Carpal
(hand) or pedal (foot)
spasm once irritated
The gallbladder (storage of bile):
Digestion of fats
When there is fat ingestion, the small
intestines produces cholecystokinin
(CCK) to stimulate gallbladder to
contract and ejects bile through cystic
duct (passage ways) to empty in the
duodenum to aid in the digestion of
fats.
Cholecystitis:
In gallbladder containing stones
(cholelithiasis), during contraction, one
of this stones may lodge in the cystic
duct. If large enough, this causes
backflow of bile to gallbladder and
causes inflammatory response.
Continuous squeezing (contraction)
causes the pain as the classic sign.
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Jaundice:
Bile leaks into
blood
Murphy’s
Sign
Remember: Pneumoperitoneum
Patients who undergone
laparoscopic procedure is at risk
for accumulation of air in the
peritoneum. CO2 is used in
insufflating the abdomen during
the procedure. If the CO2 is
retained, it can irritate the
phrenic nerve causing
respiratory failure. Patient should
be instructed to ambulate asap
to eliminate CO2. Turning sideside may also help.
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Acute pancreatitis
Acute cholecystitis
Mechanism
Autodigestion: The enzymes itself are
digesting the pancreas d/t premature
activation of zymogen. This causes
cascade of mechanisms leading into
massive inflammatory response.
Inflammatory response: d/t large
bile stones (cholelithiasis) blocking
the cystic duct. Infection may also
occur since E.coli, clostridium etc.
are all over the gut.
Etiology
▪ Alcohol abuse: alcohol enhances
early activation of zymogen. It
becomes clogged up in the
pancreatic duct (ducts are
passageways of enzymes towards
the duodenum for digesting food).
Subsequently, these contamination
of zymogen in the pancreas is
activated to become trypsin
(digestive enzyme). This cascade
also promotes activation of other
digestive enzymes. Remember that
alcohol has a dehydrating effect, it
favors the same mechanism. In
addition, alcohol also promotes
inflammatory response.
▪ Gallstones: blocking d/t gallstones
promotes backflow of pancreatic
enzymes, thereby auto digesting the
tissues.
▪ Abdominal pain: epigastric
radiating to back
▪ Fever
▪ Nausea/Vomiting
▪ Tachycardia
▪ Loss of appetite
Classic S/S
▪ Hemorrhagic type: d/to rupture of
the small vessels
Grey turner’s sign -bluish
discoloration of the flanks
Cullen’s sign – bluish discoloration
of the umbilicus
Gallstone: Predisposes the Fs
▪ Fair complexion: more prevalent
to Caucasians
▪ Fat: high fat intake
▪ Female, Fertile, Forty (age ≥40:
Estrogen are made up of fat
cells itself. Estrogen imbalance
predisposes fat deposition
▪ Familial
Abdominal pain: Mid epigastric to
RUQ (radiates to scapula and
shoulders). Rebound tenderness
when palpated. It is also usually
in response to eating high fatty
food due to continuous release
of CCK.
Murphy’s sign: Positive when RUQ is
palpated while patient is
instructed to inhale and suddenly
stops, complains of pain and
catches breath. (pain upon
inhalation)
Jaundice: if the stone lodges
further down to common bile
duct, the bile from the liver
backflows to itself. Increase bile
in the bile ducts of the liver
causes increase pressure and
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bile is pushed into the blood
vessel.
Others S/S:
▪ Fever
▪ Nausea/Vomiting
▪ Tachycardia
▪ Loss of appetite
Remember: Acute pancreatitis is a
very severe kind of inflammation. It
means you expect severe
complications.
Complications
▪ Hypovolemic shock: d/t
hemorrhage
▪ Disseminated intravascular
coagulation (DIC): the body used up
the coagulation function, in effect, if
there is needed coagulation it
cannot produce more coagulants,
causing bleeding.
▪ Cyst abscess: d/t a massive
inflammatory response
▪ Hypocalcemia: necrosis (fat
necrosis) d/t massive inflammation
consumes a lot of calcium.
Peritonitis: d/t rupture or the
microorganisms invading the wall
of the gallbladder and into the
peritoneum.
Remember: Pancreatic function
depends on the precise flow of
calcium within the acinar cells. In
short, calcium is a way of life for
pancreas
▪ ARDS (non-cardiogenic pulmonary
edema): d/t massive inflammatory
response that affects the lung
tissues.
Diagnostics
Elevated Lipase(more specific)
Elevated Amylase
CT scan, USD
Endoscopic retrograde
cholangiopancreatography (ERCP)
▪ Magnetic resonance
cholangiopancreatography (MRCP)
▪
▪
▪
▪
▪ Elevated alkaline phosphatase:
Necrotic ductal cells release
these enzymes
▪ CT scan, USD
▪ HIDA scan (Cholescintigraphy):
Measures gallbladder bile
ejection
▪ Endoscopic retrograde
cholangiopancreatography
(ERCP)
▪ Magnetic resonance
cholangiopancreatography
(MRCP)
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Treatment
▪ REST BOWEL: NPO, NGT if severe
vomiting
▪ Nutritional support while NPO: TPN
▪ Pain management:
IV Morphine
Remember: There is no conclusive
study suggests that morphine causes
spasm in sphincter of oddi.
▪ Anti-nausea/emetic:
Zofran (ondansetron)
▪ Antipyretic
▪ Hydration: IV Fluids, replace
electrolyte
▪ Treat complications:
Oxygen, Antibiotics
▪ REST BOWEL: NPO, NGT to low
intermittent suction (LIS)
▪ Pain management:
IV NSAIDs: Ketorolac
IV Morphine
▪ Anti-nausea/emetic:
▪ Zofran (ondansetron)
▪ Antipyretic
▪ Hydration: IV Fluids, replace
electrolyte
▪ Treat complications: Antibiotics
▪ Surgery: Open cholecystectomy,
Laparoscopic cholecystectomy
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Common GIT disorders: Appendicitis
Appendicitis:
The appendix is a blind pouch
located at the junction of the ileum of
the small intestine and the beginning
of the large intestine (cecum). When
infected or obstructed (foreign body,
fecal material, tumor, lymph tissue),
the appendix becomes inflamed,
causing acute appendicitis.
Appendicitis is an acute condition
that needs immediate surgical
intervention to prevent appendix
rupture and subsequent peritonitis
and sepsis.
Causes: Obstruction
▪ Fecalith: hard fecal matter
▪ Undigested seeds
▪ Pinworm infections: intestinal
parasites
▪ Lymphoid hyperplasia: common in
children and adolescent when
growing, also caused by viral
infections.
Mechanism: Inflammation
The inflammatory process causes
increase pressure and eventually
migration of E. coli (common gut
flora).
S/S:
▪ Fever, Elevated WBC: d/t
inflammatory process
▪ Nausea/vomiting
▪ RLQ (Mc Burney’s point) pain: d/t
inflammation irritating the nearby
nerves. Radiates to umbilicus.
Complications: Further pressure
Compression of the blood vessels
leads to ischemia and the
appendiceal walls becomes weaker
and ruptures. Leakage means
peritonitis and eventually septic
shock.
Management:
▪ REST BOWEL: NPO, NGT if severe vomiting
▪ Pain management:
IV Morphine: Nowadays, there are no concerns of
masking the symptoms of peritonitis iv giving analgesics
▪ Anti-nausea/emetic
▪ Antipyretic
▪ Hydration: IV Fluids, replace electrolyte
▪ Treat complications: Antibiotics
▪ Surgery: Open, Laparoscopic appendectomy
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Other signs:
Appendicitis
Psoas Sign
Irritation or pain
upon Hip
Flexion
Obturator Sign
Irritation or pain on
hip flexion and
abduction
Rouvsing Sign
Pain on RLQ upon
palpation of the
LLQ Flexion
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Blumberg Sign
Rebound tenderness on
palpation of abdomen
(indicates peritonitis)
Areas of referred pain in the abdomen:
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Common GI disorders in children:
Pyloric stenosis vs Intussusception vs Hirschsprung’s disease
Pyloric stenosis
Stenosis of the pyloric
sphincter causing backflow
of food into stomach and
esophagus due to increasing
pressure.
▪ Projectile vomiting: d/t
increasing pressure in the
stomach
▪ Non bilious vomitus:
because food is not
drained yet to duodenum
d/t stenosis
▪ Olive shaped mass: visible
swollen stomach
Intussusception
Hirschsprung’s
One part of the intestine
prolapses and then
telescopes into another part.
It is one of the most frequent
causes of intestinal
obstruction during infancy.
Aka Aganglionic megacolon:
the segment lacking neurons
(aganglionic) becomes
constricted, causing the
normal, proximal section of
bowel to become distended
with feces. Aganglionic also
means loss of bowel tone or
movement leading to fecal
impaction
▪ LLQ pain: d/t fecal
impaction that usually
▪ RLQ pain (intermittent
affects the recto-sigmoid
cramping): guarding
colon
behavior or drawing up legs.
▪ Meconium ileus: unable to
It usually affects the terminal
pass out stool within 24 hour
part of ileum to ascending
after birth d/t constricted
colon (small-large space)
portion. This sign can be
▪ Currant jelly stool: mixed
present in cystic fibrosis (d/t
mucus and blood d/t
dehydrated stool)
adhesions
▪ Ribbon like stool: passing
▪ Sausage shaped mass:
out stool resulting from a
visible mass d/t telescoping
constricted portion in the
rectum.
Complication: dehydration
d/t vomiting
Complication: dehydration
d/t diarrhea, Bowel ischemia
(Necrosis)
Complication: Toxic
megacolon develops due to
relative fecal stasis including
sepsis
Surgical repair: Pylorotomy
▪ Enema to push the
telescoping out:
Air enema is better than
barium d/t relative effects
of constipation or fecal
impaction
▪ Surgery: for bowel ischemia
Surgical resection (removal):
colostomy can be done and
reversed.
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Common GI diagnostic procedures :
Upper GI series vs Lower GI series, ERCP vs MRCP
Procedure
Mechanism
Nursing care
Pre-procedure:
▪ NPO 8 hours before the
Radiographic (X-ray)
test
examination of the
Post-procedure:
upper gastrointestinal
▪ Expect the passage of
(GI) tract. The
chalky, white stool until
esophagus, stomach,
all barium contrast has
and duodenum are
been expelled
made visible on X-ray film
▪ Take a laxative (e.g.,
Upper gastrointestinal series by a liquid suspension.
magnesium
This liquid suspension
(barium swallow)
hydroxide[Milk of
may be barium or a
Magnesia]) to assist in
water-soluble contrast. If
expelling the barium.
only the pharynx and
Retained barium can
esophagus are
lead to fecal impaction
examined with barium,
▪ Drink plenty of fluids to
the procedure is called a
promote hydration and
barium swallow.
eat a high-fiber diet to
prevent constipation.
Pre-procedure:
▪ Take a cathartic (e.g.
magnesium citrate,
Uses fluoroscopy to
polyethylene glycol) to
visualize the colon
empty stool from the
outlined by contrast to
colon.
detect polyps, ulcers,
▪ Clear liquid diet the
tumors, and diverticula.
day before the
procedure: (avoid red
Lower gastrointestinal series Remember: This
and purple liquids)
procedure is
(barium enema)
▪ NPO 8 hours before the
contraindicated for
clients with acute
test
diverticulitis as it may
Post-procedure:
rupture inflamed
▪ Take a laxative (e.g.,
diverticula and cause
magnesium
subsequent peritonitis.
hydroxide[Milk of
Magnesia])
▪ Drink plenty of fluids
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An invasive procedure in
which an endoscope is
passed through the
mouth into the
duodenum to assess the
pancreatic and biliary
ducts. Using fluoroscopy
with contrast media
(iodine dye) during the
procedure, the ducts
can be visualized and
treatments including
Endoscopic retrograde
cholangiopancreatography removal of obstructions,
dilation of strictures, and
(ERCP)
biopsies can be
performed.
Pre-procedure:
▪ NPO 8 hours before the
test
▪ Assess for iodine allergy
(dye allergies)
▪ Assess kidney status:
BUN creatinine d/t use
of contrast dye
(nephrotoxicity)
Post-procedure:
▪ You will not be allowed
to eat or drink anything
until your gag reflex has
returned.
▪ Instruct patient to
report:
Fever or chills,
abdominal pain, N/V:
may indicate
pancreatitis
▪ Black, tarry, or bloody
stools (perforation)
Remember:
Perforation or irritation of
these areas during the
procedure can cause
acute pancreatitis, a
potentially lifethreatening
complication after an
ERCP.
A noninvasive diagnostic
Pre-procedure:
test used to visualize the
biliary and hepatic ducts ▪ Assess for
contraindications prior
via MRI. MRCP uses oral
to the procedure,
or IV gadolinium
Magnetic resonance
including presence of
(noniodine contrast
cholangiopancreatography
certain metal implants
material) and is a safer,
(MRCP)
(e.g. pacemaker,
less invasive alternative
aneurysm clip,
to ERCP to determine the
cochlear implant),
cause of cholecystitis,
pregnancy.
cholelithiasis, or biliary
obstruction.
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13
Musculoskeletal
Anatomy and Physiology
How does muscles contract?
Skeletal muscles:
Neuromuscular junction
Calcium triggers release of
ACH (action-potential). ACH
binds to nicotinic receptors
(cholinergic receptors) in the
muscle cells to cause
contraction.
A smooth muscle is excited by external
stimuli, which causes contraction. Smooth
muscle contractions are involuntary
movements triggered by impulses that travel
through the autonomic nervous system
(ANS) to the smooth muscle tissue.
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Common disorders: Arthritis
Rheumatoid arthritis (RA)
Chronic inflammatory
(autoimmune): Human
leukocyte antigen (HLA),
which are present in these
individuals are triggered by
environmental factors (e.g.
smoking, pathogens) to
cause inflammatory
process. The process
involves immune cells (RH
ABs, IgM Abs) that attack
the synovium (joints). It is
also associated with other
autoimmune diseases such
as SLE, scleroderma etc.
Osteoarthritis (OA)
Progressive loss of articular
cartilage (a connective
tissue that allows gliding of
joints without friction): This
results in significant friction
of bones and eventually
generates inflammation.
The high tensile strength
and elasticity of articular
cartilage helps weight
bearing joints (knees &
hips) distribute the weight
from one bone to the
other. The progressive loss
of elasticity in years
promotes inflammatory
responses to the whole
synovium.
Gouty arthritis (GA)
Hyperuricemia: Levels of
uric acid exceeds the level
of solubility and excretion
through urine. This results
into formation of urate
crystals (sharp crystals)
which usually accumulates
in areas with low blood
flow. Overtime, this
promotes inflammation to
joints (chronic gout)
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▪ Autoimmune
▪ Genetics
▪ Environment
▪ Symmetrical: affects
same joint groups at the
same sides of the body
▪ Peripheral to Weight
bearing joints (as disease
progresses)
PAIN:
▪ Cyclical (from AM-PM)
▪ Last in several hours
▪ Not relieved by rest
▪ AM pain last > 1hr
▪ Pain with swelling
DEFORMITIES:
▪ Boutonnière deformity
▪ Swan-Neck deformity
Others non-specific S/S:
Fever, malaise, low
appetite
▪ Blood test:
Rheumatoid factor (RH
Ab)
▪ Imaging: X-rays
Low bone density, bone
erosions, narrowing of the
joint space, soft tissue
swelling
▪
▪
▪
▪
Age
Joint injury
Obesity
Mechanical stress:
overuse
▪ Asymmetrical: can affect
only one knee, hip joints
▪ Weight bearing to
peripheral joints (as
disease progresses)
PAIN:
▪ AM – PM (worst in PM) d/t
overuse
▪ Last in few hours,
Relieved by rest
▪ AM pain last < 1hr
▪ Pain without swelling
DEFORMITIES:
▪ Bouchard’s deformity
(proximal
interphalangeal)
▪ Heberden’s deformity
(distal interphalangeal)
▪ Imaging: X-rays
Joint space narrowing,
osteophytes (bony
projections from outward
growth)
Primary hyperuricemia:
Unknown
Secondary hyperuricemia:
▪ Acquired
▪ Diet: increase purine
▪ Obesity
▪ Chemotherapy &
radiation (Tumor lysis
syndrome)
▪ CKD
▪ Medications: Thiazide
diuretics and aspirin
▪ Variable symmetry
▪ Usually affects “big toe”
(aka Podagra)
PAIN:
▪ AM or anytime of the day
precipitated by high
purine intake
▪ Podagra: In AM (big toe
burning pain)
▪ May last in several hours
▪ May not be relieved by
rest
▪ AM pain last > 1hr
▪ Burning pain, tender,
swelling
DEFORMITIES:
▪ Tophi (uric deposits): d/t
repeated gouty attacks
▪ Synovial fluid: definitive
(+) urates
▪ Blood test: Elevated uric
acid
▪ Imaging: X-rays
Bone erosions
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Disease modifying antirheumatic drugs (DMARDs):
Acronym: ELISA +
Methotrexate
E: Etanercept
L: Leflunomide
I: Infliximab
S: Sulfasalazine
A: Anakinra
Methotrexate
Remember:
This medications are
aimed to modify the
disease by minimizing the
symptoms of chronic
inflammation and minimize
chances of flare-ups as an
autoimmune disease. This
leads to longer remissions
than exacerbations.
▪ Non-pharmacologic:
▪ Weight loss (exercise)
▪ Physical therapy
▪ Pharmacologic: reducing
pain and inflammation
▪ NSAIDs
▪ Hyaluronic injections to
joints
▪ Surgery:
▪ Hip replacement
▪ Knee replacement
▪ Non-pharmacologic:
▪ Low purine diet
▪ Hydration (promotes
solubility of uric acid)
▪ Pharmacologic: reducing
pain and inflammation
▪ NSAIDs
▪ Steroids
DOC:
▪ Colchicine: Antiinflammatory (acute
gout)
▪ Allopurinol: decrease uric
acid levels (chronic gout)
▪ Probenecid: increases
excretion of uric acid
(chronic gout)
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Dietary modifications:
▪ Increasing fluid intake (2 L/day):
to help eliminate excess uric acid
▪ Implementing a low-purine diet:
particularly avoiding organ meats
(e.g. liver, kidney, brain) and
certain seafood (e.g. sardines,
shellfish)
▪ Limiting alcohol intake, especially
beer: alcohol competes with the
excretion of uric acid in kidneys
▪ Low-fat diet: as excess dietary fats
impair urinary excretion of urates
Hip and knee replacement:
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Nursing: Preventing complications
▪ Provide abduction pillow
between the legs- to prevent
adduction of the affected leg
(prosthesis dislocation)
▪ Do not flex the affected hip more
than 90 degrees – prevent
prosthesis dislocation
▪ Provide elevated toilet seats and
chairs that do not recline.
▪ Assess for signs of hip dislocationincluding shortening and internal
rotation of the leg.
Assess for s/s of complications: DVT
or PE, infections, hemorrhage
Complications:
▪ Bleeding
▪ Prosthesis dislocation
▪ Deep vein thrombosis (DVT)
▪ Infection
Average stay post operatively:
3-5 days (full weight bearing by
discharge)
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Common disorders: Developmental dysplasia of the hip
(DDH) aka Congenital hip dysplasia
Normal development:
▪ Femoral head stays fitted
with the acetabulum
▪ Grow together
DDH:
▪ Femoral head dislocates out
of acetabulum
▪ Grow out of proportion
▪ Unable to form stable joint
S/S: <2-3 months
▪ Extra gluteal or inguinal
folds/Asymmetrical folds
▪ Affected leg shorter when flexed
together (Galeazzi sign)
▪ Laxity/instability: (+) Barlow and
(+) Ortolani maneuvers (done
only by physician)
Remember: If DDH is not treated,
these signs disappear after age
2-3 months d/t the development
of muscle contractures.
Etiology:
▪ Unknown
▪ Breech position of baby: too
much force against fetal thigh
▪ First borns: uterus is not yet
stretch-out putting pressure to
fetal thigh
▪ Low amniotic fluid: not enough
room for fetus’ legs
Key management: Maintain
abduction
▪ Proper swaddling technique
▪ Choosing infant carriers or car
seats with wide bases-infant
seats. Avoiding any positioning
device, seat, or carrier that
causes hip extension with the
knees straight and together.
▪ Pavlik harness (1-6 mos. old)
▪ Closed reduction with Spica
cast (6-18 mos.)
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Ortolani maneuver:
Done after Barlow
maneuver. If (+) dislocation
is determined (Barlow
maneuver), abducting the
adducted leg results into a
clicking sound, (+) Ortolani.
Galeazzi sign:
performed by flexing an
infant's knees when they
are lying down so that the
feet touch the surface and
the ankles touch the
buttocks. If the knees are
not level then the test is
positive, indicating a
potential DDH
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Pavlik harness:
▪ Regularly assess skin for redness or
breakdown under the straps
▪ Dress the child in a shirt and knee socks
under the harness to protect the skin
▪ Avoid lotions and powders to prevent
irritation and excess moisture
▪ Lightly massage the skin under the straps
every day to promote circulation.
▪ Only apply 1 diaper at a time (wearing
≥2 diapers increases risk of incorrect hip
placement
▪ Apply diapers underneath the straps to
keep harness clean and dry
Spica cast:
▪ Keep the cast clean and dry
▪ Check carefully beneath the cast
edges for skin impairment (redness, etc.)
▪ If the cast becomes damp, it can be
dried by exposing it to air during the
child's nap or dryer on a cold setting
▪ Assess for s/s of abdominal pain. This
can be a sign of Cast syndrome
(superior mesenteric artery syndrome). A
rare condition which compresses the
SMA (major artery) that leads to GI
ischemia and necrosis.
Common disorders: Fat embolism
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Medullary cavity:
Located in the center of long bones
▪ Red marrow – for blood cell formation
▪ Yellow marrow – contains mainly fats
Fat embolism syndrome (FES):
A rare, but life-threatening complication that
occurs in clients with long bone and pelvis
fractures. It can also occur in non-trauma–
related conditions, such as pancreatitis and
liposuction. It usually develops 24-72 hours
following the injury or surgical repair.
S/S: The FES triad
(Respiratory/Neurological/Petechiae)
▪ Respiratory problems (e.g. dyspnea,
tachypnea, hypoxemia) after a fat
embolus travels through the pulmonary
circulation and lodges in a pulmonary
capillary, leading to impaired gas
exchange and acute respiratory failure
(similar to PE)
▪ Neurologic changes (e.g. AMS, confusion,
restlessness) d/t cerebral embolism and
hypoxia
▪ Petechial rash (e.g. pin-sized purplish spots
that do not blanch with pressure), which
appears on the neck, chest, and axilla d/t
microvascular occlusion. This is a
distinguishing characteristic from PE.
Fever : d/t a cerebral embolism leading to
hypothalamus dysfunction.
Management: Non specific
Minimizing movement of a fractured long
bone and early stabilization of the injury with
surgery reduce the risk for fat emboli.
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Common disorders: Acute compartment syndrome
ACS:
Is a serious complication due
to neurovascular compromise
from swelling and increased
pressure in a confined space.
This swelling of the soft tissues
surrounding the blood vessels
compresses the blood and
lymphatic vessels further,
causing more fluid to enter the
extracellular spaces, leading
to additional compression. This
worsening cycle can
eventually lead to tissue
ischemia and necrosis.
Classic S/S: The 6 Ps
Early:
Pain: Increasing despite
elevation, analgesics, and ice.
Pressure: Digits are firm and
tense; shiny tight skin
Paresthesia: Tingling,
numbness, burning sensation,
(nerve ischemia)
Pallor: Capillary refill is >3
seconds (poor perfusion)
Late:
Pulselessness
Paralysis: Loss of function
(e.g. Volkmann paralysis)
Diagnosis:
▪ Clinical signs/symptoms (6Ps)
▪ Posterior compartment: Pain
upon dorsiflexion
▪ Anterior compartment: pain
upon plantar flexion
▪ Blood test: Elevated myoglobin,
elevated CK-MB
Remember:
Elevated amounts of myoglobin
overwhelms kidney that leads to
kidney failure. This condition is also
known as rhabdomyolysis.
Management:
▪ Hydration: to eliminate
myoglobin thereby preventing
kidney failure
▪ Fasciotomy: a large incision to
decompress the
compartments. It remains
exposed for several days (upto
2 weeks). Risk for infection is a
priority.
▪ Amputation: if treatment
options are ineffective
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Common disorders: Carpal tunnel syndrome
Carpal tunnel syndrome (CTS):
CTS is caused by compression of a
median nerve within the carpal
tunnel at the wrist. Any swelling in
the canal puts pressure on the
nerve and produces pain and
paresthesia in the median nerve
distribution (first 3½ digits).
Symptoms often worse at night
when the wrists are flexed during
sleep after a day of use.
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Etiology:
▪ Genetics
▪ Work related: Stress to d/t
repetitive tasks (e.g. typing),
force, posture, & vibration
Associated conditions:
▪ Arthritis
▪ Acromegaly
▪ Obesity
▪ Pregnancy: d/t hormonal
changes (fluids retention)
Management:
▪ Behavior modification (e.g.
wrist support while typing)
▪ Physical therapy: isometric
exercise and stretching
▪ Splinting
▪ Steroids
▪ Surgery: relieving pressure in
median nerve (Pain and
tingling may last several
months after surgery which
normally subsides gradually)
Diagnosis:
▪ Physical symptoms
▪ Phalen’s maneuver: flexing
wrist as far as possible for 1
min. (+) tingling or pain
▪ Tinel’s maneuver: tapping
the median. (+) tingling or
pain
▪ Durkan’s test: manually
compressing the median
nerve. (+) tingling or pain
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Assistive devices: Crutches and cane
2 point gait:
1. Advance bad leg and
crutch on the side of good
leg together
2. Advance good leg and
crutch on the side of bad
leg together.
3 point gait:
1. Advance both crutches
2. Advance bad leg
3. Advance good leg
4 point gait (most stable):
1. Advance crutch on the
side of good leg
2. Advance bad leg
3. Advance crutch on the side
of bad leg
4. Advance good leg
Remember:
In assistive devices using cane and crutches, the acronym “good goes to
heaven” and “bad goes to hell” applies. It means, good leg first on going up
and bad leg first on going down using stairs. In addition, assistive device should
always go together with the bad leg, one or the other advances or
simultaneously.
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Using stairs:
Going up: Modified 3 point gait
1. Advance good leg
(goes to heaven)
2. Advance both crutches
3. Advance bad leg
Going down: 3 point gait
1. Advance both crutches
2. Advance bad leg
(goes to hell)
3. Advance good leg
Remember: Acronym “COAL” in holding cane
C – Cane held O – Opposite from A – Affected L – Leg
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Using stairs:
Going up:
1. Advance good leg
(goes to heaven)
2. Advance cane
3. Advance bad leg
Going down:
1. Advance cane
2. Advance bad leg
(goes to hell)
3. Advance good leg
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Tractions: Skin vs skeletal traction
Principles:
▪ Must produce pulling effect
▪ Counter traction must be
maintained
▪ Traction and counter
pull/traction must be
opposite direction
▪ Ropes must move freely
▪ Precise amount of weight
must be applied and must
hang freely
Purpose:
▪ Relieve spasms/promoting
comfort
▪ Promotes alignment
▪ Maintains immobilization
Buck’s (skin traction): A type of skin traction used for fracture of
the hip and femur. The upper body must be flat on bed to
promote counter traction. The affected leg is placed with pillow
to prevent swelling and decrease tension.
Types:
▪ Skin
▪ Skeletal (uses tong, metal
pins and wires)
Russel’s (skin traction): A type of skin traction used for fracture
of the femur similar to Buck’s traction. However, it uses upward
pull as a counter traction in addition to own upper body
traction. It can also utilize metal pins and tongs, in this case it is
called a skeletal traction.
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Nursing care: Traction
Bryant’s (skin traction): A type of skin traction used for fracture
of the femur in children age 2 years or under 20-30 lbs. Buttocks
should be off the bed and legs at right angle to the body
Dunlop’s (skin traction): A type of skin traction
used for fracture of the arm (humerus, radius,
ulna). Used when closed reduction is difficult or
traumatic. Elbow flexed at 45 ° (radial/ulnar
fracture as illustrated above), horizontal elbow
(humerus fracture).
T – Temperature checks for
infection d/t applied metal
pins and tongs aka pin
tract infection (skeletal
traction)
R – Ropes hanging freely
maintaining counter
traction
A – Analgesia (relieve pain)
C – Circulation (check
neurovascular status - 6Ps)
T – Trapeze bar to assist in
mobility (prevents
pneumonia)
I – Infection (assess for s/s of
associated infection e.g.
pneumonia, pin tract
infection)
O – Output and intake
(maintain hydration)
N – No weights on the floor
(must be hanging freely)
Cervical (skeletal traction): A type of skeletal
traction that uses tongs (e.g. Crutchfield tongs)
to promote traction to patients with cervical
fractures. Weights are used as counter tractions.
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Scoliosis:
Characterized by lateral curvature
and spinal rotation to the spine.
Caused by congenital or
pathologic conditions, it is most
often determined to be idiopathic
(unknown cause). Commonly first
noticed during periods of rapid
growth, particularly during early
adolescence in girls.
Screening for early detection:
Girls (age 10-12)
Boys (age 13-14)
Braces for scoliosis: A type of skin traction device that
uses with the same purposes such in traction. Boston
brace, Wilmington brace are thoracolumbosacral
orthosis (TLSO) braces. Milwaukee brace is cervical
thoracolumbosacral orthosis (CTLSO)
Nursing care:
▪ Perform proper skin care
▪ Wear a cotton t-shirt under the
brace
▪ Do not use lotion or powder can
cause skin irritation beneath the
brace.
▪ Most braces are worn for up to
23 hours/day and removed for
bathing and exercise
▪ Address psychosocial needs (e.g.
body image, socialization)
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14
Integumentary
Anatomy and Physiology
The Skin
Function:
Protection: an anatomical barrier from pathogens
and damage
Sensation: contains a variety of nerve endings that
react to heat and cold, touch, pressure, vibration,
and tissue injury
Heat regulation: contains a blood supply greater
than its requirements, allows control of energy loss
by radiation, convection, conduction.
Control of evaporation: provides a relatively dry and
semi-impermeable barrier to fluid loss
Storage and synthesis: storage center for lipids and
H20, and synthesis of vitamin D
Excretion: sweat contains urea
Skin flora: competes with transient pathogens for
nutrients, secreting chemicals against them, or by
stimulating the skin's immune system.
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Common disorders: Burns
Burns Classification
SUPERFICIAL
DEEP
Characteristics:
▪ Painful, swelling
▪ Normal capillary refill
▪ Blanchable redness
SUPERFICIAL
Affects: Dermis
▪ Dry/red (erythema)
▪ Painful
Remember: This is not
included in TBSA (rule
of 9 calculation)
EPIDERMIS (1°)
Characteristics:
▪ Minimal – No pain
▪ Non blanchable
redness
SUPERFICIAL
Partial Thickness
Affects:
Parts of dermis
▪ Red and moist
with blisters
▪ Very painful
DEEP
Partial Thickness
Affects: All dermis
▪ Pale to red
▪ Minimal pain
▪ Damaged blood
vessels
▪ Extravasation
DERMIS (2°)
Full Thickness
Affects:
Hypodermis (SQ)
▪ Leathery gray or
charred black
▪ No pain d/t
damaged nerves
HYPODERMIS (3°)
Associated Problems:
Evaporation: 30-50 ml/hr. evaporation
leading to hypovolemia
Anemia: d/t destruction of RBC by
injury
Hyperkalemia: d/t shifting of
electrolytes resulting from cellular
injury
Infection: d/t loss of barrier function
Pain: d/t inflammatory process and
affecting nerve endings
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Rule of 9: Total body surface area (TBSA)
Remember: Burns needing
referral to HCP
▪ ≥ 10% TBSA
▪ Deep thickness (partial or full)
▪ Circumferential/around the
area (leads to compartment
syndrome)
▪ Inhalation burns
▪ Chemical burns
▪ Electrical burns
Remember: Use rule of
palm (1%) to each
scattered small wounds.
Remember: Does not need
referral (minor burns)
▪ < 10% TBSA
▪ Superficial burns
First aid:
▪ Flush with cool (not ice cold)
water
▪ Prevent further burning
▪ Manage pain
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Burns management:
1
2
Resuscitative/Emergent phase:
Burns with ≥ 15% TBSA given 24-48
hrs. Goal: Prevent hypovolemia
▪ Parkland Rule (ml/day)
____% (TBSA) X WT (kg) X 4 ml
Isotonic solution:
▪ Hartman Solution/PLR (Preferably
d/t added electrolytes & stays
longer in the serum)
Acute phase: After hemodynamically
stable
Goal: Prevent infection, Pain
management
▪ IV antibiotics (≥60% TBSA)
▪ Wound care
▪ NSAIDs, Morphine
Example: Parkland (ml/day)
50 % (TBSA) X 80 kg X 4 ml
= 16,000 ml/day
1st 8 hrs. 50% = 8,000 ml
2nd 8 hrs. 25% = 4,000 ml
3rd 8 hrs. 25% = 4,000 ml
Total:
16,000 ml/day (24°)
Rehabilitative phase:
Goal: Return of optimum function
3
▪ Emotional support
▪ Surgical debridement (if needed)
Common disorders:
Hospital acquired pressure ulcer (HAPU)
HAPU classification
Affects: Epidermis
Affects: Epidermis to
dermis (e.g. blister)
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Affects: Epidermis to
hypodermis (SQ)
Unstageable: Mostly covered
by slough or necrotic tissue
Affects: Epidermis to
muscles and bones
SDTI: Skin is intact but with
purple discoloration d/t
possible deep tissue injury
Common types of dressing:
Transparent dressing: For
stage 1 pressure ulcer
(protective dressing)
Foam dressing: For stage 2
exudative pressure ulcer
(absorbent)
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Duoderm dressing: For stage 2
pressure ulcer (moist wound
healing). The wound moist itself
promotes debridement.
Hydrogel dressing: For stage 3 or 4
pressure ulcer (hydrates and
promotes debridement)
Question: A client is brought to the emergency department after sustaining thirddegree burns over 50% of the body. Which solution is the best choice for
fluid resuscitation in this client?
1. 0.45% normal saline
2. 5% dextrose in 0.9% normal saline (D5NS)
3. 5% dextrose in water (D5W)
4. Lactated Ringer's solution
Answer: 4
Rationale: Hypovolemic shock and electrolyte imbalance is a priority in patients
with burns. In the emergent/resuscitative phase of burn management, it is
critical to establish an airway and replace fluids and electrolytes.
LR remains in the intravascular space longer than other solutions, which
helps to stabilize blood pressure and avert shock.
Hypotonic solutions (e.g. 0.45% normal saline) quickly leave the intravascular
space and are not useful in replacing intravascular volume. They may also
contribute to peripheral and interstitial edema, which can lead to
pulmonary complications. Hypertonic solutions (e.g. D5NS , 3% saline) can
cause further electrolyte imbalances in a client with severe burns, resulting in
hypernatremia and arrhythmias.
Although technically an isotonic solution, D5W once infused and
metabolized by liver is a hypotonic solution and free water is released to the
tissues rather than remaining in the intravascular space.
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Visual & Auditory
Anatomy and Physiology
Eye
Important components:
▪ Cornea, the anterior
chamber, and lens:
Refraction (focusing ability
of the eye)
▪ Ciliary body:
Accommodation, aqueous
humor production and
resorption
▪ Aqueous humor: Providing
oxygen, nutrients, and
metabolic waste removal
to the lens and the cornea
(which do not have their
own blood supply) and
provides structural support
of the eye (keeping the
shape of the eye)
Remember: Intraocular
pressure depends on the
levels of production and
resorption of aqueous
humor (IOP: 12 -15 mmHg)
▪
▪
Retina: Translates image
into electrical neural
impulses to the brain to
create visual
perception (Rods:
Black/white, Cones:
Color)
Macula: Responsible for
the central, highresolution, color vision.
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Common disorders:
Macular degeneration vs Retinal detachment
Age related Macular
degeneration (AMD)
Age related degeneration
Mechanism
Etiology
▪ Dry AMD (90%): related to
decrease blood supply
▪ Wet AMD (10%): Related to
abnormal formation of blood
vessels
▪ Environmental: Smoking, HTN,
Atherosclerosis, Hyperlipidemia,
Exposure to UV
▪ Genetics
Classic S/S
Los of central vision
Diagnostics
▪ Amsler grid: Grid of horizontal and
vertical lines used to monitor a
person's central visual field.
▪ Fundoscopy: aka
ophthalmoscopy
▪ Fluorescein angiography:
Technique for examining the
circulation of the retina and
choroid using a dye & a
specialized camera.
Treatment
▪ Preventive: Lifestyle modification
▪ Laser coagulation: for wet AMD
▪ Stem cell implant
Retinal detachment
Involves a break or separation in the
retina that allows the fluid in the eye
to get behind the retina. Can be
caused by injury or inflammation of
the eye.
▪ Trauma/Injury: Cataract
surgeries, high impact sports,
glaucoma
▪ DM retinopathy
▪ Painless (d/t absent pain
receptors in retina)
▪ Floaters
▪ Curtain sensation
▪ Flashes of light
▪ Clinical S/S
▪ Fundoscopy: aka
ophthalmoscopy
▪ Ocular ultrasonography
▪ Laser coagulation
▪ Pneumatic retinopexy: a gas
bubble is injected into the eye
after which laser or freezing
treatment is applied to the retinal
hole to push the retinal back.
▪ Scleral buckling: Silicone bands
push the wall of the eye inward
against the retinal hole
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Loss of central vision
Amsler grid
Pneumatic retinopexy
Curtain sensation
Scleral buckling
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Common disorders: Glaucoma (COAG vs ACAG)
Glaucoma: Characterized by increase IOP (normal: 12-15 mmhg) which results to
damage in the optic nerve and cause vision loss. IOP is a function of production
of aqueous humor by the ciliary processes of the eye, and its drainage through
the trabecular meshwork. Aqueous humor flows from the ciliary processes by the
lens posteriorly and anteriorly by the iris. It then flows through the pupil of the iris
into the anterior chamber. Furthermore, trabecular meshwork drains aqueous
humor via the scleral venous sinus (Schlemm's canal) into scleral plexuses and
systemic blood circulation. Any problem to its drainage system causes increase
in IOP in a fixed space like the eye. Increase IOP (intraocular hypertension)
means at ≥25 mmhg causes symptoms of glaucoma.
Chronic open angle glaucoma
(COAG)
Acute close angle glaucoma
(ACAG)
Most common: Open angle
between cornea and iris. However,
the drainage system slowly gets
clogged overtime. This results
gradual (chronic) increase IOP to
optic nerve.
▪ Age
▪ Genetics
▪ Prolonged use of steroids (steroidinduced glaucoma)
▪ DM retinopathy: d/t restricted
blood
Close (narrow) angle between
cornea and iris. This results into
backflow of aqueous humor and
thereby pushing the lens against the
iris. This build-up of fluid is rapid
enough to cause acute symptoms.
Classic S/S
▪ Does not have acute S/S
▪ Loss of peripheral vision (tunnel
vision): d/t atrophy of the outer
rim of the optic nerve. Eventually
leads to central vison loss.
▪ Eye pain, Headache, Nausea
▪ Blurred vision, Eye redness,
▪ Visual halos, Loss of peripheral –
central vision (if not treated
promptly)
Diagnostics
▪ Tonometry: assess IOP
▪ Visual field testing
▪ Gonioscopy: anterior chamber
angle examination
▪ Optical coherence tomography
(OCT): To obtain detailed images
from within the retina.
Same
Mechanism
Etiology
▪ Trauma
▪ Surgery
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Goal: Early detection, Decrease IOP
Treatment
Medication:
▪ Alpha 2 adrenergic agonist: ↓
aqueous humor production &
↑outflow. (e.g. Brimonidine)
▪ Prostaglandin analogs: ↑outflow
(e.g. Bimatoprost)
▪ Beta blockers: ↓ aqueous humor
production(e.g. Timolol)
▪ Carbonic anhydrase inhibitors:↓
aqueous humor secretion (e.g.
acetazolamide)
▪ Laser trabeculoplasty (ALT): Used
to treat open-angle glaucoma
temporarily (not a cure)
▪ Trabeculectomy: Partial thickness
flap is made in the scleral wall
and a window opening is made
under the flap to remove a
portion of the trabecular
meshwork
Goal: Decrease IOP, preventing
further damage
▪ Medication: same with COAG
▪ Trabeculectomy
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Loss of peripheral vision (tunnel vision)
Errors of refraction: Myopia (nearsightedness), Hyperopia
(farsightedness), Astigmatism
Myopia:
Light rays focus in front
of the retina d/t
irregular shape lens.
Correction with
biconcave lens (thinner)
to reach the retina
Hyperopia:
Light rays focus behind
the retina d/t irregular
shape lens. Correction
with biconvex lens
(thicker) just enough to
reach the retina
Astigmatism:
Light rays focus on more
than one point
(unequal refraction).
Correction with lens
depending on the
errors.
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Common disorders affecting external, middle, inner ear
Otitis externa
(Swimmer’s ear)
Mechanism
Etiology
Alteration in the
protective environment
of the external ear that
results into infection. It
can also lead into otitis
media.
▪ Swimming
▪ Minor trauma from
cleaning
▪ Using hearing aids and
ear plugs
Pathogens:
Pseudomonas, E. Coli,
S. Aureus
Otitis media
Inflammation or
infection of the middle
ear. The eustachian
tubes in infants and
young children are
short, wide, and fairly
horizontal, which results
in ineffective draining of
respiratory secretions
and a potential for
recurrent infections.
Age group: < 2 YO
▪ Recurring exposure to
tobacco smoke
▪ Regular pacifier use,
after age 6 months
(d/t constant sucking)
▪ Drinking from a bottle
while lying down
▪ Lack of immunization
Pathogens:
S. Pneumoniae, H.
influenza (HIB), R.
syncytial virus (RSV)
Classic S/S
▪ Ear pain
▪ Fever, irritability
▪ Ear pain: upon pulling ▪ Conductive and
sensorineural hearing
the tragus
loss (if not treated)
▪ Ear discharge,
itchiness
Remember: Sudden
▪ Temporary conductive absence of fever and
hearing loss
pain is a sign of
perforated tympanic
membrane.
Diagnostics
▪ Clinical S/S
▪ History of URTI
▪ Ear examination:
Otoscope (bulging
tympanic membrane
distinguish OM from
otitis externa)
▪ Clinical S/S
▪ Ear examination:
Otoscope
Meniere’s disease
(Endolymphatic hydrops)
Endolymphatic hydrops:
excessive build-up of the
endolymph fluid, which
fills the hearing and
balance structures of the
inner ear. This build-up of
fluid may be caused by
immune response.
▪ Autoimmune
▪ Genetics
Triad:
▪ Vertigo
▪ Ringing in the ears
(tinnitus),
▪ Hearing loss
(sensorineural)
Clinical S/S
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DOC: Amoxicillin
Treatment
Prevent further infection
DOC: Ciprofloxacin
If failed:
Myringotomy/tympanos
tomy: incision is
created in the
eardrum (tympanic
membrane) to relieve
pressure caused by
excessive buildup of
fluid, or drain pus.
Tympanostomy tube
(grommet) to keep the
middle ear aerated to
prevent reaccumulation of fluid.
DOC:
▪ Thiazide diuretics
▪ Acetazolamide
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How to distinguish conductive hearing loss (reversible) from
sensorineural hearing loss (irreversible)?
Conductive hearing loss is temporary and it affects external and middle ear.
Sensorineural hearing loss affects inner ear and is irreversible kind of hearing
loss.
Remember:
Weber and Rinne tests are done on an existing hearing loss of an affected
ear. This is to distinguish what kind of hearing loss the patient is manifesting.
Weber test:
Tap a tuning fork and placed on
top of the head.
Interpretation: Considering the
patient complained of a hearing
loss in the right ear.
▪ If the patient cannot hear on that
right ear, patient is having a
sensorineural hearing loss
▪ If the patient hears louder on that
affected right ear (lateralization),
the patient is experiencing
conductive hearing loss.
Rinne’s test:
1. Tap a tuning fork and place in
front of the affected ear
2. If the patient does not hear
anymore sound from the tuning
fork, place behind the ear.
Interpretation: Considering the
patient complained of a hearing
loss in the right ear.
▪ After placing the tuning fork (step
2) behind the ear and still hears it:
sensorineural hearing loss
▪ If the patient does not hear it
otherwise: conductive hearing
loss.
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Question: The nurse is planning care for a client experiencing an acute attack of
Meniere disease. Which action is a high priority to include in the plan of care?
1. Initiate fall precautions
2. Keep the emesis basin at bedside
3. Provide a quiet environment
4. Start intravenous fluids
Answer: 1
Rationale: Clients with Meniere disease (endolymphatic hydrops) can have severe
vertigo, tinnitus, hearing loss, and aural fullness. It is a priority for the nurse to institute
safety measures, such as fall precautions, for these clients. All other choices are
correct but are not priority.
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16
Hematology/Oncology
Anatomy and Physiology
Hematopoiesis
Bone marrow
(hematopoietic
stem cells)
Myeloid
(Blast cells)
Erythrocyte
(RBC): Gas
exchanges
Megakaryocyte
(Platelet): Blood
coagulation
Lymphoid
(Blast cells)
Monocyte
Migrates to
tissues and
become
macrophages
(e.g. Alveolar
macrophages in
the lungs, Kupffer
cells in the liver,
Microglia in the
brain)
Granulocyte
Basophils: Allergic reaction
Eosinophils: Allergic reactions,
parasitic infections
Neutrophils: Most abundant,
bacterial infections
Agranulocytes:
T-cells and
B-cells
B-cells:
Mature in bone
marrow (B)
T-cells:
Mature in
Thymus gland (T)
Plasma B-cells:
T-cells:
Antibody
/immunoglobulin
(Ig) production
IgG – Crosses
placental barrier
(most abundant)
IgA – abundant in
secretions, found
in breastmilk
IgM – First Ig to
migrate in the
area of infection
Cytotoxic (CD8)–
destroys virus,
tumor cells
Suppressor/regula
tory: Shuts down
immunity
T-helper (CD4) –
Orchestrates
immune response
Memory T-cells Specific immunity
to previous
pathogen
IgE – Allergic
reaction
IgD – Unknown
function
Memory B-cells:
Specific immunity
to previous
pathogen
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Common disorders affecting RBCs: Anemias
Hemoglobin:
Heme: iron containing
compound where O2 binds.
Globin: protein chains where
hemes are wedged. Heme
and globin are both
involved in binding and
transport of O2.
2 alpha, 2 beta chains
Anemia:
Is a decrease in the total
amount of RBC or
hemoglobin in the blood, or
a lowered ability of the
blood to carry O2.
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Anemias
Mutations to
globin chains
Alpha Thalassemia:
Major: 4 mutations
(hydrops fetalis)
Minor: 2 mutations
Beta Thalassemia:
(Cooley’s anemia)
Major: 2 mutations
Minor: 1 mutation
Sickle cell anemia:
Mutation to beta
chains
Deficiencies
Megaloblastic:
▪ Vit B12 (Pernicious
anemia)
▪ Vit B9 (Folic acid
def. anemia)
Iron deficiency
Bone marrow
suppression
Aplastic anemia:
(Fanconi’s anemia)
(Low RBCs, WBCs,
Platelets Pancytopenia)
Remember:
The 4Fs (Classic S/S of anemia)
Fatigue
Forgetfulness
Fainting
Fast heartbeat (tachycardia)
Differentiating anemias: Microcytic vs macrocytic
Hypochromic vs hyperchromic
Remember:
There are various types of anemias. In order to distinguish these types, microscopic
test is made to determine the size and the color (morphology). On the other hand,
a complete blood count test (CBC) is a more convenient test. Mean corpuscular
HgB (MCH) for color and mean corpuscular volume (MCV) is for size. A normal
sized RBC is normocytic while normochromic pertains to its normal red color.
MCV: Determines size
Normal: 80-90%
Microcytic: <80%
Macrocytic: >90%
MCH: Determines color
Normal: 27-33%
Hypochromic: <27%
Hyperchromic: >33%
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Anemias
Overview
Morphology
Alpha thalassemia
Major
Minor
Alpha thalassemia results in
decreased alpha-globin
production. This leads to a
relative excess of beta globin
chains. The degree of
impairment is based on how
many genes are affected. Alpha
thalassemia major is associated
with hydrops fetalis (e.g.
hemolytic disease in newborn)
where hemolysis is evident
leading to accumulation of
water in newborn.
Microcytic, Hypochromic
Beta Thalassemia:
(Cooley’s anemia)
Major
Minor
Characterized by reduced or
absent synthesis of the beta
chains of hemoglobin that results
in severe anemia. In beta
thalassemia major, it involves
lifelong blood transfusion which
later cause iron overload as a
complication.
Microcytic, Hypochromic
Megaloblastic:
Vit B12 deficiency
(Pernicious
anemia)
Vit B9 (Folic acid
deficiency
anemia)
Megaloblastic as the name says
forms macrocytic type of RBCs.
This is a result from abnormal RBC
production d/t low vitamin B12
(cyanocobalamin) and vitamin
B9 (folic acid), main components
to create RBCs.
Vit B12 (Pernicious anemia):
Characterized by “red beefy
tongue”. The deficiency is mainly
d/t absence of parietal cells
which secretes intrinsic factor
necessary in Vit B12 absorption.
Can be caused by low dietary
intake, PUDs, gastritis, Zollinger
Ellison (gastric cancer)
Remember: Vitamin B12 is
obtained only from animal
proteins, so clients who follow a
vegan diet are at high risk.
Macrocytic, Normo/Hypochromic
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Vit B9 (FADA): Associated with
neural tube defects in infants
(spina bifida), chronic alcoholism
and gastritis.
Remember: Contrary to Vit B12,
leafy green vegetables are the
best dietary sources of folic acid.
Other sources include, fortified
grain products (e.g. cereals,
bread, pasta)
Iron deficiency
(IDA)
IDA is the most common chronic
nutritional disorder in children.
Iron-rich foods are leafy green
vegetables, red meats, poultry,
dried fruit and fortified cereals. It
is also important to limit milk
intake (16-24 oz/day) in toddlers
to ensure a balanced diet.
Microcytic, Hypochromic
Remember: Over consumption
of cow's milk (poor source of
available iron) before age 1 year
is a common cause.
Aplastic anemia:
(Fanconi’s anemia)
Characterized by bone marrow
suppression which leads to
pancytopenia. The main cause is
unknown. However, heredity,
autoimmune response, or
exposure to chemicals (benzene:
major chemical in gasoline) and
radiation can play a role.
Normocytic, Normochromic
Common disorders affecting RBCs: Sickle cell disease
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Sickle cell disease/anemia (SCD):
Is a hereditary hemoglobinopathy in which normal hemoglobin is replaced with
abnormal hemoglobin S in red blood cells (genetic mutation to beta chain). The
cells change to a sickle shape with triggers such as dehydration, infection, stress,
high altitude and extremes in temperature. In general, this triggers cause greater
demand of O2 in the body. The sickling causes occlusion of small blood vessels
with ischemia and damage to organs. Another reason is that the mutated beta
chain has less affinity (attachment) to O2. Person with SCD survives as long as the
environment has good oxygenation.
SCD
Increase levels of
reticulocytes
(immature RBCs)
A counterregulatory
mechanism by bone
marrow in response to
abnormal levels of RBCs d/t
hemolysis.
Effects:
Hepato/splenomegaly: d/t
crowding of the
reticulocytes
Enlarged cheeks: d/t new
bone formation from
expanded medullary
cavities (overcrowding)
Risk for infection: d/t
splenomegaly (spleen: role
in immune system)
DOC:
Hydroxyurea - Increases
formation of fetal Hgb
which has higher affinity to
O2. Fetal Hgb is present at
birth until 6 months, the
primary reason why infants
are asymptomatic with
SCD.
Vasoocclusive crisis
Hemolysis
Sickled cells stocked in the
small capillaries impeding
the circulation and causes
variety of symptoms
Repeated sickling causes
premature destruction of
RBCs (hemolysis) leading to
Effects:
Pain crisis: primary symptom
of SCD
Remember: Generalized
pain is a common and a
chronic symptom of SCD.
Localized pain on the other
hand is acute and needs to
be addressed immediately.
Dactylitis (swollen hands
and feet in infants): Initial
sign of SCD
Splenic sequestration:
characterized by severe
abdominal pain which is a
life threatening symptom.
CVA: involving cerebral
vessels
Renal necrosis: causing
hematuria and proteinuria
Acute chest syndrome:
characterized by chest pain
affecting lung vasculature
Priapism: prolonged painful
erection as it affects
vasculature in penis
Effects:
Anemia
Hyperkalemia: as K+ leaks
into the serum d/t RBC
destruction
Elevated bilirubin:
biproduct of RBC
metabolism is bilirubin
Jaundice: d/t elevated
bilirubin
Gallstone formation: d/t
elevated bilirubin
Triggers: Promote sickling
▪
▪
▪
▪
▪
Dehydration
Infection
Stress
High altitude areas
Extremes in temperature.
Remember: Hypoxia and
deoxygenation of the RBCs
in general causes the
sickling, so administration of
oxygen is the priority
intervention.
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Management:
▪ Prevent triggers
▪ O2 supplement - to prevent further sickling
▪ Hydration - aggressive intravenous and oral
hydration is recommended (to reduce the
viscosity of the blood)
▪ Pain control: Often need large doses of
narcotics (round the clock)
▪ Infection prevention – age-appropriate
vaccination
▪ Diet - the client is encouraged to have a
high-protein, high-calorie diet with folic acid
and a multivitamin without iron (IDA is
uncommon to SCD)
▪ Folic acid - to help in the creation of the new
red blood cells needed due to the hemolysis
Question: A 32-year-old patient with sickle cell anemia is admitted to the hospital
during a sickle cell crisis. Which action prescribed by the health care provider
will you implement first?
1. Give morphine sulfate 4 to 8 mg IV every hour as needed.
2. Administer 100% oxygen using a nonrebreather mask.
3. Start a 14-gauge IV line and infuse normal saline at 200 mL/hr.
4. Give pneumococcal and Hemophilus influenzae vaccines.
Answer: 2
Rationale: Hypoxia and deoxygenation of the RBCs are the most common cause
of sickling, so administration of oxygen is the priority intervention here. Pain
control and hydration are also important interventions for this patient and
should be accomplished rapidly. Vaccination may help prevent future
sickling episodes by decreasing the risk of infection, but it will not help with
the current sickling crisis.
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Common disorders affecting platelets: Thrombocytopenia
Thrombocytopenia:
Disseminated Intravascular
coagulation (DIC)
“consumption
coagulopathy”
Mechanism:
Hemostasis out of control.
Too much platelet is
consumed d/t a massive
injury in a certain area. As a
result, other body parts
tend to bleed.
Etiology: Trauma, Abruptio
placenta, sepsis, leukemia
Diagnosis:
▪ Low platelet
▪ Elevated PT/INR, PTT
▪ Elevated D-dimer
Management:
▪ Treat cause
▪ Blood transfusion
▪ Prevent bleeding
Heparin induced
thrombocytopenia (HIT)
Mechanism: Due to
administration of various forms
of heparin. Regardless of its
cause, thrombocytopenia
usually results in bleeding.
However, in HIT this usually
leads to paradoxical venous
and/or arterial thrombosis
and less commonly to
bleeding. The mechanism for
thrombosis is unclear. The
danger of HIT is risk of organ
damage from local thrombi
and/or embolization, leading
to CVA or PE.
Remember: Bleeding risk
A priority assessment in a
client with low platelets is
any change in LOC (e.g.
disorientation, lethargy,
restlessness). This indicates
intracranial bleeding and
increased ICP.
Thrombotic
thrombocytopenic
purpura (TTP)
Mechanism: An immune
response characterized by
thrombosis in small blood
vessels, d/t elevated Von
Willebrand factor (clot
creator). The platelet are
stocked into fibrin
(stabilizer) strands made by
VWF resulting to low
platelet count with
hemolysis of the RBCs.
Elevated VWF is d/t
deficiency of ADAMTS
enzyme (clot buster)
Etiology: Autoimmune
Remember: FAT RN
F - Fever: immune response
A – Anemia: hemolysis
T – Thrombosis: ↑ VWF
R – Renal: AKD d/t massive
hemolysis
N – Neuro: thrombotic CVA
Diagnosis:
▪ Normal platelet
▪ Normal PT/INR, PTT
▪ Elevated Von Willebrand
factor (VWF)
Management:
▪ No platelet transfusion
(worsens the problem)
▪ Plasmapheresis (adding
ADAMTS enzyme)
Idiopathic/Immune
thrombocytopenic
purpura (ITP)
(Werlhof's Disease)
Mechanism:
An autoimmune disease
with antibodies against
several platelets. Primary
ITP is unknown (idiopathic)
while secondary ITP is d/t
SLE. Platelets with Ig are
rendered to spleen and
phagocytized by splenic
macrophages,
Etiology: Idiopathic,
autoimmune
Diagnosis:
▪ Low platelet
▪ Normal PT/INR, PTT
Management:
▪ Blood transfusion
▪ Prevent bleeding
▪ Steroids
▪ IV Immunoglobulins
▪ Splenectomy
Remember: HIT
Platelets <150,000 /mm3:
continue treatment
Platelet <40,000/mm3:
Discontinue treatment (risk
for bleeding)
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Common disorders affecting WBCs: Leukemia
Myeloid/Myelocytic
Affects the myeloid line
of blood cells. The
monocytes, erythrocytes
(RBCs), megakaryocyte
(platelets) and
,granulocytes (basophils,
neutrophils, eosinophils)
Chronic leukemia
Characterized by
partially immature cells.
Gradually spills out and
still causes crowding but
in a slow progression. This
mechanism also causes
pancytopenia
Acute leukemia
The fully immature cells
are >20% which more likely
crowds abruptly.
Crowding affects the
production of other blood
cells, RBCs, platelets and
other WBCs regardless of
the line originally affected
Lymphoid/lymphocytic
Affects the lymphoid line
of blood cells. The
agranulocytes (B-cells
and T-cells)
Acute
Myeloid/Myelocytic
leukemia (AML)
Rare type which usually
affects elders/adults.
Rapidly progresses as an
acute leukemia
Chronic
Lymphoid/lymphocytic
leukemia (CLL)
Usually affects elders >70
YO. Only affects the B-cells
of the lymphoid line.
Acute
Lymphoid/lymphocytic
leukemia (ALL)
B-cell leukemia affects
children and T-cell type
usually affects teenagers.
A very rare type of
leukemia which
progresses rapidly.
Chronic
Myeloid/Myelocytic
leukemia (CML)
Rare type which usually
affects elders/adults.
Characterized by
mutation of the
chromosome 22
(Philadelphia
chromosome).
Leukemia: Is a group of blood malignancies (cancer) that usually begin in the bone
marrow and result in elevated count of abnormal and immature white blood cells.
Classification is according to progression and the hematopoietic blood line affected.
These blood cells are not fully developed and are called leukemia cells. Treatment
involved are chemotherapy, radiation bone marrow transplant and supportive care.
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Remember:
Acute myelodysplastic
syndrome is not AML of
leukemic origin. This is
characterized by <20% blast
cells of myeloid blood lines
but it does progress rapidly
causing the same symptoms
such of AML.
Common disorders affecting WBCs:
Hodgkin’s vs Non-Hodgkin’s lymphoma
Lymphoma
Hodgkin’s
lymphoma
(+) Reed Sternberg
cells on biopsy
Lymphadenopathy
usually in neck and
chest
Good
Good prognosis
A group of blood
malignancies (cancers)
that affects the
lymphocytes. Most
commonly B-cells.
Mechanism:
Migration to lymphoid
tissues causing painless firm
and movable
lymphadenopathy
(classic symptom). Other
manifestations include:
fever, night sweats
(drenching type which rule
out PTB), weight loss, loss of
appetite. Treatment is
usually chemotherapy,
radiation and surgery. In
addition, Burkitt’s
lymphoma (severe form)
causes rapid deterioration
or death
Non-Hodgkin’s
lymphoma
(-) Reed Sternberg
cells on biopsy
Lymphadenopathy
usually affects
upper and lower
extremities
Good
Poor prognosis
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Common disorders affecting WBCs: Multiple myeloma
Multiple myeloma
Is a malignancy of plasma cells that
produces antibodies, particularly
affecting the IgG. The usual onset is 70
YO. Older patients are often
experiencing other serious diseases,
which affect survival.
Diagnosis:
▪ BUN, creatinine
▪ Electrophoresis
(M-protein spikes)
▪ CBC, Electrolytes (BMP)
▪ Bone marrow biopsy
▪ Ben jones proteins (tumor
markers)
▪ Bone imaging
Management:
Supportive care,
chemotherapy, bone
marrow transplant
C
R
C – Calcium
Elevated calcium
d/t lytic bone
lesions caused by
rapid growth of
cancer cell
Classic S/S:
Bone pain to lower
back
(most common
symptom)
R – Renal
Monoclonal
antibodies called
M-protein
overwhelms the
kidneys leading to
kidney failure.
Regular kidney
function is checked
to determine
disease progression
A
A – Anemia
Crowding of the
cancer cells affects
hematopoietic stem
cells in the bone
marrow. This also
leads to low levels
of WBCs and
platelets. Risk for
infection and
bleeding
B
B – Back pain
A common
symptom related
to hypercalcemia
and pathological
bone fractures.
Spine and ribs are
usually affected
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Cell cycle:
G1 checkpoint
Checks for:
▪ Cell size
▪ Nutrients
▪ DNA damage
▪ Growth factors
G2 checkpoint
Checks for:
▪ DNA damage
▪ DNA
replication and
completeness
Remember:
As cells move through the cell cycle, do they breeze through from one phase to the
next? If they're cancer cells, the answer might be yes. Normal cells, however, move
through the cell cycle in a regulated way. This regulation makes sure that cells don't
divide under unfavorable conditions (for instance, when their DNA is damaged, or when
there isn't room for more cells in a tissue or organ).
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Chromosomes, Genes, DNA:
Remember:
Cells are made up of trillions of
cells. Cells contains nucleus
where identical pairs
chromosomes are located. One
chromosome from each of its
pair is inherited from each
parent. Segments from each
chromosomes are called genes.
Lastly, genes are made up of
DNA where the genetic make-up
(information) is transcribed
intricately through group of
proteins overtime in an
organized process. Any
disturbance to this process is an
abnormality. However, the
human body has its own
mechanism to autocorrect
whatever is detected abnormal.
This happens before it regularly
undergoes cell division, carrying
DNA information from one to the
other.
Chromosome:
Humans has 23 pairs, designated 1 to 22 in order of
decreasing size and X and Y (23rd) for the female and male
sex chromosomes respectively.
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DNA damage vs Mutation:
Replication is the process of
producing two identical replicas of
DNA from one original DNA
molecule. This process is the basis for
biological inheritance. A DNA
damage during replication can be
repaired as it undergoes a process of
correction overtime. In contrast,
DNA mutation cannot be corrected
and remains present in the new DNA
strand because it is simply not
recognizable. Then every time that
strand of DNA is replicated the error
will be carried to next cycle.
Implication:
Mutation or damage supports the
idea of inheritance from one
generation to another. Ironically,
cancer occurs at anyone and at
anytime in an unpredictable
manner. How does cancer develop?
It simply remains unclear. However
there are available theories that
supports the concept.
Proto-oncogenes vs Oncogene (Tumor) suppressor theory:
Proto-oncogene
▪ A dominant gene
▪ Promotes mutation
▪ More active and mutation
becomes permanent once
activated
Oncogene suppressor
▪ A recessive gene
▪ Induces apoptosis
(programmed cell death for
damaged/non useful cells.
▪ Protects the stability of genetic
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Inheritance: Dominant vs recessive, Autosomal vs X-linked
(Sex-linked)
Dominant
It only needs to inherit one
copy of the gene for the
trait to be expressed. For
instance, if one parent has
a dominant gene of a
green eyes, there is 50 %
chances that the child will
have green eyes.
Recessive
Needs to inherit two
copies of the gene from
each parents for the trait
to be expressed. Both
parents must have
recessive genes of green
eyes for their child to have
it at a 25% chance (both
parents are carrier)
X-linked (sex linked)
The inheritance of a trait
is determined by a gene
located on one of the sex
chromosomes (23rd Ch)
Autosomal
The inheritance of a trait
is determined by a gene
located on 1-22
chromosomes.
X-linked Dominant
Every affected person
has at least one parent
with a trait. A male with
trait passes it on all his
daughters. A female ,
may pass to both sons
and daughters.
e.g. Alport syndrome
X-linked recessive
Affected fathers do not
pass to sons. Males
manifest the disease than
females. Females are
carrier (passed from
mother to son)
e.g. Hemophilias, color
blindness
Autosomal dominant
Affected fathers or
mothers passes on the
disease to both sons and
daughters e.g. Marfan’s
syndrome, polycystic
kidney disease
Autosomal recessive
Males and females can be
equally affected. Parents
are asymptomatic carriers.
e.g. Sickle cell disease,
cystic fibrosis
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Benign tumors vs malignant tumors
Benign
▪ Slow growing
▪ Capsulated
▪ Non invasive
▪ Do not metastasize
▪ Well differentiated
▪ Suffix “oma” e.g.
Fibroma
Malignant
▪ Fast growing
▪ Non-capsulated
▪ Invasive and infiltrating
▪ Metastasize
▪ Poorly differentiated
▪ Suffix “carcinoma or
sarcoma”
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Common cancers: Early and late signs/symptoms
Cancer
Early S/S
Late S/S
Brain
Headache
Loss of consciousness
Esophageal/
tracheal
Hoarseness
Dysphagia
Stomach
Indigestion/dyspepsia
Chronic indigestion
Lung
Nagging cough
Hemoptysis
Dimpling “Peau
d’orange” (breast skin is
similar to orange peel)
Asterixis (flapping
tremors)
Breast
Lump
Liver
RUQ pain
Colon
LLQ pain
Bloody stool
Bladder
Dysuria
Hematuria
Cervical/Uterine/
Ovarian
Dysplasia from pap
smear
Foul smelling vaginal
bleeding
Testicular
Dragging pain
Spongy testes
Skin
Non healing sore
Ulceration
Bone
Bone pain d/t easy
fracture
Deformity
Bone marrow
Exhaustion
Pancytopenia
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Screening tests: CDC recommendation
Cancer
Screening tests (early detection)
Breast
Breast self-examination: Monthly starting age 20 YO
Best time: End of the menstrual cycle (variable: few days
after). This is the time when hormonal changes have
the least influence on breast tissue, and the breasts are
the least tender.
Postmenopausal women/Irregular menses: Choose a day
of the month (usually single digits to easily remember)
and consistently perform breast self-exam on that
same day every month.
Mammogram: Annually starting age ≥ 40 YO
Every 2 years (age ≥ 50-70 YO)
Cervical
Colorectal/colon
Lung
Pap Smear: Every 3 years age 21-65 YO
>65 with previous positive (+) results/history of cervical
cancer: Also needs testing
>65 YO with negative (-) results: No need for testing
Colonoscopy: Every 10 years age 50-75 YO, may also have
sigmoidoscopy as an alternative (fairly quick and safe).
Done every 5 years. If high risk may do fecal occult
blood (FOB) done annually.
Chest X-ray: Every year for chronic smokers
Chronic smokers: 30 pack years or 1 pack/day and 15
pack years or 2 packs/day
>80 YO or quit smoking for 15 years: no need testing
Remember:
Other screening test such as prostate examinations and testicular test
examinations are not included according to CDC because of low probability and
specificity issues. However, this test are still done to high risk individuals
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Treatment: Chemotherapy and radiation
Chemotherapy
Non Cell
specific
Cell specific
Vina alkaloids
▪ Vincristine
▪ Vinblastine
Antimetabolites
▪ 5 Fluorouracil
(5FU)
▪ Methotrexate
Adverse: Bone marrow
suppression
DOC to increase:
WBC: Neupogen (Filgrastim)
RBC: Epoetin (Epogen)
PLT: Neumega (Oprelvekin)
Infection risk : Neutropenic
precaution
Absolute neutrophil (ANC)
Normal: 3,500 – 7000/mm3
Severe risk: <500/mm3
Moderate risk: 500-1000/mm3
Mild risk: 1000-1500/mm3
Insignificant: >1500/mm3
Acute tumor lysis syndrome (TLS):
A potential complication of
chemotherapy d/t rapid release
of intracellular components such
as potassium, phosphorus and
nucleic acids into the
bloodstream. This will cause
hyperkalemia, hyperuricemia
hyperphosphatemia. Released
phosphorus binds calcium,
producing calcium phosphate
mixture but lowering serum
calcium levels (hypocalcemia).
Both calcium phosphate and
uric acid are deposited into the
kidneys, causing renal failure.
Antibiotic
antitumor
▪ Adriamycin
▪ Bleomycin
Alkylating agents
Hormones
▪ Tamoxifen
▪Cyclophosphamide
“Those not
mentioned” e.g.
Cisplatin
Adverse for antibiotic anti tumor: Pulmonary fibrosis
Adverse for Hormones: “ACHES”
A – Abdominal pain (bowel ischemia)
C – Chest pain (PE or AMI)
H – Headache (CVA)
E – Eye problem (retinal ischemia)
S – Severe leg pain (DVT)
Remember: Hormones (estrogen, progesterone)
generally affects cardiovascular system.
Adverse for alkylating agents: Hemorrhagic cystitis
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Radiation
External
(Teletherapy)
Internal
(Brachytherapy)
Sealed
(regional)
e.g. Cobalt
Intracavitary
radiation
D
D – Distance
▪ Maintain at least 6 feet
from the radiation source
▪ Assign the client to a
private room with a
private bath
▪ Keep the door closed
▪ Ensure that caution
signages are affixed to
the door
▪ Instruct the client to
remain on bedrest to
prevent dislodgement of
the implant
Unsealed
(systemic)
▪ Radioactive
isotopes (IV)
▪ Radioactive
iodine (PO)
T
S
T – Time
S – Shielding
▪ Limit staff time spent in
the room to 30 minutes
per shift.
▪ Cluster nursing care to
minimize exposure
▪ Rotate staffing
▪ All staff must wear a
dosimeter film badge
when assigned
▪ No pregnant or under
age 18 may be in the
room
▪ All staff providing nursing
care that requires
physical contact must
wear a lead apron.
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Question: The nurse is providing medication instructions to a client with breast
cancer who is receiving cisplatin. The nurse should tell the client to take
which action?
1.Take the medication with food
2. Increase fluid intake to 2000 to 3000 mL daily
3. Decrease sodium intake while taking the medication
4. Increase potassium intake while taking the medication
Answer: 2
Rationale: Hemorrhagic cystitis is an adverse effect that can occur with the use
of cisplatin. The client needs to be instructed to drink copious amounts of
fluid during the administration of this medication. Clients also should monitor
urine output for hematuria. Remember that those that are not mentioned
from the common examples above are classified as alkylating agents.
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17
Immunology/Infectious disease
Remember: acronym “Be DR. HIP”
Age 2 and 4 months: Dr. HIP (DTaP, RV, Hib, IPV, PCV)
Age 6 months: Be Dr. HIP (Hep B, DTaP, RV, Hib, IPV, PCV)
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Active/Live vaccines:
▪ Varicella Zoster (VZV)
▪ Measles-mumps-rubella (MMR)
▪ Influenza nasal spray (out in the
market 2017)
Remember: Live vaccines
▪ Live vaccines cannot be given
to immunocompromised and
pregnant clients.
▪ The only vaccines given SQ
Routes of administration:
Oral: OPV, RV (Rota)
IM: DTaP, Hep B, IPV, HiB, PCV,
Hep A
SQ: MMR, VZV (active vaccines)
Contraindications:
Encephalopathy: DTaP
Antibiotic allergy “mycins”: IPV, MMR, VZV
Gelatin allergy: MMR, VZV
Egg, protein allergy: MMR, VZV
Baker’s yeast: Hep B
Common misperceptions:
▪ Penicillin allergy
▪ Mild illness (with or without an elevated
temperature)
▪ Mild site reactions (e.g. swelling, erythema,
soreness)
▪ Recent infection exposure
▪ Current course of antibiotics
Key points:
▪ IPV - a new form of polio vaccine
because OPV (Oral) had caused
incidences of vaccine-associated
paralytic poliomyelitis (VAPP).
▪ RV – not given with immunodeficiency or
intussusception
▪ Newborns at risk for HIV infection need to
receive all recommended immunizations
at the regular schedule; live vaccines are
not administered until HIV status is
determined
▪ Infants with (+) Hep B mothers should
receive Hep B vaccine and hepatitis B
immunoglobulin (HBIG) within 12 hours of
birth.
Key points:
▪ Hep B Vaccines – can be given to MS,
GBS, autoimmune, autoimmune diseases,
and pregnant women except allergy to
baker’s yeast.
▪ Cervical Cancer: Cervarix, Gardasil - 3 IM
Injections (6 months period) before
becoming sexually active
▪ In HIV (CD4 <200, <15%): Varicella, MMR
cannot be given
▪ MMR & Varicella if not administered on
the same day, must be separated by 28
days
▪ Hep B Vaccines should not be given if
infant weighs <2000gms.
▪ Tdap (Tetanus toxoid, diphtheria and
pertussis) is a booster vaccines for DTaP
given at age 11 YO
▪ Hib vaccine is for H. influenza Type B
bacteria to prevent bacterial croup in
children (epiglottitis). Flu vaccine (flu
shots) is for seasonal flu (NovemberMarch) caused by influenza virus (type A
and B, given annually starting age 6
months and above including elderlies.
Routinely recommended during pregnancy:
▪ Flu (influenza) shot during flu season.
Avoid influenza nasal spray (active)
▪ Tdap - given between 27 and 36 weeks
AOG.
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Common disorders: Systemic Lupus Erythematosus (SLE)
SLE: An autoimmune disorder in which the
body's immune system produces
autoantibodies that attack the body's tissues
and cells. It is characterized by alternating
periods of exacerbation (flare) and
remission (latent). The skin is one of the
target organs commonly affected by the
disease. The characteristic cutaneous
manifestation of SLE (> 50%) is a flat or raised
red rash that forms a butterfly shape across
the bridge of the nose and cheeks “butterfly
rash”. It is often related to sunlight exposure
(ultraviolet light) and is more pronounced
during a disease flare.
Mechanism:
Genetic susceptibility plays the role in the
development of the disease. If susceptible
skin is exposed to sun (environment),
apoptosis develops (programmed cell
death) and releases chemicals as
antigens. This leads to production of
autoimmune cells (antibodies) that attack
own tissues (autoimmune)
Lab tests:
Most specific:
▪ Anti-double stranded DNA (dsDNA)
▪ Anti-smith DNA
Anti-nuclear antibodies (ANA)
Anti-phospholipid
Diagnostic criteria: SOAP DISH MD
Any combination of 4 or more of 11 criteria,
well-documented at any time during a
patient's history.
Treatment:
▪ Limit stress to prevent flare-ups
▪ Disease modifying drugs (immune
suppressants: steroids)
Remember: Disease modifying drugs are
generally given to autoimmune diseases
such as arthritis, SLE, Multiple sclerosis etc.
The goal of treatment is prolong remission
thereby limiting exacerbations. Autoimmune
diseases are chronic diseases that are not
curable.
Malar rash: a rash shaped like a butterfly that is usually found of the bridge
of the nose and the cheeks “butterfly rash”
Discoid rash: a raised rash usually found on the head, arms, chest, or back.
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Common disorder: HIV-AIDS
Remember: CD4 cell or T-helper cells
orchestrates immune response.
Acquired immunodeficiency
syndrome (AIDS): A chronic,
potentially life-threatening
condition caused by the
human immunodeficiency virus
(HIV). By damaging your
immune system (CD4), HIV
interferes with your body's
ability to fight the organisms
that cause disease.
Transmission:
▪ Sexual intercourse
▪ Contaminated blood transfusions
▪ Contaminated IV drug paraphernalia
▪ During pregnancy or delivery or through
breast-feeding.
Remember:
Infected mothers may or may not pass the
virus on to their babies. HIV-positive mothers
who get treatment for the infection during
pregnancy can significantly lower the risk to
their babies.
Phases of HIV-AIDS:
1. Primary infection (Acute HIV): flu-like illness
within a month or two after the virus enters the
body.
2. Clinical latent infection (Chronic HIV):
Persistent swelling of lymph nodes occurs
during this stage. Otherwise, there are no
specific signs and symptoms. Generally lasts
around 10 years if not receiving antiretrovirals.
3. Symptomatic HIV infection: Develops chronic
signs and symptoms of infections
4. Progression to AIDS: Immune system has been
severely damaged. More likely develop s
opportunistic infections and cancers.
>5 YO-adults: CD4 cells <200/mm3
1-5YO: CD4 cells <500/mm3
<1YO: CD4 cells <750/mm3
Normal CD4: 500-1500/mm3)
Diagnosis: CDC recommendation
1. P24 antigen test (2-3 weeks result): Antigen
test contrary to the conventional ELISA
(antibody test) which takes longer (3
months). Longer results means higher
chances of transmission if the patient is (+)
2. If P24 is (+) do Differential assay
(+): Either HIV 1 or HIV 2
Western blot: Confirm HIV1 or HIV2
3. If Diff. assay is (-) do Nucleic acid test (NAT)
(+): HIV 1
(-): No HIV and P24 is false positive
For pregnant:
▪ Test is done for high risk mothers during
first and last trimester
▪ Pregnant with (+) HIV can take retroviral
to limit transmission to babies
For newborns with (+) HIV mothers:
▪ First 48 hours: PCR test (antigen test)
▪ 1-2 months: NAT (96% specificity)
▪ 3-6 month: ELISA (antibody test)
Infections common to HIV/AIDS:
▪ Tuberculosis (most common)
▪ Cytomegalovirus
▪ Candidiasis
▪ Cryptococcal meningitis
▪ Toxoplasmosis
▪ Cryptosporidiosis
▪ Kaposi's sarcoma
▪ Lymphoma
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Question: An HIV-positive patient who has been started on HAART is seen in the
clinic for follow-up. Which test will be most helpful in determining the
response to therapy?
1. CD4 level
2. Complete blood count
3. Total lymphocyte percent
4. Viral load
Answer: 4
Rationale: Viral load testing measures the amount of HIV genetic material in the
blood, so a decrease in viral load indicates that the highly active
antiretroviral therapy (HAART) is effective.
HAART: Acts by inhibiting the enzymes responsible for viral
replication
Nucleoside/nucleotide reverse-transcriptase inhibitors (NRTI):
zidovudine, abacavir, lamivudine, emtricitabine, tenofovir
Non-nucleoside reverse-transcriptase inhibitors (NNRTI):
nevirapine, efavirenz, etravirine and rilpivirine
Integrase inhibitors: elvitegravir, dolutegravir
Protease inhibitors: lopinavir, indinavir, nelfinavir, amprenavir,
ritonavir
The CD4 level, total lymphocytes, and complete blood count will also be
used to assess the impact of HIV on immune function but will not directly
measure the effectiveness of antiretroviral therapy
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Common disorders: Tuberculosis
Induration
(After 48-72 hours)
Population with positive results (Tuberculin testing)
≥ 5 mm
Immunocompromised (HIV, Autoimmune diseases)
Post organ transplant
≥ 10 mm
Health care workers, homeless, drug users, endemic
countries, <4 YO
≥ 15 mm
Unknown risk
Remember:
Latent TB (asymptomatic TB) does not need to have airborne isolation. Active TB
with symptoms are highly contagious and needs to be isolated accordingly.
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Rifampicin
Red orange secretions, hepatotoxic
Isoniazid (+ VitB6)
Peripheral Neuritis, hepatotoxic
Pyrazinamide
Increase Uric acid, hepatotoxic
Ethambutol
Optic neuritis
Streptomycin
Ototoxic, neurotoxic, nephrotoxic
Remember: Isoniazid or Rifampin may be taken alone to
prevent a latent TB infection from turning into active
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Common Infections:
Diarrheal infection
Giardiasis (Parasite)
Salmonellosis (bacteria)
Shigellosis/Dysentery
(bacteria)
Classic sign
“Greasy Stool”
“Blood in the stool”
“Blood in the stool”
DOC
Metronidazole
Penicillin, Quinolones
Penicillin, Quinolones
Macrolides
Preventive standard
vaccines:
Rotateq, Rotarix
Rotavirus
“Stomach Flu”
High fever, black tarry
with pus in the stool
Norovirus/Norwalk Virus
“Winter vomiting
disease”
Low grade fever,
Vomiting
Supportive treatment
Fluids - Priority
Sexually transmitted
Classic sign
DOC
Herpes Simplex (Virus)
Painful Genital Vesicles
(Lifelong Infection)
Genital Warts (Virus)
Syphilis/Chancre
(Bacteria)
Chancroid
(Bacteria)
Gonorrhea
(Bacteria)
Flesh colored, swollen
Cauliflower
Painful/itchy
Painless Sore
(Genital, Rectum,
Mouth)
Painful Sore
From asymptomatic to
symptomatic
genital pus, painful sex,
rectal, throat, eyes, joints
inflammation
Complication: Infertility
Epididymitis (male)
Pelvic inflammatory
disease (female)
Acyclovir (Zovirax)
Vaccines (IM):
Gardasil, Cervarix
Penicillin, Doxycycline,
Azithromycin
Azithromycin
Ceftriaxone
Azithromycin
Doxycycline
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Chlamydiasis/ “Tracho”
(Bacteria)
Same with gonorrhea
Azithromycin
Doxycycline
Moniliasis/Candidiasis
(Fungal)
Cheese-like discharge
odor free
Cotrimoxazole – Topical
Miconazole – Topical
Itraconazole – Systemic
Fluconazole - Systemic
Trichomoniasis/”Trich”
(Parasite)
Foul smelling
frothy discharge with
Itchiness
Metronidazole
Animal associated
Animal source
Classic sign
Histoplasmosis (Fungal)
Birds, bats
Flu like symptoms,
extreme tiredness
Rabies (Virus)
Racoon, dog, rat bites
Hypersalivation,
photophobia,
hydrophobia
Toxoplasmosis
(Protozoal)
Cat litter
Flu like symptoms,
lymphadenopathy
Viral encephalitis
(West Nile virus)
Mosquito bites
Bulging fontanels in infants
Lyme disease
“Borreliosis” (Bacteria)
Deer ticks
Bull’s eye rash
Infections prevented by
standard vaccines
Classic signs
Standard vaccines
Hepatitis B (Virus)
Fatigue, low grade fever,
jaundice, RUQ pain
Hep B vaccine (HBV)
Diphtheria (Bacteria)
Tetanus (Bacteria)
Skin: gray thick ulcers
Respiratory: gray thick
secretions surrounding
throat, epiglottitis
Severe muscle spasms:
Opisthotonos: arching of
neck and spine
Trismus: lock jaw
Risus sardonicus: 'sarcastic'
grimace, drawing
eyebrows
DTaP, TDaP
DTaP, TDaP
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Pertussis (Bacteria)
“whooping cough” or
violent cough
Rota virus
High fever, black tarry
with pus in the stool
Rota vaccine (RV)
Hemophilus Influenzae
Type B (HiB: bacteria)
Epiglottitis: 4 Ds
dysphonia (muffled
voice), dysphagia
(difficulty swallowing),
drooling, and distressed
respiration.
HiB vaccine
Poliomyelitis (Virus)
Infantile paralysis
Inactivated polio
vaccine (IPV)
Pneumococcal
pneumonia (Bacteria)
Purulent rusty sputum
Pneumococcal
conjugate vaccine
(PCV)
Measles (Rubeola virus)
White Koplik’s spots:
clustered, white lesions
on the buccal mucosa
Measle, Mumps, Rubella
vaccine (MMR)
Mumps (Virus)
Painful swelling of parotid
glands in the neck
Measle, Mumps, Rubella
vaccine (MMR)
German measles
(Rubella virus)
Chicken pox
(Varicella virus)
Hepatitis A
Seasonal Flu
(influenza A, B viruses)
Red Forcheimer spots:
small, red spots
(petechiae) on the soft
palate
Itchy skin rash with red
blisters
Remember:
Most contagious 1-2 days
before the rash appears
until all blisters are dried &
crusted.
DTaP, TDaP
Measle, Mumps, Rubella
vaccine (MMR)
Varicella zoster virus
vaccine (VZV)
Fatigue, low grade fever,
jaundice, RUQ pain
Hep A vaccine (HBV)
Fever, malaise, chills
Flu vaccine (flu shots)
Trivalent:
▪ H1N1(swine flu): Type A
▪ H3N2: Type A
▪ Type B
Quadrivalent: covers 2
type A and 2 type A
influenza
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Common Antibiotic
resistant infections
Associated with
Manifestation
DOC
Clostridium difficile
Fluoroquinolones,
Cephalosporins,
Carbapenems,
Clindamycin
Severe diarrhea
Vancomycin
Metronidazole
Vancomycin-resistant
Enterococcus (VRE)
Vancomycin
Severe diarrhea
Linezolid
Penicillin,
Cephalosporins
Skin and
respiratory
infections,
bacteremia
Vancomycin
Linezolid
Methicillin-resistant
Staphylococcus aureus
(MRSA)
Other infections
Classic sign
DOC
Pediculosis (Parasite)
Occipital itchiness
Permethrin cream 10%
Scabies (Parasite)
Burrowing tract
Permethrin cream 10%
Infectious Mononucleosis
“Kissing’s disease”
(Epstein Virus)
Lymphadenopathy,
splenomegaly
NSAIDs, Steroids
Legionnaire’s Disease
(Bacteria)
Pneumonia symptoms
(severe form) with high
fever and relative
bradycardia, dry cough
Fluoroquinolones,
Azithromycin, Doxycycline
5th Disease
(Parvovirus B19)
“Slapped cheek”
red rashes
Supportive treatment with
NSAIDs
Question: A parent brings her 4-month-old infant to a well-baby clinic for immunizations.
The child is up to date with the immunization schedule. The nurse should prepare to
administer which immunizations to this infant?
1. Varicella, hepatitis B vaccine (Hep B)
2. Diphtheria, tetanus, acellular pertussis (DTaP); measles, mumps, rubella (MMR);
inactivated poliovirus vaccine(IPV)
3. MMR, Hemophilus influenzae type b (Hib), DTaP
4. DTaP, Hib, IPV, pneumococcal vaccine (PCV), rotavirus (RV)
Answer: 4
Rationale: (Refer to standard vaccine schedule). Active vaccines [Varicella Zoster (VZV),
Measles-mumps-rubella (MMR) ] are given at 12 months due to low immune system
at younger age.
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18
Maternal & child
Antepartum: Signs of pregnancy
Presumptive signs
“subjective”
(as verbalized by client)
Breast tenderness
Urine frequency
Nausea/vomiting
Fatigue
Amenorrhea
Quickening (fetal
movement)
Probable signs
“objective”
(as assessed by nurse)
(+) HCG
(+)Pregnancy test (PT)
Hegar’s sign: softening
uterus
Chadwick’s sign: Bluish
discoloration of
vagina
Goodell’s sign: softening
of cervix
Braxton Hicks: false
contractions
Ballottement: fetal
bouncing after
pushing uterus
Fetal outline: Leopold’s
maneuver
Positive signs
“confirmatory”
(+) Fetal heart tone (FHT)
4-8 weeks: vaginal USD
12 weeks: doppler USD
16 weeks: Stethoscope
Remember:
Presumptive signs are verbalized by clients to which they “feel they are pregnant.
Probable signs are assessed by nurse, however there is no fetal heart rate. Fetal
heart rate is a confirmatory sign. In addition, probable signs are “signs with
medical names implicated”.
Normal values:
Amniotic fluid:
500—1000 ml
> 1500 ml: Polyhydramnios
< 500 ml: Oligohydramnios
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Additional calorie intake:
Pregnancy: 300 kcal/day
Lactating: 500 kcal/day
Weight gain:
First trimester: 1 lb/month
2nd Trimester: 1 lb/week
3rd Trimester: 1 lb/week
Protein Intake:
65 g/dl (Pre-pregnant)
45 – 50 g/dl (Female)
65 – 70 g/dl (Male)
RSA: right sacrum anterior ROP: right occiput posterior
ROA: right occiput anterior LSA: left sacrum anterior
LOP: left occiput posterior LOA: left occiput anterior
Remember: Folic acid intake on planning to get pregnant
Must consume 400-800 mcg of folic acid daily. Inadequate maternal intake of
folic acid during the critical first 8 weeks after conception (often before a
woman knows she is pregnant) increases the risk of fetal neural tube defects
(NTDs), which inhibit proper development of the brain and spinal cord.
Common NTDs are spina bifida and anencephaly (lack of cerebral hemispheres
and overlying skull).
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Approximate fundal height
Gestational age
Fundal height
12 weeks
Symphysis pubis
20 weeks
Umbilicus
36 weeks
Xiphoid process
37-40 weeks
Regression of fundal height between 36-32 cm
Postpartum:
≤ 24 hours
Umbilicus
Antepartum: Expected day of confinement (EDC)
EDC
Get first day of a woman's LMP (M/D/Y)
- 3 (M) +7 (D) + 1 (Y)
e.g. LMP 09 – 7 – 19
09 7 19
- 3 +7 + 1
= 06 14 20 (June 14, 2020)
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Antepartum:
Aortocaval syndrome (supine hypotensive syndrome)
Remember: Best position during pregnancy is LATERAL POSITION
Supine hypotensive syndrome occurs when the weight of the abdominal
contents compresses the vena cava causing decreased venous return to the
heart. This results in low cardiac output (maternal hypotension) and reflex
tachycardia as a compensatory mechanism. This leads to dizziness, pallor, and
cold and clammy skin, similar to symptoms oh hypovolemic shock. The client
should be immediately repositioned laterally (right or left side) until the symptoms
subside. Utilizing a wedge pillow prevents this condition.
Antepartum: Biophysical profile testing
Biophysical profile:
A combination of USD and nonstress test done during 26-28
weeks gestation. A score of 8
requires further evaluation such
as contraction stress test/stress
test 32 weeks near delivery.
Indication: High risk pregnancy
▪ Multiple pregnancy
▪ Hypertension, DM, CV diseases
▪ Previous pregnancy
complication
▪ RH incompatibility
▪ Obesity
▪ Pregnancy ≥ 35 YO
Criteria: Highest score 10 points
1. Fetal heart rate
20 mins: ≥ 2 Acceleration (2 points)
40 mins: No acceleration (0 points)
2. Fetal breathing
30 secs: (+) rhythm (2 points)
(-) rhythm (0 points)
3. Fetal body movement
30 mins: ≥ 3 movements (2 points)
No movements (0 points)
4. Fetal leg movement
(+) extension from flexed position (2 points)
No extension (0 points)
5. Amniotic fluid
(+) pocket of fluid (2 points)
(-) pocket of fluid (0 points)
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Non stress test vs Stress test/Contraction stress test (CST)
Non stress test
Remember that in NST, you
are looking for acceleration
(fetal heart activity).
▪ Done 26-28 weeks
(biophysical profile)
▪ A positive result (+) is
normal
▪ A negative (-) result is
abnormal
ST/CST
Remember that in ST/CST,
you are looking for
deceleration “late
deceleration” This time, the
mother is given oxytocin to
see how the fetus’ heart
responds to stress when
uterus contracts
▪ Done 32 weeks near
delivery
▪ A positive result (+) is
abnormal
▪ A negative (-) result is
normal
Both are prenatal test for high risk pregnancies by monitoring
fetal heart activity and fetal well-being in general.
Fetal Heart Monitoring: VEAL CHOP
Variable deceleration
Early deceleration
Acceleration
Late deceleration
Cord compression
Head compression
Okay!
Poor placental perfusion
Variable Deceleration
Cord compression
Variable deceleration means, at any time during uterine contraction by mother the fetus
decelerates (fetal heart rate decreases/downward deflection) due to cord compression.
Top rhythm represents the fetal activity while bottom is maternal contraction
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Early Deceleration
Head compression
Early deceleration: At each uterine contraction by mother, the fetus
decelerates (fetal heart rate decreases/downward deflection) due to head
compression. This reflects a “mirror image” on the monitor.
Acceleration
OK-normal/reassuring
Acceleration: Fetal heart activity showing upward deflection specially during
maternal contraction. This activity is reassuring and indicates fetal well-being
anticipating a stressful event during labor and delivery.
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Late Deceleration
Poor placental perfusion
Late deceleration: Fetal heart activity showing wherein fetus decelerates (fetal
heart rate decreases/downward deflection) after each uterine contractions.
This indicates that fetus responds poorly to stressful events. This can be caused
by poor placental perfusion.
Common conditions: Hyperemesis gravidarum, ectopic
pregnancy
Hyperemesis gravidarum
Overview
A disorder that causes severe
nausea and vomiting that
leads to fluid and electrolyte
imbalances, nutritional
deficiencies, ketonuria, and
weight loss up to 5 kg body
weight. Usually occurs at 8-12
weeks AOG.
Etiology
Genetics, hormonal response
to human chorionic
gonadotropin (HCG), Estrogen
decreases intestinal motility
and gastric emptying leading
to nausea/vomiting
Ectopic pregnancy
Occurs when a fertilized egg
implants and begins to grow
outside the uterine cavity, most
often in the fallopian tubes. A
growing fetus causes rupture to
fallopian and is a life
threatening to the mother.
▪ Age 35 – 40 YO
▪ Pelvic inflammatory disease
(PID)
▪ Smoking
▪ Previous ectopic pregnancy
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Classic S/S
▪ Dehydration (dry mucous
membranes, poor skin
turgor, decreased urine
output, tachycardia, and
low blood pressure
▪ Headache
▪ Hallucination
▪ Weight loss
▪ Ketonuria (breaking down
fats d/t starvation state)
▪ Electrolyte imbalance
(hypokalemia)
▪ Metabolic alkalosis
Complications
▪ Low birth weight
▪ Kidney failure
Diagnostics
▪ Electrolyte levels
▪ HCG
▪ Hemoglobin/hematocrit
Treatment
▪ Sudden-onset abdominal
pain
Referred: Shoulder pain d/t
irritation of the diaphragm
from intraabdominal
bleeding.
▪ Cullen’s sign (periumbilical
bruising)
▪ Hypovolemic shock:
Hypotension, Tachycardia,
Tachypnea
Hypovolemic shock
DOC: Ondansetron
(antiemetic)
Rehydration
Diet: Small frequent feeding,
High protein, low odor food
▪ Pregnancy test (+) HCG
▪ Physical exam
▪ CBC, BUN, Creatinine
DOC: Methotrexate
(anticancer) – to stop
proliferation of cells
preventing rupture
Treat shock: Fluid management
Surgery (if ruptured)
Types of abortion:
Type according to degree of severity
Threatened
Reversible
Inevitable
Possible or inevitable loss
Missed
Fetal loss and retained for a period of time
Incomplete
Partially retained products
Complete
All products of pregnancy removed
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Type according to cause of abortion
Spontaneous
Recurrent
Non-induced or natural passage of products of
conception before 20 weeks AOG.
A form of infertility characterized by 3 consecutive
spontaneous abortions
Induced
Use of medicine to end an undesired pregnancy.
Criminal
termination of pregnancy illegally, usually undertaken
when legal induced abortion is unavailable
Common conditions: Pregnancy induced hypertension (PIH)
Pregnancy induced
hypertension (PIH):
Is a condition characterized by
high blood pressure during
pregnancy beyond 20th week
AOG. Gestational Hypertension
can lead to a serious condition
called Preeclampsia (Triad:
HTN, Proteinuria that leads to
edema and weight gain). If left
untreated it will lead to organ
damage and eclampsia
(Triad + Seizure).
Remember:
The term eclampsia means
“shining forth” which implicates
a common aura for patients
with occurring seizure.
2oth week
AOG
Preexisting HTN
PIH
Remember:
Hypertension prior to 20th week gestation is a preexisting HTN not related to
pregnancy. Pregnancy induced hypertension (PIH) is beyond 20th week.
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Mechanism: The exact cause of PIH-Preeclampsia-Eclampsia mechanism is
unknown. However, certain facts are developed to support its pathophysiology.
Genetically, the abnormal development of placenta causing fibrosis to spiral
arteries which supplies nutrients and O2 to uterus and placenta contributes to the
disease process. This leads to inadequate blood supply leading to release of
placental factors that causes systemic damage to endothelium as it travels to
maternal circulation. Remember, once the body tissues are deprived of O2, it tends
to create dysregulation by releasing certain chemicals. In placenta, these placental
factors promote harmful effects not only within tissues but systemically.
Clinical presentation: Preeclampsia
TRIAD
HTN (>140/90 mmhg): d/t
vasoconstriction by placental
factors and retained fluids by
inadequately perfused kidneys.
Proteinuria: d/t damage glomerulus in
kidneys.
Edema: d/t loss of protein from
proteinuria
Organ damage: Eclampsia
Seizure: d/t decrease blood supply to
brain characterized by headache
and visual disturbances as an “aura”
prior to seizure.
Pulmonary edema: d/t low protein
(albumin)
HELLP syndrome: Liver malfunction
characterized by epigastric pain or
RUQ pain (cardinal sign), N/V, and
eventually hematomas and bleeding
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HELLP syndrome:
A potentially life-threatening
disorder that is usually
associated with preeclampsia.
HELLP syndrome is a disorder of
the liver and blood that can be
fatal if left untreated. The
symptoms of HELLP syndrome
are wide-ranging and vague,
and can often be difficult to
initially diagnose. The name
HELLP syndrome has three major
abnormalities seen on the initial
lab analysis. These include:
Hemolysis, elevated liver
enzymes and low platelet count
Treatment:
▪ Delivery of fetus (depends on
the severity and AOG)
▪ Seizure management
DOC: Magnesium sulfate
▪ BP management
DOC: Hydralazine, Labetalol
Diagnosis:
▪ Physical examination
▪ Blood tests: CBC, Liver profile,
BUN, creatinine
▪ Urinalysis: Urine protein
▪ CXR: pulmonary edema
▪ Biophysical profile
▪ Fetal USD
Common conditions: Abruptio placenta vs Placenta previa
Overview
Abruptio placenta
Placenta previa
Premature and abrupt
separation (full or partial) of the
placenta from the uterine wall
resulting in hemorrhage. Its
main mechanism is the
degeneration of the arteries
supplying the placenta leading
to rupture and separation.
Primarily, the word “previa”
means first. In this condition
you see the placenta first lying
on the cervical os. The
implantation is normally on the
upper part of uterus d/t high
vascularization. However, d/t
previous trauma to uterus, the
placenta is not able implant on
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a normal location.
Types:
Complete: fully covering the
cervical os
Partial: Partially covers the
cervical os
Marginal: 2 cm near the
cervical os
Etiology
Classic S/S
HTN
Chronic smoking
Trauma
Drug abuse
(Methamphetamines,
cocaine) d/t significant
vasoconstriction
▪ Multiparity
▪ Age >35 YO
▪
▪
▪
▪
▪
▪ Painful rigid abdomen: d/t
uterine spasms
▪ Usually concealed bleeding
▪ Hypovolemia (hypotension,
tachycardia, tachypnea)
▪ Painless soft boggy
abdomen: because the
bleeding is not concealed
which does not cause
contractions and spasm
▪ Bleeding: d/t cervical
thinning (effacement) in
preparation for delivery
▪ Hypovolemia (hypotension,
tachycardia, tachypnea)
▪
▪
▪
▪
Maternal:
▪ Hypovolemic shock d/t
bleeding
▪ Acute kidney injury (d/t
hypovolemia)
Complications
▪ DIC
Fetal:
▪ Intra uterine hypoxia (late
decelerations)
▪ Premature birth
Diagnostics
▪ USD
▪ Blood stained amniotic fluid
Previous CS
Abortion
Smoking
Multiparity
Age >35 YO
Maternal:
▪ Hypovolemic shock d/t
bleeding
Fetal:
▪ Intra uterine hypoxia (late
decelerations)
▪ Premature birth
▪ Prenatal USD
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Treatment
▪ IV fluids to support fluid
volume
▪ Blood products (prevent
DIC)
▪ Emergency CS (if severe)
▪ Major bleeding:
Blood products
IV fluids
▪ Corticosteroids: enhance
lung maturity
▪ Emergency CS (if severe)
Remember:
No internal examination (IE)
indicated
Placenta
previa
Marginal/low lying
placenta previa
Partial placenta
previa
Complete
placenta previa
Abruptio
placenta
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Labor and delivery: Stages of Labor
1. Cervical Dilatation (Dilatation – Duration – Interval)
Latent:
0 - 3 cm; 20 - 40 secs; 5 - 10 mins
Active:
4 - 7 cm; 40 - 60 secs; 3 - 5 mins
Transitional:
8 -10 cm; 60 - 90 secs; 1-3 mins
Number of hours:
Primipara: 10 - 14 hours
Multipara: 6 – 8 hours
Remember: No opioids 1-4 hours prior to giving birth
Do not administer opioids 1-4 hours prior to giving birth to avoid neonatal
abstinence syndrome (NAS). Initially, it causes CNS depression that may lead to
respiratory distress similar to opioid intoxication if left untreated. NAS follows after
the opioid effects has already subsided causing withdrawal effects to NB such
as agitation, increases reflexes and seizure. In addition, do not encourage
mother to bear down not until fully dilated at 10 cm to avoid laceration.
Providing emotional support is the priority concern when fully dilated as it is the
most emotionally challenging phase of labor.
2. Expulsion of baby
Hallmark:
Crowning
RBOW:
Primipara: 10 cm
Multipara: 7 - 8 cm
Acronym: “Every darn fool in Egypt eats raw eggs”
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3. Placental Separation
Signs:
Calkin’s sign (Globular shape of abdomen)
Sudden gush of blood
Lengthening of cord
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Schultz Mechanism – shiny inverted umbrella (fetal side)
Duncan Mechanism – Raw red umbrella (maternal side)
4. Immediate post-partum (1 – 4 hours)
Lochia – Psychological Task
Rubra:
1-3 days - Taking In - physiologic need
Serosa:
4-10 days Taking Hold – accepting status
Alba:
11-20 days Letting Go - adapted to roles
Remember: Post-partum blues vs. post-partum depression
Post-partum blues normally resolves within this period of psychological tasks. If
the mother does not overcome this needs and exceeds beyond, it can lead to
depression and psychosis. High risk mothers include history of depression, abuse,
smoking or alcohol use, anxiety, poor marital relationship. Newborn safety is a
priority because mothers may not adapt to roles. It can also lead to possible
suicide and homicide.
Labor and delivery: Umbilical cord prolapse
Knee chest position
uses gravity to shift
fetus out of the pelvis.
Patient’s thighs must
be at the right angles
and chest flat on bed
A gloved hand in the
vagina pushes the
fetus upward and off
the cord
The patient’s hips are
elevated with 2 pillows;
this is often combined
with the Trendelenburg
(head down) position.
Umbilical cord prolapse: Occurs when the umbilical cord slips under the
presenting part of fetus. This causes cord compression and eventually fetal
hypoxia. The prolapsed cord may be palpated during a vaginal examination or
visualized protruding from the vagina. Emergency CS may be required if it causes
severe fetal hypoxia.
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Question: A nurse is evaluating the external fetal monitoring strip of a laboring
primigravida at 36 weeks gestation. Which nursing interventions should the nurse
implement? (Select all that apply)
1. Administer supplemental oxygen by mask
2. Increase the intravenous (IV) fluid rate
3. Prepare the client for an amnioinfusion
4. Reposition the client to the supine position
5. Stop the client's oxytocin infusion
Answer: 1, 2, 5
Rationale: Late decelerations are caused by uteroplacental insufficiency. The client
should be given O2 via facemask, repositioned to the right or left side, stop
ongoing oxytocin if administered, and provide NS bolus. The nurse will need to
prepare for delivery if the deceleration persists.
Amnioinfusion is a transvaginal infusion of fluid for oligohydramnios.
Maternal hypotension:
Acronym: STOP
Stop infusion of Pitocin.
Turn the client on her left side.
Administer Oxygen.
If hypovolemia is present, Push IV fluids
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Post-partum: Hemorrhage
Contraction of uterine
muscles. Compression of
vessels prevents bleeding
Uterine atony:
Lack of uterine contraction
Post-partum hemorrhage (PPH):
Defined as the significant blood loss of more than 500 ml (vaginal delivery or 1,000 ml (CS
delivery) within the first 24 hours following childbirth. Causes include 4 Ts (Tone, trauma,
tissue and thrombin). In addition saturating a peri pad in 1-2 hours could indicate
hemorrhage. This can be assessed by a boggy fundus. The nurse should also assess the
client's vital signs for signs of shock.
Tone: Uterine atony
Causes:
▪ Repeated distention
(multipara, multifetal)
▪ Muscle fatigue from
delivery
▪ Distended bladder
▪ Anesthesia
Treatment:
▪ Fundal massage to
promote contraction
▪ Promote urination
▪ Catheterization
Tissue: Retained placental
fragments
Causes:
▪ Placenta accrete
(deep attachment of
placenta to uterus). This
also promotes uterine
atony
Treatment:
▪ Removal of retained
fragments
Trauma: Damage to genital
structures (vagina,
perineum, uterus, cervix)
Causes:
▪ Incision from delivery
▪ NB coming from vaginal
canal
▪ Medical instrument
(forceps, vacuum)
Treatment:
▪ Repair of trauma site
Thrombin: Abnormal clotting
condition
Causes:
▪ DIC caused by abruptio
placenta
▪ Preexisting coagulation
disorders
(thrombocytopenia)
Treatment:
▪ Treat the specific
underlying cause
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Post-partum: Breastfeeding
▪
▪
▪
▪
Good latch
Baby’s mouth is widely open,
like a yawn
Tongue is over his lower gum
Lips are curled out like a fish
Chin firmly touches breast
▪
▪
▪
▪
Poor latch
Baby’s mouth is barely open
Tongue behind the lower gum
Lips are curled in
Chin barely touches breast
Remember:
Proper breastfeeding technique promotes adequate intake and
emotional bonding. Normally NB will feed at least 8-12 times a day.
at approximately 15-20 minutes each breast. Remember that at
approximately every 2 hours they require attention (feeding and
diaper change). This is also an important indication of the infant’s
hydration status considering intake and output.
Breastfeeding principles:
▪ The client should hold the infant "tummy to tummy," with the
mouth positioned in front of the nipple. The head should be
facing forward keeping the body in alignment.
▪ The infant needs to grasp both the nipple and part of the areola
to ensure proper latching otherwise it will cause pain.
▪ Insert a finger to break the suction prior to moving the infant
away after feeding or in cases on incorrect latching. This
prevents trauma to nipples that may cause mastitis.
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Newborn: APGAR score
APGAR score:
Assessed during first (1st) and fifth (5th) minutes of life. Score of 7-10 is normal and
reassuring, 4-6 is guarded and needs further monitoring (repeated every 5 mins
until the 20th minute of life), 0-3 is critically low and may need resuscitation.
Newborn: Reflexes
Reflexes
Rooting
Sucking
Palmar grasp
Description
When stroked baby will turn his or her
head and open his or her mouth & follow
When the roof of the baby's mouth is
touched, the baby will start to suck
Stroking the palm of a baby's hand
causes the baby to close his or her fingers
in a grasp
Disappears
3-4 months
10-12 months
3-4 moths
Plantar grasp
Similar to the palmar reflex in that stroking
or pressing on the ball of the foot causes
the foot and toes to flex, or curl, so as to
grasp whatever caused the stimulus.
8-10 months
Tonic neck
When a baby's head is turned to one side,
the arm on that side stretches out and the
opposite arm bends up at the elbow. This
is often called the fencing position
4-6 months
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Moro (Startle)
Babinski
Stepping
The baby throws back his or her head,
extends out his or her arms and legs, cries
when startled
Occurs after the sole of the foot has
been firmly stroked. The big toe then
moves upward or toward the top surface
of the foot. The other toes fan out.
Also called the walking or dance reflex
because a baby appears to take steps
or dance when held upright with his or
her feet touching a solid surface
3 months
2 years
2 months
Newborn: Sudden infant death syndrome (SIDS)
Risk factors
▪
▪
▪
▪
▪
▪
▪
Prone or side lying while sleeping
Exposure to tobacco
Infant sleeping with adults
Low birth weight (prematurity)
Overheating during sleep
Soft mattresses
Loose linens, beddings bumper
pads to cribs
Prevention
▪
▪
▪
▪
▪
▪
▪
Supine position
Breastfeeding
Up to date vaccinations
Pacifier use during sleep (focuses
infants attention to sucking)
Sleep sack
Firm mattress
No loose items or toys
Sudden infant death
syndrome (SIDS):
Unexplained death, usually
during sleep, of a seemingly
healthy baby less than a
year old. Although the
cause is unknown, it
appears that SIDS might be
associated with defects in
the portion of an infant's
brain that controls
breathing and arousal from
sleep.
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Newborn: Jaundice (physiologic vs. pathologic)
Physiologic
Pathologic
Not present until 72 hours after birth
Present in the first 24 hours of life
Bilirubin rises <5 mg/dl/day
Bilirubin rises >5mg/dl/hour
Bilirubin peaks at <14-15 mg/dl
Bilirubin peaks up to >15 mg/dl
Direct bilirubin <10% of total
Direct bilirubin >10% of total
Resolves by 1 week (term infants)
Resolves by 2 weeks (preterm infants)
Persists beyond 1 week (term infants)
Persists beyond 2 weeks (preterm infants)
Cause: normal heme breakdown
Cause: Various conditions (e.g.
Erythroblastosis fetalis or Hemolytic
disease of the NB)
Bilirubin levels: Remember that high levels of bilirubin can cause brain damage
(kernicterus) Normal: < 1.5 mg/dl, Jaundice: ≥ 5 mg/dl, Hyperbilirubinemia: ≥ 30
mg/dl
Phototherapy:
Phototherapy:
Is the use of intense fluorescent
lights to reduce serum bilirubin
levels in the NB. Adverse effects
from treatment, such as eye
damage, dehydration, or sensory
deprivation, can occur
Nursing care:
▪ Monitor skin temperature
closely
▪ Reposition the newborn every
2 hours.
▪ Cover the newborn’s eyes with
eye shields or patch
▪ Increase fluids to compensate
for water loss
▪ The fluorescent light turned off
every 4 to 8 hours and is
monitored for bronze baby
syndrome, a grayish brown
discoloration of the skin.
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Newborn: Erythroblastosis fetalis (Hemolytic disease of the NB)
1
2
3
4
5
1. RH (+) father and RH (-) mother yields an RH (+) baby. An RH is an
antigen in the surface of the RBC
2. RH antigen is acquired by fetus from the father (RH+). At this time, there
is no antigen-antibody reaction from the mother and fetus because
there is non-mixing of blood between mother and fetus by way of
placental barrier.
3. After birth, fetal erythrocytes with RH antigen (RH+) leaks into maternal
blood due to breakage of the chorion (placental barrier).
4. The maternal B-cells develop antibodies against RH antigen and
potentially react to future pregnancies.
5. During subsequent pregnancy with acquired RH antigen (RH+) from the
father, the maternal antibodies that are developed by the mother
attack the RH antigen (RH+) of the fetus causing antigen-antibody
reaction. This leads to hemolytic reaction.
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S/S:
Hemolytic anemia: The 4Fs
Fatigue
Forgetfulness
Fainting
Fast heartbeat (tachycardia)
Jaundice
Kernicterus: neurotoxicity
Prevention: Rhogam
Given 26-28 weeks during pregnancy
or within 24-72 hours after delivery if
determined that the baby is RH (+).
Rhogam is an antibody given before
the mother is able to produce its own
by simply halting the B-cells
“signaling not to produce anymore”.
This antibodies does not cause
immune response.
Coombs test: Test for antibodies
Direct: Test that directly detects antibodies in the
surface of RBC. It can diagnose HDN. If positive it
means that these antibodies may cause Ag-Ab
reaction (hemolysis)
Indirect: Detects antibodies from the serum (plasma).
Used to determine if there are chances of
developing Ag-Ab reaction. It is an important tool in
diagnosing hemolytic diseases (e.g. HDN) or in
general, a possible BT reactions of any conditions.
Placental barrier:
The placenta is composed of
several layers of cells acting as a
barrier for the diffusion of
substances between the maternal
and fetal circulatory systems.
However, the placental barrier
between mother and fetus is the
“leakiest” barrier and is a very
poor block to chemicals.
Remember: TORCH
Infectious agents that may cross
placental barrier during first trimester
leading to congenital abnormalities
T: Toxoplasmosis,
O: Others (syphilis, varicella-zoster,
parvovirus B19)
R: Rubella (German measles)
C: Cytomegalovirus
H: Herpes simplex
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Blood compatibilities: ABO and RH
ABO blood system: Is used to symbolize the presence of one, both,
or neither of the A and B antigens on the surface of RBCs. The body
also tends to produce antibodies against a certain antigen
considered as foreign that may cause reaction. For instance, type
A (with antigen A) has developed antibodies against type B that
whenever transfused a foreign blood type B, it will cause Ag-Ab
reaction resulting into hemolysis. On the other hand, a type AB
blood can receive either A, B, O (no antigen) because it does not
have neither antibodies against A or B.
Remember:
Do not interchange RH from ABO system. RH blood system is normally
described with a positive or negative suffix after the ABO type. For
instance, if you have a blood type A(+) it means you have both
antigens A and RH (aka antigen D) in the surface of RBCs. A(-) has
antigen A but with no RH antigens on its surface. RH (+) blood does not
develop antibodies against RH (+) itself, RH (-) does. If RH (-) is exposed
to RH (+) blood, the antibodies cause immune reaction.
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Remember: ABO and RH combined
AB (+): Universal recipient since
type AB does not contain
antibodies against A or B and RH
(+) also does not have antibodies
against any antigen.
O (-): Universal donor since the
recipient blood with RH (+) does
not contain antibodies and RH (-)
recipients only contains antibodies
against RH (+). Type O blood from
a donor does not have A or B
antigen, it means there is nothing
for a recipient with a type A, B
blood to react with. Type AB does
not have antibodies.
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Growth & development
19
Theories: Psychosexual development (Freud)
Stage
Age
Sexual focus
Key task
Fixation
Oral
Birth-1
YO
Mouth
Weaning
Anal
2-3 YO
Anus
Toilet training
Obsession on cleanliness, sexual
anxiety
Identifying
gender role
Genitals
models
(masturbation)
Oedipus: boys
Electra: girls
Difficulty in intimate relationship,
inadequacy, inferiority
Obsessive eating, smoking,
drinking (alcoholism
Phallic
4-5 YO
Latency
6-12 YO
None
Social
interaction
Genital
Puberty
& later
Genitals
(sexual
intimacy)
Intimate
relationship/
Productivity
No fixation
Return to previous fixation (low
sexual interest or if no previous
fixation, may have sexual
motivation
Cognitive development (Piaget)
Stage
Age
Sensorimotor
Birth – 2
YO
Pre-operational
“mental operations”
2-7 YO
Concrete
operational
7-11 YO
Important features
▪ Object permanence: Differentiates self from objects
e.g. “If you remove the toy or object, they will think
that it does not exist anymore”
▪ Egocentric: self centered
▪ Understands symbols
▪ Classifies objects by it single feature: groups all
together red blocks regardless of shape
▪ Conservation: e.g. the same amount of fluid is what
it is even if you transfer it to a different containers.
▪ Classifies objects according to several features
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12 and
up
Formal operation
▪ Abstract: believes that there is always a
consequence of actions
▪ Moral reasoning: believes in what is right and what
is wrong
Moral development (Kohlberg)
Level and age
Stage
Preconventional
(Pre-moral)
Up to age 9 YO
Conventional
(Most
adolescents
and adults)
What determines right and wrong?
“Obey or punished”
Defined by what they get punished for. If
you get told off for stealing then that is
wrong
“Individuals have
different viewpoints”
Determined by what we are rewarded or
by doing what others want
Good boy, good girl
Being good is what pleases others. Right
and wrong is determined by the majority
Law and order
Being good is doing your duty to society.
Showing respect to society
Social contract
Determined by personal values: “Rules in
society is not absolute, people have rights”
Universal ethical
principle
In accordance with deeply held moral
principles: “human rights is more important
than the law even if you are persecuted”
(e.g. Martin Luther King, Nelson Mandela
principles)
Post
conventional
(0-15 % of over
20 YO)
Psychosocial/Personality development (Erikson)
Age
Infancy
(0-1 YO)
Toddlerhood
(1-3 YO)
Preschool
(4-6 YO)
Significant
Virtues
Crisis
Hope
Trust vs
mistrust
Mother
Can I trust the
world?
Feeding,
abandonment
Will
Autonomy
vs shame
and doubt
Parents
Is it OK to be
me?
Toilet training,
clothing their
own selves
Purpose
Initiative vs
guilt
Family
Is it OK for me to
move?
Exploring tools,
making arts
relationship
Question
Crucial events
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Can I make it in
the world of
people and
things?
School
activities, sports
Who am I? Who
I can be?
Social
relationships
Compe
tence
Industry vs
inferiority
Neighbors,
school
teachers
Adolescence
(12-19 YO)
Fidelity
Identity vs
role
confusion
Peers, role
models
Early
adulthood
(20-35 YO)
Love
Intimacy vs
isolation
Friends and
partners
Can I love?
Romantic
relationships
Adulthood
(35-65 YO)
Care
Generativity
vs
stagnation
Household,
workmates
Can I make my
life count?
Work,
parenthood
Wisdom
Ego
integrity vs
despair
Mankind,
my kind
Is it OK to have
been me?
Reflection on
life
School age
(6-12 YO)
Late
adulthood
(65 and up)
Developmental milestones: Infants - toddlers
Age
(Months)
1
2-3
Gross motor
Attempts to hold
head up when
prone
Gains head
control when
held
4-5
▪ Rolls from frontback then
back-front
▪ Sits with support
6-9
▪ Sits without help
▪ Begins to crawl
▪ May pull to
stand
10-12
▪ May walk with
help or
independent
steps
▪ Crawls up stairs
Language
Social/cognitiv
e
Maintains fisted
hand
Cries when upset
Gazes at parents
when they speak
Holds rattle when
placed in hand
Makes cooing
sounds
Smiles in response
to talking and
smiling
▪ Begins to laugh
▪ Makes some
consonant
sounds
Calms by
parent’s voice
Fine motor
▪ Holds object
with palmar
grasp
▪ Puts things in
mouth
▪ Moves objects
between hands
▪ Uses crude
pincer grasp
(using pads of
index finger)
▪ Uses 2 finger
pincer grasp
▪ Hits 2 object
together
▪ Babbles and
imitates sounds
▪ May say
“Mama”
▪ Says 3-5 words
▪ Non-verbal
gesture like
waving
goodbye
▪ Recognizes
familiar faces
▪ May have
stranger anxiety
▪ May have
stranger anxiety
▪ Searches for
hidden objects
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18
▪ Walks up/down
stairs with help
independently
▪ Throws ball
overhand
▪ Jumps in place
▪ Builds 3-4 blocks
tower
▪ Turns 2-3 book
pages
▪ Scribbles
▪ Uses cup and
spoon
▪ Says 10+ words
▪ Identifies
common
objects
▪ Has temper
tantrums
▪ Understands
ownership
“mine”
▪ Imitates others
2 YO
▪ Walks up/down
stairs alone, 1
step at a time
▪ Runs without
falling
▪ Kicks ball
▪ Builds 6-7 block
tower
▪ Turns 1 book
page
▪ Draws a line
▪ 300+ words
▪ 2-3 word
phrases
▪ States own
name
▪ Begins parallel
play
▪ Begins to gain
independence
from parents
3 YO
▪ Walks up stairs
with alternating
feet
▪ Pedals a
tricycle
▪ Jumps forward
▪ Draws a circle
▪ Feeds self
without help
▪ Grips a crayon
with fingers
instead of fist
▪ 3-4 sentences
▪ Ask “why”
questions
▪ States own age
▪ Begins group
play
▪ Toilet trained
except wiping
Others:
Readiness in toilet training:
▪ Ambulates to and sit on the
toilet
▪ Remain dry for several hours or
through a nap
▪ Pull clothes up and down
▪ Understand a two-step
command
▪ Express the need to use the
toilet (urge to defecate or
urinate)
▪ Imitate the toilet habits of adults
or older siblings
▪ Express an interest in toilet
training
Remember:
There is no magic age for toilet
training. Developmental
milestones rather than the child's
age signal a child's readiness for
toilet training
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Age
Birth to 2 YO
3-5 YO
6-9 YO
10-12 YO
Adolescent
Belief on death
▪ Does not understand death
▪ Sensitive to loss and separation
▪ Death is reversible
▪ Thoughts may include magical thinking and
fantasy
▪ Concrete finality of death
▪ Difficult in perceiving their own death
▪ May be preoccupied with the medical or
physical aspects of dying
▪ Understands that death affects everyone
▪ Thinks about how death may affect them
personally
▪ View death on an adult level and understands
that their own death is inevitable but is a
difficult concept to perceive
▪ Incorporates spiritual and religious aspects of
death
Separation anxiety:
Also known as anaclitic depression,
affects children age 6-30 months and
peaks at 10-18 months. May last until
3 years.
Stages:
Protest – Characterized by refusing
from others so the parent returns by
crying
Despair – Withdraw, quiet, displays
younger behavior
Detachment – Suddenly appears
friendly and builds relationships
Nursing care:
▪ Encouraging the parents to leave favorite toys, books, and
pictures from home
▪ Establishing a daily schedule that is similar to the child's home
routine
▪ Maintaining a close, calming presence when the child is
visibly upset
▪ Facilitating phone or video calls when parents are available
▪ Providing opportunities for the child to play and participate in
activities
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Question: The parents of a hospitalized 3-month-old have to leave the infant
while they work. One parent fears that the baby will cry as soon as they
walk out. The nurse teaches both parents about separation anxiety. Which
statement by the parent indicates that the teaching has been effective?
1. "At this age, my baby will not cry because we are leaving."
2. "I know my baby will feel abandoned when we leave."
3. "My baby is too young to sense my anxiety about leaving."
4. "My baby understands that we will return later in the day."
Answer: 1
Rationale: A 3-month-old can be soothed by any comforting voice and does not
develop separation anxiety at this time. This behavior starts around age 6
months, peaks at age 10-18 months, and can last even until age 3 years. It
produces more stress than any other factor for children in this age group.
However, this reaction is normal and resolves as the child approaches age 3
years.
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20
Therapeutic communication:
Behavioral
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Non therapeutic communication:
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Defense mechanism:
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Eating disorders: Bulimia nervosa vs Anorexia nervosa
Anorexia nervosa
vs
Purging without eating
Overview
Purging after binge eating
Weight loss of up to < 75% ideal
body weight since patient is not
eating
General
Appearance
Normal appearance, may or
may not have weight loss since
patient still eats.
Yes
May or may not use
Induced
vomiting
(purging)
Laxative use
(Abuse to
drugs)
Bulimia nervosa
Yes
Yes
Low
Potassium
Low
Low
Blood sugar
Low
Suppression as characterized by
consciously forgetting to eat
because they think they are fat
Defense
mechanism
Compulsiveness characterized
by repetitive and excessive
induced vomiting
Tricyclic antidepressants
Imipramine (Tofranil)
DOC
Tricyclic antidepressants
Imipramine (Tofranil)
Nursing
▪ Setting limits
▪ Staying after meals to ensure
intake
▪ Be alert of hidden or discarded
food wrappers (common sign)
▪ Assess for dehydration and
electrolyte imbalance
▪ Daily weights
▪ Allowing them to keep food
diary to understand disorder.
However, close supervision is
indicated
▪ Setting limits
▪ Staying after meals to ensure
intake
▪ Assess for dehydration and
electrolyte imbalance
▪ Daily weights
▪ Allowing them to keep food
diary to understand disorder.
However, close supervision is
indicated
Remember:
Common etiologies associated with eating disorders are associated with factors
such as: Individual (self-imposed), familial (perfectionist parents), social (peer
pressure). Eating disorders are potentially life threatening due to fluid and
electrolyte imbalances implicated.
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Cognitive disorder: Alzheimer’s disease
Alzheimer's disease
Accounts for 50% to 70% of cases of dementia (broad definition of brain disease
that causes a long term or chronic cognitive malfunctioning). It is one of the
most common causes of injuries resulting from fall among elderlies in the US, both
in and out patient population. Alzheimer’s implies SAFETY precautions as a
priority at any time.
Remember:
Pick’s disease is a form of dementia
with similar symptoms of Alzheimer’s
disease which is most specific to
frontotemporal degeneration of the
brain. Defining characteristic of the
disease is build-up of tau proteins in
neurons, accumulating into silverstained aggregations known as "Pick
bodies" which can only be done on
autopsy.
Acronym: 3 As
Aphasia: Language deficit
either expressive, receptive
or both
Agnosia: Unable to recognize
things
Anomia: (A form of aphasia)
unable to recall the names
of everyday objects
Safety: “Sundowning”
Also known as sundown
syndrome, is a phenomenon
associated with increased
confusion and restlessness in
patients with Alzheimer's
disease, usually before the
day ends.
Acronym: ATE
Aricept (Donepezil)
Tacrine (Cognex)
Exelon (Rivastigmine)
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Schizophrenia spectrum disorder:
Schizophrenia spectrum disorder:
Psychotic disorders Includes a range of linked conditions of schizophrenia.
Symptoms fall into two broad categories: positive and negative symptoms.
Positive symptoms are current manifestation and are not present before
diagnosis and are all present to each disorders under this spectrum. Negative
symptoms are normal characteristics of an individual before the diagnosis which
are not currently seen and may or may not be present to each disorders.
Disorder
Characteristics
Signs & symptoms
Brief psychotic
Symptoms last for 30 days
(+) symptoms
(-) symptoms
Schizophreniform
Symptoms last 30 days –
6 months
(+) symptoms
Schizophrenic
Persistent symptoms
more than 6 moths
(+) symptoms
(-) symptoms
Schizoaffective
Exhibiting symptoms of both
schizophrenia and a mood disorder
(bipolar, depression)
(+) symptoms
(-) symptoms
Delusional
Previously called paranoid disorder.
Exhibits delusion as a major
manifestation
(+) symptoms
(delusional)
Substance abuse
psychosis
Psychotic disorder with substance
abuse etiology
(+) symptoms
With or without (-)
symptoms
Schizotypal
Always fantasizing and socializes in
a strange way “awkward”. If
without (+) symptoms, can be a
cluster A personality disorder
(+) symptoms
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Positive (+) symptoms
▪ Anxiety/Akathisia/Agitation
▪ Hallucination (perception of
something not present)
▪ Delusion (false conviction to
something that is not real)
Remember:
Positive symptoms are treated
with typical anti-psychotics
with suffix “AZINE”, “DOL”
except Loxapine and
Molindone.
Example: Haloperidol,
Chlorpromazine
Remember:
Both negative and positive
symptoms are treated with
atypical anti-psychotics with
suffix “PINE”, “ONE”, “ZOLE”
Example: Olanzapine,
Quetiapine, Clozapine,
Ziprasidone, Risperidone,
Aripiprazole
Remember:
Psychotropic medications are
major tranquilizer except for
antianxiety (minor). This
medications can cause major CV
effects (hypotension).
Remember: 2-3 Rule
2-3 minutes antianxiety
medications takes effect
2-3 days anti-Parkinson
medications takes effect
2-3 weeks anti-depressant
medications takes effect
Side effects:
▪ Drowsiness, Dizziness,
▪ Tremors, Restlessness
▪ Tachycardia
▪ Blurred vision
▪ Constipation
▪ Dry mouth
▪ Skin rash
▪ Photosensitivity
▪ Muscle spasms
Negative (-) symptoms
Acronym: 6 As (except anxiety,
akathisia, agitation)
▪ Anhedonia: Loss of pleasure
▪ Avolition: Loss of motivation
▪ Ambivalence: indecisiveness
▪ Alogia: Loss of logic
▪ Anergia: Loss of energy
▪ Apathy/Affect disturbance:
Loss of feelings
Psychotropic medications are
given with food or after meals
except for antianxiety (pre-meals)
Adverse effects:
▪ Agranulocytosis: sore throat and fever
▪ Malignant hyperthermia: Fever and rigidity
▪ Neuroleptic malignant syndrome (NMS):
Fever, rigidity, etc. (all s/s)
Tardive dyskinesia (dystonia)
Minor: Puffing of cheeks, Lip smacking,
tongue protrusion
Major: Oculogyric crisis (rolling of eyes),
Torticollis (stiffed neck), Opisthotonus
(arching of back)
Hepatotoxicity, Orthostatic hypotension,
Pseudo parkinsonism
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Common disorders related to psychopharmacology:
Malignant
hyperthermia
Neuroleptic malignant
syndrome (NMS)
Serotonin syndrome
Causative drug
Succinylcholine,
Antipsychotics
Antipsychotics,
Withdrawal from
anti-Parkinson’s
Serotonergic
agents (overdose
or combination)
Onset of
symptoms
Minutes to hours
Days to weeks
Hours
Mental status
Agitation
Stupor
Agitated
Muscle
symptoms
Rigidity
Rigidity
Rigidity with tremors
Vitals
Severe hyperthermia,
Tachycardia,
Hypertension,
Tachypnea
Hyperthermia,
Tachycardia,
Hypertension,
Tachypnea
Hyperthermia,
Tachycardia,
Hypertension,
Tachypnea
Dantrolene
Bromocriptine,
Dantrolene
Chlorpromazine,
Benzodiazepines
(e.g. Diazepam)
DOC
Remember:
There must be a minimum of 14 days (2 weeks)
between the administration of anti-depressants
(e.g. MAOIs and SSRIs) to avoid serotonin
syndrome;, these medications cannot be
administered concurrently.
Serotonin syndrome:
A life-threatening condition,
develops when drugs
affecting the body's
serotonin levels are
administered in
combination or in overdose.
This include anti-depressants
such as selective serotonin
reuptake inhibitor (SSRI),
serotonin norepinephrine
reuptake inhibitor (SNRI),
monoamine oxidase
inhibitor (MAOI), tricyclic
antidepressants (TCAs),
tramadol,
dextromethorphan, St.
John's wort, ondansetron.
metoclopramide,
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Mood disorders: Depression and Bipolar disorders
Depression
(Unipolar depression)
Major depressive
disorder:
Characterized by:
Meets 5 criteria
Last ≥ 2 weeks
Persistent depressive
disorder/Dysthymia
(PDD)
Characterized by:
Meets 3 criteria
Last ≥ 2 years
Depression criteria: SIGECAPS
S: Sleep problems (Insomnia or hypersomnia)
I: Interest lost (anhedonia)
G: Guilt (worthlessness, hopelessness)
E: Energy deficit
C: Concentration deficit
A: Appetite (increased or decreased)
P: Psychomotor retardation or agitation
S: Suicidality
Bipolar Disorder
Bipolar I:
Bipolar II
Characterized by:
▪ Mania episode
▪ Positive (+) symptoms of
psychosis
▪ Psychotherapy,
cognitive therapy, and
medications
▪ Treated with
electroconvulsive
therapy
Characterized by:
▪ Hypomania episode
▪ No positive (+)
symptoms of psychosis
▪ Psychotherapy,
cognitive therapy, and
medications
▪ No electroconvulsive
therapy needed
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Antidepressants:
1
Selective serotonin reuptake
inhibitor (SSRI)
Increase the serotonin level
in the brain by preventing
it's reuptake by the
presynaptic neurons. It
simply means it will remain
available to bind to
postsynaptic neurons and
exert its mood enhancing
effects. Low serotonin levels
are a cause of depression.
Remember:
Reuptake is the reabsorption of a neurotransmitter by transporter located
along the plasma membrane of an axon terminal after it has performed its
function of transmitting a neural impulse. Reuptake is necessary because it
allows for the recycling of neurotransmitters and regulates the level of
neurotransmitter. Any abnormal amounts of neurotransmitter may affect
neuronal function easily.
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Remember: Excitatory
neurotransmitters (SEND-G)
FSF
Fluoxetine (Prozac)
Sertraline (Zoloft)
Fluvoxamine (Luvox)
▪
▪
▪
▪
▪
Nursing: SSRI
S: Sexual dysfunction
S: Sleep disturbance (Insomnia)
R: Restlessness
I: Increase weight
Serotonin
Epinephrine
Norepinephrine
Dopamine
Glutamate (most abundant)
Decrease levels in excitatory NT may
cause the opposite (depression)
than may be caused by
acetylcholine as an inhibitory NT.
2
Serotonin and
norepinephrine reuptake
inhibitor (SNRI)
Inhibits the reuptake of
serotonin and
norepinephrine in the
presynaptic neurons.
3
Venlafaxine (Effexor)
Nursing: SNRI
S: Sexual dysfunction
N: Nausea/vomiting
R: Reduced weight
I: Insomnia
IAC “ine’s, il’s”
Tricyclic antidepressants
(TCA)
Inhibits both reuptake of
serotonin and
norepinephrine as well as
inhibiting production of
acetylcholine
(anticholinergic effects)
Imipramine (Tofranil)
Amitriptyline (Elavil)
Clomipramine (Anafranil)
Nursing: TCA
T: Tension/tention (hypotension,
urinary retention)
C: Cardiovascular effects (e.g.
palpitations, hypotension,
arrhythmias)
A: Arrhythmias
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4
5
Multimodal/Atypical
antidepressants
Frequently used in patients
with major depression who
have inadequate responses
or intolerable side effects
during first-line treatment
with SSRIs or other
antidepressants. In general,
they increase excitatory NT
same with the other class.
Monoamine oxidase
inhibitors (MAOI)
Inhibits monoamine oxidase
an enzyme which is
responsible in breaking
down amines (dopamine,
serotonin, epinephrine). By
inhibiting these enzymes, it
tends to increase levels of
tyramine, a precursor of the
amines. Last line of
medication due to tyramine
Cardiovascular effects such
as hypertensive crisis.
Remember that this NT
chemicals are excitatory.
Bupropion (Wellbutrin)
Trazodone (Oleptro)
Vortioxetine (Brintelix)
Remember:
These medications are most
commonly indicated in the US these
days. Trazodone is tetracyclic
antidepressant with similar effects
such as TCA. Crushing, cutting and
chewing these medications are
contraindicated because its mostly
prepared as extended release (XR) to
minimize side effects
PAMANA
(Parnate) Tranylcypromine
(Marplan) Isocarboxacid
(Nardil) Phenelzine
Nursing: Avoid tyramine rich food
Avoid: ABC
▪ Aged cheese, avocado
▪ Bananas, beers (alcoholic beverages)
▪ Cold cuts, cured meats
Remember:
Selegiline is a MAOI that has less chances
of causing hypertensive crisis due to its
route of administration given as a patch.
Remember: Fresh cheese is OK
When I was in AMERICA, I visited my aunt RICOTTA,
she is a FARMER. I usually stay in a COTTAGE and eat
my favorite CREAM cheese.
Fresh cheeses:
American
Ricotta
Farmer’s
Cottage
Cream
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Lithium:
Lithium is a mood stabilizer most often used to treat bipolar disorders. It is usually
given with antipsychotics for the first 2 weeks to treat symptoms of mania because it
will take 2 weeks to achieve its effects. Lithium has a narrow therapeutic index or a
“thin line” between therapeutic effects and toxicity. Lithium toxicity is triggered by
dehydration, impaired kidney function (in the elderly), diet low in sodium, and drugdrug interactions (e.g. NSAIDs and diuretics).
Acute manifestations:
NAVDA (GI symptoms)
N: Nausea
A: Abdominal pain
V: Vomiting
D: Diarrhea
A: Anorexia
Prevention:
▪ Extra sodium intake to avoid
depletion: Hyponatremia,
dehydration triggers toxicity
▪ Increase fluid intake (2-3 L/day)
▪ Regular blood works for lithium
levels and kidney function
Chronic manifestations:
Neurologic symptoms
Neuromuscular excitability
(tremors, agitation, restlessness,
confusion) followed by coma if not
treated promptly. Dialysis is a
treatment of choice.
Lithium level:
0.5—1.5 mEq/L (Acute/Adult)
0.6—1.2 mEq/L (Maintenance)
0.4—1.0 mEq/L (>65 YO)
6 to 8 mEq/L: needs dialysis
Electroconvulsive therapy:
Electroconvulsive therapy:
ECT is an effective treatment for
severe form major depression with
psychotic symptoms (bipolar I).
Can be used also in clients who do
not respond to medications or
patient with severe symptoms
awaiting for the effects of
medications (2 weeks). The usual
course is 1-1 ½ months (2-3 sessions
per week)
Remember:
Confusion and memory loss are
common effects due to anesthesia
and muscle relaxants administered
concurrently during brief
convulsions.
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Anxiety disorders:
Are group of disorders characterized by significant feelings of anxiety and fear.
Anxiety is a worry about future events, and fear is a reaction to current events.
The implication is that, it may cause variety of physiological symptoms such as
tachycardia, palpitations, arrhythmias, etc. Safety is a priority because
potentially it can lead to panic attack and may cause potential death.
Generalized anxiety disorder is a common disorder that may last more than 6
months and is characterized by excessive, exaggerated anxiety and worry
about everyday life events with no obvious reasons. Below are the specific
disorders of anxiety that severely affects individuals’ various aspects of life.
Disorders
Overview
“Irrational fear or aversion to something” which is
persistent and excessive.
Example:
1. Agoraphobia - Fears and avoid places or situations
that might cause panic and make you feel trapped or
helpless. The fear they experience is out of proportion to
any actual danger. Need to get accompanied by a
relative or friend when facing situations is common.
Phobia
Common situations:
In a crowd, Traveling in a public transport, in a bridge
or in a tunnel or enclosed spaces such as malls, halls,
theaters, open spaces such parking.
2. Social anxiety disorder - Fear of “scrutiny” or
embarrassment in a public in a performance such public
speaking.
3. Specific phobias – Claustrophobia (specific to confined
spaces, not necessarily in public), Aerophobia (Airplane),
Acrophobia (heights)
Post-traumatic stress
disorder (PTSD)
“Reaction to a traumatic or disastrous event that is lifethreatening to oneself or others”
Characteristics:
▪ Flashbacks/nightmares
▪ Reminder avoidance (e.g. avoids watching news
related to traumatic event experienced)
▪ Increased anxiety and arousal
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“Pattern of unreasonable thoughts and fears (obsessions)
that lead to do repetitive behaviors (compulsions)”
Obsessive
compulsive (OCD)
Characteristics: OCD is distinguished from OC personality
disorders (OCPD) as the former suffers from depression.
They are fully aware that their obsession/compulsion is
undesirable for others, in which they could not control
leading to depression. In OCPD, they are not aware of
their behavior. For them, it’s just but part of daily routine.
This insight leads to a better outcome (no depression)
comparing to OCD.
“Unintentional, extreme focus on physical symptoms
such as pain or fatigue that causes major emotional
distress and anxiety as well as problems in functioning”
Somatic symptom
disorder
Factitious
(Munchausen)
disorder
Hypochondriasis - exaggerated symptoms of serious
illness
Body dysmorphic - perceived defects or flaws in your
appearance “feeling ugly”
Pain disorder – exaggerated symptom of pain
Conversion disorder – (aka functional neurological
symptom d/o) converting to neurologic symptom
such as seizure, loss of consciousness, blindness,
deafness with no medical basis.
“Intentional, habitual lying or faking disease in order to
play the patient role, not necessarily to achieve a
personal gain”
Munchausen by proxy syndrome – a more harmful type
in which the person involves other person (mostly
their children) to make it appear that their ill. They
intentionally injure the child. This syndrome is a form
of child abuse.
“Intentional, habitual lying or faking disease in order to
necessarily achieve a personal gain”
Malingering
Primary gain – patient wants attention to increase his/her
self-esteem (internal motivators)as a gain by faking.
Secondary gain – patient wants a sick leave even not
sick, to gain money from converted leaves (external
motivators)
Tertiary gain – Uses someone’s illness (third person) to
achieve a personal gain
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Personality disorders:
Are a group of mental illnesses involving long-term patterns of thoughts and
behaviors that are unhealthy and inflexible. The behaviors cause serious
problems with relationships and work. They are categorized into 3 clusters:
Cluster A: “Odd or weird personalities”, associated with schizophrenia
Cluster B: “Wild, overly dramatic personalities”, associated with mood disorders
and substance abuse
Cluster C: “Easily worried and anxious personalities”, associated with anxiety
disorders
Cluster A
Paranoid
Schizoid
Schizotypal
Cluster B
Overview
“Accusatory and underdeveloped trust”
Characteristics:
▪ Eager observant
▪ Mistrust
▪ Pervasive suspicion
▪ Hypersensitive
“Social withdrawal, aloof”
Characteristics:
▪ Does not socialize and distant from people
▪ Does not find socialization enjoyable
▪ Solitary in activity
“Always fantasizing and awkward”
Characteristics:
▪ Socializes but in an awkward or strange way
▪ Classified within schizotypal spectrum if with positive (+)
symptoms of schizophrenia
Overview
“No rules, disregards others rights”
Antisocial
Characteristics:
▪ Womanizer/Unfaithful
▪ Lack of empathy and guilt
▪ Highly aggressive and irritable
▪ Impulsive
▪ Consistently irresponsible
▪ Blaming others
▪ History of conduct disorder from childhood
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“Split personalities”
Borderline
Characteristics:
▪ Risk takers, suicidal
▪ Dissociates from one personality to another (from joyful
to anger/rage) “mood swings”
▪ Impulsive
▪ Also manifest antisocial behavior but they are not
persistent in disregarding rules
“Self centered”
Narcissistic
Characteristics:
▪ Sense of self-importance and entitlement
▪ Excessive admiration to self
▪ Arrogant
▪ Lack of empathy and guilt
▪ Taking advantage of people around them
“Overly acting (OA)”
Histrionic
Cluster C
Characteristics:
▪ Excessive attention seeking
▪ Seductive behavior “Flirt”
▪ Dramatic
▪ Rapid shifts of emotion (more to drama)
▪ Seeks approval from others
Overview
“Clingy”
Dependent
Characteristics:
▪ Excessive reliant from other people
▪ Inability to make his/her own decisions
▪ Fear of abandonment or being alone
▪ Helpless when relationship ends
▪ Afraid of confrontation
▪ Low self confidence
▪ Advice seekers
“Coward”
Avoidant
Characteristics:
▪ Avoids social interaction
▪ Inferiority behavior
▪ Afraid of criticism from others
▪ Low self confidence
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Obsessive
compulsive
personality
(OCPD)
“OC”
Characteristics:
▪ Dislikes unpredictable events or situations
▪ “Time is gold” character but inflexible to circumstances
▪ Excessive concern to orderliness, cleanliness, attention to
details
▪ Imposes own standards, reluctant in delegating task
▪ Rigid and determined
▪ Hoarder
▪ Aware and happy with their behavior otherwise may
lead into depression (OCD)
Autism spectrum disorders (ASD) vs Attention deficit
hyperactivity disorder (ADHD):
ASD
A group of disorders
generally characterized by
1. antisocial behavior and 2.
repetitive movements or
fixation to a certain actions
such as spinning, hand
shaking, rocking.
ASD Management
No medication is needed
unless with severe
form(CDD) to treat
symptoms. Behavioral and
enrichment of skills
education are also
indicated
ADHD
Is one of the most common
neurobehavioral disorders
of childhood. It is usually first
diagnosed in childhood
and often lasts into
adulthood. Generally
characterized by
1. Hyperactivity,
2. impulsiveness and
3. inattentiveness
ADHD management
DOC: Methylphenidate
(Ritalin). Mechanism of action
is to balance dopamine
Nursing:
▪ Given in the morning to
prevent insomnia or 4-6
hours prior to sleeping hours
▪ Monitor BP and HR since it
increases dopamine
▪ Given after meal because it
cause decrease appetite
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ASD
Overview
Classic autism
Characteristics: Antisocial and fixation
▪ Speech delay (classic sign)
▪ Low IQ autism
▪ Common in < 3 YO
Asperger’s disorder
Characteristics: Antisocial and fixation
▪ Mild autism
▪ Normal or high intelligence
▪ “High-functioning autism”
Pervasive
developmental
disorder nonotherwise specified
(PDD-NOS)
Characteristics: Antisocial and fixation
▪ Does not meet other criteria of autism
▪ Mild autism/atypical autism
Childhood
disintegrative
disorder (CDD)/
Heller’s syndrome
Characteristics: Antisocial and fixation
▪ Severe form of autism
▪ Deterioration in skills which were attained previously
▪ Late onset developmental delays
▪ Loss of bladder and bowel control
▪ May have seizures
Substance abuse: depressants and stimulants
Depressant “downers”
Chemicals or drugs that slows
down the central nervous
system (CNS) function such as
bradycardia, hypotension,
hypoventilation, drowsiness.
Commonly abused are
alcohol and narcotic or
opioid medications.
Stimulants “uppers”
Chemicals or drugs that
speeds up the central
nervous system (CNS)
function such as tachycardia,
hypertension,
hyperventilation, confusion,
agitation. Commonly abused
are amphetamines,
marijuana, cocaine, ecstasy.
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Withdrawal
Intoxication
Describes as ingestion of
large quantity of a substance
either a stimulant or a
depressant achieving it toxic
effects.
Group of symptoms that occur
upon the abrupt discontinuation
or decrease in intake of abused
chemical in which a person
develops dependence.
Remember that these chemicals
are addictive, if stopped
abruptly, the body springs off
(rebound effect) and produces
opposite effect of the
substance.
Commonly abused substance: Stimulants and depressants
STIMULANTS
Intoxication
classic sign
Withdrawal
classic sign
Chronic use
Cocaine
Epistaxis
Mental depression
Nasal septum
deviation
Amphetamines
Halitosis
Mental depression
Cachexia
(muscle wasting),
Psychosis
Marijuana
Blood shot eyes
“no withdrawal”
Memory loss,
Psychosis
DEPRESSANTS
Intoxication
classic sign
Withdrawal
classic sign
Chronic use
Alcohol
Hypoventilation,
CNS depression
Delirium tremens
“DTs”
Wernicke’sKorsakoff
syndrome
Codeine
Muscle
incoordination
Headache,
Insomnia, sweating
Impotence
Morphine
Extreme drowsiness
Piloerection
“goosebumps”
Personality
changes
Heroin
Pinpoint pupils
Rhinorrhea
Personality
changes
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General symptoms of
INTOXICATION from
depressants
Remember:
CNS depressant means
respiratory compromise as a
priority. Other effects are
cardiovascular and
autonomic.
▪ Hypoventilation resulting
to respiratory acidosis and
respiratory depression
▪ Bradypnea
▪ Bradycardia
▪ Decrease level of
consciousness
▪ Miosis (pupil constriction)
▪ Constipation
▪ Nausea/vomiting
▪ Urinary incontinence
▪ Pruritus
DOC (antidote):
Naloxone
General symptoms of WITHDRAWAL from
depressants
Remember:
Withdrawal symptoms are the rebound effects
of this substances. The body tends to “crave”
for its addictive effects by increasing the
amounts of excitatory NT. Dehydration and
seizure are the priority.
Early S/S:
▪ Hyperventilation resulting to respiratory
alkalosis
▪ Tachypnea, Tachycardia
▪ Anxiety, agitation, tremors
▪ Diaphoresis
▪ Mydriasis (pupil dilation)
Late S/S:
▪ Diarrhea
▪ Severe nausea/vomiting
▪ Piloerection (goosebumps)
▪ Rigidity
▪ Seizure
▪ Hallucination
DOC (antidote): Methadone
Remember:
Methadone is also an opioid medication.
However, due to its long half-life up to 60
hours, the drug can still remain in the body in
large amounts enough to sustain the “craving”
and limit symptoms.
Remember:
Intoxication from stimulant substances cause the same manifestations from
withdrawal to depressants, vice versa. This is caused by the rebound effects.
Neurotransmitters from the brain are sensitive to this substances.
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Alcohol use disorder:
Lethal alcohol
levels:
400 mg/dL
(> or =0.4%)
Antabuse vs Librium
Remember:
Disulfiram (Antabuse) is for
alcohol intoxication to keep
patient sober from alcohol.
Antabuse is an antidote that
blocks the enzyme necessary
in alcohol metabolism and
produces an UNPLEASANT
effects to patients making the
body get rid of it. This leads
into gradual non-craving
from alcohol. On the other
hand, Chlordiazepoxide
(Librium), a CNS depressant is
given to limit symptoms of
withdrawal such as agitation,
anxiety, restlessness, tremors
etc.
Acronym: A L cohol
Antabuse – Intoxication
Librium – Withdrawal
Nursing care: Disulfiram (Antabuse)
▪ Patient should be alcohol free for at least 12
hours before giving the medication
▪ Avoid “MOFAVS”
M: Mouthwash
O: OTC medications
F: Fermented wines
A: Aftershave
V: Vinegar
S: Skin products
Delirium tremens: Rapid onset of confusion and
other symptoms related to withdrawal from alcohol
substance. Safety is the priority for this patient (risk
for injury).
Wernicke’s – Korsakoff syndrome: is a type of brain
disorder caused by a lack of Vit B1(thiamine)and Vit
B3 (niacin) most commonly caused by chronic
alcoholism. The syndrome is actually two separate
conditions that can occur at the same time
characterized by gradual memory loss (amnesia)
specifically confabulation, a form of memory loss
wherein a patient fills in false stories during a
talkative conversation
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Question: The home health aide reports to the nurse care manager that the
client has been trying to give away possessions. When the nurse asks the
client about this behavior, the client says, "With my spouse dead, there's no
reason for me to go on." What is the best priority response by the nurse?
1. "Do you have any friends in the building?"
2. "Have you had any thoughts of hurting yourself?"
3. "Tell me more about how you're feeling."
4. "You're not thinking of killing yourself, are you?"
Answer: 2
Rationale: A suicide risk assessment is the priority nursing action for a client who
expresses thoughts about "not wanting to go on" or "wishing for death" or
engages in potential suicidal indicators such as giving away possessions.
Asking the client directly about thoughts of hurting or killing oneself is a
therapeutic approach necessary to assess risk of immediate suicide. Option 4
is a misleading statement and provokes suicide thought. Other options (1
and 3) are correct but are not priority.
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21
Miscellaneous
Normal Values:
Vital Signs:
Heart rate: 80-100 bpm
Respiratory rate: 12-16 rpm
Blood pressure: 110-120/60-70 mmHg
Temperature: 37 °C (98.6 °F)
T (°C) = (T (°F) - 32) × 5/9
T (°F) = T (°C) × 9/5 + 32
Basic Conversions
1 teaspoon (t) = 5 ml
1 tablespoon (T) = 3 t = 15 ml
1 gram (g) = 1,000 mg
1 mg = 1000 mcg
1 kilogram (kg) = 2.2 lbs.
1 grain (gr) = 65 mg
1 lb. = 16 oz
1 oz = 30 ml
1 cup = 240 ml
1 cup = 8 oz
1 quart = 2 pints
1 pint = 2 cups
1 meter = 3.28 feet
Hematologic
•
RBCs:
WBCs:
Platelets:
4.5 - 5.0 million/liter
5,000 - 10,000 /µL
200,000 - 400,000/µL
Rapid Response Team (RRT):
consists of a group of health
care providers who bring
critical care expertise to the
bedside of clients
demonstrating early signs of
deterioration. It differs from
the "Code" team that is
called when a client stops
breathing or goes into
cardiac arrest.
Criteria in activating RRT:
1. Nurse is worried
2. An acute change in any of
the following:
▪ Heart rate: <40 or
>130/min Systolic BP: <90
mm Hg
▪ RR: <8 or >28/min
▪ O2 Sat: <90 despite O2
▪ Urine output: <50 mL/4 hr.
▪ Decrease LOC
Safety Alert: Critical results
Are tests and diagnostic
procedures that fall
significantly outside the
normal range and may
indicate a life threatening
situation. The objective is to
provide the responsible
licensed caregiver these
results within an established
time frame so that the patient
can be promptly treated.
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Hemoglobin (Hgb): 12 - 16 gm (f) 14 - 18 gm (m)
Hematocrit (Hct): 37 - 47 (f) 40 - 54 (m)
Acronym: Never Let Monkeys Eat Bananas
(WBC percentage amount)
Neutrophils:
Never
54 - 62%
Lymphocytes: Let
25 - 32%
Monocytes:
Monkeys
3 - 7%
Eosinophils:
Eat
1 - 3%
Basophils:
Bananas
<0.75%
Comprehensive Metabolic Panel (CMP)
Sodium:
Potassium:
Serum Glucose:
Calcium:
BUN:
Creatinine :
Chloride:
CO2:
Total Protein:
Albumin:
Bilirubin:
Alkaline Phosphatase (ALP):
Aspartate aminotransferase (AST):
Alanine aminotransferase (ALT):
135 -145 mEq/L
3.5 - 5.5 mEq/L
70-110 mg/dl
9 -10.5 mEq/L
10 – 20 mg/dl
0.5 – 1.5 mg/dl
90 - 110 mEq/L
35 – 45 mmHg
6 – 8 g/dl
3.5 – 5 g/dl
<1.5 mg/dL
44 to 147 U/L
10 - 50 IU/L
5 - 35 IU/L
Remember: CMP
Is a frequently ordered panel of 14 tests that gives a healthcare
provider important information about the current status of a person's
metabolism, including the health of the kidneys and liver, electrolyte
and acid/base balance as well as levels of blood glucose and blood
proteins.
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Others:
Magnesium:
Phosphorus:
Ammonia:
LDH:
Total Cholesterol:
Triglyceride:
HDL (Good Cholesterol):
LDL (Bad Cholesterol):
HBA1C:
1.7 - 2.2 mEq/L
Tumor lysis syndrome (TLS):
3 - 4.5 mEq/L
A potential complication of
15 - 110 ug/dl chemotherapy is acute TLS,
a rapid release of
100 - 190 U/L
intracellular components
<200 mg/dL
into the bloodstream. TLS
<150 mg/dL
include rising blood uric
>45 mg/dl (m) acid, potassium, and
phosphate levels, with
>50 mg/dl (f)
decreasing calcium levels.
60 - 80 mg/dl
With diabetes:
< 7% Good control
> 9% Poor Control
> 12% Very Poor Control
With no diabetes:
4 - 5.6% normal level
5.7 - 6.4% high chance of diabetes
≥6.5% Diabetes
1.010 - 1.030
3.5 - 7.5 mg/dL
Urine Specific Gravity:
Uric Acid:
Heart failure:
B-Type Natriuretic Peptide (BNP):
<125 pg/mL (0 - 74 YO)
<450 pg/mL (75 - 99 YO)
•
•
Brain (or b-type) natriuretic
peptide (BNP):
Secreted in response to
ventricular stretch and wall
tension when cardiac filling
pressures are elevated. The
BNP level is used to
differentiate dyspnea of
heart failure from dyspnea of
noncardiac etiology.
Remember: Refeeding syndrome
A serious complication of
nutritional replenishment. It is
marked by declines in serum
phosphorus, potassium, and/or
magnesium (mnemonic PPM).
Most common to homeless and
anorexia when abruptly giving
food after periods of starvation.
Electrolytes should be monitored
frequently.
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Acute Coronary Syndrome (ACS):
In order rising:
Myoglobin: 0 - 85 ng/ml
Troponin:
< 0.6 ng/ml (most specific and most sensitive)
CPK:
12 - 70 U/ML (m), 10 - 55 U/ml (f)
AST:
10 - 50 IU/L
LDH:
100 - 190 U/L
Anticoagulant Therapy:
Heparin – Antidote: Protamine sulfate
aPTT:
30 - 40 sec (more sensitive)
(1.5 - 2X is therapeutic)
Risk for Bleeding: > 80 secs
PTT:
25 - 35 sec (less sensitive)
(1.5 - 2X is therapeutic)
Risk for Bleeding: > 70 secs
Warfarin (Coumadin) - Antidote: Vitamin K
PT:
10 - 12 sec
(1.5 - 2X is therapeutic)
Risk for Bleeding: > 24 secs
INR:
0.9 - 1.18
(up to 3X is therapeutic)
Risk for Bleeding: > 3.5 secs
Drug Therapeutic Levels:
Carbamazepine (Tegretol):
Phenobarbital :
Digoxin (Lanoxin):
Theophylline (Aminophylline):
Phenytoin (Dilantin):
4 - 10 mcg/ml
15 - 0 mcg/mL
0.8 - 2.0 ng/ml
10 - 20 mcg/dL
10 - 20 mcg/dL
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Valproic Acid (Depakene):
50—100 mcg/ml
Lithium:
0.5 - 1.5 mEq/L (Acute/Adult)
Remember:
0.6 - 1.2 mEq/L (Maintenance)
Toxic levels mean
0.4 - 1.0 mEq/L (>65 YO)
compromised KIDNEY
function. Always check for
6 - 8 mEq/L (Severe toxicity)
renal panel. (BUN,
Vancomycin:
creatinine)
20 - 40 mcg/ml (peak)
5 - 15 mcg/ml (trough)
Remember: Vancomycin
Peak (effectivity): Blood
Magnesium Sulfate:
draws 15 - 30 mins after the
4 - 8 mg/dl (therapeutic level)
dose
8 - 10 Absence of reflexes
Trough (toxicity): Blood
10 - 12 Respiratory depression
draws 15 – 30 mins before
the next dose
> 15 Coma/death
Poisoning:
Lead:
5 U - Safe Level
10 U - Toxic Level
70 U - Medical Emergency
Lead poisoning in children:
Can lead to many severe complications of the kidneys & neurological system
(e.g. developmental delays, cognitive impairment, seizures). A common source
of exposure is lead-based paints found in houses built before 1978, when such
paint was banned. Blood lead level (BLL) screenings are recommended at ages
1 and 2, and up to age 6 if not previously tested.
Carbon Monoxide:
10 to 20% (Headache)
> 20 % (Generalized weakness)
> 30% (Chest Pain)
> 40% (Seizure, unconsciousness)
> 60% (Coma - Death)
Remember:
The priority action is to
administer 100% oxygen
using a nonrebreather mask
to treat hypoxia and help
eliminate CO.
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Aspirin:
50 - 100 mg /ml
Remember:
Aspirin should not be given to those under the age of 16 years, unless
specifically indicated in Kawasaki disease or in the prevention of blood
clot formation. Severe liver damage is closely associated with
acetaminophen & aspirin overdose or Reye syndrome.
Pressures (mmHg):
ICP:
0 - 10 mmHg
IOP:
12 - 15 mmHg
Airway Suction Pressure:
100 - 120 mmHg (adults)
80 - 100 mmHg (children)
60 - 80 mmHg (infants)
ET/Tracheostomy cuff pressure:
15 mm Hg (20 cm H2O)
Chest tube negative pressure:
20 cm H2O
Hemodynamics
Remember:
Permissive hypertension
is allowed within the
first 24-48 hours of an
acute ischemic stroke
provided that the BP is
<220/120 mm Hg. This
practice allows
adequate cerebral
perfusion to keep the
stroke from extending.
Mean arterial pressure
(MAP) formula:
= 2 (DBP) + SBP
3
Pulse Pressure formula:
= SBP - DBP
MAP:
70-105 mm Hg
Pulse Pressure: 40 mm Hg
Central Venous Pressure (CVP)/Right Atrial Pressure (RAP):
2 - 8 mmHg
Right Ventricular Pressure (RVP):
15 - 25 mmHg (systolic)
0 - 8 mmHg (diastolic)
Pulmonary Artery Pressure (PAP):
20 - 30 mmHg
Pulmonary Capillary Wedge Pressure (PCWP):
8 - 13 mmHg
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Positioning:
Above Knee Amputation: Elevate for first 24 hours on pillow, position
on prone daily to prevent Hip Flexion Contractures
Air/Pulmonary embolism: Turn to left side and lower HOB to promote
resistance, preventing emboli going towards pulmonary artery
Asthma: Orthopneic position, patient sitting up and bent forward with
arms supported on a table or chair . Promotes O2 and lung
expansion
Autonomic Dysreflexia: Sitting position (elevate HOB) first
before any other implementation. Promotes comfort, breathing
Below Knee Amputation: Foot of bed elevated for first 24 hours,
position prone daily to prevent hip flexion contractures
Bronchiolitis: Tripod position to promote drainage of secretion,
improves lung expansion
Buck’s Traction: Elevate foot of bed for counter-traction
Cardiac Catheterization: Seep site extended. Preventing impede
circulation
Cast: Elevate extremity to prevent edema
Cerebral Aneurysm: High Fowler’s to prevent rupture
Cleft-lip: Position on back or in infant seat to prevent trauma to the
suture line. While feeding, hold in upright position to prevent
aspiration
Cleft-palate: Prone to promote drainage of secretion
Cleft Lip and Palate: Supine or side to prevent rubbing
Detached retina: Area of detachment should be in the dependent
position to promote reattachment of retina
Dumping Syndrome: Eat in reclining position, lie down after meals for
20-30 minutes to slow down food movement
Enema Administration: left-side lying (Sim’s position) with knees flexed
to rest rectum
Epistaxis: Lean forward to prevent aspiration
Flail Chest: Affected side to facilitate expansion of unaffected lung
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Fracture of the neck of femur: Internal rotation of the leg with
extension of the knee to promote alignment
Head Injury: HOB 30° to prevent Increased ICP
Hemorrhoidectomy: Assist to lateral position to promote comfort
Hemorrhagic Stroke: HOB elevated 30 degrees to reduce ICP and
facilitate venous drainage.
Hiatal Hernia: Upright position to prevent reflux
Increased ICP: High Fowler’s to facilitate venous drainage.
Internal radiation implant: Complete bed rest while implant is in place
to prevent dislodgement
Intestinal Tubes: Right side lying to facilitate passage into duodenum
Laminectomy: Back as straight as possible; log roll to move and sand
bag on sides to promote alignment
Liver Biopsy: Right side lying with pillow, or small towel under puncture
site for at least 3 hours to prevent bleeding
Lobectomy: Semi fowlers to promote breathing
Mastectomy: Elevate affected side with pillow to prevent
lymphedema
Myelogram: (Water-based dye) semi Fowler’s for at least 8 hours to
promote drainage (Oil-based dye) flat on bed for at least 6-8
hours to prevent leakage of CSF, (Air dye)Trendelenburg to
suspend air promoting drainage to venous circulation
Nasogastric Tubes: Elevate HOB 30°, Maintain elevation for
continuous feeding or 1hour after intermittent feedings, prevents
aspiration
Paracentesis: Flat on bed or sitting, promotes comfort, lung expansion
Peritoneal Dialysis: When outflow is inadequate turn patient side to
side before checking for tube kinks to mobilize fluids
Post abdominal aneurysm surgery: Fowler’s position to improve
circulation
Post Bronchoscopy: Flat on bed with head hyperextended to
promote patent airway
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Post cataract surgery: Sleep on unaffected side with a night shield for
1-4 weeks to prevent increase IOP
Post infratentorial surgery (incision at nape of neck):
Flat and lateral on either side to prevent trauma to incision site,
to promote patent airway and drainage of secretions
Post Lumbar puncture: Flat for 2-3 hours to prevent headache and
leaking of CSF.
Post myringotomy: On the side of affected ear post-surgery to allow
drainage of secretion
Post Supratentorial surgery (incision behind hairline): Elevate HOB 3045 degrees, neutral position, to promote patent airway and
drainage of secretions
Post Total Hip Replacement: Don’t sleep on operated side, don’t flex
hip more than 45-60 degrees, don’t elevate HOB more than 45
degrees. Maintain hip abduction by separating thighs with
pillows to prevent displacement.
Postural Drainage: Lung segment to be drained should be in the
uppermost position to allow gravity
Prolapsed cord: Knee-chest position or Trendelenburg to prevent
compression
Pyloric stenosis: Right side lying after meals to facilitate entry of
stomach contents into intestines
Rectal Exam: Knee-chest position, Sim’s, or dorsal recumbent to
promote access to rectum
Seizure: Side lying to promote airway, facilitate drainage of secretions
Shock: Bed rest with extremities elevated 20°, knees straight, head
slightly elevated (modified Trendelenburg) to promote venous
return
Spina Bifida: Infant on prone to prevent sac rupture
Spinal Cord Injury: Immobilize on spine board, with head in
neutral position. Immobilize head with padded C-collar, maintain
traction and alignment of head manually. Log roll client, don’t
allow to twist or bend
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Thoracentesis: Sitting on the side of the bed and leaning over the
table (during procedure) to promote lung expansion; affected
side up (after procedure) to promote re-expansion of the
affected side and prevent leaking. If leaking, position on the
affected
Thyroidectomy: Semi fowlers, avoid hyperflexion & hyperextension of
neck to prevent tension of suture
Tonsillectomy: Side lying or prone to promote drainage
Total Parenteral Nutrition (TPN): Trendelenburg during insertion to
prevent air embolism
Tracheoesophageal fistula (TEF): Supine with HOB elevated 30° to
minimize reflux, prevent aspiration
Tube feeding for patients with decreased LOC: Right side to promote
emptying of the stomach with HOB elevated to prevent aspiration
A must have bedside equipment:
Amputation – Tourniquet
Autonomic Dysreflexia – Urinary Catheter
Chest Tube Drainage – Extra sterile bottle with sterile H20,
clamp/forceps, Vaselinized gauze
Cholinergic crisis – Tracheostomy/ET tube
Hydrocephalus – Tape measure
Laryngotracheobronchitis – Tracheostomy
Myasthenic Crisis – Tracheostomy/ET tube
Parkinson’s Disease – Suction equipment
Radium Implant – Lead container, long handled forceps
Seizure– Suction equipment
Spinal Cord Injury – Tracheostomy
Tamponade tube (Sengstaken–Blakemore)– Scissors
Thyroidectomy – Tracheostomy
Tonsillectomy – Flashlight
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Tracheostomized Patient – Obturator, hemostat (Dilator), one size
smaller tracheostomy tube, Ambubag
Wired Jaw – Suction equipment, Wire cutter
Diets:
Acute Glomerulonephritis: Low Na, low protein
Addison’s disease: High Na, low potassium
ADHD: High-calorie, finger foods
Bedsore: High Protein, High Vitamin C
Bipolar Disorder: Finger foods
Burns: High protein, high caloric, high Vitamin C
Cancer: High-calorie, high-protein.
Celiac Disease: Gluten-free diet (no BRW: barley, rye, and wheat)
selected oats only
Cholecystitis: High protein, High carbohydrate, Low fat
Chronic Renal Disease: Low protein, low sodium and potassium , Low
phosphate, fluid-restricted
Cirrhosis (stable): Normal protein
Cirrhosis with hepatic insufficiency: Low protein, Low Sodium
Constipation: High-fiber, increased fluids
COPD: Soft, high-calorie, low-carbohydrate, high-fat, small frequent
feedings
Crohn’s disease: High protein, high carbohydrate, low fat
Cushing’s disease: High potassium, Low Na
Cystic Fibrosis: High fluids & Na, High Calorie
Cystitis (Stones):
Acid ash for alkaline stones (Uric, Cystine), Alkaline ash for acid
stones (Calcium, Struvite), Increase OFI
Diarrhea: Liquid, low-fiber, regular, fluid & electrolyte replacement
Diabetes Mellitus: Balanced
Diverticulitis: Low residue
Diverticulosis: High Residue
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Dumping Syndrome: High fat, high protein, drink 30 - 60 minutes
before or after meals (no fluids with meals)
Gallbladder diseases: Low fat, low calorie, regular
Gastritis: Low-fiber, bland diet
Gouty Arthritis: Low purine
Hepatitis: Regular, high-calorie, high-protein
Hirschsprung’s: High Calorie, high protein, low residue
Hyperlipidemias: Fat-controlled, Low calorie
Hyperparathyroidism: Low calcium
Hypertension, CHF, CAD: Low sodium, low-calorie, fat - controlled
Hyperthyroidism: High calorie, high protein
Hypoparathyroidism: High Calcium, low phosphate
Hypothyroidism: Low calorie, low fat
Kawasaki disease: Clear liquid
Meniere’s disease: Low sodium
Nephrotic Syndrome: Low sodium & potassium, high calorie & protein
Osteoporosis: High calcium, high vitamin D
Pancreatitis: Low-fat, regular, small frequent feedings; tube feeding or
TPN
Peptic ulcer: Bland, high carbohydrate, low protein
Phenylketonuria: Low phenylalanine
Pregnancy Induced Hypertension (PIH): High protein
Pernicious Anemia: High Vitamin B12 (Cobalamin)
Renal Failure (Acute): High protein, high-calorie, fluid-controlled,
sodium and potassium controlled
Renal Failure (Chronic): Low sodium, potassium, low protein
Sickle Cell Anemia: Increase fluids
Stroke (CVA): Mechanical soft, regular, or tube- feeding
Tonsillitis: Clear Liquid
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Classic signs:
Acute coronary syndrome – Levine’s sign (clenched fist held over the
chest to describe ischemic chest pain)
Infective endocarditis – Janeway lesion, splinter hemorrhages, Osler’s
node, Roth spots
Cardiac tamponade – Beck’s triad: Narrowed pulse pressure
(hypotension), muffled/distant heart sound, distended neck
veins
Rheumatic heart disease – JONES criteria: Joint problem, O (looks like
a heart) carditis, nodules (subcutaneous), erythema
marginatum, Sydenham’s chorea. CAFE PAL criteria: CRP
increased, arthralgia, fever, elevated ESR, prolonged PR interval,
anamnesis (history) of rheumatism, leukocytosis
Kawasaki Disease – CRASH and Burn (fever): Conjunctivitis, rash,
adenopathy (cervical), strawberry tongue, hands (palmar
erythema, swelling), fever
Patent ductus arteriosus – Machinery like murmur
Tricuspid atresia – Holosystolic murmur
CHF in children – Brow or scalp sweating
Abdominal aortic aneurysm – Pulsatile lump with abdominal pain
(enlarging aneurysm)
Aortic dissection - Moving, "ripping" back pain
Deep vein thrombosis (DVT) – Virchow’s triad (venous stasis, vein
trauma/endothelial injury, hypercoagulability)
Peripheral arterial disease (PAD) – Intermittent claudication
Asthma - High-pitched, sibilant wheezing on expiration
Emphysema – Barrel chest, pursed lip breathing (pink puffers)
Bronchitis (Chronic) – Obese and cyanotic (blue bloaters)
Cystic fibrosis – Layered sputum, steatorrhea, salty skin, meconium
ileus on birth
Obstructive sleep apnea (OSA) - Loud snoring, witnessed apnea
episodes, morning headaches
Acute Respiratory Distress Syndrome (ARDS) aka non cardiogenic
pulmonary edema – Refractory hypoxemia
Superior vena cava syndrome (SVC) – Facial edema
Epiglottitis - 4 Ds: dysphonia (muffled voice), dysphagia, drooling, and
distressed respiration
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Trigeminal neuralgia - Severe, intense, burning, or electric shock-like
pain
Bell’s palsy – Facial drooping
Traumatic brain injury (TBI) - “Lucid interval”, followed by a quick
decline in mental function
Basilar skull fracture - Otorrhea, racoon’s eye, post-auricular
ecchymosis (battle’s sign)
Increase intracranial pressure (IICP) – Late sign: Cushing’s triad:
Irregular respiration, bradycardia , widened pulse pressure
(systolic HTN)
Myasthenia gravis - Ptosis/diplopia, Bulbar signs (difficulty speaking or
swallowing)
Multiple sclerosis - Lhermitte’s sign, Charcot’s Triad: Intentional
tremors, Nystagmus, Scanning speech (staccato speech)
Guillain-Barre Syndrome (GBS) – Ascending paralysis
Meningitis - Brudzinski Sign, Kernig Sign
Alport syndrome - Hematuria (Tea colored), proteinuria,
hypoalbuminemia
Nephrotic syndrome – Proteinuria, hypoalbuminemia, hyperlipidemia,
low anti-thrombin
Nephritic syndrome - Hematuria (Tea colored), proteinuria,
hypoalbuminemia
Kidney stones - Flank pain (mid-lower back), renal colic (constant
sharp pain)
Syndrome of inappropriate ADH (SIADH) - Dilutional hyponatremia
(water intoxication)
Diabetes insipidus - Polyuria (2-3L/H), polydipsia
Cushing’s - Truncal obesity, buffalo hump, moon shaped face
hypernatremia, hypokalemia, hypocalcemia, hirsutism, acne,
gynecomastia (males)
Addison’s disease (primary adrenal insufficiency) - Bronze skin
(hyperpigmentation), hyponatremia, hyperkalemia,
hypercalcemia
Diabetes mellitus (DM) – Polyphagia, polyuria, polydipsia, glucosuria
Gastric ulcer – Pain while eating (relieved by vomiting), weight loss
Duodenal ulcer – Pain if not eating (relieved by food), weight gain
Crohn's disease (Regional enteritis) – Crampy RLQ abdominal pain,
diarrhea (3-4 /day)
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Ulcerative colitis – Crampy LLQ pain abdominal pain, diarrhea (More
severe and painful: 10 or more x /day)
Diverticulitis (inflamed diverticula) - Painless rectal bleeding,
hematochezia, LLQ abdominal pain
Acute pancreatitis - Epigastric pain radiating to back, Grey turner’s
sign, Cullen’s sign
Acute cholecystitis - Mid epigastric to RUQ radiating to scapula and
shoulders, Murphy’s sign
Appendicitis - RLQ (Mc Burney’s point) abdominal pain, Psoas Sign,
Obturator Sign, Rouvsing sign, Blumberg Sign
Pyloric stenosis - Projectile vomiting, non-bilious vomitus, olive shaped
mass
Intussusception - RLQ pain (intermittent cramping), currant jelly stool,
sausage shaped mass
Hirschsprung’s disease - LLQ pain, meconium ileus, ribbon like stool
Rheumatoid arthritis – Joint pain, Boutonnière deformity, Swan-Neck
deformity
Osteoarthritis - Joint pain, Bouchard’s deformity, Heberden’s
deformity
Gouty arthritis – Joint pain, podagra, tophi (uric deposits)
Developmental dysplasia of the hip (DDH) - Extra gluteal or inguinal
folds/asymmetrical folds, Galeazzi sign, Barlow Sign, Ortolani sign
Fat embolism – Petechial rash on the neck, chest, and axilla (defining
characteristic from PE)
Acute compartment syndrome - The 6 Ps: Pain, Pressure, Paresthesia,
Pallor, Pulselessness, Paralysis
Carpal tunnel syndrome – Tingling pain on Phalen’s maneuver, Tinel’s
maneuver, Durkan’s test
Age related Macular degeneration (AMD) - Los of central vision
Retinal detachment – Painless, floaters, curtain sensation, flashes of
light
Chronic open angle glaucoma (COAG) - Loss of peripheral vision
(tunnel vision)
Acute close angle glaucoma (ACAG) - Eye pain, headache, nausea,
blurred vision, eye redness, halos, tunnel vision
Meniere’s disease (Endolymphatic hydrops) – Triad: Vertigo, tinnitus,
sensorineural hearing loss
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Anemia - 4Fs: Fatigue, Forgetfulness, Fainting, Fast heartbeat
(tachycardia)
Hodgkin’s lymphoma - (+) Reed Sternberg cells on biopsy,
lymphadenopathy usually in neck and chest
Non-Hodgkin’s lymphoma - (-) Reed Sternberg cells on biopsy,
lymphadenopathy affects upper and lower extremities
Multiple myeloma – CRAB: Calcium (hypercalcemia), Renal, Anemia,
Bone pain (spine and ribs)
Systemic Lupus Erythematosus (SLE) – SOAP BRAIN MD: Serositis, oral
ulcers, arthritis, photosensitivity, blood disorders, renal
involvement, ANA (+), immunologic, neurologic, malar rash
(butterfly rash), discoid rash
Pregnancy induced hypertension (PIH) - Triad: HTN, proteinuria,
edema
Abruptio placenta - Painful rigid abdomen, concealed bleeding
Placenta previa - Painless soft boggy abdomen, bleeding
Alzheimer's disease - 3 As: Aphasia, Agnosia, Anomia, “Sundowning”
Drug causing urine discoloration:
Amitriptyline – Blue or blue green
Daunorubicin or Doxorubicin - Red/Pink
Ferrous / iron dextran - Dark / Brown
Heparin - Orange/yellow, Red/Pink
Ibuprofen - Red/Pink
Levodopa - Dark / Brown
Methyldopa - Dark / Brown, Red/Pink
Metronidazole - Dark / Brown, Yellow-brown
Nitrates - Dark / Brown
Nitrofurantoin - Dark / Brown, Yellow-brown
Phenazopyridine - Orange/yellow
Phenothiazines - Red/Pink
Phenytoin - Red/Pink
Rifampin - Orange/yellow, Red/Pink
Salicylates - Red/Pink
Sulfasalazine - Orange/yellow
Sulfonamides - Dark / Brown, Yellow-brown
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Triamterene - Blue or blue green
Warfarin - Orange/yellow
Herbal remedies:
Remember:
Avoid the G’s (ginseng,
ginger, gingko, garlic)
when on anticoagulants.
Do not combine with
drugs with the same
effects
Di Huang – Diabetes Mellitus
Ma Huang – Weight Loss
Echinacea – Immune booster
Black Cohosh – Flushing in menopause
Blue Cohosh – Uterine tonic
Saw Palmetto – BPH
Arnica – Post operative bruising
Ginger – Anti emetic, anti-inflammatory – Bleeding risk
Ginkgo Biloba – Memory enhancement – Bleeding risk
Ginseng – Improve mental performance – Bleeding risk
Garlic – HPN, cholesterol – Bleeding risk
St. John’s wort – Depression, Insomnia
Kava – Anxiety, Insomnia
Valerian - Insomnia
Licorice – Bronchitis, anti-ulcer
Ephedra – Colds & flu, weight loss, improve athletic
performance
Sample calculations:
A HCP prescriptions reads phenytoin 0.2 g orally twice daily. The
medication label states that each capsule is 100 mg. The RN prepares
how many capsule(s) to administer 1 dose? Fill in the blank.
Answer: ______ capsules
Formula:
Ordered dose x quantity
Stock on hand
= 0.2 g x 1000 mg (1000 mg in 1 g) x 1 capsule
100 mg
= 2 capsules
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A HCP prescription reads potassium chloride 30 mEq to be added to
1000 ml NS and to be administered over 10 hour period. The label on
the medication bottle reads 40 mEq/20 ml. the RN prepares how
many ml of potassium chloride to administer the correct dose of
medication? Fill in the blank.
Answer: ______ ml
Formula:
Ordered dose x quantity
Stock on hand
= 30 mEq x 20 ml
40 mEq
= 15 ml
A HCP prescribes 1 unit PRBC to infuse over 4 hours. The unit of blood
contains 250 ml. The drop factor is 10 drops/1 ml. The RN prepares to
set the flow rate at how many drops per minute? Fill in the blank.
Record your answer in the nearest whole number.
Answer: ______ drops/min
Formula:
Volume (ml) x drop factor (drops/ml)
Duration x 60 mins/hr.
250 (ml) x 10 drop factor (drops/ml)
4 hours x 60 mins/hr.
= 2500
240
= 10.42 drops/min
= 10 drops/min (nearest whole number)
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Give Nitroprusside 5 mcg/kg/min via continuous infusion for a patient
weighing 205 lbs. Nitroprusside is available in a solution of 200 mg in
250 ml D5W. What rate on the infusion pump will deliver the correct
dose? Record answer using 1 decimal place.
Answer: ______ ml/hour
Formula:
Ordered dose (mcg/kg/min) x Weight (kg) x 60 min/hr x quantity (ml)
Stock on hand in mcg (1000 mcg=1mg)
Convert lbs. to kg = 202 lbs. / 2.2 = 93.18 kg
= 5 mcg/kg/min x 93.18 kg x 60 min/hr x 250 ml
200,000 mcg (200 mg x 1000)
= 34. 9 ml/hour
A health care provider prescribes regular insulin, 8 units/hour by
continuous intravenous (IV) infusion. The pharmacy prepares the
medication and then delivers an IV bag labeled 100 units of regular
insulin in 100 mL normal saline (NS). An infusion pump must be used to
administer the medication. The nurse sets the infusion pump at how
many milliliters per hour to deliver 8 units/hour? Fill in the blank.
Answer: ______ ml/hr
Formula:
Ordered dose (units/hr) x quantity (ml)
Stock on hand
= 8 units/hr x 100 ml
100 units
= 8 ml/hour
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You have an order to administer heparin sodium IV 1000 units per
hour. It is supplied by tour pharmacy as 25,000 units in 250 ml of D5W.
How many ml per hour will you set on the infusion pump? Record your
answer in the nearest whole number.
Answer: ______ ml/hr
Formula:
Ordered dose x quantity (ml)
Stock on hand
= 1,000 units x 250 ml
25,000 units
= 10 ml/hour
Your patient has an order of heparin SC 2500 units BID. You have on
hand heparin 5000 units/ml/. How many ml will you administer?
Record your answer using 1 decimal place.
Answer: ______ ml
Formula:
Ordered dose x quantity (ml)
Stock on hand
= 2,500 units x 1 ml
5,000 units
= 0.5 ml
HCP orders 10 mcg/kg/min of Dopamine infusion. The patient weighs
170 lbs. Dopamine is supplied as 500 mg/500 ml. How many ml/hr will
you administer? Record your answer using 1 decimal place.
Answer: ________ ml/hr
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Formula:
Ordered dose (mcg/kg/min) x Weight (kg) x 60 min/hr x quantity (ml)
Stock on hand in mcg (1000 mcg=1mg)
Convert lbs. to kg = 170 lbs. / 2.2 = 77.27 kg
= 10 mcg/kg/min x 77.27 kg x 60 min/hr x 250 ml
500,000 mcg (500 mg x 1000)
= 46.362 ml/hour
= 46.4 ml/hour (1 decimal place)
You have an order to run epinephrine at 10 mcg/min. You have a
solution of 3 mg in 250 ml fluid. What rate you will set for your IV
pump? Record your answer using 1 decimal place.
Answer: _______ ml/hr
Formula:
Ordered dose (mcg/min) x 60 min/hr
x quantity (ml)
Stock on hand in mcg (1000 mcg=1mg)
= 10 mcg/min x 60 min/hr x 250 ml
3,000 mcg (3 mg x 1000)
= 0.5 ml/hour
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6
The Day
On the day of exam make sure you avoid the things that you think
might affect your performance. You have spent a lot of hours and
sacrifices to achieve your goals, only to be beaten by things you
can easily avoid. For instance, anxiety might be a reason to lose
what you have mastered. A day before the exam you must have
turned your worry into confidence. Following are the habits on your
way to success.
1.
Get plenty of sleep not only a night before the exam but
starting from the days ahead before the exam. Hydrate
adequately.
2. Avoid distractions the day before exam. You may have some
relaxation activities.
3. Don’t isolate yourself, get out of your room and have some light
exercise
4. Don’t cram, but you need to calibrate your level of confidence,
too much is dangerous.
5. Plan to dress comfortably
6. Plan to arrive at least 30 minutes early in your testing center. If
the Test Center is in a busy district, you may come visit days
ahead of the exam.
7. Take along with you a high-energy snack, a chocolate bar for
instance.
8. Try not to focus on the length of your exam. Your goal is passing
at 75 items but it might be a little longer. That is where your
good sleep a night before will take its job.
9. Plan something fun to do after the exam. You’ll need at least a
reward after a series of hard work on studying.
10. Above all, don’t forget to put your faith into action. Pray hard,
claim your success and give back the glory.
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7
Destination RN
Absolutely it is OK to be anxious at this moment
of waiting for the result. This might be the
longest 48 hours of your life waiting for the
quick results. If you are to inflict more anxiety
to yourself then wait for 6 weeks for NCSBN to
release your result.
Then came the SUCCESS. Passing NCLEX® is
not easy, it is a culmination of hardwork and a
result of free will to welcome a future made by
the Almighty. Get going, get it and be a
NURSE.
Created by: Jay Padong, RN, USRN
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