lOMoARcPSD|22650627
Med-Surg Study Guide
Table of Contents
Burns 2
Cancer 8
Cardiac 12
Cardiac Basics 12
Heart Failure 14
Coronary Artery Disease 16
Angina Pectoris 18
Myocardial Infarction 20
Electrolyte Imbalances 22
Sodium 22
Potassium 23
Calcium 24
Magnesium 25
Phosphorus 26
Chloride 27
Relationships 28
Endocrine 29
Endocrine System 29
Thyroid Gland and Disorders 32
Hyper- and Hypoparathyroidism 37
Adrenal Glands and Disorders 40
DI vs SIADH 45
Diabetes Mellitus 48
Gastrointestinal 58
The Digestive System 58
Gastroesophageal Reflux Disease 61
Peptic Ulcer Disease 62
Inflammatory Bowel Disease 63
Diverticulosis and -itis 67
Celiac Disease 69
Hepatitis 71
Cirrhosis 77
Pancreatitis 80
Cholecystitis 83
Appendicitis 85
Hematologic Disorders 87
Musculoskeletal 89
Musculoskeletal System 89
Fracture 92
Osteoarthritis 95
Rheumatoid Arthritis 97
Osteoporosis 100
Gout 103
Neurology 105
Brain Anatomy and Physiology 105
Stroke 108
Seizure 114
Increased Intracranial Pressure 118
Multiple Sclerosis 123
Parkinson's Disease 126
Myasthenia Gravis 130
Guillain-Barre Syndrome 133
Renal 136
Kidneys, Nephrons and RAAS 136
Chronic Kidney Disease 139
Acute Kidney Injury 141
Renal Calculi 143
Urinary Tract Infections 146
Glomerulonephritis 149
Nephrotic Syndrome 151
Dialysis 152
Diuretics 154
Respiratory Disorders 159
Lung Anatomy and Physiology 159
Pneumonia 160
COPD 161
Asthma 162
ARDS 163
Pleural Effusion 164
Shock 165
lOMoARcPSD|22650627
BURNS
Damage to the skin's integrity by some kind of energy source
Types of Burns
Thermal - Most common - caused by flame, flash, scald or contact with hot
objects (liquid, steam, fire); e.g. from cooking, burning leaves, smoking
Chemical - caused by contact with acids, alkali or organic compounds - no heat
needed
acids (e.g. hydrochloric, oxalic, hydrofluoric)
alkali (e.g. cement, oven/drain cleaners, heavy industrial cleaners); harder
to treat because adheres to tissue
organic compounds (e.g. phenols and petroleum products)
Electrical - caused by intense heat generated from an electric current that
passes through the body and damages tissue
hard to determine extent of damage because most of damage is below the
skin - 'iceberg effect'
Cold - caused by cold exposure to skin; frostbite
Radiation - caused by sun or cancer treatment
Friction - caused by abrasion to skin
road rash (car accident)
rope burn
Epidermis
Superficial partial
thickness (1st degree)
Deep partial
thickness
(2nd degree)
Full
thickness
(3rd & 4th
degree)
Sweat
gland
Dermis
Hair
Follicle
Fat
Muscle
Bone
lOMoARcPSD|22650627
Burn Severity Depends on:
Depth of Burn
Extent of Burn
Calculated in % of TBSA
Use Rule of 9s (see next page)
Location of Burn
Patient risk factors
If they experienced an inhalation
injury or not
Depth of Burn
st Degree
Superficial partial thickness
Epidermis only
Least severe
Heals in 7 days
Erythema
Blanching on pressure
Pain/mild swelling
Skin pink/red
Warm to touch
No blisters
Usually no scarring
nd Degree
Deep partial thickness
Epidermis and dermis
Very painful
Blisters
Redness that blanches
Swelling (mild - moderate)
Shiny red/pink and moist
If severe, may need skin
grafting
rd Degree
Full thickness
All layers are damaged
Not painful due to damage to nerves
Skin will NOT heal - needs skin
grafting
Will take months to heal
Dry, leathery hard skin (eschar)
May be black, yellow, red, waxy
white
th Degree
Eschar - dead tissue - dangerous if
around torso or extremity; will need
to be removed via escharotomy
Deep full thickness
All layers destroyed and extends to
muscles, bone, ligaments
NO pain sensation
Black, charred with eschar
Months to heal
Will need skin grafts
In Full Thickness, watch for acute
tubular necrosis (ATN), due to the
release of myoglobin and hemoglobin
that block kidney tubules.
lOMoARcPSD|22650627
Extent of Burn
To determine the extent of burn, calculate the TBSA burned using the Rule
of Nines and then use the Parkland Formula to calculate the fluids needed
Rule of Nines
Purpose:
4.5%
To calculate the total body surface area burned
(TBSA%) for 2nd, 3rd and 4th degree burns
To determine the amount of fluid therapy needed
18%
4.5% Front 4.5%
using the Parkland Formula
4.5%
To determine if the patient meets criteria for
burn unit
Add the percent of each body
part burned.
Use for 2nd
This number equals the
degree burns
or greater
TBSA%.
1%
9% 9%
4.5%
18%
Back
4.5%
9% 9%
Parkland Formula
Purpose: To calculate the total volume
of fluids (mL) that a patient needs
24 hours after experiencing a burn.
Make sure TBSA is NOT a decimal!
For instance, if a patient has a TBSA% =
45%, use 45 in the equation, NOT .45
4 mL X TBSA (%) X Body weight (kg) =
total mL of fluid (lactated Ringer's) needed
Give first half of
the solution in
the first 8 hours
Give second half of
the solution over the
next 16 hours
Location of Burn - potential problems
Respiratory - face, mouth, neck, trunk (due to edema or eschar)
Disability - Eyes, hands, feet, joints (due to damage to nerves)
Infection - Perineum (due to infection from urine/feces) and ears, nose (thin skin)
Trouble Healing - Ears, nose (due to thin skin and poor blood supply)
Compartment syndrome - Full thickness circumferential burns
lOMoARcPSD|22650627
Patient Risk Factors
Preexisting heart, lung, kidney
disease (body already taxed)
Diabetes
Peripheral Vascular Disease
Any chronic disease that causes
weakness
If burn patient also has fractures,
head injuries, other trauma
Age - children or elderly
Inhalation Injury
Damage to respiratory system due to
breathing in toxic substances
Affects: Upper & lower airways
Signs:
Burned in enclosed space
Burned on face
Spit, mouth, nose have soot
Hair singeing (head & nose)
Brignt red skin
Hoarse voice
Pre-Hospital and Emergency Care
At scene Remove from source of burn
Stop the burning process
Small thermal burns (10% or less TBSA)
Cover with cool, clean, tap water-dampened towel
If >10% TBSA or electrical/inhalation burn and patient unresponsive:
Focus on CAB
C - Circulation - check for pulse and elevate burned limb(s)
A - Airway - check for patency, soot around nose and on tongue,
singed nasal hair, darkened oral or nasal membranes
B - Breathing - check for ventilation
If patient is responsive, do A B C
Cool large burns no longer than 10 minutes
Do not immerse in cool water
Do not cover with ice
Do remove as much burned clothing as possible
Do wrap in sheet/blanket
Chemical burns - remove all chemicals from skin; remove clothing containing
chemical and then flush skin with water
Monitor patient with inhalation injury for signs of respiratory distress
→ →
lOMoARcPSD|22650627
Phases of Burn Management
Emergent Phase
Onset of burn until 24 - 48 hours post
Time required to resolve the immediate, life-threatening problems
Main concerns: onset of hypovolemic shock and edema formation
Hypovolemic shock is the greatest initial threat to a patient with a major burn
Phase ends when fluid mobilization and diuresis begin
Monitor for:
Pathos:
Increased capillary permeability causes:
Plasma fluid to leave intravascular
space
Na+ & Albumin follow
Fluids shift to interstitial tissue
Edema results
Blood thickens
Hct, K+, Na+, WBC
Fluid may lead to hypovolemic
shock:
HR
CO
BP
↑
↓
↑ ↓ ↓
↑
↓
↓
Wound Care:
Intervention:
Hypovolemic shock
Electrolyte imbalances
Renal failure
GI problems
IV access (2)
Calculate fluids (lactated Ringer's) using
formula
Electrical burns need higher fluids and
possibly osmotic diuretic (mannitol)
Catheter to monitor urinary output
Monitor every hr
Goal >30cc/hr
Albumin may be administered
Monitor urine for Hg and Mb (ATN)
Elevate extremities above heart level
Pain meds via IV initially; opioids
May need intubation (esp face/neck burn)
Wound care can begin once proper airway,
circulation and fluid replacement achieved
Open or Closed
Open: open to air with topical antimicrobial - often limited to facial burns
Closed: topical antimicrobial and area covered with sterile dressing
Debridement - necrotic tissue removed
Positioning - no pillows (esp with neck/ear burns); rolled towel under shoulders
Elevate extremities - helps prevent edema and contractures
Do not let 2 burn areas touch (to prevent webbing)
ROM/splints to prevent contractures
Premedicate w/pain meds before dressing changes or debridement!
Graft types: autograft (self), allograft (cadaver), CEA (grown from pt own skin), artificial skin
lOMoARcPSD|22650627
Acute Phase
48 - 72 hours after burn until wound heals
↑
Fluid has mobilized and subsequent diuresis has begun ( urine production)
May last weeks to months
Focus: prevent infection, pain management, nutrition, wound care
Monitor:
Interventions:
Proper urine output
Signs of GI distress (pain, vomiting, blood
in stool - may be Curlings ulcer;
constipation)
Bowel sounds (no sounds may be
paralytic ulcer)
May need NG tube for suctioning (to
remove fluids, gas)
Compartment syndrome if
circumferential burns
Distal extremity pulse absent/weak,
cool to touch, abnormal color
Respiratory status esp with chest, face,
neck burn or inhalation injury
Electrolyte imbalances:
sodium and potassium
Infection signs ( HR, RR, BP,
UO, confusion, chills, appetite)
Will need systemic abx
Neurology: watch for signs of delirium
↓
↑ ↑ ↓
↓
Rehabilitative Phase
NPO until bowel sounds + order to eat:
Will need Cal/Pro/Carb diet
May need enteral
Watch for hyperglycemia
Early nutrition will complications
and mortality and healing
Tetanus shot, antibiotics, ulcer meds
May also need: sedative, hypnotics,
antidepressants
Pain meds- IV best route b/c skin layer
may be damaged as well as muscle
Avoid infection: sterile linens, gowns,
gloves, protective isolation
Stretch ROM and move as much as
possible to avoid contractures
Keep room temp at least 85F
↑
↓
↑
wound closure to patient's optimal level
Burn has healed and patient functioning again (physically and mentally)
May happen as early as two weeks post-burn to 7-8 months after
Focus: psychosocial, ADLs, PT, OT, cosmetic correction
Goals:
Prevent scars/contractures (ROM & splints)
Activities of daily living (ADLs)
Psychosocial
PT/OT/Cosmetic consults
Educate:
Moisturizing for scar
management
Sun management
PT and OT importance
lOMoARcPSD|22650627
Cancer
Disease characterized by uncontrolled and unregulated growth of cells
1.
2.
Pathophysiology
Defective cell proliferation:
Normal cells proliferate only at cell
death or when physiologically necessary
(such as infection) and exhibit contact
inhibition (respect cell boundaries)
Cancer cells proliferate indiscriminately
and have no contact inhibition; form
tumor
Defective cell differentiation:
Normal cells mature and perform one
specific function
Cancer cells have a defect and perform
more than one function
Cancer
Occurs in all ages,
higher in men than
women
The second most
common cause of
death in U.S
1/3 of all cancerrelated deaths in U.S.
due to tobacco use,
unhealthy diet,
physical inactivity
and/or obesity
3 Stages of Cancer
Initiation - mutation/change in DNA occurs (exposure to carcinogen)
Most cancers not due to inherited genes, but to damage during lifetime
Carcinogens (cancer-causing agents)
Chemical - e.g. benzene, arsenic, formaldehyde
Radiation - e.g. UV radiation
Viral - e.g. Epstein-Barr virus, HIV, Hep B
Promotion - proliferation of ALTERED cells by promoters (e.g. dietary fat,
obesity, cigarette smoke, alcohol consumption); Reversible at this stage
Latent period - 1-40 yrs between initial genetic alteration and clinical
evidence
Progression - Increased growth rate of tumor, increased invasiveness, metastasis
(spread of cancer to a distant site). Most frequent sites of metastasis are lungs,
liver, bone, brain and adrenal glands
lOMoARcPSD|22650627
Types of Cancer
Leukemias and lymphomas - cancers of the blood and blood-forming tissues
Carcinomas - cancers of the cells that line the skin, lungs, digestive tract, and
internal organs
Sarcomas - cancers of the mesodermal cells (e.g. muscles, blood vessels, bone)
Cancer Classification Based on:
Anatomic Site
Histology (grading) - I, II, III, IV, X (better prognosis worse)
Anatomic extent of disease (varies widely per cancer type)
→
Prevention ** KEY
↓exposure to carcinogens (smoking, tanning beds, sun)
Diet - ↑veggies/fruits/whole grains, ↓dietary fat and preservatives
Limit alcohol intake
Regular exercise
Healthy weight
6-8 hrs sleep/night
stress
Regular physical exam
Follow cancer screening guidelines
Self-exam
Know 7 warning signs
↓
C hange in bowel or bladder habits
A sore that does not heal
U nusual bleeding or discharge
Thickening or a lump in the breast/body
I ndigestion or difficulty swallowing
O bvious change in a wart or mole
N agging cough or hoarseness
Diagnosis - ** Depends on the suspected site of cancer **
Pathologic evaluation of a tissue sample is the only definitive
means to diagnose cancer
Cytology studies (e.g. Pap)
Tissue biopsy
Chest x-ray
CBC
Liver function studies
Endoscopic exam (upper GI,
sigmoidoscopy, colonoscopy)
Radiographic studies (mammogram,
ultrasound, CT scan, MRI)
Radioisotope scans (e.g. bone, hair, lung, brain)
PET scan
Tumor markers
Genetic markers
Bone marrow examination
lOMoARcPSD|22650627
Treatment
Surgery - to eliminate or reduce the risk of cancer development; includes prophylactic removal of non-vital
organs (e.g. mastectomy, thyroidectomy, hysterectomy)
Chemotherapy (antineoplastic therapy); a systemic therapy and a mainstay of cancer tx for most solid
tumors and hematologic malignancies (e.g. leukemia, lymphomas)
Goal is to eliminate or reduce the number of cancer cells in the primary tumor and metastatic tumor site
Methods: oral or IV (most common; may cause local tissue breakdown/necrosis)
Regional chemotherapy - delivery of drug directly to the tumor site; reduced systemic toxicity
Chemotherapy agents cannot distinguish between normal cells and cancer cells
Side effects are result of destruction of normal cells, especially rapidly proliferating ones (e.g. bone
marrow, lining of GI system, skin/hair/nails)
Long-term side effects: damage to heart, lungs, liver, kidneys
Radiation therapy - local therapy; high-energy beams delivered into tissue to break the chemical bonds in
DNA; only has effect on tissues within tx field
Teletherapy - exposed to radiation via machine
Brachytherapy - implanting radioactive material directly into tumor
Immunotherapy (biologic therapy); uses the immune system to fight cancer; e.g. cytokines, vaccines,
monoclonal antibodies (most successful)
Targeted therapy - acts on specific targets associated with cancer; does less damage to normal cells than
chemo; e.g. tyrosine kinase inhibitors
Hormone therapy - can block the effects of certain hormones that enhance the growth of cancer (e.g.
corticosteroids, estrogen receptor blockers, androgen receptor blockers)
Hematopoietic stem cell transplantation (HSCT)- originally called BMT or PSCT
Goal is to eradicate diseased tumor cells and/or clear the bone marrow of its components to make way
for engraftment of transplanted, healthy stem cells; used for pt w/tumors resistant to chemo or rad tx
Uses high levels of chemo and/or radiation to clear the bone marrow; healthy stem cells are infused
afterwards
Intensive procedure with high risks
Complications: bacterial, viral, fungal infections; graft-vs-host disease
Complications of Cancer
Malnutrition - Seen as fat/muscle depletion
Small meals/ cal/ pro
Encourage nutrition supplements (Ensure);
cal/ density foods (e.g. oils, butter)
Weigh at least 2x/wk
Oncologic emergencies - life-threatening
Obstructive - tumor obstruction of an organ
or blood vessel (e.g. superior vena cava
syndrome, spinal cord compression)
Metabolic - hypercalcemia, SIADH, tumor
lysis syndrome
Infiltrative - Cardiac tamponade
↑ ↑
↑ ↓
↑
Cancer cachexia - Wasting syndrome ( morbidity risk)
Anorexia, unintended weight loss and appetite
Tissue wasting, skeletal muscle atrophy, immune
dysfunction
Cannot be reversed nutritionally
Best management is to treat cancer; nutrition
intake; Megace may help
Infection - a primary cause of death in pt with cancer
Instruct - call HCP if temp is 100.4 F or higher
Dysgeusia - altered taste sensation
Encourage experimenting with different foods and
spices
↑
lOMoARcPSD|22650627
Potential Side Effects of Chemotherapy or Radiation and Management
Mucositis/Stomatitis/Esophagitis
Assess oral mucosa daily
Instruct to avoid hot/spicy foods
Saline oral rinse
Artificial saliva
No tobacco or alcohol
Topical anesthetics (e.g. viscous lidocaine)
Nausea/Vomiting
Antiemetics (Zofran, Reglan)
Before chemo and as needed
Monitor for dehydration
Diarrhea
Antidiarrheal drugs
At least 3 L fluid/day
Constipation
Stool softeners
fiber foods
fluids
Activity if tolerated
Thrombocytopenia
Watch for bleeding (e.g. petechiae)
Monitor PLT
Neutropenia
Prevent infection! Hand washing
Monitor temp
Intracranial Pressure
Monitor neurologic status; may need
corticosteroids
Pneumonitis
Monitor for dry, hacking cough; fever
Pericarditis/Myocarditis
Monitor for CV symptoms (e.g. dyspnea)
Alopecia
Avoid excessive brushing, shampooing, hair
drying, curling, etc
Suggest hair pieces, scarves, wigs
Cognitive changes (brain fog) - Encourage:
Exercise brain (word puzzles, etc)
Use detailed planner; no multitasking
Sleep/rest
↑
↑
Fatigue (universal symptom) look for any
reversible cause:
Anemia
Hypothyroidism; Dehydration
Depression; Anxiety
Encourage rest/exercise as tolerated
Anorexia
Small, frequent meals high pro/cal
Monitor wt and look for dehydration
Nutr supplement drinks (Ensure, etc)
If severe- parenteral or enteral nutrition
Bone Marrow suppression (one of most common
symptoms) anemia
Monitor: neutrophils, PLT, RBC
Iron supps/erythropoetin
Leukopenia
Monitor WBC (esp. neutrophils)
Monitor body temp/signs of infection
May need WBC growth factors
Hepatotoxicity
Monitor liver fnx tests
Nephrotoxicity
Monitor BUN/CR
May need Sodium Bicarbonate and allopurinol
Cardiotoxicity
Monitor EKG
Hyperuricemia
Monitor UA levels; fluids
Allopurinol prophylactically
Skin changes
Erythema (patches of red skin)
Protect from temp extremes, tight
garments, harsh chemicals
Lubricate dry skin, aloe vera gel
Photosensitivity/hyperpigmentation
Avoid sun exposure
Pain management - moderate to severe in 50% pt
NSAIDs, opioids, morphine, fentanyl
Monitor for constipation
→
↑
lOMoARcPSD|22650627
The Heart
To body
Flow of Blood
through
the heart
Superior
Vena
Cava
Aorta
Pulmonary
Artery
Pulmonary
Veins
Right
Pulmonary
Atrium
Valve
Right Side - Deoxygenated blood
1.
2.
3.
4.
5.
6.
Left
Atrium
Mitral Valve
Aortic
Valve
Tricuspid Valve
Inferior
Vena
Cava
Superior/Inferior Vena Cava (from body)
Right Atrium
Tricuspid Valve
Right Ventricle
Pulmonary Valve
Pulmonary Artery (to lungs)
Pulmonary
Veins
Left
Ventricle
Right
Ventricle
Left Side - Oxygenated blood
7. Pulmonary Veins (from lungs)
8. Left Atrium
9. Mitral Valve
10. Left Ventricle
11. Aortic Valve
12. Aorta (supplies body)
Heart Sounds
S1
Closing of the atrioventricular valves; high-pitched, use diaphragm. NORMAL
S2
Closing of the semilunar valves; high-pitched, use diaphragm. NORMAL
S3
Heart may be in fluid overload or failure; low-pitched, use bell. MAY BE ABNORMAL
S4
Ventricle resistance; low-pitched, use bell. ABNORMAL
Murmurs May indicate wall defect or valve problem; low-pitched, use bell.
MAY BE ABNORMAL
lOMoARcPSD|22650627
The Heart
Cardiac Terms
Preload:
Volume of blood in the ventricles at end
of diastole
The resistance the left ventricle must
overcome during systole
afterload=
Stroke Volume:
The amount of blood pumped out of the
ventricles with each beat
Normal = 60-100 ml/beat
Cardiac Output:
The amount of blood the heart pumps in
1 minute (in liters)
Ejection Fraction:
Volume of blood expelled with every
contraction
Afterload:
cardiac workload
CO = HR X SV
(Normal = 4-8L/min)
Normal = 50-70%
Cardiac Biomarkers
Normal
Protein released into the bloodstream when the heart
muscle is damaged. BEST INDICATOR OF ACUTE MI!
Cardiac Troponin:
(cTnT)
0-0.4 ng/mL
>1.5 = critical
Creatine Kinase:
(CK-MB)
0-5 ng/mL
Enzyme released into the bloodstream when heart, brain
or skeletal muscle damaged.
Brain Natriuretic
Peptide (BNP):
<100 pg/mL
Peptide released into the bloodstream when ventricles fill
with too much fluid and STRETCH.
5-70 ng/mL
Found in heart and skeletal muscles; released into
bloodstream with MI or severe muscle damage. Not a
specific indicator of MI, but good to rule out.
Myoglobin:
(MB)
Cardiac Index:
(CI)
2.5 -4.0 L/min/m2
Central Venous
Pressure (CVP):
2 - 8 mmHg
Mean Arterial
Pressure (MAP):
70 - 100 mmHg
Average arterial pressure. Indicates perfusion of organs
and tissues.
Pulmonary Artery
Wedge Pressure:
(PAWP)
6-12 mmHg
Measures left ventricular preload. Indicates left-sided
heart function.
Cardiac Output adjusted for body surface area. More
accurate measure of cardiac function.
Measures right ventricular preload. Indicates fluid
volume status.
lOMoARcPSD|22650627
Heart Failure
When the heart is not able to supply enough blood to meet the body's need for blood and oxygen.
Two types: Left-sided and Right-sided
Left-sided
Systolic: Weakened heart
muscle can't squeeze blood
to the body
Left-sided
Right-sided
Diastolic: Stiff heart muscle
can't relax and fill with
blood
Inability to pump blood
from body to lungs
Right-sided
Right chamber has lost
its ability to PUMP.
Fluid backs up
peripherally
Often occurs due to
left-sided heart failure
Causes and Risk Factors
CAD
MI
HTN
Damaged valves
Myocarditis
Congenital heart defects
Heart arrhythmias
Family history
Left-sided
Two types: Diastolic and Systolic
Diastolic
Left ventricle doesn't
FILL properly
STIFF heart muscle
Normal EF
Systolic
Left ventricle doesn't
EJECT properly
WEAK heart muscle
Decreased EF
Signs and Symptoms
Left-sided
Dyspnea
Shallow respirations
Weakness/fatigue
Dry, hacking cough
Orthopnea
Crackles
S3 + S4 heart sounds
PMI displaced
Right-sided
Swelling of legs and hands
Fatigue
Weight gain
Ascites
JVD
Edema
Anorexia
lOMoARcPSD|22650627
Diagnosis
Blood test for BNPsecreted when there is increase pressure in the ventricles
level is high in heart failure
X-ray - check for enlarged heart and pulmonary infiltrates
Echocardiogram to look at ejection fraction, back flow and valve problems
ejection fraction is decreased in most heart failure
Heart cath
Nuclear stress test
Heart failure can be
acute or chronic
and exacerbated by:
BNP Levels
<100 pg/mL
No failure
100-300 pg/mL
Present
300 pg/mL Mild
600 pg/mL Moderate
900 pg/mL Severe
High salt intake or fluids
Uncontrolled atrial fib
Infection
Renal failure
Interventions
Monitor
Heart rate (Digoxin)
Respiratory status
Blood pressure (vasodilators)
Diuretics
strict I/Os
daily weights
monitor electrolytes (esp K+)
Labs:
BNP
BUN/Creatinine
Troponin
Edema
Instruct
Restrict fluids
Increase activity
gradually (balance with
rest)
Monitor wt and report
gain of 3 lbs in 2 days
Monitor for edema
Flu vaccine
Smoking cessation
Limit alcohol
Diet
Low sodium
2-3 gm/day
Low fat (trans/sat)
Low sugar
No caffeine
<2 L fluids/day
Spread fluids out
over day
Medications
Diuretics (Loop, Thiazide, K+ Sparing)
ACE inhibitors
Angiotensin II receptor blockers
Beta Blockers
Anticoagulants
Vasodilators
Digoxin
lOMoARcPSD|22650627
Coronary Artery Disease
Build up of fatty plaques due to atherosclerosis in the coronary artery.
Can lead to restriction of blood flow to the heart and heart damage or death.
Coronary Arteries
Left coronary
artery
Right coronary
artery
Left circumflex
artery
Right marginal
artery
Left anterior
descending artery
Normal
coronary artery
Posterior descending
artery
Atherosclerosis
(Plaque buildup)
Atherosclerosis
with blood clot
Risk Factors
Not Modifiable
Modifiable
Age
Gender
Men > 45 yrs
Women > 55 yrs
Race (African American)
Family history
Diabetes
HTN (>140/90)
High LDL cholesterol
Smoking
Sedentary lifestyle
Obesity
Metabolic syndrome
High stress
Unhealthy diet
Possible Factors
Sleep apnea
High hs-CRP levels (highsensitivity C-reactive
protein)
High TG levels
High homocysteine levels
Preeclampsia
Heavy alcohol use
Autoimmune diseases
lOMoARcPSD|22650627
Coronary Artery Disease
Signs and Symptoms
Chest pain during activity
(angina)
Heaviness
Tightness
Burning
Squeezing
SOB
Very tired
Sweating
Weakness
Dizziness
Nausea/vomiting
Racing heartrate
Palpitations
Pain in the arms or
shoulders
Coronary Artery
Disease can lead to:
Women's symptoms often
include:
Nausea/vomiting
Back pain
Jaw pain
SOB with no chest pain
Angina
Heart attack
Heart failure
Arrhythmia
Interventions
Diagnosis
Blood test (TC, LDL, HDL,
TG)
EKG- to assess if MI or not
Stress test- for any EKG
changes during exercise
Nuclear stress test- to
assess blood flow
Heart cath- to identify any
blockages
Heart CT scan- to check
for calcium deposits
Early on most are
ASYMPTOMATIC
Goal is to prevent further progression of CAD by reducing
or eliminating risk factors.
Goal: HDL >40mg/dL and LDL<100 mg/dL
Diet
Instruct
Smoking cessation
Exercise
Weight loss
Stress management
Lowering BP
Lowering cholesterol
Managing DB
Decrease alcohol intake
Monitor s/s
Low fat
Cholesterol <200 mg/day
Adequate fiber
Monitor sodium
Add in healthy fat (omega-3)
Encourage fruits, vegetables
and whole grains
Medications
Statins
Beta Blockers
ACE Inhibitors
Niacin
Aspirin/Plavix
Nitrates
lOMoARcPSD|22650627
Angina Pectoris
Chest pain caused by reduced blood flow to the heart.
Three types: Stable, Unstable and Variant
Stable
** Most common **
Predictable
Occurs with exertion or
stress
Short duration
Symptoms relieved by
rest or nitroglycerin
Unstable
Variant
** Most dangerous **
Unpredictable
Occurs at rest, exertion
or stress
Symptoms unrelieved
by rest or meds
** Rare **
Pain at rest
Caused by spasm in
coronary artery
Reversible ST
elevation
Atherosclerosis
(Plaque buildup)
Causes
**Atherosclerosis Main Cause **
Atherosclerosis
Coronary artery spasm
Thrombosis
Heart failure
Valve disorders
Aortic stenosis
Risk Factors
Obesity
Sedentary lifestyle
Smoking
Poor DB management
High cholesterol/TG
High BP
Family history
Age
Men > 45 yrs
Women >55 yrs
Emotional stress
Weather extremes
Heavy meals
lOMoARcPSD|22650627
Angina Pectoris
Signs and Symptoms
Chest pain that may radiate
to jaw, neck, shoulders, back
Pressure
Squeezing
Burning
Fullness
SOB
Diaphoresis
Weakness/fatigue
Pallor
Dizziness
Nausea/vomiting
Diagnosis
EKG
Stress test
Echocardiogram
Coronary angiography
Chest x-ray
Blood tests (troponin, lipids)
Cardiac catherization
Cardiac MRI
Surgery
(if necessary)
PCI: stent in artery OR
CABG: reroute around artery
Feeling of gas, indigestion
Women:
Nausea
SOB
Abdominal pain
Discomfort in neck, jaw, back
Interventions
Instruct
Diet
BP control
Smoking cessation
Diet modification
Control DB
Exercise
Flu vaccine
Decrease chol levels
Flu vaccine
Low fat
Cholesterol <200
mg/day
Adequate fiber
Monitor sodium
Add in healthy fat
(omega-3)
Encourage fruits,
vegetables and whole
grains
Medications
Immediate relief: Nitroglycerin to
dilate heart arteries
Store pills out of light
Patch for unstable
Ca channel blockers
Beta Blockers
Antiplatelet/Anticoagulant
Statins
lOMoARcPSD|22650627
Myocardial Infarction
(AKA Heart Attack)
Decreased blood flow in a coronary artery leads to decreased oxygen to the heart muscle
which causes damage to the heart
Heart changes after MI
Early signs of
MI
Heart muscle not
physically
changed yet
Enzymes released:
Myoglobin 1 hr post
Troponin 2-4 hrs post
CK-MB 4-6 hrs post
24-36 hrs
post MI
Inflammation sets in
Neutrophils arrive
Heart fails to pump
efficiently
Arrhythmias may
develop
Risk Factors
Diabetes
HTN
Obesity
High cholesterol levels
Smoking
Gender (male)
Sedentary lifestyle
Stress
Age (45+ men, 55+ women)
Family history
Race- African American
10 days
post MI
2 months
post MI
Macrophages
arrive to clean
up dead cells
New tissue is
weak
Scarring occurs
Heart size and
functionality
changed due to
increased collagen
Signs and Symptoms
Chest pain (left
substernal) with no relief
with rest or meds
Jaw and/or left arm pain
Heart burn
Increased HR
SOB
Nausea/vomiting
Diaphoresis
Anxious, scared
When a coronary artery
becomes 100% blocked,
the muscle cells die
Women present with
different symptoms:
Fatigue
Shoulder blade
discomfort
SOB
Silent MI
No chest pain
Occurs mainly in DB
due to neuropathy
Cell death is
irreversible
after 30 minutes
lOMoARcPSD|22650627
Myocardial Infarction
Normal EKG
ST Elevation (STEMI)
Full blockage (No O2)
ST Depression
Partial Blockage (Low O2)
Diagnosis
EKG
ST elevation - full blockage (no O2), worst type of MI b/c most damage
ST depression - partial blockage (low O2)
Blood tests: Troponin, CK-MB, myoglobin
Echocardiogram - to check for damage
Heart cath - to check for blockages and muscle damage
Stress test
Interventions
Immediate
12-lead EKG
Monitor BP/HR
Oxygen
Bed rest
Collect enzymes
Administer meds
Monitor lungs for
'crackles'
Surgery
If necessary
PCI or
CABG
Instruct
Low salt and fluid
Decrease stress,
alcohol, caffeine
Smoking cessation
Increase exercise
Weigh daily
Potential Complications
of MI
Cardiogenic shock
Dysrhythmias
Heart failure
Cardiac tamponade
Medications
Nitrates
ARBs
Statins
Calcium channel blockers
Anti-thrombotic agents
Antiplatelets
Morphine
Beta Blockers
ACE Inhibitors
lOMoARcPSD|22650627
Sodium
Major Extracellular Fluid (ECF) cation.
Assists in acid-base balance and fluid balance.
Helps regulate nerve function and muscle
contraction
Helps maintain stable blood pressure levels.
Inverse to Potassium
Normal: 135-145 mEq/L
Hyponatremia <135 mEq/L
Hypernatremia >145 mEq/L
Signs and Symptoms
Signs and Symptoms
Fatigue
Nausea/vomiting
Confusion
Seizures
Weakness
Muscle cramps
Tachycardia
Thirst
Agitation
Confusion
Irritability
Restlessness
HTN and fluid retention
Decreased urine output
Low
Causes
Increased Na+ excretion:
Vomiting/Diarrhea
Sweating
Diuretics
NG suction
Fluid overload:
CHF
Hypotonic fluids
Liver failure
High
Causes
Na+ intake
insufficient:
Fasting
NPO
ADH
oversecretion
(SIADH)
Excess oral/IV Na+ intake
Excess hypertonic IV fluids
Fever
Watery diarrhea
Dehydration
Overproduction of aldosterone (Cushing's)
GI tube feedings
Impaired thirst
Management
Management
Increase oral Na+ intake
Decrease fluids
Diuretics if due to hypervolemia
ADH antagonist (for SIADH)
If due to hypovolemia, IV NaCl infusions
at low rate (only in critical situations-hard
on veins, risk of fluid overload)
Decrease oral Na+ intake
If due to fluid loss, administer IV
infusions slowly to avoid cerebral edema
If due to decreased excretion of Na+,
provide diuretics that increase Na+ loss
High Sodium Foods
Encourage!
Soups, canned foods
Ham, bacon, sausage
Most processed foods
Cheese, dressings
Avoid!
Pizza, hot dogs
Cold cuts
lOMoARcPSD|22650627
Potassium
Major Intracellular Fluid (ICF) cation.
Helps regulate fluid balance, muscle
contractions and blood pressure.
Assists in sending nerve impulses.
Inverse to Sodium
Similar to Magnesium
Normal: 3.5-5.0 mEq/L
Hypokalemia <3.5 mEq/L
Hyperkalemia >5.0 mEq/L
Signs and Symptoms
Signs and Symptoms
Weakness
Thready pulse
Muscle leg cramps
Shallow respirations
Hypoactive bowel sounds
Constipation
Inverted T wave
Low
Irregular heartbeat
Nausea and diarrhea
Abdominal cramping
Tall peaked T wave
Tingling in hands, feet
and mouth
Weakness
Muscle cramps
Causes
Causes
Diuretics
Vomiting
Diarrhea
Drains (NG tubes)
Corticosteroids
Long-term laxative use
Fasting, NPO
IV therapy with K- deficient solutions
Magnesium deficiency
Tissue damage, burns, trauma
Kidney disease
Adrenal insufficiency (Addison's disease)
K-retaining diuretics
Acidosis
ACE inhibitors
Uncontrolled diabetes
Excessive K intake
Management
Management
Oral K- supplements (given with food)
Liquid potassium chloride
K-retaining diuretic
Hold K-wasting diuretics
In very low levels (<2.5), potassium IV
infusion (SLOWLY)
Discontinue IV and PO K
Initiate K-restricted diet
K-excreting diuretics
IV Calcium
IV Insulin
Albuterol
Dialysis
High Potassium Foods
Encourage!
Baked potato
Sweet potato
High
Banana, avocado
Watermelon
Avoid!
Spinach
Canned clams
lOMoARcPSD|22650627
Calcium
Assists in formation of bones and teeth, muscle
contraction, normal functioning of many
enzymes, blood clotting and normal heart
rhythm
Regulated by PTH and calcitonin
Inverse to Phosphorus
Similar to Vitamin D and Magnesium
Normal: 9-11 mg/dL
Hypocalcemia <9 mg/dL
Hypercalcemia >11 mg/dL
Signs and Symptoms
Signs and Symptoms
Tingling fingers, face and
limbs
Muscle spasms
Arrhythmias
Tetany
Muscle cramps
Laryngospasms
Low
Muscle weakness
Decreased DTR
Arrhythmias
Bone pain
Nausea and vomiting
Anorexia
Excessive urination
Thirst
Causes
Causes
Decreased Mg levels
Insufficient Ca or Vit D intake
Increased serum phosphorus
Hypoparathyroidism
Pancreatitis
Kidney disease
Diarrhea
Phenytoin
Hyperparathyroidism
Malignancy (bone destruction from
metastatic tumor)
Thiazide diuretics
Kidney disease
Antacids with calcium
Severe dehydration
Inactivity (e.g. paralysis)
Management
Management
Encourage foods high in Ca
Supplements PO or IV: Ca, Mg, Vit D as
prescribed
Calcium IV must be administered
SLOWLY
Move clients carefully as they are at risk
for fractures
Discontinue:
Vit D supplements
IV or PO calcium
Thiazide diuretics
Administer calcitonin and/or
biphosphonates
Avoid foods high in calcium
Last resort: dialysis
High Calcium Foods
Encourage!
Dairy foods
Sardines
High
Green leafy vegetables like
curly kale, okra, spinach
Avoid!
Brazil nuts
Canned salmon
lOMoARcPSD|22650627
Magnesium
Regulates:
Muscle contraction and nerve function
Blood sugar levels
Blood pressure
Helps make protein, bone and DNA
Similar to Calcium
Normal: 1.5-2.5 mg/dL
Hypomagnesemia <1.5 mg/dL
Hypermagnesemia >2.5 mg/dL
Signs and Symptoms
Signs and Symptoms
Hyperreflexia (increased DTR)
Seizures
Lethargy
Tachycardia
Disrhythmias
Hypertension
Nausea/vomiting
Weakness
Low
Hypotension
Decreased DTR
Bradypnea (Low RR)
Vomiting
Nausea
Coma (severe)
Causes
Diuretics
Chronic alcoholism
Diarrhea
Malnutrition
Crohn's disease
Celiac disease
Fluid loss via NG suction
Causes
Kidney failure (decreased renal excretion
of Mg)
Large intake of Mg-containing antacids
Excessive Mg-containing laxative use
Hyperkalemia from Addison's disease
Hypothyroidism
Management
Magnesium sulfate IV (slowly)
Oral magnesium salts
Encourage high-magnesium foods
Management
Diuretics
IV Calcium Gluconate
Dialysis
Decrease Mg-containing foods
Avoid laxatives and antacids containing
Mg
High Magnesium Foods
Encourage!
Pumpkin seeds
Dark chocolate
High
Almonds and cashews
Spinach and avocados
Avoid!
Brazil nuts
Salmon
lOMoARcPSD|22650627
Phosphorus
Builds and repairs bones and teeth
Helps nerve function
Assists in energy production in cells
Makes muscles contract
85% of the body's phosphorus located in bones
Inverse to Calcium
Vit D and Phosphorus assist in each other's absorption
Normal: 2.5-4.5 mg/dL
Hypophosphatemia <2.5 mg/dL
Hyperphosphatemia >4.5 mg/dL
Signs and Symptoms
Signs and Symptoms
Confusion
Irritability
Muscle weakness
Lethargy
Bone pain and fractures
Numbness
Loss of appetite
Decreased ability to breathe
Most are asymptomatic
Bone pain
Muscle spasms (calves
and feet)
Itchy skin
Increased DTR
Low
Causes
Causes
Hyperparathyroidism
Malabsorption from long-term antacid use
Vitamin D deficiency
Chronic diarrhea
Long-term diuretic use
Severe malnutrition
Excessive alcohol use
Burns
Hypoparathyroidism
Overuse of Vit D
Diabetic ketoacidosis
Severe kidney disfunction
Chemotherapy
Management
Management
Oral phosphorus
Oral vitamin D
Encourage high-phosphorus foods
IV phosphate- monitor kidney fx, Ca level,
EKG
Calcium carbonate or calcium acetate
given with food
Avoid phosphate enemas
Decrease high-phosphorus foods in diet
Last resort= dialysis
High Phosphorus Foods
Encourage!
Milk and cheese
Egg yolks
High
Chocolate
Soft drinks and beer
Avoid!
Fish, beef, chicken
Nuts and beans
lOMoARcPSD|22650627
Chloride
Helps keep the ICF and ECF in balance
Helps maintain blood volume, blood pressure
and pH of body fluids
Level controlled by the kidneys
Normal: 95-105 mEq/L
Hypochloremia <95 mEq/L
Hyperchloremia >105 mEq/L
Signs and Symptoms
Signs and Symptoms
Difficulty breathing
Muscle spasms
Dehydration
Weakness
Fatigue
Diarrhea
Vomiting
Low
Muscle weakness
Excessive thirst
Hypertension
Fatigue
Fluid retention
Irregular heartbeat
Causes
Causes
Renal failure
Prolonged diarrhea and vomiting
Diuretic therapy
NG tube suctioning
Chronic lung disease
CHF
Metabolic alkalosis
Chemotherapy
Severe diarrhea
Extremely high ingestion of dietary salt
Renal or metabolic acidosis
Respiratory alkalosis
CKD
Diabetes insipidus or diabetic coma
Chemotherapy
Management
Management
Treat underlying cause
IV fluids (like normal saline)
Encourage more sodium chloride in diet
Meds to curb nausea, vomiting, diarrhea
Hydration if dehydrated
Decrease saline IV
Maintain blood glucose levels
Stop meds if they are contributing to the
problem
High Chloride Foods
Encourage!
Table salt
Seaweed
High
Rye
Tomatoes
Avoid!
Lettuce and celery
Olives
lOMoARcPSD|22650627
Electrolyte Relationships
Sodium / Potassium = INVERSE
+
Na =
K+
Calcium / Phosphorus = INVERSE
+
Ca =
PO4
Calcium / Vitamin D = SIMILAR
+
Ca =
Vit. D
Calcium / Magnesium = SIMILAR
+
Ca =
Mg
Magnesium / Potassium = SIMILAR
Mg =
K+
Magnesium / Phosphorus = INVERSE
Mg =
PO4
lOMoARcPSD|22650627
The Endocrine System
A network of glands and organs that regulate and control various body
functions by producing and secreting hormones.
Pineal
Hypothalamus
Pituitary
Parathyroid
Thyroid
Thymus
Adrenal
Pancreas
Ovaries
(female)
Testes
(male)
Major Endocrine Glands
1.
2.
3.
4.
5.
Hypothalamus
Pituitary
Pineal
Parathyroid
Thyroid
6. Thymus
7. Adrenal
8. Pancreas
9. Ovaries
10. Testes
lOMoARcPSD|22650627
Hypothalamus Gland
Location: Base of brain
Function: Major role in endocrine system; maintains body's homeostasis; releases hormones
that stimulate the pituitary gland
Main Hormones: Oxytocin, Anti-Diuretic Hormone (ADH/Vasopressin)
Pituitary Gland - AKA 'Master' gland
Location: Connected to hypothalamus in brain
Function: Secretes hormones that send signals to other endocrine glands to release or inhibit
their own hormone production
Main Hormones and target organ:
Growth hormone - Bones, muscles, organs
Prolactin - Breasts (mammary glands) to stimulate milk production
Luteinizing hormone (LH) ovaries to produce estrogen/progesterone
testes to produce testosterone
Follicle-stimulating hormone (FSH) - same as LH
Adrenocorticotropic hormone (ACTH) - adrenal glands to produce
corticosteroids
Thyroid-stimulating hormone (TSH) - thyroid to produce thyroid
hormones
ADH (made in hypothalamus but stored in pituitary) - kidneys to ↑
water absorption in blood
Oxytocin (made in hypothalamus but stored in pituitary) - breasts
(for milk production) and uterus (for contractions)
Pineal Gland
Location: Between two hemispheres in brain
Function: Regulates circadian rhythm and
reproductive hormones
Main Hormone: Melatonin
Parathyroid Glands
Location: Four glands in the neck BEHIND the thyroid
Function: Regulate calcium and phosphate levels
Main Hormone: Parathyroid hormone (PTH)
Thyroid Gland
Location: Lies just below the Adam's
apple in the neck
Function: Regulates the body's
metabolism
Main Hormones: T3 (Triiodothyronine),
T4 (Thyroxine- converts to T3),
Calcitonin
No relation other
than name
lOMoARcPSD|22650627
Thymus Gland
Location: Behind sternum between lungs
Function: Stimulates the development of T cells which are sent to lymph nodes to help fight
disease. Only active until puberty then shrinks and becomes fat!
Main Hormone: Thymosin
Adrenal Glands - AKA Suprarenal
Location: Two glands located one on top of each kidney
Function: Two parts to each gland (Medulla and Cortex), each with its own function.
Medulla: Secretes epinephrine and norepinephrine to help control activities of
sympathetic nervous system (blood pressure, heart rate, sweating)
Cortex: Secretes two types of corticosteroid hormones:
1. Glucocorticoids:
a. Hydrocortisone (cortisol) - helps convert food to energy
b. Corticosterone - regulate immune response
2. Mineralcorticoids: The main one is aldosterone - maintains balance of salt and
water to control blood pressure
Main Hormones: Epinephrine, Norepinephrine, Hydrocortisone, Corticosterone, Aldosterone
Pancreas - belongs to both endocrine and digestive systems
Location: Next to stomach, connected to duodenum
Function: Main endocrine function is to regulate blood glucose levels; only 5% of pancreas is
endocrine cells (Islets of Langerhans)
Main Hormones:
1. Gastrin - stimulates cells in stomach to produce acid for digestion
2. Glucagon - stimulates cells to release glucose to raise blood glucose levels
3. Insulin - regulates blood glucose levels by allowing cells to absorb & use glucose (thus
lowering blood glucose levels)
4. Somatostatin - released when insulin and glucagon get too high
5. Vasoactive intestinal peptide (VIP)- controls H2O secretion/absorption from intestines
Ovaries
Location: On either side of uterus
Function: For proper physical development
of girls and to ensure fertility
Main Hormones: Estrogen, Progesterone
Testes
Location: Within the scrotum
Function: For proper phys. development of
boys, then libido, muscle strength, bone dens.
Main Hormone: Testosterone
lOMoARcPSD|22650627
The Thyroid Gland
Location: Lies just below the Adam's apple in the neck
Function: Regulates the body's metabolism
Main Hormones: T3 (Triiodothyronine), T4 (Thyroxine- converts to T3), Calcitonin
Thyroid uses iodine in food we eat
to make the 2 main hormones (T3
and T4)
T3 & T4 function:
Regulate metabolism
Affect:
Heart rate
SNS
Growth/development
Body temperature
Fertility
Digestion/burning calories
Muscle contraction
Calcitonin helps incorporate
calcium into bone
Hypothalamus releases
Thyrotropin-releasing
Hormone (TRH) Pituitary
releases Thyroid-stimulating
Hormone (TSH) thyroid
produces T3 & T4
Too much T3 & T4 in blood
stimulates pituitary to stop
releasing TSH (negative
feedback loop)
→
→
If thyroid is enlarged, a goiter may
appear below or to the sides of the
Adam's apple
Thyroid Function Tests
Blood tests:
TSH - Best indicator of thyroid function
Need to test along with T4 & T3 to see if problem lies with thyroid or
pituitary
T4 & T3
TRH
Thyroid Binding Globulin (TBG) (carries T3 & T4 in blood)
Antibodies (to check for autoimmune disease)
Biopsy (if cancer suspected)
Ultrasonography (if growths are detected)
Radioactive iodine uptake test (to measure thyroid activity)
lOMoARcPSD|22650627
Hyperthyroidism
Condition that occurs when there is a high level of thyroid hormones
in the blood - AKA Overactive Thyroid
Causes:
Graves Disease (see Graves
Disease section) - most common
Toxic multinodular goiter Plummer Disease - many nodules
that secrete excess thyroid
hormones
Thyroiditis - Inflammation caused
by:
Virus
Autoimmune
Single toxic nodule - abnormal
tissue within the thyroid produces
excess thyroid hormones
Certain meds
Iodine (too much)
Overactive pituitary gland - rare
Treatment
Will depend on cause
Iodine - not used long-term; given
when tx needed fast (i.e. thyroid
storm - see Thyroid Storm section)
Radioactive iodine - destroys part or
all of thyroid gland; may need HRT
for rest of life
Thyroidectomy - removal; will need
HRT for rest of life
Beta-blockers - ↓ HR, tremors and
anxiety
Meds
Signs and Symptoms - think FAST
Enlarged thyroid gland (goiter)
Sped up body functions
↑ HR/BP
Palpitations due to arrhythmias
Excess sweating/hot
Shaky hands
Nervous/anxious/irritable
Insomnia
Wt loss/ ↑ appetite
Frequent BM/diarrhea
Change in menstrual cycles
Elderly - 'Masked' hyperthyroidism
Weak
Confused
Withdrawn
Depressed
Other s/s if caused by Graves (see
Graves Disease section)
Meds
Antithyroid meds:
Methimazole - most common
Propylthiouracil (PTU) - watch
for liver damage
Stop the production of T3 & T4
Educate pt:
Do not abruptly stop
Same time each day
Avoid iodine-rich foods
No aspirin/salicylates
Watch for thyroid storm and
hypothyroidism
lOMoARcPSD|22650627
Intervention
Cool, calm environment
Daily wts
Monitor EKG, HR, BP
Monitor for thyroid storm
Educate on:
Radioactive iodine therapy
Thyroidectomy
If thyroidectomy:
Monitor for possible parathyroid issues
and thyroid storm
Watch Ca levels
Keep pt in Semi-Fowler's position
Keep trach kit, oxygen nearby
Graves Disease
Autoimmune disorder where the antibody (Thyroid Stimulating
Immunoglobulin - TSI) stimulates the thyroid to produce and secrete excess
thyroid hormones into the blood; often hereditary
Signs/Symptoms include those for hyperthyroidism PLUS :
Protruding eye balls/puffy eyes
Double vision; sensitive to light
Pretibial Myxedema - red, swelling on the skin, lower legs and feet (has
an orange peel texture)
TX- same as for hyperthyroidism, PLUS
For eyes: Elevate HOB, eye drops, selenium, diuretics
Corticosteroid cream for itchy skin
Thyroid Storm- a life-threatening emergency!
Sudden, extreme overactivity of the thyroid gland
Cause: Pt w/hyperthyroidism that is unmanaged/ill-treated or is ill (sepsis;
DKA; surgery); post-thyroidectomy; taking salicylates; pregnant, or exposed to
radioactive iodine therapy
S/S: Typical hyperthyroidism s/s to the EXTREME! Fever, HTN and
tachycardia (may lead to CHF or MI), RR (may lead to resp failure), restless
and confused (may lead to seizures, delirium, come)
Interventions: Monitor HR, BP, RR, EKG, temperature; sedatives, no iodine
Meds: Antithyroids (Methimazole, PTU) - block synthesis; Iodide solution blocks secretion; Tylenol (no salicylates), Beta Blockers (Inderal) - block
conversion; Glucocorticoids (Dexamethasone) - suppresses immune system
↑
lOMoARcPSD|22650627
Hypothyroidism
Condition that occurs when there is a low level of thyroid hormones in the blood
Causes:
Primary
Hashimoto's thyroiditis - most
common- autoimmune disorder
where body attacks thyroid
Thyroiditis - usually temp
Tx for hyperthyroidism or
thyroid cancer
Low iodine in diet (rare in U.S.)
Radiation to head & neck
Genetic disorder
Secondary- rare
When pituitary gland fails to
secrete enough TSH
**Affects mainly women
middle to older aged**
Signs and Symptoms- think SLOW
Possible enlarged thyroid gland
(goiter)- usually w/Hashimoto's
Slowed down body functions
Fatigued- usually 1st sign
Eyelids droop
Eyes/face puffy (myxedema)
Voice hoarse/speech slow
Hair sparse, coarse, dry
Skin coarse, dry, scaly
Wt gain
Constipated
Muscle cramps
No tolerance to cold
↓ HR
Change in menstrual cycles
Elderly may appear depressed,
confused, forgetful, demented
Treatment - Meds
Thyroid hormone replacement
Synthroid
Thyrolar
Cytomel
NO sedatives/narcotics - increase
risk for myxedema coma (see
Myxedema Coma section)
lOMoARcPSD|22650627
Intervention
Monitor for myxedema coma
(see next section)
Administer meds as prescribed
Don't take within 4 hrs:
Carafate
Aluminum Hydroxide
Simethicone
Multivitamin
Monitor for hyperthyroidism
NO sedatives or narcotics
Educate pt:
Don't abruptly stop taking
meds
Take same time every day
Medication interactions
Myxedema Coma - a life-threatening emergency!
Sudden, extreme underactivity of the thyroid gland
Cause: Pt w/hypothyroidism that is unmanaged/ill-treated or is ill, abruptly
stops taking thyroid replacement meds, takes sedatives or lithium, or thyroid
gland is removed
S/S: Typical hypothyroidism s/s to the EXTREME!
HR, BP
Temp
RAREBG
Occurs mainly in
Na
elderly women
Resp failure
Myxedema (swelling of eyes/face)
Drowsy
May lead to confusion, stupor, coma
Interventions:
Monitor HR, BP, EKG, Wt
Monitor resp status (may need mech vent)
Keep warm
IV solutions as prescribed:
Normal saline and glucose
Synthroid (monitor for toxicity)
Glucose
No sedatives or narcotics
↓ ↓
↓
↓
↓
lOMoARcPSD|22650627
Hyper- and Hypoparathyroidism
Two disorders caused by too much or too little parathyroid hormone.
The main purpose of the parathyroid glands is to control blood calcium levels.
Role of Calcium in body
Nerve impulse
transmission
Muscle contraction
Bone health
Blood clotting
It's all
about the
calcium!
Parathyroid glands monitor
the Ca level 24 hrs/day.
When the level , the glands
make and release parathyroid
hormone (PTH).
When the level , the glands
make less PTH or stop the
release altogether. (PTH
negative feedback loop)
↓
↑
When Ca level is low, PTH is sent to:
Bones to release Ca into blood
Normal Ca levels =
Intestine to ↑ absorption of Ca from diet
8.6 - 10.0 mg/dL
Kidneys to:
Reabsorb Ca (and stop the release into urine)
Stimulate the production of active Vit D (needed to absorb Ca)
Block phosphate form being reabsorbed (excretes in urine instead)
Hyperparathyroidism
Disorder caused by over-production of PTH by a parathyroid gland.
Leads to Hypercalcemia and Hypophosphatemia
2 types:
Primary - Caused by enlarged PT gland(s)
Noncancerous growth - ** Most common
Enlargement (hyperplasia)
Cancerous tumor (very rare)
Secondary - Caused by another condition that causes
↓Ca levels in the body
Severe Ca deficiency
Severe Vit D deficiency
Chronic kidney failure (kidneys can't covert Vit D so SI can't absorb Ca)
lOMoARcPSD|22650627
Risk Factors
Radiation tx for cancer in
neck area
Lithium (bipolar disorder)
Complications
Osteoporosis
Kidney stones
CVD
In pregnant women may
cause neonatal
hypoparathyroidism
Signs and Symptoms
Osteoporosis
Kidney stones (↑ Ca levels cause kidney to reabsorb Ca)
Excess urination (↑ Ca levels cause ↑ urine production)
N/V
No appetite
Ab pain (↑ stomach acid)
Constipation
Feeling ill in general
Tired/weak
Bone and joint pain
Depressed/forgetful
Intervention
Admin meds per MD order
Monitor:
Vitals
EKG
Ca/PO4 levels
Renal status
I/Os, encourage fluids
Diet: ↓ Ca, ↑ PO4
Post-op:
Monitor respiratory status
Keep in Semi-Fowler's position
Keep trach kit, oxygen, suction on hand
Watch for ↓ Ca levels:
Tingling
Twitching
+ Trousseau's Sign
+ Chvostek Sign
Laryngeal nerve damage (voice changes,
trouble swallowing or speaking)
Diagnosis
Blood tests:
Ca
PO4
Mg
PTH
Sometimes:
Urine for Ca
EKG
Bone density
Surgery
(parathyroidectomy)
is the main treatment
for Primary
Hyperparathyroidism
Meds
Calcimimetics 'Senispar' - mimics role
of Ca in blood to ↓ PTH levels - used in
pt w/secondary hyperparathyroidismtake w/food to avoid GI distress
Calcitonin - injected or nose spray - ↓
osteoclasts and ↑ kidney excretion of
Ca
Loop diuretics 'Lasix' - ↓ Ca
reabsorption in renal tubules- monitor
K+ levels
Bisphosphonates 'Aredia' or 'Fosomax'
- slows down osteoclasts
lOMoARcPSD|22650627
Hypoparathyroidism
Disorder caused by decreased production of PTH by the parathyroid glands.
Leads to Hypocalcemia and Hyperphosphatemia
Very
RARE
Causes:
Following thyroid or PT surgery
Accidental removal during thyroid surgery
Parathyroidectomy (usually transient)
Inability of kidneys and bones to respond to
PTH (pseudo-hypoparathyroidism)
Congenital (Neonatal hypoparathyroidismdue to pregnant mom with
hyperparathyroidism)
Immune system develops antibodies against
PT tissue
Hypomagnesemia
Usually caused by chronic alcoholism
Signs and Symptoms
Parathesia - tingling,
numb skin
+Trousseau's Sign
+Chvostek Sign
Severe tetany bronchospasm,
laryngospasm,
hand/feet spasm,
seizures, EKG changes
↓ Ca, ↑ PO4
Intervention
Meds
IV calcium - slowly, can cause tissue
sloughing, watch if pt on Digoxin (risk
of toxicity)
Oral Ca w/Vit D - give separate times
than Fe and thyroid hormone
PO4-binders - Aluminum carbonate given after meals to ↑ excretion of PO4
by GI system
PTH replacement - Natpara - Monitor
Ca levels; watch for GI distress,
paresthesia
Monitor Ca and PO4 levels
Have trach kit, oxygen and suction at
bedside
Diet - ↑ Ca, ↓ PO4
Meds per MD order
Diet
Encourage:
Beans
Almonds
Dark green, leafy veges
Dairy
Fortified cereals, OJ
Avoid:
Soft drinks, coffee
Eggs, red meat
Alcohol, tobacco
lOMoARcPSD|22650627
The Adrenal Glands
Location: Two glands located one on top of each kidney
Function: Two parts to each gland (Medulla- inner layer and Cortex- outer layer),
each with its own function.
Medulla: Secretes epinephrine and norepinephrine to help control activities
of sympathetic nervous system (blood pressure, heart rate, sweating)
Cortex: Secretes two types of corticosteroid hormones:
Glucocorticoids:
Hydrocortisone (cortisol) - regulates metabolism
Corticosterone - regulate immune response
Mineralcorticoids: The main one is aldosterone - maintains balance of
salt and water to control blood pressure
Main Hormones: Epinephrine, Norepinephrine, Hydrocortisone, Corticosterone,
Aldosterone
Adrenal glands
Hypothalamus releases Corticotropinreleasing Hormone (CRH)
Pituitary
releases Corticotropin (ACTH)
adrenal glands release glucocorticoids
In response to stress, the hypothalamus
stimulates the medulla to release
epinephrine and norepinephrine
The renin-angiotensin-aldosterone
system (regulated by kidneys)
stimulates adrenal glands to produce
more or less aldosterone
→
Kidneys
Adrenal
Cortex
Adrenal
Medulla
Kidney
→
lOMoARcPSD|22650627
Cushing's Syndrome
Condition due to very high level of cortisol released from adrenal glands
Causes:
Large doses of corticosteroids (ex.
Prednisone, Dexamethasone)
Asthma, rheumatoid arthritis,
lupus
Tumor in adrenal glands
Tumor outside the pituitary glandsproducing corticotropin (ACTH)
Cushing's Disease
Very high level of cortisol due to
pituitary gland producing too
much ACTH. Usually caused by a
tumor in the pituitary. The adrenal
glands are normal.
Treatment
Will depend on cause
↓ corticosteroids if possible (weigh
benefits)
↑ pro, ↑ K diet
Meds to ↓ cortisol and its effects:
Metyrapone
Ketoconazole
Mifepristone
Radiation tx
Surgery
Remove tumors
Adrenalectomy (may need
corticosteroids for life)
Signs and Symptoms
Excessive fat on torso & top of back
(known as buffalo hump)
Large round face (moon face)
Weak muscles
Thin skin, bruise easily
Striae on abdomen/chest
Fatigue, depression
↑ BP
↑ BG
↓K
Osteoporosis
Irregular menstrual cycles in women
ED in men
↑ body and facial hair, women balding
Hirsutism in women
Children: grow slowly, short stature
Diagnosis
Measure cortisol in
urine/saliva/blood for 24 hr pd
(will be ↑ all day in Cushing's)
CT, MRI, chest x-ray to look for
tumors
Intervention
Prep for surgeries
Monitor for infection/skin
breakdown
Monitor BG, K, Na, Ca
lOMoARcPSD|22650627
Addison's Disease
Deficiency of cortisol and aldosterone due to underactive adrenal glands
AKA Primary Adrenal
Insufficiency
(See next page for Secondary
Adrenal Insufficiency)
Causes:
Autoimmune reactions - body
attacks adrenal cortex
Cancer
Tuberculosis/infections
Trauma to adrenal cortex
In infants/children: genetic
Diagnosis
S/S slow to show, no definitive
blood test so difficult to dx
Blood tests may show ↓ Na, ↑ K,
↓ cortisol, ↑ ACTH
Treatment
Goal is to replace cortisol &
aldosterone with meds- will
need for life
Meds
Cortisol replacement:
Hydrocortisone (divided
doses each day)
Prednisone
Dexamethasone
Aldosterone replacement:
Fludrocortisone
Signs and Symptoms
Develop slowly over time, vary/person
Weak, tired, dizzy
Dark patches of skin (knuckles, scars,
creases, gums)
Black freckles
Wt loss/No appetite
Muscle aches
N/V/Ab pain/Diarrhea
No tolerance to cold
↓ BP, dehydration
Crave salt
Depression
↓ Na, ↓ BG, ↑ K, ↑ Ca
Irregular menstruation in women
ED in men
Intervention
Monitor BG and K
Administer meds as prescribed
Educate:
Don't abruptly stop meds
Report ↑ stress levels (may
need adjustment)
Carry injection of cortisol for
emergency
Wear med alert bracelet
Diet ↑ Prot/carbs, include Na
Avoid undue stress and
strenuous exercise
Watch for Addisonian Crisis (see
next page)
lOMoARcPSD|22650627
Secondary Adrenal Insufficiency
Decrease in cortisol due to lack of ACTH from pituitary gland
Causes:
S/S:
Similar to Addison's Disease, except:
No dark patches of skin
No dehydration
Na & K levels normal
Corticotropin level is LOW
Treatment: Prednisone or hydrocortisone
Chronic steroid use *Most common
Pituitary tumor
Removal of pituitary gland
Head injury
Addisonian Crisis (Adrenal Crisis)
Extremely low cortisol levels. Life-threatening emergency!
Causes:
Pt has Addison's Dz and:
Not treated properly
Experiencing extreme stress,
accident, injury, surgery, severe
infection
Adrenalectomy
Pituitary gland not producing ACTH
Treatment:
IV Solu-Cortef/IV fluids (D5NS)
**STAT!**
Intervention:
Monitor for:
Infection
Neuro status
Electrolyte status (Na, K, BG)
S/S:
Severe Ab/low back/leg pain
Sudden, extreme weakness
Extremely BP
Dehydration
Severe vomiting/diarrhea
May lead to
Kidney failure
Shock
Loss of consciousness
↓
lOMoARcPSD|22650627
Pheochromocytoma
Tumor in the adrenal medulla that produces excessive amounts of catecholamines
Normally, the adrenal medulla secretes
catecholamines (epinephrine,
norepinephrine, dopamine) in response
to stress. They cause:
HR, BP, BG, BMR
Fat metabolism
Thermogenesis
Feelings of anxiety/fear
However, in pheochromocytoma, the
tumor causes these reactions without
stress.
↑ ↑ ↑ ↑
↑
↑
Diagnosis
24 hr urinary catecholamines &
metanephrines (breakdown products)
Serum catecholamines
MRI/CT to look for tumor
Treatment
Tumor removal or complete
adrenalectomy
Until surgery, ↓ catecholamines
and BP with meds
Meds
Alpha-adrenergic blockers:
Cardura, Minipress, Hyrtin
Beta-adrenergic blockers:
Labetalol or Inderal
Tumors are mostly benign
Usually in one gland
Affect mostly adults (20-40 yrs)
Signs and Symptoms
Severe HTN, ↑ BG
Severe headaches
Tachycardia
Excess sweating
N/V
Back/Ab/chest pain
Tremors in hands
Anxiety/fear
Heat intolerance
Flush face
Intervention
Monitor:
BP, HR, BG
Look for hypertensive crisis:
>180 systolic or >120 diastolic
S/S: Headache, changes in
vision or neuro, seizures, SOB
Chest pain
EKG changes
Meds as ordered
Educate pt:
High cal diet
No stimulants
Hormone therapy post-surgery
lOMoARcPSD|22650627
DI vs SIADH
Diabetes Insipidus vs Syndrome of Inappropriate Antidiuretic Hormone
It's all about
Antidiuretic
Hormone
(ADH)!
ADH
aka
Vasopressin
ADH is produced in hypothalamus and
stored/secreted in pituitary gland.
ADH secreted or withheld due to changes
in hydration status
ADH function: to cause the body to retain
water and constrict blood vessels.
How? By causing the renal tubules to
retain water.
Diabetes Insipidus
SIADH
D = DRY
S = Soaked
Too little ADH
Too much ADH
↓ADH
Cannot retain water
↑urine output
↑Na
Dehydrated
↑ADH
Retains too much water
↓ urine output
↓Na
Overhydrated
lOMoARcPSD|22650627
Diabetes Insipidus
Condition in which the kidneys are unable to retain water.
Types/Causes:
Central DI - Pituitary gland does not secrete ADH - Most common
Damage to hypothalamus or pituitary gland
Brain damage: Head trauma, stroke
Brain tumor
Aneurysm
Certain drugs: Declomycin (tx. for SIADH)
Too little ADH
Nephrogenic DI - Kidneys do not respond to ADH
Hereditary
Acquired
Certain drugs: Lithium, Declomycin
Polycystic Kidney Disease, Sickle Cell Disease
↓ADH
Cannot retain water
↑urine output
↑Na
Dehydrated
Gestational - Rare
Placenta produces vasopressinase which can cause ADH to breakdown
Signs and Symptoms
Polyuria - LOTS of urine - 4-24L/day
Polydipsia - crave water/ice
Dehydrated - dry mucous
membranes/skin; ↓ skin turgor
Urine diluted (↓ spec gravity)
↑ Na - due to ↓ water levels
Hypotension - due to severe dehydration
and vessels dilated
Extreme fatigue
Muscle pain/weakness
Intervention
Strict I/Os, daily wts
Monitor electrolytes (Na, K)
Meds as prescribed
↓ Na diet
Avoid caffeine: tea, coffee,
energy drinks
Diagnosis
Water deprivation test - 12 hours no fluid
Measure urine , electrolytes, wts regularly
Then inject ADH after 12 hrs
If ↓ urination, urine concentrated, BP rises,
HR normal = Central DI
If not = Nephrogenic DI
Treatment
No cure
Give adequate water
↓ Na diet
Meds
Meds
Chlorpropamide (Diabinese)
↑ ADH hormone
May cause ↓ BG, photosensitivity
Desmopression (DDAVP, Stimate)
Nasal spray/tablet/injection/or IV
May cause ↓ Na
Thiazide diuretics
lOMoARcPSD|22650627
SIADH
Condition in which the body makes too much ADH
Causes:
Lung cancer (ADH produced outside the pituitary)
Damage to hypothalamus or pituitary gland
Infection/germs
Pneumonia
CNS disorder - stroke, hemorrhage, trauma
HIV
Certain drugs
Carbamazepine
Chlorpropamide (tx. for DI)
Too much ADH
↑ADH
Retains too much water
↓urine output
↓Na
Overhydrated
Signs and Symptoms
Diagnosis
↑ fluid retention (wt gain)
↓ Na - causes most of outward symptoms
Sluggish, confused
Muscle cramps, fatigue
↑ HR
↓ Urine output; concentrated (↑ spec gravity)
↑ HTN
Seizures (later on)
Intervention
Daily wts/monitor wt gain
Strict I/Os
Restrict fluids
Safety due to confusion
Admin meds per MD order
Blood and urine tests
(Na & K)
Difficult to diagnose - need to rule
out other conditions
Treatment
Treat cause
Restrict fluids
Meds
Meds
IV Hypertonic Saline - slowly
Loop diuretics - monitor K
Demeclocycline or lithium
↓ effect of ADH on kidneys
Conivaptan or tolvaptan
Block ADH receptors and prevent kidneys
from responding to ADH
lOMoARcPSD|22650627
Diabetes Mellitus
Disorder in which the amount of glucose in the blood is elevated.
What happens in diabetes mellitus?
The food we eat is broken down into glucose and absorbed
into our blood.
Simple carbs are broken down fastest, followed by complex
carbs and then protein and fats.
Important!!
Once the glucose is in the blood, the pancreas releases insulin
to move the glucose out of the blood and into our cells.
From the cells, the glucose is either used by the body
immediately or stored in the liver and muscles as glycogen or in
our body as fat (if liver and muscle glycogen stores are full).
In diabetes, the pancreas either doesn't release enough
insulin, doesn't release any at all OR the cells do not respond
to the insulin.
All situations lead to high levels of glucose in the blood
(hyperglycemia).
lOMoARcPSD|22650627
Insulin/Glucagon Feedback Loop
↑→
→
Blood glucose
Pancreas releases INSULIN glucose
enters cells to be used or saved as glycogen or fat Blood
glucose
↓
↓→
↑
→
→
Blood glucose
Pancreas releases GLUCAGON liver
releases stored glycogen (converts to glucose in blood)
Blood glucose
→
Types of Diabetes
Prediabetes
Type I
Type II
Gestational
Prediabetes
Blood glucose levels too high to be considered normal but not high
enough to be labeled Diabetes
Fasting blood glucose levels are 100-125 mg/dL
Decreasing body weight by 5-10% can usually return BG levels back to
normal and decrease risk of developing DB in future
lOMoARcPSD|22650627
Type I Diabetes
Pancreas produces LITTLE TO NO INSULIN because the insulin-producing
cells have been destroyed
Usually diagnosed at a young age
Happens suddenly
Pt MUST take insulin each day for life
Causes: Genetic, auto-immune (virus)
Signs and Symptoms
Pt usually young and thin
Experiencing the 3 Ps:
Polyuria - When BG levels (above 160-180 mg/dL), glucose spills
into urine kidneys will excrete add'l H2O to dilute glucose
Polydipsia - Excess urination will trigger thirst response
Polyphagia - Calories (glucose) will be lost in urine causing hunger
Breath smells of acetone - due to DKA (see Complications section)
Blurred vision
Drowsiness
Nausea
Decrease endurance during exercise
Wounds heal slowly
Rashes
Yeast infections
→
↑
lOMoARcPSD|22650627
Type II Diabetes
Pancreas produces insulin, however, the cells do not respond to it
(Known as Insulin Resistance)
Glucose can't get into cells
Pancreas continues to produce insulin; leads to Hyperinsulinemia
Hyperinsulinemia leads to Metabolic Syndrome
Causes: Obesity, sedentary lifestyle,
Metabolic Syndrome
poor diet (lots of refined carbs), stress,
BP, BG, TG
plus a genetic component
HDL
Pt usually overweight adult
Excess fat around waist
↑ ↑ ↑
↓
Signs and Symptoms
May take years before diagnosed - Symptoms subtle at first
↑ urination
↑ thirst
Fatigue
Blurred vision
Dehydrated
Slow wound healing
Rashes
Yeast infections
Glycosuria
Gestational Diabetes
Similar to Type II Diabetes
Cells not receptive to insulin
May need to take insulin during pregnancy
Must monitor BG levels and diet throughout pregnancy
Goes away after birth
lOMoARcPSD|22650627
Treatment/Intervention of DB
Diet
Exercise
BG
Monitoring
Medication
DB Management Triad
Patients with DB need to monitor their BG throughout the day
Diet, exercise and meds all work together to help maintain proper BG
levels
The nurse's goal is to educate the pt on all 3 parts of the triad: Diet,
Exercise and Meds
Diet
Each diet will vary per pt as each individual's
BG responds differently to different foods
Begin with the Diabetes Plate Method:
1 = Nonstarchy vegetables: Broccoli,
tomatoes, lettuce, etc
2 = Carbohydrate foods: breads, pasta, etc
3 = Lean beef, chicken, eggs, beans, etc
4
1
Nonstarchy
vegetables
2
Water or 0
calorie drink
Carbohydrate
foods
3
Protein
Foods
Exercise
Pt should test BG prior to exercising
If < 100 mg/dL, eat small carb snack before exercise and monitor for
hypoglycemic symptoms while exercising (have simple carb on hand)
If glucose >300 mg/dL wait until glucose before exercising
If exercise for extended pd of time, monitor BG during exercise
Add'l food may be needed as intensity and duration rises
↓
lOMoARcPSD|22650627
Medications
Oral meds may be necessary for Type II pt when diet and exercise aren't
enough to control BG
Biguanides (Metformin) - liver stores of glycogen, body's
sensitivity to insulin; side effects: N/Ab pain/Bloating/Diarrhea
Sulfonylureas (Glyburide, Glipizide, Glimepiride) - helps body secrete
insulin; avoid with ETOH; side effects: hypoglycemia, wt gain
Meglitinides (Repaglinide) - helps body secrete insulin (fast-acting);
side effects: hypoglycemia, wt gain
Thiazolidinediones (Avandia, Actos) - makes tissues more sensitive
to insulin, glucose production in liver; side effects: risk for heart
failure, bladder cancer, bone fractures, chol, wt gain
Alpha-glucoside Inhibitors (Precose, Glyset) - block the breakdown of
starchy foods; take with first bite of each meal; side effects: gas,
diarrhea, stomachache
Instruct pt:
Watch for hypoglycemia with:
Beta blockers; ASA, MAO inhibitors, Bactrim, ETOH
Watch for hyperglycemia with:
Thiazide diuretics, glucocorticoids, estrogen therapy
Type I pt (and some Type II) will need to take insulin daily
↓
↓
↑
↑
↑
Insulin
Important points to remember:
4 types: Rapid-Acting, Short-Acting (Regular), Intermediate-Acting
(NPH), Long-Acting
Regular is the only insulin given IV
If Regular given at same time as NPH, can be in same syringe
If Regular given with long-acting, must be in a different syringe
NPH: If mixed, clear-to-cloudy (Regular is clear; NPH is cloudy)
Long-acting: Do NOT mix
Rotate injection site and do not massage area
lOMoARcPSD|22650627
Rapid-Acting
Aspart
Lispro
Glulisine
Take with meal
Onset: 15 minutes
Peak: 1 hour
Duration: 3 hours
To remember: Ralph Rapidly Ate Lots of Grapes: 15 Red, 1 green, 3 seedless
Short-Acting (aka Regular)
Take 30-40
minutes
before
eating
Onset: 30 minutes
Peak: 2 hour
Duration: 8 hours
To remember: Steelers came up short against the Ravens 30 to (2) 8
Intermediate-Acting (aka NPH)
Covers
insulin
needs for
1/2 day
Onset: 2 hours
Peak: 8 hours
Duration: 16 hours
To remember: In the Night, Paul Had 2 8-oz glasses of water and peed 16 times.
Long-Acting
Detemir
Lantus
Glargine
Onset: 2 hours
Peak: None
Duration: 24 hours
Do NOT mix
Covers
insulin
needs for
FULL day
To remember: During the Long Game: 2 goals, No penalties, 24 min on ice.
No mixups!
Watch for:
Somogyi Effect: Drop in BG in middle of night causes rebound hyperglycemia in
a.m.; treat with bedtime snack of carbs and/or change in bedtime insulin
Dawn Phenomenon: Natural increase in BG right before waking; in DB there is
no insulin to deal with BG leading to hyperglycemia; treat with bedtime insulin
change
lOMoARcPSD|22650627
Complications of Diabetes
Diabetic Ketoacidosis (DKA) - mostly affects Type I
Hyperglycemia (exceeding 300 mg/dL)
No insulin body burns fats for energy produces ketones
(byproduct) excess acid in body acid/base imbalance (metabolic
acidosis)
Kidneys attempt to reabsorb glucose but there is too much glucose
leaks into urine osmotic diuresis polyuria and excretion of
electrolytes (Na, K, Cl) dehydration
Pt usually young; will lead to coma and death if not treated
Causes: Type I diabetics: undiagnosed, not taking appropriate insulin, not
eating, or experiencing sepsis/illness/extreme stress
→
→
→
→
→
→
→
→
Signs and Symptoms
Polyuria/Polydipsia
Dehydration
Wt loss
Fatigue
Fruity smell to breath (ketones)
Tachycardia
↓ HTN
Kussmaul breathing (to correct
the blood's acidity)
Ab pain in kids
Blood ph < 7.35
HCO3 <15 mEq/L
Intervention - Needs tx STAT
↑ hydration, ↓ BG and correct acid-base imbalance.
Goal is to
Treat hydration first:
0.9% NS then progress to
0.45% NS
D5W added to 0.45% NS once
BG 250-300 mg/dL
Treat BG:
IV regular insulin (make sure K
is normal > 3.3)
Monitor BG hourly
Monitor K levels; add K to IV if
needed
Monitor for cerebral edema
lOMoARcPSD|22650627
Hyperosmolar Hyperglycemic State (HHS) - mostly affects Type II
BG extremely high (exceeding 600 mg/dL)
Passing large amounts of urine severe dehydration blood
abnormally concentrated (hyperosmolar)
Differs from DKA in that pt has some insulin, so there is no breakdown of
fats (no ketosis or metabolic acidosis)
Kidneys attempt to reabsorb glucose but there is too much glucose
leaks into urine osmotic diuresis polyuria and excretion of
electrolytes (Na, K, Cl) dehydration
Causes: Type II DB with illness or infection or taking corticosteroids or
diuretics; usually older adults
→
→
→
→
→
→
Signs and Symptoms
Mental change
Main outward symptom
Confusion to drowsiness to
coma
Hyperglycemia: >600 mg/dL
Polyuria
Polydipsia
Dehydration
Fever
Fatigue
Intervention
↑
↓
Goal is to hydration and BG
Hydrating patient will help solve BG problem so focus on that 1st.
Treat hydration first:
0.9% NS then progress to
0.45% NS
D5W added to 0.45% NS once
BG 250-300 mg/dL
Treat BG:
IV regular insulin (make sure K
is normal > 3.3)
Monitor BG hourly
Monitor K levels; add K to IV if
needed
Monitor for cerebral edema
lOMoARcPSD|22650627
Hypoglycemia:
BG < 60 mg/dL or drops rapidly
Signs/Symptoms:
Sweating
Clammy
Confused
Lightheaded
Double vision
Tremors
Treatment:
Simple carbs PO (fruit juice, honey, hard
candy, glucose tablets or gel packs)
IVD50 if unconscious
Other Complications
Atherosclerosis which can lead to:
Angina
Heart failure
Stroke
Diabetic retinopathy
Neuropathy
HTN
Chronic Kidney Disease
Fatty liver disease
Yeast infections
Ulcers/infections of feet/hands
lOMoARcPSD|22650627
The Digestive System
The digestive system consists of the gastrointestinal tract and accessory
organs of digestion. The system is responsible for breaking food down into
nutrients, absorbing nutrients into the bloodstream and eliminating the
indigestible parts of food from the body.
Mouth
Throat
Esophagus
Liver
Stomach
Gallbladder
Pancreas
Small Intestine
Large Intestine
Anus
The gastrointestinal tract
1.
2.
3.
4.
5.
6.
Mouth
Throat and esophagus
Stomach
Small intestine
Large intestine
Rectum and anus
Rectum
Accessory organs of digestion
1. Liver
2. Pancreas
3. Gallbladder
lOMoARcPSD|22650627
Mouth
Throat and Espophagus
Receives food; process of
digestion begins here via
digestive enzymes released by
salivary glands
Throat (AKA Pharynx) is where food goes after it is
swallowed.
Esophagus: channel that connects the throat with the
stomach. Either end has ring-shaped muscles (Upper and
Lower Esophageal Sphincters) to prevent stomach
contents from flowing back into throat or esophagus
Cardia
Body
Antrum
Stomach
3 parts: Cardia, Fundis (body), Antrum
Cardia and body store food, waiting for antrum to
contract. Once contracted, the antrum mixes food with
acid enzymes and grinds it.
3 substances secreted: Mucus, HCl, and
precursor to pepsin (to break down protein)
Duodenum
Jejunum
Ileum
Small Intestine
3 segments: Duodenum, Jejunum, Ileum
Duodenum- receives food from the stomach via pyloric sphincter.
Pancreas sends pancreatic enzymes. Liver and gallbladder send bile.
Jejunum and Ileum- Absorb fat and other nutrients
The entire surface area of the jejunum and ileum and most of the
duodenum are covered in villi and microvilli to aid absorption.
Transverse
Cecum
Only a few substances, such as
alcohol and aspirin, can be
absorbed directly into the
bloodstream from the stomach
Ascending
(rt)
Descending
(lt)
Sigmoid
Rectum
Anus
Appendix
connected
to cecum
(no known fnx)
Absorbs most of
the nutrients of
the food
Large Intestine
Consists of: Cecum & Ascending (rt) colon,
Transverse colon, Descending (lt) colon and
Sigmoid colon
Secretes mucous and is largely responsible for
absorption of water from the stool
Has lots of
bacteria for
digestion,
creating gas
Rectum & Anus
Rectum connects to sigmoid colon. Stays empty until the descending
colon becomes full and passes stool, causing urge to move bowels.
Anus- opening through which stool leaves the body
lOMoARcPSD|22650627
Accessory Organs in Digestion
Liver
- Produces many chemicals.
- Produces cholesterol which is used to make bile and some
hormones
- Produces many proteins, such as those needed to clot
blood and albumin (to maintain pressure in the
bloodstream)
- Stores sugar (as glycogen) to use when needed
- Breaks down harmful substances
Second largest
organ in the
body after skin.
Pancreas
Has 2 types of tissue: Pancreatic acini and Islets of Langerhans
Pancreatic acini cells- Produce the digestive enzymes and secrete them
into the duodenum. Also secrete large amounts of sodium bicarbonate
which neutralizes acid from the stomach.
The Islets of Langerhans- Produce hormones which are secreted into
the blood. The hormones are:
Insulin - Decreases the level of sugar (glucose) in the blood
Glucagon - Raises the level of sugar in the blood (stimulates liver to
release its stores)
Somatostatin - Stops the release of insulin and glucagon
3 Digestive
Enzymes:
Amylase-digests
carbohydrates
Lipase - digests
fats
Trypsin - digests
protein
Gallbladder
The gallbladder holds and releases bile. It is connected to the liver via
biliary tracts (ducts). Bile aids in digestion and eliminating some waste
products.
Gallstones are hard masses made of cholesterol that may form in
gallbladder or bile ducts.
Gallbladder is not
needed and can be
removed if
necessary.
lOMoARcPSD|22650627
Gastroesophageal Reflux Disease
Contents of stomach flow backward from the stomach into the esophagus. The acid and
bile cause inflammation in the esophagus and pain in the bottom of the chest.
Cause
** Occurs when LES (Lower esophageal sphincter) does not
function properly and hold bottom of esophagus closed.
** Esophagus has no lining to protect against acid and bile
LES
Signs and Symptoms
Heartburn
Regurgitation
Sore throat
Hoarseness
Cough
Feeling of lump in throat
Occasional wheezing
Dyspepsia
Dysphagia
Diagnosis
- Usually not necessary Endoscopy with biopsy
pH testing
Meds
PPIs
H2 Blockers
Antacids (watch interaction
w/other meds)
-AKA GERD and
Acid Reflux Disease
VERY COMMON!!
Long-term Complications
Inflammation of the esophagus
(esophagitis)
Ulcers of the esophagus
Narrowing of the esophagus
Abnormal cells that may become cancer
(Barrett's Esophagus)
Risk Factors
Overeating
Overweight
Pregnancy
Increased intake of foods that irritate (i.e.
alcohol, coffee)
Anticholinergetics
Hiatal hernia
Intervention
Meds as prescribed
Raise HOB after eating +/or while sleeping
Refrain from eating 2-3 hrs before bed
Lose wt if needed
Avoid foods that irritate (peppermint,
coffee, alcohol, fatty foods, acidic juices,
cola drinks)
Surgery (fundoplicationAvoid smoking
to wrap part of stomach
Eat small meals
around esophagus)
lOMoARcPSD|22650627
Peptic Ulcer Disease (PUD)
A sore in the lining of the stomach or duodenum caused by stomach acid and digestive juices.
Pathophysiology
3 Types of Peptic Ulcers
Acid penetrates the lining histamine
released parietal cells release more HCl
resulting in a more acidic environment
1. Duodenal - Most common
2. Gastric - usually in lower part of
stomach
3. Esophageal - not as common
→
→
Cause
Long-term Complications
2 main causes:
Bleeding (most common)
Penetration
Perforation (requires immediate
surgery)
Obstruction
Cancer
1. H. pylori infection - spread from consuming
something contaminated with the bacteria
2. Long-term use of NSAIDS prostaglandins
bicarb in stomach
acid in stomach
↓
↑
→↓
→
Signs and Symptoms
Vary with location of ulcer and pt age
Duodenal ulcer:
Gastric ulcer:
Food decreases pain (pain returns
3-4 hours post eating)
Pain at night
Gnawing pain
Normal weight
If severe, black tarry stool from
GI bleed
Risk Factors
Smoking
Alcohol
Stress (psychological)
Food increases pain
Dull/achy pain
Weight loss
If severe, vomiting (bright red and
looks like coffee grounds) from GI
bleed
Diagnosis
Meds
Blood/stool test
Breath test
Upper endoscopy
Antibiotics
PPIs/H2 Blockers
Antacids
Intervention
Meds as prescribed
Diet: Low fiber and avoid: spicy
and acidic foods, caffeine,
chocolate, cola drinks, fried and
fatty foods, alcohol
Surgery may be needed for:
Obstruction that recurs
Perforation
Bleeding ulcers (2 or more)
Cancerous ulcer
lOMoARcPSD|22650627
Inflammatory Bowel Disease (IBD)
Disease where the intestine is inflamed, causing recurring abdominal pain and diarrhea.
2 main types of IBD: Crohn's and Ulcerative Colitis
Inflammatory Bowel Disease is NOT the same as Irritable Bowel Syndrome
(IBS). IBS is a group of symptoms, not a disease. People with IBS do not
experience increased inflammation, hospitalization or increased risk of
cancer as people with IBD experience.
Crohn's Disease
An IBD characterized by inflammation and ulcers in the GI tract. May affect ANY part of
the digestive tract, but most commonly occurs in the last part of the small intestine
(ileum) and the large intestine. Affects the entire bowel wall (through the layers) in a
scattered pattern (not continuous) giving it a cobblestone appearance.
Cause
**Exact cause unknown**
Possibly: Dysfunction of the immune system
causing an overreaction to something in the
environment, diet or an infectious agent. May be
hereditary. Cigarette smoking and oral
contraceptives may increase risk.
5 Types of Crohn's
Ileocolitis: Most common - end
of SI and LI
Ileitis: Only ileum
Gastroduodenal: stomach and
duodenum
Jejunoileitis: Jejunum
Granulomatous (Crohn's
Colitis): Only LI
Patches of
inflammation in
SI and LI from
Crohn's
Diagnosis
Blood & stool tests to check:
Anemia
WBC count
Albumin
C-Reactive protein
CT or MRI of abdomen
Colonoscopy
lOMoARcPSD|22650627
Crohn's Disease
Signs and Symptoms - Pt has flare-ups and remission cycles
Adults:
Crampy ab pain in RLQ
Abdominal bloating
Chronic diarrhea
Fever
Loss of appetite
Children:
Wt loss
Ulcers (mouth & GI tract)
Anal fissures (w/bleeding)
Malnourished
May not show digestive symptoms
Slow growth
Joint inflammation
Fever
Weakness
Fatigue
Complications
Obstruction - due to scarring
Perforation - from ulcers
Abscesses - pockets of infection
Fistulas - due to ulcer or abscess formation
Anal fissures
Colon cancer
Other parts of body:
Gallstones
Urinary tract infections
Kidney stones
Intervention
**No cure**
Meds as prescribed
Educate pt on disease - no cure
Encourage no smoking
May require TPN in severe cases
Monitor I/O and GI symptoms
Surgery
May be necessary w/complications
May end up with ileostomy
Ostomy care
Diet:
Goal is to avoid flare-ups (individual to
each person)
May cause flare-ups:
High fiber foods
Hard to digest foods
Typical allergen foods (i.e. dairy,
wheat)
Preferred diet: Low fiber and high protein
Meds
Anti-inflammatory - Sulfasalazine;
Prednisone
Immuno-suppressors - Azathioprine;
Imuran
Biologic agents - Adalimumab;
Infliximab
Antibiotics - Ciprofloxacin
Probiotics
Anti-diarrheal - take PO before meals
No NSAIDS! Cause flare-ups
lOMoARcPSD|22650627
Ulcerative Colitis
An IBD characterized by inflammation and ulcers in the large intestine and rectum.
Affects the inner lining in a continuous pattern, starting in the rectum.
Cause
Diagnosis
**Exact cause unknown**
Possibly: Overactive immune response to something in
the environment, diet or an infectious agent. May be
hereditary.
Blood & stool tests to check:
Anemia
WBC count
Albumin
C-Reactive protein
Barium enema w/x-ray
Colonoscopy
→
→
Intense inflammation in LI cells die ulcers form,
bleed and create pus LI can no longer absorb water
stool remains watery diarrhea (bloody) flareup cycles cause polyps and scar tissue to form bowel
narrows due to scar tissue LI loses shape and
becomes smooth
→
→
→
→
→
→
Continuous
inflammation in
the LI from
Ulcerative
Colitis
Signs and Symptoms
Symptoms will depend on severity
of flare-up and how much of LI is
affected
Frequent BM
Wt loss
Anemia
Painful abdominal cramps
Rectal bleeding
Severe diarrhea
Fever
Blood/mucus in stool
4 Types of UC
Complications
Bleeding - most common (leads to anemia)
Toxic colitis - (rare, severe)
May lead to toxic megacolon - LI
becomes paralyzed and may rupture
Colon cancer
Peritonitis - leaking intestinal contents into
abdominal cavity
Ulcerative Proctitis: Rectum Mildest
Proctosigmoiditis: Rectum and
Sigmoid colon
Pancolitis: entire colon SEVERE
Left-sided colitis: Descending
colon, sigmoid colon, rectum
lOMoARcPSD|22650627
Ulcerative Colitis
Intervention
**Only cure is surgery**
Meds as prescribed
May be NPO w/IV hydration
Monitor:
Bowel movements
Wts
GI system- sounds, distention
Educate pt on disease - no cure
Surgery
Proctocolectomy - complete removal of
colon and rectum - will end in ileostomy
Ileoanal anastomosis (J-pouch) - colon
and rectum removed - pouch attached to
ileum - no ileostomy needed
Diet:
Goal is to avoid flare-ups (individual to
each person)
May cause flare-ups:
High fiber foods
Hard to digest foods (nuts, seeds)
Typical allergen foods (i.e. dairy,
wheat)
Preferred diet: Low fiber and high protein
Meds
Anti-inflammatory - Sulfasalazine;
Prednisone
Immuno-suppressors - Azathioprine;
Imuran
Biologic agents - Adalimumab;
Infliximab
Antibiotics - Ciprofloxacin
Probiotics
Anti-diarrheal - take PO before meals
No NSAIDS! Cause flare-ups
Differences between Crohn's and UC
Crohn's
Can affect any part of GI tract mouth → anus
Can affect entire thickness of bowel wall
Scattered patches
No cure
Ulcerative Colitis
Only colon and rectum affected
Affects inner-most lining of LI only
Continuous (starts in rectum)
Colectomy is cure
Similarities between Crohn's and UC
Pt has flare-ups and remission
Cause unknown
↑ risk of colon cancer
Prescribed diets similar
Prescribed meds similar
lOMoARcPSD|22650627
Diverticul -osis and -itis
Two types of diverticular disease: a condition where small sacs called diverticula form in
the intestine (usually the wall of the large intestine).
Diverticula are created when the thin inner layer
of the bowel bulges out through a defect in the
middle layer. May be caused by spasms of the
muscular layer of the intestine. Found most
often in the sigmoid colon.
Large Intestine
Diverticulosis: Presence of 1 or more diverticula
Diverticulitis: When diverticula become inflamed
(with or without infection)
Diverticulosis
Cause
**Exact cause unknown**
Possibly: Low-fiber diet, sedentary lifestyle, obesity, smoking,
certain drugs (NSAIDs), constipation/straining during bowel
movements; risk increases with age
Signs and Symptoms
Usually asymptomatic
Sometimes:
Painful cramps
Sudden
constipation/diarrhea
Abdominal bloating
Complications
Diverticulitis
GI Bleed
Bowel obstruction
Fistula
Diagnosis
Colonoscopy
CT scan
Intervention
None if symptom-free
Diet changes if symptoms present:
High-fiber diet (Fruits/vegetables/whole grains)
Adequate fluids for fiber
May need daily fiber supplement (psyllium)
Treat bleeding that does not stop on own
Colonoscopy to coagulate
Angiography
Surgery to remove part of LI (rare)
lOMoARcPSD|22650627
Diverticulitis
Cause
**Exact cause unknown**
Possibly:
Stool stuck in diverticulum infection
Pressure from straining during bowel movement tears the
diverticulum leading to inflammation
→
Signs and Symptoms
Pain/tender (LLQ)
Fever
Nausea/vomiting
Abdominal bloating
Cramps
Constipation
Bloody stool
Risk Factors
Over age 40
Corticosteroid
use
HIV +
Chemotherapy
Diagnosis
Colonoscopy
CT scan
MRI (pregnant or
young)
Complications
Fistula - When inflamed diverticulum touches another
organ
Abscess - Pocket of pus around diverticulum
Peritonitis - Infection of the abdominal cavity, which
develops if wall of diverticulum ruptures
Obstruction - due to inflammation and scarring of tissue
Intervention
Mild case:
Liquid diet, rest
After a few days, ↓ fiber diet, then once
recovered, ↑ fiber diet (same as diverticulosis)
Severe case:
IV fluids/ABx/TPN
Bed rest
NPO
Then clear liquids, then ↓ fiber diet until recovered
and then ↑ fiber diet (same as diverticulosis)
Drain abscess if necessary
Surgery rarely: partial colectomy
lOMoARcPSD|22650627
Celiac Disease
A hereditary autoimmune disorder involving intolerance to gluten. The intolerance causes
damage to the lining of the small intestine, resulting in malabsorption.
Gluten is a protein found in wheat, barley and rye. It is comprised of
gliadin and glutenin. In celiac disease, gliadin is seen as a foreign
invader (like a bacteria or virus) because it cannot be broken down
properly.
Cause
Gluten stimulates the immune system to produce certain
antibodies which damage the lining of the small intestine (mostly
the jejunum). This flattens the villi that line the SI. These villi are
necessary for absorption so malabsorption results.
Normal
VIlli
Signs and Symptoms
Adults:
May or may not have digestive
symptoms
Weak
No appetite
Diarrhea/oily or greasy stool
Mild wt loss
Anemia
Mouth sores/inflamed tongue
Osteoporosis/osteopenia
Dermatitis herpetiformis (rash
with blisters)
Lactose intolerance
-AKA Gluten Enteropathy
Villi are finger-like
projections along the
lining of the SI that aid
in the absorption of
nutrients
Flattened
VIlli
Develops in children OR adults
Children:
Upset stomach
Abdominal bloating
Steatorrhea
Failure to thrive
Weak, pale, listless
Short stature
Anemia
Edema (due to ↓ protein)
Nerve damage ( due to
malabsorption of B12)
Broken bones, tooth discoloration
(due to ↓ calcium absorption)
lOMoARcPSD|22650627
Celiac Disease
Diagnosis
Blood test to
measure
antibodies
Biopsy of SI to
check villi
Intervention
May need test for vit deficiencies
Vit/Min supps such as folate & Fe
If severe in children, may need
IV feeding at first
Strict gluten-free diet for life
Encourage to join Celiac Support
Group
If gluten-free diet does not
cure symptoms, pt may have
refractory celiac disease
which is then treated with
corticosteroids (such as
prednisone)
Celiac Diet
Avoid:
Wheat
Barley
Rye
Malt
Triticale
Beer
Pasta (made from wheat)
Most seasonings
All breads not gluten-free
Many processed foods
Breadings, coatings
Soups, dressings
Look for 'Gluten-free'
on the label!
If it does not have it,
avoid it!
Always check the label
for hidden ingredients
that may contain
gluten.
Encourage:
Choose WHOLE FOODS over
PROCESSED FOODS
Meats
Rice, corn, soy, millet, quinoa,
tapioca, chia, buckwheat
Vegetables and fruits
Nuts, beans, legumes
Dairy (if pt is not lactose
intolerant)
Eggs
Fish/seafood
lOMoARcPSD|22650627
Hepatitis
Inflammation of the liver
Can be either ACUTE: lasting < 6 months or CHRONIC: lasting > 6 months
The Liver
Functions
Makes about 1/2 the body's cholesterol
Cholesterol is used to make bile (aids in digestion)
Cholesterol also used to make many hormones
Makes clotting factors and albumin (to maintain fluid pressure in
the bloodstream)
Stores sugar as glycogen and releases it into bloodstream as
needed
Breaks down harmful substances and secretes them
Metabolizes drugs
Produces immune factor proteins and eliminates bacteria from
blood
Turns ammonia (from breakdown of proteins) into urea via urine
Breaks down RBCs into bilirubin which is excreted via stool
(gives it brown color)
Hepatic
vein
Gallbladder
Causes
of Hepatitis
Virus - A, B, C, D, or E
**Main cause**
Excessive alcohol intake
Nonalcoholic fatty liver
disease
Certain drugs
Liver
Portal
vein
Hepatic
artery
LARGEST ORGAN IN
BODY NEXT TO
SKIN
VERY COMPLEX
AND IMPORTANT!!
MANY
FUNCTIONS
Receives blood via the portal vein (oxygenpoor, rich in nutrients, filtered in liver)
and the hepatic artery (oxygenated blood
from heart). Blood leaves liver via the
hepatic vein.
AKA: Viral Hepatitis
When a virus attacks the
cells of the liver causing
them to malfunction
Most cases of acute
hepatitis are caused
by a virus and
resolve on their own,
but some progress to
chronic
lOMoARcPSD|22650627
Transmitted
Hepatitis A
Via contaminated food or water by the
stool of an infected person
(fecal oral route)
→
Most common cause of acute viral
hepatitis.
Acute infection only!
Signs and Symptoms- for ALL types of Hepatitis
May be asymptomatic at first
Jaundice, itchy skin
Whites of eyes turn yellow
Nausea/vomiting
Stomach pain (URQ)
No appetite
Fever
General ill feeling
Dark urine
Clay-colored stool
Diagnosis
Blood test to check for:
anti-HAV
IgM (active)
IgG (recovered, has
immunity)
When liver does not filter bilirubin out of
blood, it builds up in blood and deposits in
skin (jaundice) and whites of eyes.
Bilirubin is normally secreted in intestine
and excreted in stool. Instead, with
Hepatitis, it is eliminated in the urine.
Hence, pale stool and dark urine.
Pt may be
contagious 2 weeks
before s/s appear
and 1-3 weeks after
they appear
Prevention
Handwashing - especially after
using bathroom, after changing
diaper, and before handling food
Vaccine
Immune globin (IG) if came in
contact with virus (contains
antibodies)
Avoid water supply in developing
countries
Treatment
Rest
Supportive care
Avoid alcohol until
healed
Cholestyramine for
itching
Recovery usually
complete
Vaccines available
for Hepatitis A and
Hepatitis B only!
lOMoARcPSD|22650627
Transmitted
Hepatitis B
Via blood and body fluids
IV drug use (sharing needles)
Reusing needles to apply tattoos
Sexual contact
Birth if mom is Hep B+
Second most common cause of
acute viral hepatitis.
Acute and chronic infections!
Signs and Symptoms
Diagnosis
See s/s for Hepatitis A, plus:
Blood test to check for:
HBsAg (shows infectious)
Anti-HBs (pt recovered and immune)
Joint pain
Itchy red hives on skin (wheals)
~ 5-10% of people with
acute Hep B develop
chronic. The younger
the person the higher
the chance of
developing chronic.
Treatment
Acute:
Rest
Supportive care
Avoid alcohol until
healed
Cholestyramine for
itching
Chronic:
Antiviral meds
Liver transplant if
severe
Chance of developing
chronic after acute:
Infants 90%
Children 1-5 yrs
old 25-50%
Adults 5%
If Hep B becomes
chronic, severe
scarring of liver
(cirrhosis), liver
failure or cancer can
develop.
Prevention
Avoid sharing needles
Avoid multiple sex partners
Pregnant mothers tested
Vaccine
Those exposed but not vaccinated
should receive Hep B immune
globulin
lOMoARcPSD|22650627
Hepatitis C
Transmitted
Via blood and body fluids
IV drug use (sharing needles)
**Most common
Reusing needles to apply tattoos
Sexual contact
Long-term dialysis
Acute and chronic infections!
Signs and Symptoms
Often asymptomatic. If symptoms
present, see s/s for Hepatitis A
Diagnosis
Having the antibody to Hep C
does NOT protect from
getting it again (unlike A & B)
Blood test to check for:
Antibodies to Hep C
75% of people
with acute Hep C
develop chronic
Hep C.
Treatment
Antiviral meds
Avoid alcohol until
healed
Chronic Hep C is
usually MILD but
may develop
cirrhosis or liver
cancer over time.
There is no
vaccine for
Hep C!
Prevention
Avoid sharing needles
Avoid multiple sex partners
Blood and organ donor screening
lOMoARcPSD|22650627
Transmitted
Hepatitis D
Via blood and body fluids
IV drug use (sharing needles)
Reusing needles to apply tattoos
Sexual contact
Signs and Symptoms
See s/s for Hepatitis A.
Makes current symptoms of
Hepatitis B more severe!
Only affects a person who already has
Hepatitis B! Hepatitis D is an
incomplete virus and needs Hepatitis
B to reproduce.
Prevention
Treatment
Diagnosis
Avoid sharing needles
Avoid multiple sex partners
Vaccine for Hep B (no vaccine for
Hep D or post-exposure IG)
Antiviral meds
Interferon alfa
Avoid alcohol until
healed
Blood test to check for:
HDAg
anti-HDV
Transmitted
Acute and chronic infections!
Very rare in the U. S.
Hepatitis E
Via contaminated food or water by the
stool of an infected person
(fecal oral route)
→
Signs and Symptoms
Almost all acute infections.
Chronic infections rarely with
immunosuppressed people.
Can cause severe symptoms,
especially in pregnant women.
See s/s for Hepatitis A.
Diagnosis
Blood test to check for:
anti-HEV
Treatment
Rest
Supportive care
No alcohol until healed
Ribavirin for chronic
Prevention
Handwashing - especially after
using bathroom, after changing
diaper, and before handling food
No vaccine in the U. S.
lOMoARcPSD|22650627
Cirrhosis
Disease of the liver where healthy liver tissue is replaced with scar tissue due to repeated
or continuous damage. The damage and scar tissue are permanent.
The liver consists of 2 main lobes.
Within these lobes are thousands of
lobules. Within the lobules are
hepatocytes and Kupffer cells.
Hepatocytes- make up 80% of
liver's mass and do most of the
metabolic, endocrine and secretory
functions
Kupffer cells- macrophages that
remove bacteria, debris, parasites
and old RBCs
The liver receives blood via the
portal vein (oxygen-poor, rich in
nutrients, filtered in liver) and the
hepatic artery (oxygenated blood
from heart). Blood leaves liver via
the hepatic vein.
Hepatic
vein
Gallbladder
Liver
Portal
vein
Hepatic
artery
The liver performs many important
functions in the body. In cirrhosis, the
liver is not able to perform these
functions and the whole body suffers.
Healthy Liver
Cirrhosis Liver
Causes of Cirrhosis
Chronic alcohol use (one of most
common)
Chronic Hep C or B (one of most
common)
Fatty liver (nonalcoholic): obesity,
diabetes, hyperlipidemia
Any disorder, drug or toxin that
causes fibrosis (e.g. autoimmune)
Bile duct problems: bile remains in
liver and damages cells
lOMoARcPSD|22650627
Cirrhosis
Signs and Symptoms
None at first
1/3 never develop symptoms
Tired
↓ appetite
↓ wt
Fingertips enlarged (clubbing)
Jaundice, itchy skin
Stools affected:
Light color, soft, bulky
Oily, steatorrhea (bad odor)
Hepatic foeter - pungent, sweet,
musty smell to breath (buildup of
toxins)
Impaired Liver Function
Detoxification (break down and
secretion of harmful substances):
RBC breakdown into bilirubin to
excrete in stool:
Makes cholesterol (used to make
bile to aid digestion):
Muscle wasting
Asterixis (hand tremors)
Due to ↑ estrogen in blood:
Enlarged breasts in men
Red palms
Spider angiomas
Renal failure
Ascites
Confusion
Splenomegaly
↓ platelets, ↓ WBCs
Edema - legs
Varices
Complication
Toxins accumulate in bloodstream, side
effects of meds , alcohol not excreted as
well, estrogen not metabolized
↑
Leaks into blood then skin/eyes- Jaundice
↓ fat absorption and digestion is affected
Turns ammonia (from
breakdown of protein) into urea
excreted via urine:
Neuro changes, asterixis, hepatic
encephalopathy
Stores excess sugar as glycogen
and releases as BG level :
Blood glucose levels may be high as excess
is not turned to glycogen OR blood glucose
levels may be low as liver not able to
release stored glycogen as needed.
Produces blood clotting
factors and albumin:
Fluid pressure interrupted, clotting
problems
↓
lOMoARcPSD|22650627
Cirrhosis
Complications
Portal Hypertension - Portal vein narrows due to scar tissue → ↓
blood flow to liver → ↑ pressure in portal vein
Most serious complication
Leads to enlarged spleen (splenomegaly)
Spleen cannot release platelets and WBCs → ↓ platelet and
WBC count
Leads to esophageal/gastric/rectal varices
Increase pressure in veins may rupture and may be lifethreatening due to ↓ platelets, ↓ clotting factors, ↓ vit K
Ascites - fluid in abdomen - due to portal HTN plus ↓ albumin levels
This fluid may become infected (spontaneous bacterial
peritonitis)
Jaundice (↑ bilirubin)
Poor absorption of fats/vits
Lead to osteoporosis (vit D), ↑ bleeding (vit K)
Bleeding problemsToo much bleeding (↓ vit K, ↓ platelets)
↑ risk of infection (↓ WBCs)
Hepatic encephalopathy- brain function deteriorates
↑ ammonia and toxins
Kidney failure - Hepatorenal syndrome
↓ urine produced → ↑ toxins in blood
May require dialysis
Liver cancer
Diagnosis
Blood tests: albumin, PLT, PT/INR,
Hep B or C, bilirubin
Liver biopsy
lOMoARcPSD|22650627
Cirrhosis
Treatment
No cure
Treat cause
Stopping alcohol use, drugs, etc
Hepatitis - give antivirals
Transplant
Treat complications:
↓ fluids/diuretics
Vit supps
Beta blockers (to ↓ BP in liver's blood vessels)
Shunting surgery - blood rerouted to bypass liver
Alleviates ascites
Vit K (help with clotting)
Lactulose (↓ ammonia level)
Paracentesis (remove fluid from abdomen)
Intervention
Monitor:
Bleeding (PT/INR)
Vomiting/coughing blood (for esophageal varices)
Mental status - irritable, confused, asterixis
BG levels
I/Os, daily wt, swelling, ascites
Diet:
If neuro problems → ↓ protein
If not, ↑ lean protein (no raw seafood - bacteria)
No ETOH
Restrict fluids
Vits/lactulose per MD orders
lOMoARcPSD|22650627
Pancreatitis
Inflammation of the pancreas that occurs when the pancreatic digestive enzymes start
digesting the pancreas itself. Can be either ACUTE: lasts up to a few weeks or CHRONIC:
persists and destroys pancreatic function
Pancreas
Leaf-shaped organ located behind the lower part of the stomach and duodenum. Has 2 types
of tissue: Pancreatic acini and Islets of Langerhans
Pancreatic acini cells- Produce the digestive enzymes and secrete them into the duodenum
where they are activated. Also secrete large amounts of sodium bicarbonate which
neutralizes acid from the stomach.
The Islets of Langerhans- Produce hormones which are secreted into the blood. The
hormones are:
Insulin - Decreases the level of sugar (glucose) in the blood
Glucagon - Raises the level of sugar in the blood (stimulates liver to
release its stores)
Somatostatin - Stops the release of insulin and glucagon
3 Digestive Enzymes:
Amylase-digests
carbohydrates
Lipase - digests fats
Trypsin - digests protein
**Enzymes not activated until
they reach the duodenum**
Bile sent to pancreas from
gallbladder to increase absorption
of fats
Stomach
Liver
Gallbladder
Sphincter
of Oddi
Duodenum
Pancreatic
duct
Pancreas
lOMoARcPSD|22650627
Acute Pancreatitis
The digestive enzymes inside the pancreas are activated and the pancreas begins to
digest itself. Can be reversed with prompt proper treatment.
Causes
Gallstones (stones stuck in common
bile duct - enzymes collect and begin
to digest cells) - 40% of cases
Alcohol use (damaged cells produce
thick fluid that clog ducts)- 30% of
cases
Hereditary
Some medications
Viruses
Tumor
Diagnosis
Blood tests - amylase, lipase, WBC,
BUN (all ↑)
Imaging - x-ray, CT, ultrasound
Urine test - trypsinogen (↑)
Endoscopic Retrograde CholangioPancreatography (ERCP)- uses
scope to assess; can also remove
gallstones
Signs and Symptoms
Severe upper ab pain (felt in back)
Quick onset- gallstones
Slow onset- alcohol
Sitting up and moving forward
makes the pain recede
N/V, dry heaving
Hyperglycemia
↓ BP
Fever
Swelling upper abdomen
Sweaty
↑ HR
Shallow, rapid breathing
↑ amylase/lipase
Severe case: (due to
retroperitoneal bleeding)
Cullen's Sign - bluish skin
around belly button
Greg-Turner's Sign - bluish
skin around flanks
Complications
Pancreatic pseudocyst: Collection of fluid that forms in and around the pancreas may become infected
Necrotizing pancreatitis: Severe - parts of pancreas die and fluid leaks into
abdominal cavity → ↓ blood volume → ↓ BP → shock/organ failure
Organ failure: activated enzymes and toxins enter bloodstream → ↓ BP and damage
to organs such as lungs and kidneys
lOMoARcPSD|22650627
Intervention - Tx depends on severity
IV fluids
NPO, then liquids, then ↓ fat, soft diet
May need tube feed or TPN
Monitor:
BG for hyperglycemia
WBC, BUN
Stools
Daily wts, I/Os
Pain meds - NO morphine - will cause
spasm of Sphincter of Oddi
No supine position
PPIs, H2 blockers, antacids (to ↓ acid
secretion)
Pancreatic enzymes - give b4 meals
with acidic foods
Abx (for any infection)
Pseudocyst - drained via endoscope
NG tube - remove fluid and air
Chronic Pancreatitis
Chronic inflammation that has led to
irreversible damage.
Causes
Heavy alcohol use
(50% cases in U.S.)
Smoking
Cystic fibrosis
Hereditary
Autoimmune
Tumor
Diagnosis
Imaging - CT, x-ray, ERCP
Blood tests - amylase, lipase, BG
(all ↑)
Complications
Pancreatic pseudocyst
Diabetes
Pancreatic cancer
Signs and Symptoms
Severe upper ab pain (until late, then stops)
Worse after greasy, fatty meals & ETOH
Lessens sitting upright or leaning forward
Pancreatic insufficiency - ↓ amt of dig enz in
pancreatic fluid → malabsorption →
steatorrhea, light colored, oily stool
Wt loss
Possible mass in abdomen due to pseudocyst
Jaundice - due to damaged bile duct
Dark urine
Signs of diabetes b/c Islet of Langerhans not
working (regulating BG)
Intervention
No ETOH
No smoking
Pain control:
4 or 5 small meals; ↓ fat
Opioids w/antidepressants, SSRIs
Corticosteroids for autoimmune
ERCP - drain duct
Pancreatic enzymes w/meals
H2 blockers, PPIs
Fat supps - A, D, E, K
Manage DB
lOMoARcPSD|22650627
Cholecystitis
Inflammation of the gallbladder usually caused by a gallstone blocking the cystic duct. can
be ACUTE: high intensity, rapid onset or CHRONIC: lower intensity, lasting long time
Gallbladder
Small, pear-shaped storage sac located under the liver that holds bile and is connected to the
liver by ducts. Secretes bile post-meal into duodenum.
Bile: greenish, yellow/brown thick sticky fluid (created by liver). Composed of bile salts,
electrolytes, bile pigments (specifically bilirubin), cholesterol and other fats. Two main
functions:
Aid in digestion of fats - If gallbladder not working we can't digest fats and they exit the
body via stool (steatorrhea/light color)
Eliminate certain waste products - excess cholesterol and Hg (breaks down into bilirubin)
- If gallbladder not working the bilirubin builds up in blood and leaks into skin and eyes
(yellow) and urine (dark)
Bile flows out of liver via
hepatic ducts which connect
with cystic duct to form
common bile duct. From there
it enters SI at the Sphincter of
Oddi.
Gallbladder not necessary for
body to function. If removed, the
bile will move directly from liver
to SI.
Right Hepatic
Duct
Gallbladder
Cystic
Duct
Duodenum
Liver
Left Hepatic
Duct
Stomach
Common Bile
Duct
Sphincter of
Oddi
Gallstones: Hard masses made of cholesterol. May form in gallbladder or bile ducts.
Usually no symptoms unless they block bile flow out of gallbladder.
Cause not completely known.
lOMoARcPSD|22650627
Acute and Chronic Cholecystitis
Cause
ACUTE: Almost always gallstones
blocking the cystic duct. Bile then
becomes trapped in the gallbladder
causing irritation and pressure that
leads to inflammation.
CHRONIC: Gallstones and
prior attacks of acute. Gallbladder
may become thick-walled, scarred
and small.
Acute Acalculous
Rare form of acute cholecystitis
without gallstones. VERY serious.
Bile becomes very thick, gallbladder
not contracting. Occurs in very ill
patients (usually already in
hospital): Mech. vent, sepsis, severe
burns or trauma, prolonged TPN.
May be overlooked: Look for fever
and swollen, tender abdomen.
Risk Factors
Women
Obese
> 60 yrs
Pregnant
Estrogen replacement
therapy
Birth control
Large wt loss
↑ fat diet
Complications
Abscess
Perforation
Pancreatitis
Diagnosis
Ultrasound
CT
HIDA scan
Signs and Symptoms
Severe upper ab pain radiating to right
shoulder blade (Chronic less severe)
Peaks after 15-60 minutes and remains
constant
Breathing deeply worsens pain
(+ Murphy's sign)
N/V
Fever (Chronic no fever)
Chills
Elderly - no appetite, tired, weak, vomiting
Jaundice
Steatorrhea, dark urine, light stools
Intervention - Hospitalization for both acute and chronic
NPO, recover → clear liquids, adv as tol per
MD order
IV fluids/electrolytes/ABx
GI suction
Analgesics / antremics
ERCP to remove gallstones
If not candidate for surgery Cholecystostomy - C-tube to remove bile
Maintain at waist level
Record drainage; monitor color
Flush per MD order only
Most will need surgery (Cholecystectomy)Bile will then drain from liver via bile duct
into duodenum
Laparoscopic procedure
Monitor for infection
Ambulate post-procedure
Encourage deep breathing
T-tube (drains excessive bile)
Keep upright in Semi-Fowler's
position; monitor drainage
MD order to flush and clamp (to allow
bile into SI)
lOMoARcPSD|22650627
Appendicitis
Inflammation of the appendix
Appendix
Finger-shaped tube connected to the large intestine at the end of the ascending colon
Not an essential organ. May play a role in immune function or maintaining healthy flora in
the GI tract
Over 5% of population in U.S. develops appendicitis at some point in their lives (usually in
adolescence or 20s)
In women, appendicitis may cause ovaries and fallopian tubes to become infected which
could cause scarring and infertility
Cause
Not 100% known. Most likely:
Blockage/obstruction
From hard, small piece of
stool (fecalith)
Foreign body
Worms (rare)
Swollen lymph nodes
Trauma
Diagnosis
Imaging test:
CT
Ultrasound
Laparoscopy
Blood test
↑ WBCs
Treatment is surgery!
Open or laparoscopic.
Transverse
Ascending
(rt)
Cecum
Descending
(lt)
Sigmoid
Rectum
Anus
Appendix
Pathophysiology
Blockage causes:
Build up of mucous, fluids,
bacteria
Increased pressure
Venous obstruction
Occlusion of blood flow
Stagnant blood coagulation
Clot formation
Ischemia
Break down of walls
Leak contents into ab. cavity
Abscess and peritonitis
→
→
→
→
→
→
→
→
→
lOMoARcPSD|22650627
Signs and Symptoms
Pain upper abdomen around navel
N/V
Pain moves after ~1-2 hours to rt lower
part of abdomen
Worst pain at McBurney's point
Rebound tenderness: press and release →
pain WORSE
Fever
Fetal position feels best
Constipation or diarrhea
Some pt: pain widespread, less severe and
less tender
Watch for:
**Pain lessening for several hours**
Appendix may have burst!
Peritonitis will occur and then pain
and fever severe: may lead to shock
Without surgery or abx: >50% pt with
appendicitis will die
If rupture repeated operations may be
necessary and long recovery
Can rupture 36 hrs after onset of symptoms
→
Intervention
Pre-OP
NPO
Monitor vitals
Watch for:
Signs of rupture
Pain lessens for several hrs, then
intense pain and fever
Signs of peritonitis
↑ HR, resp, temp, pain
Pain relief
Avoid: heat, enemas, laxatives (↑ risk of
rupture)
Post-OP
Monitor:
Vitals
Incision site for infection
Bowel sounds
Maintain drain if have one
Keep pt on right side
Ambulate
Encourage coughing/deep breathing
IV abx/pain relief per MD order
NG tube (NPO until removed)
Diet: clears → full liquid → solids as tol
lOMoARcPSD|22650627
Hematologic Disorders
Components of Blood
Plasma
White Blood Cells
Liquid component of blood
Where RBCs, WBCs and platelets are
suspended
AKA leukocytes
Fewer than RBCs
Defend against infection
When low called leukopenia
Infections more likely
When high called leukocytosis
May indicate underlying
disorder
Red Blood Cells
AKA erythrocytes
40% of blood volume
Contain hemoglobin
Gives blood red color
Helps to carry oxygen to tissues
Carry C02 from tissues to lungs
When low called anemia
Low oxygen → fatigue
When high called erythrocytosis
Blood thickens
Clot risk increases
↑ risk of stroke and MI
Normal Lab Values
WBC: 4,500-11,000
RBCs: 4.5-5.5
PLT: 150,000-450,000
Hgb:
Female: 12-16 g/dL
Male: 13-18 g/dL
Hct:
Female: 36-48%
Male: 39-54%
PT: 10-13 seconds
PTT: 25-35 seconds
aPTT: 30-40 seconds
INR:
NOT on warfarin:
<1 sec
ON warfarin: 2-3 sec
MCV: 80-100 fL
Platelets
AKA thrombocytes
Help in clotting process
When low called thrombocytopenia
Bruising and abnormal bleeding
When high called thrombocythemia
Blood clotting may cause
transient ischemic attack
Thrombocytopenia
Pathology:
Causes:
Signs:
PLT <150,000
↓ platelets → ↓ clotting → bruising and
abnormal bleeding
Anemia
Leukemia
Platelet disorders
Enlarged spleen
Prolonged bleeding time
Petechiae on lower legs
Purpura (bruising)
Bleeding gums
Blood in stool/urine
Heavy menstrual cycles
↑ INR, ↑ PT/PTT
Toxins
Cirrhosis
Infections
RBC transfusions
Treatment:
Treat cause
No aspirin
Avoid injury
Use electric razors
Possible:
Platelet transfusion
BMT
lOMoARcPSD|22650627
Anemia
Condition is which the number of RBCs is
low. Blood cannot get enough oxygen!
Iron-Deficiency Anemia
Diagnosis:
Pathology:
Low or depleted
iron stores
(needed to
produce RBCs)
Most
Common
Anemia
Blood test: ↓ Fe,
↓ Hct, ↓ Hgb
Treatment:
Stop bleeding
Iron supplements
Causes:
Usually PO, large
Excessive bleeding
amounts by IV
(GI tract, menstrual)
Side effects: stool
Inadequate dietary
dark, constipation
intake
Take 30 min b4
Decreased Fe absorption breakfast with Vit C
Iron-rich foods:
Signs:
Weak
Shortness of breath
Pale
Fatigue
Pica
Egg yolks
Spinach
Red meat
Beans
Seafood
Raisins/apricots
Aplastic Anemia
Pathology:
Damage to bone
marrow cells
causes bone
marrow failure
Causes:
Autoimmune
Infection
Toxins
Chemo tx
Pregnancy
Hepatitis
Diagnosis:
Signs:
Fatigue
Weakness
Paleness
Treatment:
Stem cell transplant
Transfusion
Meds to help
regenerate bone
marrow
Blood test (↓RBCs,
↓WBCs, ↓PLT)
Bone marrow exam
Vitamin B12 Deficiency Anemia
Pathology:
Signs:
↓ levels of B12
Weak, pale
SOB
Nerve malfunction
Tingling
Loss of sensation
Muscle weakness
Causes:
Gastric Bypass
PPI use
Alcohol
Low dietary intake
(esp. vegans)
Diagnosis:
Blood test:
↓ B12,
MCV>100
Treatment:
B12 injection/nose spray/tablet
High-B12 foods (eggs, chicken,
red meat, milk)
Folate Deficiency Anemia
Pathology:
↓ levels of folate
Signs:
Pale
SOB
Dizzy
Irritable
Weight loss
Causes:
Alcoholism
Malabsorption
Chrohn's/Celiac
Pregnancy
Diagnosis:
Blood test:
↓ folate,
MCV>100
Treatment:
Folate tablet PO
High-folate foods
(oranges, peanuts, lentils,
leafy greens)
Sickle Cell Disease
Pathology:
Inherited genetic abnormality of
Hgb → sickle-shaped RBCs
Signs:
Chronic anemia
Jaundice
Fatigue/weakness
Diagnosis:
Pain on exertion
Blood testelectrophoresis
Treatment:
Stem cell transplant
Oxygen therapy
lOMoARcPSD|22650627
Musculoskeletal System
Purpose: To protect body organs, provide support and stability for the
body and allow coordinated movement
Key Definitions
Bone
Function: support, protect internal organs,
voluntary movement, blood cell production and
mineral storage
Classified as cortical (compact and dense) or
cancellous (spongy)
Bone Cells
Osteoblasts - synthesize collagen; the basic boneforming cells
Osteocytes - mature bone cells
Osteoclasts - assist in the breakdown of bone
tissue
Joints
Place where the ends of 2 bones are in proximity
and move in relation to each other
Muscle
3 types:
Cardiac - involuntary; in heart only
Smooth - involuntary; found in airways,
arteries, GI tract, urinary bladder, uterus
Skeletal - voluntary; half of body's weight,
requires neuronal stimulation to contract
Contractions:
Isometric - Increased tension within muscle
but no movement
Isotonic - Shortens muscle and produces
movement
Flexion: bending a joint
Extension - straightening a joint
Fascia
Layers of connective tissue that surround muscles,
nerves, blood vessels, organs and holds them in
place
Bone
Ligament
Muscle
Cartilage
Bursa
Tendon
Bone
Cartilage
Flexible tissue that is the main connective tissue
in body
3 types:
Hyaline - most common; contains mostly
collagen fibers
Elastic - more flexible; contains collagen and
elastic fibers
Fibrous - tough, shock absorber; contains
mostly collagen fibers
Ligaments
Dense connective tissue connecting bones to
bones
Tendons
Dense connective tissue connecting muscles to
bones
Bursae
Small sacs of connective tissue filled with synovial
fluid; located in joints to decrease pressure &
friction
lOMoARcPSD|22650627
Musculoskeletal Assessment
Muscle Strength Scale
Assess
Range of motion
Goniometer - measures ROM of joint
Muscle strength
Look for normal spinal curvatures
Asymmetry
Joint swelling / tenderness
Look for abnormalities
Atrophy - size/strength of muscle
Ankylosis - Stiffness and fixation of joint
Kyphosis - exaggerated thoracic curvature
Swayback - exaggerated lumbar curvature
Scoliosis - asymmetric elevation of shoulders
0 = No muscle contraction
1 = A barely detectable contraction
2 = Active movement of body part without gravity
3 = Active movement of body part against gravity
4 = Active movement of body part against gravity
and some resistance
5 = Active movement of body part against full
resistance without evident fatigue
↓
Older Adults
Inquire about exercise practices; type and
frequency
Determine age-related changes of
musculoskeletal system on functional status (ADL,
etc)
risk of falls due to muscle mass and
strength and changes in patient's balance
Bone resorption increases and bone formation
decreases with age which leads to osteopenia and
osteoporosis
30% of muscle mass lost by age 70
Tendons and ligaments less flexible with leads to
rigid movement
Joints often have osteoarthritis
↑
Older Adults - instruct
Use ramps in buildings and at street corners
instead of steps
Eliminate scatter rugs at home
Use a walker or cane
Avoid excessive weight gain
Get regular and frequent exercise
Use shoes with good support
Avoid walking on uneven ground and wet floors
Avoid sudden change in position to prevent
dizziness, falls, etc
↓
R est →
I ce →
C ompression →
E levation →
To prevent further injury
To reduce inflammation and pain
To prevent edema and encourage
fluid return
To mobilize excess fluid and prevent
further edema
lOMoARcPSD|22650627
Musculoskeletal Trauma
Soft tissue injury - damage to any skin, muscle, tendon or ligament
Sprains and Strains
Sprain - an injury to ligaments surrounding a
joint usually caused by wrenching or twisting
motion in ankle, wrist or knee joint
Strain - excessive stretching of a muscle, its
facial sheath or a tendon
S/S of strain or sprain: pain, edema, fnx in
injured area, contusion; usually occur during
vigorous activities
Tx: RICE to local inflammation & pain; ice &
elevate 24-48 hrs post injury; full function
returns in 3-6 weeks
↓
↓
Repetitive Strain Injury
Injuries resulting from prolonged force or
repetitive movements and awkward postures
Tendons, ligaments and muscles are strained
causing tiny tears that become inflamed
At risk: musicians, dancers, those who use
mouse/keyboard often, competitive athletes
S/S: pain, weakness, numbness
Tx: stop activity causing RSI, heat/cold, NSAIDs,
rest, PT
Rotator Cuff Injury
Rotator cuff = 4 muscles in the shoulder
May be gradual, degenerative process or from
injury while falling
Often due to repetitive motions
S/S: shoulder weakness, pain and ROM;
positive drop arm test
Tx: rest, ice and heat, NSAIDS, corticosteroids,
PT, surgery
↓
Anterior Cruciate Ligament (ACL) Injury
Most commonly injured knee ligament
Usually occurs in athletes while pivoting or
landing from jump
S/S: hear 'pop,' then pain, swelling, knee
unstable
Tx: rest, ice, NSAIDs, elevate, crutches, knee
brace, PT, surgery; full recovery 6-8 months
Dislocation
Complete displacement of the joint
Results from severe injury of the ligaments
surrounding the joint
Usually in thumb, elbow, shoulder, hip, kneecap
Subluxation - partial displacement of the joint
S/S - deformity, local pain, tenderness, loss of
fnx of injured area, swelling near joint
Tx: requires prompt attention; orthopedic
emergency b/c may include vascular injury;
realignment 1st action, then immobilize to allow
to heal
Carpal Tunnel Syndrome
Caused by compression of the median nerve in
the wrist
May be caused by hormones - often occurs
during PMS, pregnancy, menopause
At risk: those with DB, PVD, rheum arthritis
S/S: weakness, pain, numbness, impaired
sensation in thumb, index and middle fingers
Tx: stop repetitive motions, fix ergonomics,
splint, PT, corticosteroids, surgery
Meniscus Injury
Menisci - cartilage in the knee, AC and other
joints
Usually caused by rotational stress when knee is
in flexion and foot is planted or fixed
At risk: athletes (basketball, football, soccer)
S/S: pain upon flexion, unstable, 'pops' in knee
Tx: ice, immobility, crutches, PT, surgery;
instruct importance of warming up b4 exercise
Bursitis
Inflammation of the bursa from repeated or
excessive trauma/ friction, or from gout,
rheumatoid arthritis or infection
Affects hands, elbows, shoulders, knees, hip
S/S: warmth, pain, swelling, limited ROM in
affected part
Tx: rest, splint, ice, NSAIDs, corticosteroids
lOMoARcPSD|22650627
Fracture
A break or crack in a bone caused by traumatic injury or disease such as cancer
or osteoporosis
Classifications
Open (Compound) or Closed (Simple)
Open - Skin broken, bone exposed, soft tissue injury
Closed - Skin remains intact
Complete or Incomplete
Complete - Break goes completely through the bone
Incomplete - fracture goes partly across bone shaft
Displaced or Nondisplaced
Displaced - 2 ends of broken bone separated and out
of alignment
Comminuted - 3 or more fragments
Oblique - fractured at a slant
Nondisplaced - bone fragments aligned
Transverse - fracture straight across bone
Spiral - fracture in spiral direction down bone
Greenstick - one side of bone bent, other side
splintered; incomplete; common in pediatrics
Oblique
Comminuted
Transverse
Spiral
Greenstick
Types of Fractures
Colles' fracture - in distal radius (forearm); most common; > 50 years old; risk w/osteoporosis
Humeral shaft - shaft of humerus (long bone in arm); common among young and middle-aged
Pelvic fracture - small percentage; associated with mortality rate
Hip - common in older adults; > 95% resulting from fall
Stable vertebral fracture - car crashes, falls; fragments unlikely to cause spinal cord damage
↑
Signs and Symptoms
Immediate, localized pain, tenderness
function in affected part
Unable to bear weight on affected part
Edema and swelling
↓
Deformity (abnormal position)
Contusion/bruising
Crepitation - grating or crunching of bone
fragments; audible sounds
lOMoARcPSD|22650627
Treatment
Goal:
Realign bone fragments (via closed or
open reduction)
Immobilize to maintain realignment
Restoration of normal function
Closed reduction
Nonsurgical, manual realignment
Under local or general anesthesia
Traction, cast, splint, or brace used after
Open reduction
Correction of alignment through surgery
Wires, screws, pins, plates internal or
external
Traction, cast, splint, or brace used after
Facilitates early ambulation
Traction
Aligns the bone with a constant steady
pulling action
Electrical Bone Growth Stimulation
To facilitate the healing process
Increases Ca uptake of bone, activates
intracellular Ca stores, increases
production of bone growth factors
Electrodes in band applied to skin 10-12
hrs/day (sleeping)
Meds
Muscle relaxants - Soma, Robaxin
Tetanus shot if open fracture
Bone-penetrating Abx (Kefzol)
Nutrition
Protein 1g/kg BW
Vits B, C, D; Ca, Ph, Mg
Intervention
Immediately after injury - immobilize
w/splint
Apply pressure w/sterile dressing if open
Elevate extremity
Apply ice to swelling
NPO until evaluated by surgeon
X-ray
Pain meds - monitor to see if pain relieved
Monitor for:
Compartment syndrome (see next page)
Fat embolism (see next page)
Asses 6 Ps (see next page)
Prep for surgery if needed
Post op:
Monitor vitals and Assess 6 Ps
Watch dressing for bleeding or excessive
drainage
↓
Traction Wts need to hang freely (not on floor)
Monitor pin sites for infection
Encourage pt to participate in ROM
activities (as allowed)
Casts
Keep elevated above heart level
1st 2 days ice packs
Monitor for hot spots, pain, foul odor,
swelling, 6 Ps
Monitor skin integrity - use moleskin
around top edge of cast
Keep dry!
lOMoARcPSD|22650627
Complications of Fractures
Infection Open fractures and soft tissue injuries have incidence of infection
May require aggressive surgical debridement
May have IV Abx 3-7 days post op phase
Compartment syndrome Swelling causes pressure within muscle compartment
Fascia surrounding muscle has limited ability to stretch
Continued swelling decreases function of blood vessels and nerves and decreases blood
flow to muscle
2 causes:
Decreased compartment size from restrictive dressings, splints, casts, traction
Increased compartment contents from bleeding, inflammation, edema
Usually associated with:
Trauma, large bone fractures, extensive tissue damage and crush injury
MUST be treated within 6 hours or nerve damage will result!
S/S: Look for the 6 Ps:
Pain - out of proportion to injury and not managed with meds -- early sign!
Paresthesia - numbness/tingling -- early sign!
Poikilothermia - affected limb cooler than non-affected limb
Pallor - coolness, loss of normal color in distal extremity
Paralysis - loss of function in extremity; late sign
Pulselessness - decreased or absent peripheral pulse; late sign
Intervention:
Regular neuro assessments on all patients with fractures
Notify HCP of pain and paresthesia as these are the 1st signs!
Keep extremity at heart level and NOT below
Monitor UO: look for dark reddish-brown color, may be from damaged muscles
Fat Embolism Syndrome Systemic fat globules from fractures travel to tissues, lungs and other organs after a
traumatic skeletal injury
Usually seen with long bone, rib, tibia, pelvis fractures
Need to recognize early on!
Usually occurs 24-48 hours post injury
S/S: chest pain, tachypnea, cyanosis, dyspnea, tachycardia, PaO2, changes in mental
status, restlessness, confusion, petechiae
Tx: fluid resuscitation, correct acidosis, blood transfusion
Intervention: Encourage coughs/deep breathing, O2 for hypoxia
↑
↑
↓
lOMoARcPSD|22650627
Osteoarthritis
Progressive joint disorder that develops due to the deterioration of
articular cartilage.
AKA Degenerative Arthritis and Degenerative Joint Disease
*Most common type of arthritis*
Pathophysiology
Articular cartilage (hyaline cartilage found in synovial
joints) begins to deteriorate due to tissue damage
Normally soft, smooth, white cartilage becomes less
elastic, dull, yellow and granular
Joint space decreases bones begin to grate against
each other bone erosion follows along with
osteophyte (bone spur) formation
Pieces of cartilage and bone break off and float
around in the joint space
→
→
Joint
Capsule
Bone
Bone
Synovial
Membrane
Synovial
Fluid
Bone ends
rub together
Cartilage
Bone
spur
Thinned
cartilage
Hyaline - most
common - end of
bones (joints),
ribs, nose
Fibrous intervertebral
discs, knee
Elastic - external
ear, epiglottis
Causes / Risk Factors
Bone
Healthy Joint
3 Types of
Cartilage:
Bone
Osteoarthritis
Broken
pieces of
cartilage and
bone
A condition damages cartilage
(gout, rheumatoid arthritis)
An event damages cartilage
or causes joint instability (e.g.
ACL knee injury)
Low estrogen at menopause
Obesity (increases stress on
joints)
Repetitive motions (e.g.
occupations that require
frequent kneeling and
stooping have high risk of
knee OA)
Genetics
lOMoARcPSD|22650627
NOT a normal part of aging process
Begins between 20 - 30 yrs and the majority of adults affected by age 40. Symptoms
appear after age 50 - 60 yrs
Men affected more than women before age 40
Women affected more than men between 40 -70 yrs, then both the same after 70 yrs
Signs and Symptoms
*Joint pain * - Main sign - gets worse with use
Early stages gets better w/rest
Later stages pain still at rest
Pain leads to disability and loss of function
Early morning stiffness - disappears after 30
minutes
Crepitation - grating caused by bones rubbing or
loose cartilage
Deformity, bone spur formation and tenderness at
specific joints
Heberden's Node (joint closest to fingernail)
Bouchard's Node (joint in middle of finger)
Affects hands, knees, hips and spine
Asymmetrical
Diagnosis
No single test
Analyze symptoms and rule
out other disorders such as
rheumatoid arthritis and gout
X-ray to see:
Dense bone
Osteophytes
Decreased joint space
Treatment / Intervention
No cure - Focus on managing pain and joint inflammation and maintain/improve joint function
Rest when joints acutely inflamed
Exercise - necessary to preserve articular
Use splints/brace if needed during acute
cartilage health
inflammation but not longer than 1 week
Low-impact (walking, water aerobics),
Knee OA: avoid standing/kneeling/squatting
weight training, ROM exercises
for long periods
Avoid high-impact
Assistive devices to decrease joint stress
Meds
Heat/cold to decrease pain and stiffness
Tylenol for mild pain
Ice for acute inflammation
Capsaicin cream
Heat best for stiffness
Bengay, Arthricare (contain camphor,
Nutrition - educate on weight loss if
eucalyptus oil, menthol)
overweight
Topical Salicylates (Aspercreme)
Alternative therapies:
NSAIDs
Acupuncture, Massage, Tai Chi
Intraarticular injections:
Surgery - arthroscopy for knee OA
corticosteroids (temp relief 1-2 mos)
lOMoARcPSD|22650627
Rheumatoid Arthritis
Chronic autoimmune disease that causes inflammation in the joints.
Pathophysiology
Starts with initial immune response to antigen
The antigen triggers formation of an abnormal immunoglobulin G (IgG)
The body reacts with autoantibodies known as rheumatoid factor (RF) which land on
the synovial membranes and cartilage in joints
Inflammation results which triggers release of neutrophils (Stage 1 Synovitis)
Proteolytic enzymes released damage to cartilage and thickening of synovial lining
Pannus (layer of vascular fibrous tissue) forms (Stage 2)
Pannus grows and damages bone & cartilage (Stage 3)
Cause
Ankylosis develops (fusion of bone) (Stage 4)
→
Healthy Joint
Bone
Exact cause unknown- most
likely a combination of genetics
and environmental trigger
(smoking, infection, etc)
Joint
Capsule
Stage 1: Synovitis
Synovial
Membrane
Synovial membrane
inflamed & fluid
thickened
Synovial
Fluid
Bone
Stage 2:
Pannus
Pannus forms,
cartilage
eroded, bones
exposed
Bone & cartilage
gradually eroded
Cartilage
Stage 3: Fibrous
Ankylosis
Stage 4: Bony
Ankylosis
Fibrous
connective
tissue
invades joint
Bones fused
lOMoARcPSD|22650627
Signs and Symptoms
Occurs at any age, peaking between 30-50 yrs
Occurs in women 3x more than men
Onset slow, insidious
Fatigue, anorexia, wt loss, generalized
stiffness
Stiffness becomes localized
Joints become painful, stiff with limited ROM
Joints soft and inflamed (hot, swollen, tender)
Symmetrical (Bilateral)
Typically in small bones of hands, wrists, feet
But may also be in elbows, shoulders, knees,
hips, ankles and jaw
Morning stiffness lasting 60+ minutes
Rheumatoid nodules - develop in 50% of pt
Firm masses subcutaneous (usually on
fingers and elbows)
Late stages - Deformity and disability
May spread to other parts of body:
Cataracts, vision loss
Pleurisy
Pleural effusion
Pericarditis
Pericardial effusion
Cardiomyopathy
Sjogren's syndrome:
dry mouth/eyes
photosensitivity
Felty syndrome:
enlarged spleen
WBC count
Depression
self-care capabilities
↓
↓
Treatment
No cure
Meds (main tx):
DMARDs (Disease-modifying antirheumatic
drugs), helps slow disease progression; may
be prescribed more than 1 at a time:
Methotrexate (Trexall) Side effect: bone marrow
suppression; hepatotoxicity (rare);
Needs frequent lab monitoring
Sulfasalazine (Azulfidine) - May cause
neutropenia
Hydroxychloroquine (Plaquenil)- may
cause vision problems; needs vision
check-ups regularly
Leflunomide (Avava)- teratogenic cannot be pregnant and need adequate
contraception
BRMs (Biologic Response Modifiers) for moderate to severe cases who do
not respond to DMARDs
Enbrel, Remicade, Humira, Cimzia,
Simponi
Immunosuppressants Azathioprine/cyclosporine (side
effects: liver dz, infections)
Corticosteroids - Prednisone (oral for
a limited time, injection into joint for
acute relief)
Celebrex, NSAIDs/salicylates
Surgery - may be needed to relieve
severe pain and increase fnx of
severely damaged joints
Synovectomy - remove joint lining
Arthroplasty - total joint
replacement
lOMoARcPSD|22650627
Diagnosis
Blood tests to check:
+RF (Rheumatoid factor)
ESR (Erythrocyte Sedimentation Rate)
CRP (C-Reactive Protein)
ANA (Antinuclear antibody) titers
Anti-CCP (Antibodies to citrullinated
peptide)
Check synovial fluid for:
WBC
MMP-3 (enzyme)
X-ray to show joint deterioration (will see
later in disease process)
↑
Intervention
Flare-ups
Inflamed joints - rest and ice
Splints
Heat for stiffness
Monitor for anemia (pale, fatigued, SOB on
exertion, palpations)
May need supplements: Fe, folic acid, Vit
B12
Monitor for GI bleed (look for dark, tarry
stool)
Educate:
On disease; no cure, how to manage
Importance of balanced diet and
maintaining healthy weight
Exercise - importance of; as tolerated;
low-impact; ROM exercises
Schedule rest and activity so no overexertion
Meds to take and side effects
Importance of follow-up visits
Difference between Osteoarthritis and Rheumatoid Arthritis
Osteoarthritis
Deterioration of articular hyaline cartilage
of bones
Non-symmetrical
Hands/knees/hips/spine
Not systemic (joints only)
Cause: Wear and tear/overuse/injury
Older adults
No systemic inflammation
Osteophytes
AM stiffness < 30 minutes
Rheumatoid Arthritis
Autoimmune disease that causes
inflammation of the synovium in joints
Symmetrical
Fingers/wrists/feet
Systemic
Cause: Unknown
Any age
Systemic inflammation
No osteophytes
AM Stiffness > 60 minutes
lOMoARcPSD|22650627
Osteoporosis
Chronic, progressive bone disease characterized by decreased bone mass
and deterioration of bone tissue, leading to increased bone fragility
Pathophysiology
There are 2 types of bone:
Compact: rigid, outer bone
Spongy (cancellous): porous, inner bone
Bones are in a constant state of remodeling
Bone is deposited by osteoblasts (built up)
Bone is resorbed by osteoclasts (broken down)
Usually this remodeling is in a state of equality
In osteoporosis, bone resorption > bone deposition
This inequality causes bone (specifically spongy bone)
to become very porous and thus bone density
decreases, making the bone weak
Stages of Osteoporosis
Normal Bone
Osteopenia
Osteoporosis
Severe
Osteoporosis
Hormones involved in bone health
Parathyroid Hormone - When blood Ca levels are low, the PTH gland secretes PTH.
This causes osteoclasts to break down stores of Ca in the bone and enter the blood.
PTH also increases SI reabsorption of Ca and decreases kidney excretion of Ca.
Calcitonin - When Ca levels are too high, the thyroid creates calcitonin to decrease
the activity of osteoclasts
Growth hormone - Stimulates osteoblasts to build bone
Estrogen - keeps bones strong by preventing bone resorption by the osteoclasts
Testosterone - converts to estrogen and thus helps keep bones strong
Osteoporosis is more common in women
than in men because:
Women consume less calcium
Women have less bone mass due to smaller frames
Bone resorption begins earlier in women and
becomes more rapid at menopause
Pregnancy and breast feeding deplete a woman's
skeletal reserves (unless Ca intake is adequate)
Women live longer (higher chance of developing it)
Known as the
'Silent Thief'
because it slowly
steals a person's
bone health
lOMoARcPSD|22650627
Risk Factors
> 65 years old
Female (8x more common than men)
BW (BMI < 19)
White/Asian ethnicity
Cigarette smoking
Sedentary lifestyle
Family history
Estrogen-deficient (surgical or agerelated menopause)
↓
During menopause
there is rapid bone
loss when
estrogen decline is
greatest, then
bone loss slows to
equal men's loss
Low intake of Ca and/or Vit D Deficiency
> 2 alcohol drinks/day
testosterone in men
Long-term use: Corticosteroids (major
contributor), thyroid replacement, heparin,
long-acting sedatives, aluminum-containing
antacids, anticonvulsants (phenobarbital,
Dilantin, Depakote, Tegretol),
glucocorticoids (for > 3 months)
↓
Signs and Symptoms
Early sign - pain in back, neck, hip
or spontaneous fracture
Osteoporosis most common in
spine, hips, wrists
Loss of height and humped
thoracic spine (kyphosis dowager's hump) - happens over
time from vertebral fracture
and wedging
Diagnosis
Bone mineral density (BMD) test
All women over 65+ yrs should get tested
Measured by:
Quantitative ultrasound (QUS) - for
heel, kneecap, shin
Dual-energy x-ray absorptiometry
(DXA) - *Gold standard - for spine,
hips, forearm - (No Ca supplements
24 hr before test)
Results listed as T-score and
compared to healthy 30-yr old
0 = normal for healthy young adult
+1 to -1 is normal
-1 to -2.5 = osteopenia
-2.5 or lower = osteoporosis
Diseases associated with
Osteoporosis
Inflammatory Bowel Disease
Intestinal malabsorption
Kidney disease
Rheumatoid arthritis
Hyperthyroidism
Alcoholism
Cirrhosis of the liver
Hypogonadism
Diabetes
lOMoARcPSD|22650627
Treatment/Intervention
Treatment focuses on: proper nutrition, calcium supplements, meds, exercise, fall prevention
Loss of bone cannot be significantly reversed but further loss can be prevented
Treatment begins when:
T-score less than -2.5 OR
-1 to -2.5 with add'l risk factors OR
History of hip or vertebral fracture
Goal for Ca intake:
1000 mg/day for women 19-50 yrs and men 19-70 yrs
1200 mg/day for women 51+ yrs and men 71+ yrs
Calcium Supplementation
Ca supps hard to absorb in single doses > 500 mg
Take in divided doses to absorption
Ca Carbonate - has 40% elemental Ca
Take w/meals because stomach acid needed to
dissolve and absorb
Ca Citrate - has 20% elemental Ca
Not dependent on stomach acid to absorb
Better for pt on PPIs or H2 Blockers
Ca Lactate and Ca Gluconate NOT recommended
Vit D important for Ca absorption and function and
bone formation
Get it from sun 20+ min/day
Supplemental D recommended for postmenopausal women or those homebound, in LTC
or northern climates
↑
Nutrition
High calcium foods
Ice cream
Milk, cheese
Sardines, salmon
Yogurt
Spinach
Turnip Greens
Tofu, almonds
Cottage cheese
alcohol intake and quit smoking
↓
Exercise
Important for building and maintaining bone
mass
Best exercises are weight bearing
Walking, hiking, weight training, tennis, etc
Rec 30 min 3 x/week
Fall Prevention
Educate patient:
Rooms clutter-free
Non-slip socks, shoes
Avoid throw rugs
Assistive devices
Meds
Biphosphonates Fosamax - Daily or weekly oral tablet
Boniva - once-per-month oral tablet
Actonel - daily, weekly, monthly dep on dose
Reclast - once yearly IV infusion to treat
osteoporosis or every 2 yrs for prevention
Main side effect is GI upset:
Take with full glass of water in morning
on empty stomach with no other meds;
sit upright for 30-60 min and nothing to
eat for 1 hr
Rare side effect is osteonecrosis (bone
death) of jaw so pt should be evaluated by
dentist before starting meds
Calcitonin - interacts with osteoclasts
IM, subcutaneous, intranasal (alternate
nostrils)
Side effects - nausea, facial flushing, nasal
dryness
Monitor for hypocalcemia
Evista - selective estrogen receptor modulator
(SERM) - mimics estrogen Side effects - leg cramps, hot flashes, blood
clots (monitor for DVT)
Forteo - form of PTH, increases action of
osteoblasts; for severe osteoporosis
Side effects - leg cramps/dizziness
Prolia - used for postmenopausal women with
osteoporosis who are at a high risk for fractures
Subcutaneous injection every 6 months
lOMoARcPSD|22650627
Gout
Type of acute arthritis characterized by hyperuricemia and deposits of
uric acid crystals in one or more joints. AKA Gouty Arthritis
Uric acid (UA) is the major end product of purine catabolism; excreted by kidneys via urine
Hyperuricemia - 2 types
Primary - hereditary error of purine metabolism leading to overproduction or retention
of UA
Secondary Related to another disorder such as: acidosis/ketosis, diabetes, renal insufficiency,
atherosclerosis
Caused by certain drugs: Thiazide diuretics, B-blockers, ACE inhibitors, niacin,
aspirin, cyclosporine
Gout can be acute or chronic
Causes
Decreased excretion of UA by
kidneys (most common)
Increased in UA production
High intake of
foods/beverages containing
purines (small factor)
Diagnosis
Synovial fluid aspiration to look for
monosodium urate crystals; also helps
decompress a swollen joint capsule;
* main diagnostic test
24-hr urine test to see if disease is from
decreased renal excretion or
overproduction of UA
Risk Factors
Obesity **
Excessive alcohol consumption
Prolonged fasting ( ketoacids
inhibit UA excretion)
CKD
Metabolic syndrome
Dehydration
Physical stress on body
More common in men
Pt on cyclosporine
↑
High Purine Foods/Beverages
Red meat
Organ meats (liver, kidney, sweetbread)
Beer
Shellfish (sardines, herring, mussels)
Fructose drinks (fruit juice, soda)
Venison, goose
Anchovies
lOMoARcPSD|22650627
Signs and Symptoms
Marked by painful flares lasting days to weeks with long periods of no symptoms
Sharp urate crystals form around the joints causing intense inflammation/pain/redness
Most commonly occurs in BIG toe (podagra), but also affects fingers, elbows, knees, wrists
Cool areas: crystals form more readily in cool areas on the body than warm areas
Acute
Chronic
Usually starts in big toe in middle of night
Inflammation
Joints dusky or cyanotic
Sudden swelling
Severe pain - peaks within several hours
Area sensitive to touch
Random flare-ups, may have 1-2 episodes
and no more
Attacks end in 2-10 days with or w/o tx
Multiple joint involvement
Visible deposits of sodium urate crystals
(tophi)
Tophi - white/yellow nodules under skin;
appear years after onset
Joints become damaged; cartilage
destruction may lead to secondary OA
Excessive UA excretion may lead to
kidney or urinary tract stone formation
Treatment
Main treatment: Colchicine (antiinflammatory agent) within 12-24 hrs
of attack
Usually combined w/NSAIDs
NO Aspirin
Weight loss if needed
Avoid alcohol and foods high in purine
Corticosteroids or ACTH for acute
attack
Maintenance meds (to prevent future attacks):
Drugs to lower urate level: Allopurinol
(Zyloprim, Aloprim); helps prevent attacks
Drugs to increase excretion of UA in urine:
Probenecid
Uloric for chronic gout
Krystexxa for those who can't take allopurinol
(given via IV)
Serum UA monitored regularly if on meds
Intervention
Acute attack:
Cold and warm compresses (alternating)
If on Colchicine:
Monitor for GI upset, neutropenia (slow
wound healing), toxicity (muscle pain,
easy bleeding)
Do not give with grapefruit juice
If on Allopurinol:
No vit C Supplements
Encourage regular eye exams
Hydrate 2-3 L/day
Bed rest with cradle or foot board
Educate:
Weight loss if needed
Discuss flare-ups and possible
contributor
Low-purine diet
Regular assessment of UA levels if on
meds
Avoid fasting
lOMoARcPSD|22650627
Brain Anatomy & Physiology
The brain is composed of the cerebrum, cerebellum and brainstem
Cerebrum - largest part; split into right and left hemispheres and 4 main lobes;
for higher functions like speech, reasoning, emotions, learning
Cerebellum - coordinates muscle movement, maintains posture and balance
Brainstem - relay center; connects cerebrum and cerebellum to spinal cord;
performs many automatic functions
The central nervous system is composed of the brain and spinal cord
The peripheral nervous system is composed of the spinal nerves and cranial nerves
rip rip
t
r s ry st
o
Frontal Lobe ot nso
M Se Parietal Lobe
Broca's
Wernicke's
Area
Area
Occipital
Temporal Lobe
Lobe
Brainstem
Cerebrum
Cerebellum
The Brain Lobes and Functions
Frontal Lobe
Behavior/emotions
Planning/problem solving
Thinking/concentration
Expressive speech (Broca's
area) - if damaged, can
understand speech but not
speak clearly
Body movement (Motor
strip)
Parietal Lobe
Temporal Lobe
Senses Hearing
touch/pain/temp
Memory
(Sensory strip)
Understanding language
Interprets signals (Wernicke's area) - if damaged,
cannot understand speech and
vision/hearing/motor
Interprets languages
speaks in sentences with no
and words
meaning
Occipital Lobe
Interprets vision - color/light/movement
lOMoARcPSD|22650627
Left Side vs Right Side Functions
**Nerves in the brain cross over to the other side of the
body. The left side of the brain controls the right side of
the body and vice versa.**
Left Side Functions
Logical Side
"Dominant side"
Speaking/Language
Reading
Writing
Math
Analysis
Planning
Right Side Functions
Creative Side
Creativity
Imagination
Music Awareness
Showing emotions
Art awareness
Function of Cranial Nerves I-XII
I - Olfactory - Smell
II - Optic - Sight
III - Oculomotor - eye movement, pupil dilation
IV - Trochlear - vertical eye movement
V - Trigeminal - moves face muscles, face sensations
VI - Abducens - lateral eye movement
VII - Facial - moves face, salivate
VIII - Vestibulocochlear (Auditory) - hearing, balance
IX - Glossopharyngeal - taste, swallowing
X - Vagus - heart rate, digestion, gag reflex
XI - Accessory - head and shoulder movement
XII - Hypoglossal - tongue movement
lOMoARcPSD|22650627
Blood Supply to the Brain
Cerebral arteries
External
carotid
artery
External
carotid
artery
Circle of
Willis
Internal carotid
arteries
Vertebral
arteries
Common carotid artery
Common carotid artery
Neurons
The neuron is the basic
working unit of the brain
that transmits information
to other nerve cells
Comprised of the cell body
(with nucleus), dendrites and
axon (covered by a myelin
sheath)
The impulse starts in the
nucleus and travels through
the axon to the axon
terminals
The dendrites receive nerve
impulses from the axon
terminals of other neurons
Blood is supplied to the brain
from the heart via the
internal carotid arteries and
the vertebral arteries
These arteries join the Circle
of Willis where they branch
off into cerebral arteries
that supply blood to the two
hemispheres
The carotid arteries and
vertebral arteries
communicate in the Circle of
Willis. If a vessel becomes
blocked, blood from the
other side can be supplied to
prevent brain damage
Dendrites
Cell
body
Nucleus
Direction
of impulse
Myelin Sheath
Axon
terminals
Neuron
Axon
lOMoARcPSD|22650627
Stroke
Blockage or rupture of an artery in the brain that results in death of
brain cells. AKA Cerebrovascular Accident (CVA)
Cerebral arteries
External
carotid
artery
External
carotid
artery
Circle of
Willis
Internal carotid
arteries
Vertebral
arteries
Common carotid artery
Common carotid artery
Blood Supply to the Brain
Ischemic Stroke
Types of Stroke
Ischemic Stroke
80% of all strokes
Usually due to a blocked artery
(often blocked by a blood clot)
Brain cells do not receive enough
oxygen/glucose and can soon die
Causes:
Embolism - clot forms in
another part of the body and
travels to the brain
Thrombosis - clot forms in the
artery in neck or brain
Blood supply to the brain comes from the
heart through the internal carotid
arteries and the vertebral arteries
These arteries branch into the cerebral
arteries that feed the brain
Collateral arteries (not shown) are small
arteries that run between other arteries,
making connections
These collateral arteries can form
different pathways for blood when an
artery becomes blocked.
People with small collateral arteries are
more likely to experience a stroke than
those with large collateral arteries.
Hemorrhagic Stroke
Hemorrhagic Stroke
20% of all strokes
Due to bleeding blood vessel in and
around the brain
Blood vessel ruptures, blood leaks
into brain tissue or around the
brain
blood to brain cells and
swelling in brain
Causes:
Rupture of brain aneurysm
Uncontrolled HTN
Age of blood vessels
↑
→↓
Transient Ischemic Attack (TIA) - AKA Ministroke
Early warning sign of impending stroke
Caused by a brief interruption of the blood supply to part of the brain
Blood supply restored quickly, no tissue dies, brain function returns quickly
lOMoARcPSD|22650627
Strokes usually damage one side of the brain
Signs, symptoms and effects of strokes will depend on the location of the
stroke
The nerves in the brain cross over to the other side of the body. The left side
of the brain controls the right side of the body and vice versa.
Left Side
Functions
Logical Side
"Dominant side"
Speaking/Language
Reading
Writing
Math
Analysis
Planning
Effects when stroke
on LEFT side of brain
Right side hemiplegia
(paralysis)
Trouble forming words
and comprehending
them
Cautious
Aware of deficits
Depressed
Right Side
Functions
Creative Side
Creativity
Imagination
Music Awareness
Showing emotions
Art awareness
Effects when stroke
on RIGHT side of brain
Left side hemiplegia
(paralysis)
Impulsive
Unable to recognize
people
Short attention span
Denies problems / ignores
damaged side (neglect
syndrome)
The Brain Lobes and Functions
Frontal Lobe
Behavior/emotions
Planning/problem solving
Thinking/concentration
Expressive speech (Broca's
area) - if damaged, can
understand speech but not
speak clearly
Body movement (Motor strip)
Temporal Lobe
Hearing
Memory
Understanding language
(Wernicke's area) - if damaged,
cannot understand speech and
speaks in sentences with no
meaning
Parietal Lobe
Senses - touch/pain/temp (Sensory strip)
Interprets signals - vision/hearing/motor
Interprets languages and words
Occipital Lobe
Interprets vision - color/light/movement
p
rip
st stri
r
y
o
r
Frontal Lobe ot nso
M Se Parietal Lobe
Broca's
Wernicke's
Area
Area
Occipital
Temporal Lobe
Lobe
Brainstem
Cerebellum
Cerebrum
lOMoARcPSD|22650627
Risk Factors
Conditions that lead to strokes develop over time
95% of strokes are the result of modifiable risk factors
More common among older people and women vs men
Black people 2x more likely to have a stroke than white people
Also higher incidence in Hispanics, Native Americans and Asian Americans
than in white people
Risk factors:
↑BP (single most important factor)
↑ cholesterol
Diabetes
Insulin Resistance
Smoking
Obesity
Older age
alcohol use
physical activity
Diet - salt, sat fat, trans fat and calories
↑
↓
↑
Cocaine, amphetamine use
Previous stroke
Heredity
Oral contraceptives (when combined
with smoking and BP)
Atherosclerosis (ischemic)
Blood thinners (hemorrhagic)
Clotting disorders (ischemic)
Afib (ischemic)
Cerebral aneurysm (hemorrhagic)
↑
Signs and Symptoms - SUDDEN!!
Will depend on location of blockage or
bleeding:
Weakness or paralysis, loss of sensation on
one side of body
Difficulty speaking; slurred speech;
confusion
Loss of vision in one eye
Dizziness; problems with coordination
TIA s/s same as above but disappear
within minutes to 1 hr.
Hemorrhagic s/s also include:
Severe headache, N/V
Loss of consciousness
Very BP
National Stroke Association Signs of
a Stroke:
-- Face Drooping
-- Arm Weakness
-- Speech Difficulty
-- Time to Call 911
↑
Call rapid response (or 911 if not in hospital). Record signs/symptoms
and the exact time they occurred.
lOMoARcPSD|22650627
Effects
Effects of an ischemic stroke are usually greatest immediately after the stroke
With a hemorrhagic stroke effects progress between minutes to hours after
the stroke
Some function may be regained- due to plasticity (healthy areas of brain take
over for damaged areas)
However, many effects remain and a stroke is a lifelong change for the patient
and family
Effects may include:
Motor - most obvious effects
Mobility
Respiratory
Dysphagia - problems swallowing (weak muscles)
Gag reflex
Self-care
Hemiparesis - weakness on one side of the body
Hemiplegia - paralysis on one side of body
Communication
Aphasia - Inability to speak
Receptive - unable to comprehend speech (damage to Wernicke's area)
Expressive - comprehends speech but can't respond (damage to Broca's area)
Global - inability to understand speech and speak
Dysarthria - slurred speech due to weak muscles
Affect - trouble controlling emotions
Intellectual
Memory
Judgment (left-side damage = cautious; right-side damage = impulsive)
Agraphia- loss of ability to write
Alexia - loss of ability to read
Agnosia - does not understand sensations or recognize familiar objects
Spatial-Perceptual alterations
Denies illness, ignores damaged side
Hemianopia - sees only half of visual field in each eye
Agnosia - inability to recognize objects
Apraxia - inability to carry out normal movements (despite muscles working fine)
Elimination - typically temporary; may be due to inability to communicate
lOMoARcPSD|22650627
Complications
Aspiration may lead to aspiration
pneumonia
Malnutrition from undereating
Difficulty breathing
Muscle loss, pressure sores, blood clots,
contractures from not moving
Clots may lead to pulmonary embolism
Urinary tract infections
Hemorrhagic - herniation where brain
pushes through structures that separate
brain; may lead to loss of consciousness,
coma, death
Diagnosis
CT scan or MRI
To distinguish what type
of stroke and identify
location and size
CTA or MRA (angiography)
Cardiac imagery to check
heart
Blood tests- platelets,
glucose, PT
Prognosis
The sooner the patient is treated, the less severe brain damage will result
Strokes that impair consciousness or effect a large part of the left side (language)
fair worse
Faster improvement in the few days post stroke better chances of good recovery
Ischemic - at 12 months post, problems that remain will most likely be permanent
Hemorrhagic - If not massive, outcome better than ischemic with similar symptoms
Depression common
→
Prevention
Decrease risk factors:
Normal BP
Normal BW
physical activity
No smoking
Limit alcohol
Diet:
salt/sat fat/trans fat/chol
fruits/veges
↑
↓
↑
Antiplatelet drugs - reduce risk if
already had ischemic stroke or TIA
Aspirin
Clopidogrel (Plavix)
Aggrenox
Anticoagulants (for pt w/Afib)
Warfarin
Dabigatran
Apixaban
Rivaroxaban
lOMoARcPSD|22650627
Treatment
Hemorrhagic may need:
Measures to support vitals (if needed):
Help to get blood to clot (Vit K and
O2, mechanical vent
plasma/platelet transfusion)
IV hypertensives
Meds to control BP
swelling in brain, HOB, head in midline
Shunt in skull to pressure
Adequate hydration
Stent to treat ruptured brain aneurysm
Ischemic may need:
Antiplatelet drugs, anticoagulants, BP meds
Mechanical thrombectomy, angioplasty, stent insertion
Intervention for tPA
tPA - Tissue plasminogen activator
Monitor vitals during and 24 hrs
To reestablish blood flow through a blocked artery
post
MUST be given within 3-4 1/2 hrs post stroke
Monitor labs
MUST be screened closely before administering
Watch for bleeding
Make certain not hemorrhagic stroke
Watch for neuro changes
No recent: GI bleeding, head trauma,
Will go to ICU for monitoring
major surgery, active internal bleeding
No heparin or anticoagulants
Labs normal: Glucose, INR, platelets
BP: SBP < 185 and DBP <110
↓
↑
↓
Intervention
Record time of onset of symptoms
Assess using NIH Stroke Scale (NIHSS)
0 - 42 scale
0 = No symptoms
21 - 42 = severe symptoms
Monitor vitals and neuro - BP VERY important
Airway - at risk for aspiration pneumonia
Kept at NPO until screened for ability to
swallow
Elevate HOB, encourage deep breathing
Monitor:
Cardiac rhythms
Murmurs
I/Os
Lung sounds for crackles and wheezes
Keep pt moving
ROM exercises (active and passive)
Monitor for ICP
Headache/ BP/ HR
N/V
Pupils not responding
Monitor for neglect syndrome and hemianopsia
↑
↑ ↓
Turn every 2 hrs - to optimize musculoskeletal fnx
and maintain skin integrity
Side - back - side (weak side only 30 min)
GI - May need stool softener or laxative
take to bathroom on regular schedule
Nutrition Speech therapist for evaluation before oral
intake initiated
Check gag reflex (tongue blade - back of
throat)
Food - should be easy to swallow; will need
assistance eating; monitor for food left in
mouth
Communication - Assess ability
Use gestures, visual cues, picture board
Short phrases
Be patient
Use questions with simple answers
Family Provide info and emotional support
Family and pt will have varying feelings
Social service referral will be needed
lOMoARcPSD|22650627
Seizure
A brief, uncontrolled electrical discharge of neurons in the brain that
interrupts normal function.
Provoked seizure - a seizure that has a direct cause (head injury, hypoglycemia,
infection, reaction to drug, alcohol or drug withdrawal)
Unprovoked seizure - a seizure that does NOT have an immediate cause
Epilepsy - a chronic disorder, characterized by recurring, unprovoked seizures
Seizures are the primary sign of epilepsy, but not all seizures are a sign of epilepsy
Neurotransmitters
Neuron
Neuron
Receptor
Pathophysiology
Neurons release different types of neurotransmitters
Some are Excitatory neurotransmitters that tell the neuron receptors to relay
an electrical message
Others are Inhibitory neurotransmitters that tell the neuron to stop the
electrical message
During a seizure, a cluster of neurons become impaired and start sending out a
ton of excitatory signals
lOMoARcPSD|22650627
Type of Seizures
Two main types - Generalized Onset and Focal Onset
Generalized Onset
Affects both sides of brain
Most cases lose consciousness
Tonic-Clonic - formerly known as Grand Mal
Most common Generalized Onset
Pt loses consciousness and falls to ground if
upright
Stiffens body (tonic phase) for 10-20 seconds
Jerkiness follows (clonic phase) for 30-40 sec
Cyanosis, salivating, tongue or cheek biting,
incontinence
In postictal phase - muscle soreness, tired, sleep
No memory of seizure
Absence - formerly known as Petit Mal
Usually in children; rarely continues to
adolescence
Brief staring spell (looks like daydreaming) <10
seconds
No memory of seizure
May take months to years to recognize
Atypical absence Staring with eye blinking or movement of lips
Usually continues into adulthood
Lasts 10-30 seconds
Clonic Loss of muscle tone then jerking
Not very common
Myoclonic Sudden jerkiness of body
Lasts a few seconds
Remains conscious and aware
Atonic - AKA drop seizure or drop attack
Loss of muscle tone; usually falls to ground
Lasts <15 seconds
Usually not aware; risk of injury
Tonic Sudden stiff muscles, usually occurs in sleep
<20 seconds
Remains conscious and aware
Focal Onset (formerly known as Partial Onset)
Affects specific part of brain
Focal to Bilateral Tonic-Clonic - AKA Secondary
Symptoms based on area of brain affected
Generalized Tonic-Clonic
Focal Onset Aware - formerly Simple Partial
When focal seizure spreads to other side of
Experiences unusual feelings and sensations
brain
May hear/taste/see things not real
Any Tonic-Clonic seizure preceded by an aura is
Remains conscious and aware
a focal seizure that generalized secondarily
Called an aura if happens before another seizure
May result in a brief residual neurologic deficit
Focal Impaired Awareness - formerly Complex Partial
in postictal phase called Todd's Paralysis
Loses awareness
(resolves itself)
Eyes open - cannot interact
Displays automatisms - repetitive actions (e.g. lip
smacking)
Lasts 30 seconds - 2 minutes
Tired and confused after
Generalized
Focal Onset
Aura may happen before it
Onset
lOMoARcPSD|22650627
Phases of a Seizure
**Not everyone will go through each phase**
Prodrome - feelings, sensations, changes in behavior
hours or days before seizure
Aura - doesn't happen with all types of seizures; first
symptom, happens within seconds to minutes before
seizure; sudden weird feelings (fear, panic, racing
thoughts), dizzy, headache, nausea
Ictal - actual seizure, electrical activity in brain
occurs; symptoms vary widely
Postictal - after the seizure; recovery period; may
recover immediately or take minutes to hours; may be
extremely tired, confused, have difficulty talking
Causes
Cause often dependent on age of seizure
1st 6 months of life - severe birth injury,
congenital defects of CNS, infection
2-20 years - birth injury, infection, trauma,
genetic factors, fever
20-50 years - structural lesions (trauma,
brain tumors, vascular disease)
50 + years - stroke, metastatic brain
tumors
1/3 of all cases no cause known
Genetic link- epilepsy often runs in
families
Complications
Status epilepticus - continuous seizure activity in which seizures recur in rapid succession without return to
consciousness between seizures
OR any seizure lasting longer than 5 minutes
Neurologic emergency! Can lead to brain damage if not treated
Any injury that may have occurred during a seizure
Mortality rate of people with epilepsy = 2-3x the rate of the general population
Psychosocial - difficult to cope with seizures; depression; social stigma; transportation and employment are
difficult
Diagnosis
Thorough review of history of seizures and health history needed
EEG - may show abnormal findings which will help determine type of seizure
Should be done within 24 hours of seizure
Usually need repeated EEGs or continuous EEG monitoring
NOT definitive test (false + and false -)
Magnetoencephalography (with EEG)
CBC, check on liver/kidney function, urinalysis - to rule out metabolic disorders and recreational drugs
as cause of seizures
CT/MRI - to rule out structural lesions
lOMoARcPSD|22650627
Treatment
No cure, goal is to prevent seizures with minimal
side effects from drugs
Medications Antiseizure drugs (primary treatment)
Tonic-Clonic and focal seizures Phenytoin (Dilantin)
Tegretol
Phenobarbital
Divalproex
Mysoline
Absence and Myoclonic Zarontin
Divalproex
Klonopin
For status epilepticus Rapid-acting IV antiseizure drug
Lorazepam (Ativan)
Diazepam (Valium)
Most drugs have a long 1/2 life, so given in once
or twice daily doses
Side effects:
Diplopia, drowsiness, ataxia
Mental slowness
Phenobarbital - watch for respiratory
depression and hypotension
Phenytoin - watch for gingival hyperplasia
(instruct on good oral hygiene); hirsutism,
rash (report immediately); avoid taking
with milk or antacids
Older adults: respond better to meds but side
effects are worse
Surgery If unresponsive to drug therapy
Remove part of brain causing the seizure
Vagal nerve stimulation Used when a specific area of brain cannot be
identified
Interrupts the brain wave activity to stop the
neurons
Sends electrical impulse to vagus nerve
Ketogenic diet - fat, carb diet
↑ ↓
Intervention
Seizure precautions Suction and O2 ready
IV access
Padded side rails
Pillow under head
Bed lowest position
Remove restrictive clothing/glasses
During seizure Lie pt down; turn on side
Ensure pt airway cleared
Protect from injury - side rails, pillow under
head, remove anything that may break
Remove/loosen tight clothing
Do NOT restrain
Stay with pt until seizure passes
IV access for meds if needed
Suction as needed
Note time start/stop
If > 5 minutes or no return to baseline =
Status Epilepticus activate ESR team
→
Note how pt acted immediately prior to
seizure and during
Which body part affected 1st
After seizure Assess pt status - responsive/tired/any
injury?
Maintain airway
Monitor vitals, LOC, O2 sat, pupil
size/reactivity
Clean pt if incontinence occurred
Educate patient Importance of taking meds regularly
All side effects - plus need to report them
Assist in finding resources (Epilepsy
Foundation), social worker
Suggest med alert bracelet/necklace/ID card
Factors that may cause seizure:
Stress, trauma to head, pregnancy, lack of
sleep, hypoglycemia, dehydration, fever,
strobe lights, recreational drugs, alcohol
lOMoARcPSD|22650627
Increased Intracranial Pressure
Potentially life-threatening condition where the pressure builds within
the skull.
The skull is an enclosed space with 3 essential
volume components:
Brain tissue, blood and cerebrospinal fluid
(CSF)
Intracranial Pressure (ICP) - the pressure in
the skull created by the 3 components
Normal ICP = 5-15 mm Hg
Under normal circumstances, ICP is influenced
by:
Posture
Arterial pressure
Temperature
Venous pressure
Intraabdominal pressure Blood gases
(esp. CO2)
Intrathoracic pressure
CSF
Blood
Brain tissue
Components of the Brain
The Monro-Kellie doctrine states that the 3 components must remain at a
relatively constant volume within the skull. If the volume of 1 component
increases and the volume of another component decreases, the total
intracranial volume will not change (provided the skull is closed).
The body adapts to volume changes within the skull in 3 different ways:
CSF volume: by altering CSF absorption and production or displacing CSF
Intracranial blood volume: by collapsing cerebral veins & dural sinuses;
cerebral vasoconstriction or dilation; changes in venous outflow
Brain tissue volume: by distention of the dura or compression of brain tissue
The ability to compensate for changes in volume is limited!
As the volume continues to increase, the ICP rises and decompensation ultimately
occurs, resulting in compression and ischemia.
lOMoARcPSD|22650627
Cerebral blood flow (CBF) - amount of blood in ml passing through 100 g of brain
tissue in 1 minute
Maintenance of blood flow to brain is critical because the brain requires a
constant supply of O2 and glucose
The brain regulates its own blood flow via autoregulation
Autoregulation - the automatic adjustment in the diameter of the cerebral blood
vessels by the brain to maintain constant blood flow during changes in arterial
blood pressure; also helps maintain cerebral perfusion pressure
Cerebral perfusion pressure (CPP) - the pressure needed to ensure blood flow to
the brain.
If CPP falls too low autoregulation fails CBF decreases
Normal CPP = 60-100 mm Hg
CPP = MAP - ICP
CPP < 50 mmHg = ischemia and neuronal death
MAP = SBP + 2 (DBP)
CPP < 30mmHg = ischemia and incompatible with life
3
CPP = MAP (mean arterial pressure) - ICP
SBP = systolic BP
Critical to maintain MAP when ICP is elevated!
DBP = diastolic BP
→
→
Mechanisms of Increased Intracranial Pressure
ICP begins to increase due to tissue edema from head injury, hemorrhage or
another cause (see list next page)
ICP leads to CPP which leads to cerebral blood flow
CBF leads to ischemia, swelling and more edema
Brain will try to maintain cerebral perfusion by increasing systolic BP
This will lead to systolic HTN, widening pulse pressure, bradycardia with a full,
bounding pulse and altered respirations = CUSHING'S TRIAD = neurologic
emergency!
Leads to herniation (shifting inside the skull) and displacement
Herniation forces the brainstem downward respiratory arrest due to
compression of the respiratory control center in the medulla
↑
↓
↓
↓
→
lOMoARcPSD|22650627
Causes of
↑ ICP
Head Injury
Hemorrhage
Hematoma
Brain tumor
Brain abscess
Encephalitis
Meningitis
Cerebral Infarction
Hydrocephalus
Hepatic encephalopathy
Diagnosis
CT
MRI
EEG
Cerebral angiography
ICP mmnt
Transcranial Doppler studies
Evoked potential studies
PET
Signs and Symptoms
Change in LOC - Earliest sign
BEST indicator of pt neurologic status
Appears restless or confused; level of attention
Headache - nocturnal or early morning
Vomiting - without nausea (unexpected vomiting), may be projectile
Seizures
Change in body temperature
Irregular breathing
Ocular:
Double vision
Swelling of optic nerve (papilledema)
Pupils - increase or decrease in size or unequal in size
No response to light
Check oculocephalic reflex - if eyes stay midline = brain stem damage
Muscular Weakness on one side
Decorticate - stiff with arms bent in toward body, clenched fists, legs held out
straight/rotated internally
Decerebrate - arms and legs straight, feet flexed - worst of the two- more serious
damage
Change in vitals - Cushing's triad - appears late- emergency!
↓
lOMoARcPSD|22650627
↑
Treatment
Identify/treat underlying cause of ICP
Support brain function
Maintain adequate oxygenation, may need:
Endotracheal tube
Tracheostomy
Mechanical vent
Removal of brain lesion if necessary
Meds Mannitol (Osmitrol) - osmotic diuretic given via IV
Decreases ICP by plasma expansion and osmotic effect
Draws the water pooling in the brain back to the blood
Hypertonic saline solution
Moves water out of swollen brain cells
Corticosteroids - not for TBI, used for tumors and abscesses
Monitor glucose, GI bleeds - H2 Blockers and PPIs to prevent GI ulcers/bleeding
Barbiturates (help ICP and cerebral edema), opioids
↓
Intervention
↑
Focus on preventing further ICP and
monitor current ICP
Respiratory - Maintaining airway critical!
Need to prevent hypoxia and
hypercapnia ( O2 or CO2 can
cause ICP)
Suction only as little as possible as may
ICP
Elevate HOB 30 degrees, head midline,
no flexion of neck or hips
NG tube to aspirate stomach contents
(prevents abdominal distention)
Temp Prevent elevated temp (will ICP)
Antipyretics, room temp, cool bath
(but prevent shivering)
Quiet, calm environment
Attempt to avoid: coughing/ sneezing/
valsalva maneuver/ rapid movements
↑
↓
↑
↑
↓
↑
Monitor Glasgow Coma Scale (see next page)
Neuro checks
Monitor ICP - usually via
ventriculostomy:
Catheter in lateral ventricle
coupled to external transducer
Levels >20 mm Hg report to MD
I/Os
Electrolytes - glucose, Na, K, Mg,
osmolality
Turn at least every 2 hours
Restraints only if absolutely necessary
Nutrition - enteral/parenteral as
prescribed
Watch for FVO from diuretics
Renal function
s/s of heart failure, pulmonary edema
lOMoARcPSD|22650627
Glasgow Coma Scale
Behavior
Motor Response
Verbal Response
Eye Opening Response
Response plus points
+1
+2
+3
+4
+5
+6
+1
+2
+3
+4
+5
+1
+2
+3
+4
No response
Abnormal extension (decerebrate)
Abnormal flexion (decorticate)
Flexion withdrawal from pain
Moves to localized pain
Obeys commands
No response
Incomprehensible sounds
Inappropriate words
Confused conversation
Oriented to time, person, place
No response
Responds to pain
Responds to speech
Spontaneously opens eyes
Severe head injury: Score of 8 or less
Moderate head injury: Score of 9-12
Mild head injury: Score of 13-15
ICP should be monitored in patient with GCS score of 8 or less and abnormal
CT scan or MRI
lOMoARcPSD|22650627
Multiple Sclerosis
Disorder where patches of myelin and underlying nerve fibers in the
brain and spinal cord are damaged or destroyed.
Neurons
The neuron is the basic
working unit of the brain
that transmits information
to other nerve cells
Comprised of the cell body
(with nucleus), dendrites and
axon (covered by a myelin
sheath)
The impulse starts in the
nucleus and travels through
the axon to the axon
terminals
The dendrites receive nerve
impulses from the axon
terminals of other neurons
Dendrites
Cell
body
Nucleus
Direction
of impulse
Myelin Sheath
Axon
Axon
terminals
Neuron
Pathophysiology
Unknown trigger in genetically susceptible person activates T cells which then
migrate to brain and spinal cord
This causes an inflammatory response which leads to demyelination of the
axons
At first, nerve fibers are not affected and transmission of nerve impulses
occurs but is slowed
Myelin regenerates, symptoms disappear, patient goes into remission
Inflammation later occurs again but this time myelin loses its ability to
regenerate axon then becomes damaged
Nerve impulse transmission halted and permanent loss of nerve function
occurs
→
lOMoARcPSD|22650627
Risk Factors
Causes
Unknown
Possibly autoimmune where immune
system attacks myelin sheath
Develops in genetically susceptible people
as a result of exposure to (possibly):
Infection
Smoking
Emotional stress
Excessive fatigue
Pregnancy
The autoimmune reaction results in
inflammation which damages the myelin
sheath and nerve fiber
Genetic
Climate during first 15 years of
life:
Temperate climates worst
Tropical and near equator
best
May be related to Vitamin D
level from sun
Smoking
2-3x more likely in women than
men
Shows up between 20 - 40 years
old
Diagnosis
No single test to diagnose
Assess symptoms, history and tests
MRI - detects areas of demyelination of CNS
MRI with contrast agent - used to determine recent vs old areas of damage
Spinal tap (lumbar puncture) - to detect oligoclonal bands (immunoglobulins);
shows inflammation
Evoked responses - electric signals sent to CNS to activate certain areas;
brain's responses recorded
Other test to rule out MS:
AIDS
Guillain-Barre
Lupus
Lyme
Most people with MS have periods of good health (remissions) alternating with
periods of worsening symptoms (flare-ups/relapses). Recovery during remission
is good but often incomplete leading to MS worsening slowly over time.
lOMoARcPSD|22650627
Signs and Symptoms
Will vary depending on which nerve fibers are
damaged
Symptoms begin long before diagnosed
Fatigue
Dizziness/vertigo
Tingling, numbness (face, extremities)
Pain in arms, legs, trunk
Involuntary tremors
Muscle spasms
Muscle weakness
Speech impediment
Loss of dexterity/coordination
Vision problems- blurred, double, red-green
color distortion, pain moving eyes
Nystagmus - problems controlling eye
movement
Lhermitte's sign - feels like an electric shock
radiating down the spine into the limbs upon
flexion of neck
Bowel/bladder Constipation
Spastic bladder - urinary
urgency/frequency/incontinence
Flaccid bladder - No sensation to void
Sexual dysfunction; no libido
Cognitive - problems with short-term
memory, attention, information processing
Emotion - anger, depression, euphoria
Romberg's sign - sway when eyes closed and
standing with feet together
Uhthoff's sign - symptoms get worse with
heat
Treatment
No cure so need to treat disease process and provide symptom relief
Ideally start early in course of MS better prognosis
For spasticity - muscle relaxants (Baclofen,
Medications:
Immunomodulator drugs - to inflammation Diazepam)
For fatigue - Amantadine, Modafinil
and immune system response
For bladder - Overactive -anticholinergics
Beta interferon (Rebif, Plegridy,
Avonex, Betaseron, Extavia, Copaxone) (Oxybutynin) or underactive - cholinergics
(Bethanechol)
Corticosteroids - to treat exacerbations
For walking - Dalfampridine (Ampyra)
Methylprednisolone, Prednisone
For tremors - Propranolol (beta blocker),
IV immunoglobulin G - may be needed when
Isoniazid (antibiotic)
steroids not sufficient
→
↓
Intervention
Assist patient in identifying triggers that
cause exacerbations (heat, overexertion, etc)
May need to be taught self-catherization
Speech and PT consult
Safety considerations (vision, coordination)
Encourage - light exercise and rest, well
balanced diet ( fiber), stool softeners,
caffeine, adequate fluids (1-2 L/day)
Administer meds as prescribed and educate
pt on meds
↓
↑
lOMoARcPSD|22650627
Parkinson's Disease
Chronic, progressive neurodegenerative disorder.
Basal Ganglia in the Brain
Cerebrum
Basal Ganglia
1
2
3
4
Caudate nucleus
5
Substantia nigra
1
Globus pallidus
Putamen
Subthalamic nucleus
2 3
4
5
Thalamus
Amygdala
Brain stem
Cerebellum
The basal ganglia are collections of nerve cells deep in the brain
They help initiate and smooth out voluntary muscle movements, suppress
involuntary movements and coordinate changes in posture
Pathophysiology
In Parkinson's Disease, the nerve cells in the substantia nigra (in the basal
ganglia) degenerate
These cells produce dopamine which helps increase nerve impulses to muscles
When they degenerate, dopamine level decreases and the number of
connections between nerve cells in the basal ganglia decrease
This leads to the inability of the basal ganglia to control muscle movement
properly
Plus, the levels of acetylcholine and dopamine are altered (normally equal)
with an excess of acetylcholine floating around (contributes to tremors)
PD symptoms do not show up until at least 80% of neurons in the substantia
nigra are lost
lOMoARcPSD|22650627
Cause
Risk Factors
Exact cause unknown
May be presence of Lewy bodies in
the substantia nigra
Lewy bodies are clumps of synuclein
(a protein in the brain)
60+ years old
Slight genetic link
Possibly:
Well water
Pesticides/herbicides
Rural residence
Signs and Symptoms
Will begin subtly and progress gradually
May start on one side/extremity and progress to the other side
Tremors
Often 1st sign and starts in hand
Affects handwriting
Appears to be rolling a pill or coin between
thumb and forefinger (pill-rolling)
Coarse and rhythmic
Occurs at rest (resting tremor)
May move to tongue, jaw, voice
Rigidity
Muscles become stiff, making movement
difficult
Muscles resist passive movement
Cogwheel rigidity - jerky movement
Akinesia
No control over voluntary movement
Bradykinesia - slowness of movements,
especially automatic movements (blinking
eyelids, swallowing, postural adjustments)
Seen as stooped posture, masked face,
drooling, shuffling
Postural instability
Unable to stop moving forward (propulsion)
or backward (retropulsion)
Depression
Anxiety
Apathy
Fatigue
Pain
Constipation
Urinary retention
Erectile dysfunction
Memory changes
Sleep problems
REM sleep behavior disorder (limbs
move suddenly and violently)
Urinate frequently
Scales on scalp and face
Loss of smell
ADL all become difficult due to stiff
muscles and tremors
Turning in bed
Getting out of car
Standing up
Dressing, combing hair
Eating
Writing
lOMoARcPSD|22650627
Complications
Diagnosis
Falls/injury
Aspiration (esophagus moves contents slowly)
Sudden BP (orthostatic hypotension)
Malnutrition
Dementia - 1/3 develop late in disease
Hallucinations, delusions, paranoia - may be caused by
disease OR meds
↓
Treatment
Difficult to diagnose due to same s/s as
aging
No specific test
Based on evaluation
Positive response to antiparkinsonian drugs
provides confirmation of PD
No cure, so focus is on symptom management
Medications Antiparkinsonian drugs
Main one is Levodopa combined with Carbidopa (Sinemet) - has many side effects
May stop working after several years (called 'on-off effect')
Levodopa
Converted into dopamine in the basal ganglia
Reduces muscle stiffness; improves movement; reduces tremors
May take up to 3 weeks to take effect
MANY side effects (N/V, orthostatic hypotension, flushing, nightmares, hallucinations,
confusion, obsessive compulsive behavior)
MD must find best dose by balancing control of disease with side effects
Don't take with foods high in B6 or high protein foods
Carbidopa
Prevents levodopa from being converted to dopamine in intestine and CV system (helps
decrease GI side effects)
Anticholinergic drugs - Cogentin - used to treat tremors; may be taken alone or with Levodopa; NO
alcohol
Dopamine agonists - may be used instead of Sinemet
Mirapax or Requip (taken PO- drowsiness major side effect)
Neupro (skin patch)
Apomorphine (injected under skin) - can be used as rescue therapy for 'off' effects of Sinemet
MAO Inhibitors - Eldepryl, Azilect - used w/Levodopa or alone; beware taking with foods containing
tyramine- risk of hypertensive crisis
Amantadine - may help with on-off effect; used alone or w/Levodopa; only provides MILD relief
COMT Inhibitors - Comtan, Tasmar (Help Levodopa last longer)
Domperidone- treats side effects (N/V, orthostatic hypotension)
Antipsychotics if needed - Quetrapine, Clozapine
Exelon or Aricept for dementia
Amitryptyline for depression
Surgery- For those unresponsive to drug therapy; 3 types
Deep Brain Stimulation - electrodes in basal ganglia; electricity sent to areas responsible for tremors
Ablation - ultrasound waves applied to areas of the brain affected by Parkinson's
Stem cell transplantation - ongoing research in this area
lOMoARcPSD|22650627
Intervention
Goal for patient:
Maintain good health (eating/movement)
Maintain independence
Avoid complications
Stay safe
Optimize psychosocial well-being
Major concerns - exercise and well-balanced diet
Exercise to limit:
Muscle atrophy
Contractures
Constipation
Nutrition
At risk for wt loss due to difficulty chewing/swallowing
Foods need to be soft and easy to swallow
2 L of fluids - goal during day
fiber diet; may need stool softener
Don't take meds with protein meals (will absorption)
Educate on dosages and side effects of meds (see Treatment)
Discuss environmental changes to assure safety
Removing area rugs
Removing excess furniture
Elevated toilet seat
Handrails
Use of cane
Clothing
Slip on shoes (rather than shoelaces)
Hooks and velcro rather than zippers and buttons
Educate on how to deal with freezing episodes - patient feels like feet stuck to ground and
unable to move
Change direction
Think about stepping over imaginary line on floor
Rock from side to side
Take a step back then try to go forward again
Discuss support groups and need for stress as stress may increase symptoms
↑
↑
↓
↓
lOMoARcPSD|22650627
Myasthenia Gravis
Autoimmune disorder of the neuromuscular junction that results in
muscle weakness.
Pathophysiology
The neuromuscular junction is where the
motor neuron and muscle fiber meet and
send signals
Acetylcholine (ACh) is released from the
motor neuron
Receptors on the muscle fiber are
stimulated by the ACh
The receptors contract the muscle fibers
causing movement
AChE then breaks down the ACh to avoid
constant muscle stimulation
However, in Myasthenia Gravis the
receptors are attacked by antibodies from
the immune system
This leaves fewer receptors on the fiber to
contract the muscles
Leads to muscle weakness
Neuromuscular Junction
Motor
Neuron
(Nerve)
Acetylcholine
(ACh)
Antibody
ACh
Receptors
Muscle
Acetylcholinesterase
(AChE)
Signs and Symptoms
Cause
Exact cause unknown
May be malfunction of
thymus gland where it
does not decrease in size
after puberty and
develops tumors
These tumors may
produce autoantibodies
Main sign: Weakness of skeletal muscles that
becomes worse with activity and BETTER with
rest
Usually noticed first in eyes:
Weak, drooping eyelids (ptosis)
Weak eye muscles - double vision
(strabismus)
Difficulty speaking/swallowing
Energy fades as day progresses
No expression on face
Shortness of breath
lOMoARcPSD|22650627
Diagnosis
Symptom assessment - muscles tested with repetition, patient rests and
then tested again improvement shows possible MG
EMG to show response to muscle stimulation
Blood tests - to show antibodies
Tensilon test - Injection with Edrophonium Chloride (Tensilon). If shows
improved muscle contractility = myasthenia gravis
MRI or CT - to evaluate thymus for tumors
↓
→
Treatment
No cure
Medications Anticholinesterase (Pyridostigmine)
Stops acetylcholinesterase from breaking down acetylcholine
This leaves more acetylcholine floating around and prolongs its action
Therefore more chance for muscle contraction
May cause Myasthenic Crisis (see next page)
Corticosteroids (Prednisone) - given on alternate days
Immunosuppressants - Azothioprine (Imuran), Mycophinolate (CellCept), Cyclosporine
(Sandimmune)
Thymectomy - remove thymus gland (not a cure but decreases symptoms)
Plasmapheresis (plasma exchange) or IV immunoglobulin G - Both used to provide shortterm results in myasthenic crisis or before surgery when avoiding corticosteroids
Contraindications
The following meds are contraindicated in patients with MG
Anesthetics
Antidysrhythmics
Antibiotics
Quinine
Antipsychotics
Barbiturates
Diuretics
Opioids
Cathartics
Muscle relaxants
Thyroid preparations
Tranquilizers
lOMoARcPSD|22650627
Intervention
Assess severity: Fatigue level, muscles affected, muscle strength, swallowing, speech, cough
and gag reflexes
Acute phase Monitor: respiratory (RR, O2 Sat), vision, voice, swallowing, strength, cranial nerves,
aspiration
Nutrition May have feeding tube
If not, instruct:
Balanced diet, foods easily chewed and swallowed
Schedule meds 30 - 60 minutes before eating to take advantage of strong muscles
Instruct Plan day with activities early when strength is best
Necessity of medication adherence
Adverse reactions to meds to look for
Avoid activities that risk of crisis
↑
Myasthenic Crisis
Severe episode of MG due to infection,
surgery, stress, starting
corticosteroids or not taking enough
anticholinesterase
Leads to not enough ACh at receptor
site
Signs and Symptoms:
Respiratory failure (may need
vent)
Muscle weakness
Difficulty speaking
No cough/gag reflexes
BP
Bowel/bladder incontinence
Pupils normal
↑
Cholinergic Crisis
vs
Reaction to too much anticholinesterase
Leads to too much ACh at receptor site
Signs and Symptoms:
Respiratory failure (may need vent)
Muscle weakness
Muscle fasciculation (twitching)
Blurry vision
BP
Pupils constricted
Lacrimation
salivation
Diarrhea
N/V
Ab cramps
Sweating
↓
↑
To determine if pt is experiencing MC or CC, Tensilon test will be administered.
If pt weakness improves = positive test for MC = Give anticholinesterase per MD order
If pt weakness worsens = negative test for MC = Administer Atropine per MD order
Downloaded by REGINA CARLA ARQUINES (rica.arquines@gmail.com)
lOMoARcPSD|22650627
Guillain-Barré Syndrome
Disorder in which the immune system attacks the peripheral
nervous system.
Peripheral Nervous System (PNS)- System of nerves that provides connection
between brain/spinal cord and rest of body. Consists of Somatic Nervous System
and Autonomic Nervous System. SNS = Voluntary functions (muscles, etc) ANS =
Involuntary functions (BP, HR, RR, Temp, Vision, Renal, Digestion)
Neurons
The neuron is the basic
working unit of the brain
that transmits information
to other nerve cells
Comprised of the cell body
(with nucleus), dendrites and
axon (covered by a myelin
sheath)
The impulse starts in the
nucleus and travels through
the axon to the axon
terminals
The dendrites receive nerve
impulses from the axon
terminals of other neurons
Dendrites
Cell
body
Nucleus
Direction
of impulse
Myelin Sheath
Axon
Axon
terminals
Neuron
Pathophysiology
Patient experiences illness, then 1-2 weeks later the immune system begins to
attack the PNS and cranial nerves
The myelin sheath (necessary for nerve conduction) begins to deteriorate
Demyelination occurs, transmission of nerve impulses stops
Muscles innervated by these nerves undergo denervation and atrophy
Most common type of GBS: Acute Inflammatory Demyelinating
Polyneuropathy (AIDP) - discussed in this study guide
lOMoARcPSD|22650627
Causes/Risk Factors
Most likely autoimmune reaction 1-2 weeks
after one of the following:
Viral or bacterial infection
Viral - Cytomegalovirus
Bacterial - Campylobacter Jejuni
(thought to be the most common)
Surgery
Vaccination
Flu
Typically upper respiratory illness or GI
infection is the starting incident
Miller-Fisher Syndrome
Variant of GBS
Only few symptoms develop:
Eye paralysis
Walking unsteady
Normal reflexes disappear
Signs and Symptoms
Main feature is ascending, progressive, symmetrical weakness in limbs
Begins in both legs
Pain
Paresthesia (numbness & tingling)
Hypotonia ( muscle tone)
Max symptoms reached in 2-4 weeks
Leads to paralysis
after start, then recovery begins.
Leads to Areflexia (lack of reflexes)
Damage stops at 8 weeks.
Then moves to ANS in severe cases:
No treatment = improve slowly over
BP fluctuates
several months
Cardiac dysrhythmias
Early treatment = improve quickly in
Urine retention
days or weeks
Severe constipation
Recovery takes 1-2 years to return to
Body temp fluctuations
baseline
Facial flushing
Cranial nerve involvement soon after:
Facial weakness/paresthesia
Eye movement problems
Dysphagia
Respiratory failure if progresses (most serious complication)
↓
lOMoARcPSD|22650627
Treatment
Diagnosis
Can worsen rapidly so treat as a medical emergency
Ventilation may become necessary
Feeding- enteral or parenteral
IV fluids
If within 1st 2 weeks of symptom onset, one of the
following:
IV immunoglobulin
From donor, stops antibodies
Plasmapheresis
Filters antibodies from blood
Assess symptoms plus test results
CSF analysis via spinal tap (lumbar
puncture)
Looking for elevated protein
without elevated WBCs
Electromyography and nerve
conduction studies
Looking for demyelination of
nerves
Intervention
During acute phase:
Monitor:
Motor function for ascending paralysis
Reflexes
Cranial nerve function
Gag
Cornea
Swallow
LOC
ABGs
Vital capacity
BP
Cardiac rate/rhythm for dysrhythmias
I/Os
Respiratory status ***
Bowel sounds
Pain- provide meds as needed
Turn patient every 2 hours
Encourage movement if possible
May need to provide passive ROM
stretching
Provide enteral/parenteral nutrition
as prescribed
Support/communicate with pt often
as this is a scary time for him/her and
family - Let them know this is a
temporary condition
Around 28 days after first symptom, patient will start to recover spontaneously.
~80% completely recover within a few years
~65% have minor residual symptoms
lOMoARcPSD|22650627
The Kidneys
Major function: To remove waste products and excess fluid from the body
Bean-shaped organs about the size of a fist
located on either side of the spine at lowest
level of rib cage
Kidneys filter 150-200 qts of blood and
produce 1-2 qts of H2O every 24 hrs
Each kidney contains over a million nephrons
(the functional unit where blood is filtered
and urine is produced)
Each kidney connects to a ureter which leads
to the bladder
Glomerulus Filtration Rate (GFR) measures
the total amount of filtrate formed/min by
the kidneys. Normal = 90-120ml/min
All Functions
Remove waste products from blood
Remove drugs from the blood
Help balance the body's fluids
Release hormones that regulate
blood pressure
Produce active form of Vitamin D
for bones
Control production of RBCs
Kidney
Anatomy of Kidney
1. Renal Capsule - outermost layer; gives kidney
shape an protects from infections
Ureter
2. Renal Cortex - outer layer within the kidney;
where the majority of the blood filtration and
urine production occurs; contains most of the
nephron structure minus the loop of Henle
3. Renal Medulla - inside layer; hypertonic; helps
maintain water and salt balance; contains part
of the nephrons (loop of Henle)
4. Renal Artery - Brings fresh oxygenated blood
from heart to be filtered; branches off into
afferent and efferent arterioles
5. Renal Vein - takes filtered blood back to heart
to be re-oxygenated and pumped to body
Bladder
3. Medulla
4. Artery
5. Vein
Ureter
2.
Cortex
1.
Capsule
Kidney Cross Section
lOMoARcPSD|22650627
Nephrons
Functions
Each nephron consists of two parts:
Renal Corpuscle (Glomerulus and Bowman's
Capsule)
Renal Tubule
Blood enters glomerulus, is filtered, then passes out to
the body, the filtrate drips into the Bowman's capsule
and then passes into the tubule
In the tubule chemicals and H2O are added to or
removed from the fluid and then excreted down
ureters, stored in bladder, voided out via the urethera
Filters blood (in the renal
corpuscle)
Reabsorbs minerals/H2O
and secretes waste (in
renal tubule)
Produces urine (drains
into ureters)
Glomerulus filters out: H2O,
ions, AA, glucose,
creatinine, urea from blood
Filtered blood exits via
efferent arteriole to
renal vein
In the glomerulus (in Renal Cortex); very
high pressure causes ultrafiltration;
filtrate collects in bowman's capsule
Unfiltered blood enters
nephron from renal artery
Glomerulus Efferent
Arteriole Afferent
Proximal
Arteriole
Convoluted
Tubule
Filtrate flows through
Proximal Convoluted
Tubule; where it
reabsorbs: H2O, ions,
urea, glucose, AA
Filtrate enters loop of Henle
(in the Renal Medulla). Goal
here is to concentrate urine.
In descending limb permeable to H2O
only- H2O leaves
filtrate
Distal
Convoluted
Tubule
Bowman's
Capsule
Renal Cortex
Leaves as urine
to ureter
Collecting
Tubule
Renal Medulla
Loop of
Henle
Nephron
To Ureter
In ascending limb permeable to ions
only- Na, Cl, K
pumped out of
filtrate
In Collecting
tubule reabsorbs
Na, H2O, urea
In distal convoluted
tubule - Reabsorbs Na,
H2O, Cl, Ca, HCO3;
Secretes K, H
lOMoARcPSD|22650627
RAAS: Renin-Angiotensin-Aldosterone System
A series of reactions designed to help regulate blood pressure.
1.
Blood pressure falls
→ Kidneys release RENIN
2. Renin activates ANGIOTENSINOGEN (from
liver)
3. Angiotensinogen turns into ANGIOTENSIN I
4.
ACE Inhibitors
work by blocking
this step
Angiotensin-Converting Enzyme (ACE) from lungs
converts Angiotensin I into ANGIOTENSIN II (the
main product of RAAS). Then:
ANGIOTENSIN II:
Causes vasoconstriction of venous and arterial
vessels
BP
→↑
Triggers release of Aldosterone from adrenal glands:
Causes kidneys to retain Na and H2O
Causes kidneys to secrete K
Triggers release of ADH from pituitary gland:
Causes kidneys to retain H2O
Increased Na and H2O retention causes increased blood pressure
lOMoARcPSD|22650627
Chronic Kidney Disease
Slow and progressive decline in the kidneys' ability to filter blood properly.
Causes
Diabetes - glucose sticks to artery
walls → ↓ blood supply to kidneys ** Most common
↑ BP - constant pressure damages
artery walls → ↓ blood supply to
kidneys - ** Most common
Urinary tract obstruction
Polycystic kidney disease
Autoimmune disorder (ex. lupus)
Infections
Certain meds (NSAIDS,
aminoglycosides, chemotherapy
drugs)
Diagnosis
Blood and urine tests to look for:
↑ urea and creatinine
↑ K, PO4 and PTH
↓ Ca and calcitrol
↓ Hg
Blood more acidic
Ultrasonography to rule out
obstruction
Risk Factors
Diabetes
↑ BP
Heart Disease
Family history
Stages of Kidney Disease
Normal GFR = 90-120 ml/min
Stage 1: Damage with normal renal fnx:
GFR: > 90 ml/min
Stage 2: Mild loss of renal fnx:
GFR: 60-89 ml/min
Stage 3: Mild-severe loss of fnx:
GFR: 30-59 ml/min
Stage 4: Severe loss of fnx:
GFR: 15-29 ml/min
Stage 5: End stage renal disease
GFR: < 15 ml/min
Signs/Symptoms
-Usually asymptomatic at firstEarly stages:
Nocturia (early on)
Fatigue/weak (due to metabolic waste in
blood and anemia)
↓ appetite, N/V
SOB
Unpleasant taste in mouth
Easily bruise and bleed
Gout/joint pain/swelling
Advanced stages:
Muscle: twitches/weakness/cramps/pain
Restless legs syndrome
Encephalopathy
Heart failure; pericarditis
GI ulcers
Uremic frost (deposits of urea crystals
on skin)
lOMoARcPSD|22650627
The progressive decline in kidney function will cause many problems:
Inability to remove waste from blood:
Uremia
Metabolic Acidosis
Proteinuria
Hematuria
Gout (from uric acid levels)
Filtering less H2O kidney
thinks BP is low
renin
release
BP
↑
→↑
→
→↑
Inability to balance body fluids:
Hypervolemia
Edema
BP
↑
Inability to Activate Vit D:
Vit D not available to help
reabsorb Ca
Ca
→↓
Intervention
Monitor for Kussmaul breathing
(due to metabolic acidosis)
Iron supps: IV, subq, or blood
transfusions
Monitor EKG (cardiac events)
Monitor lab values (esp. K)
May provide Keyexalate
PO4 binders (with food)
Avoid antacids/laxatives with Mg
IV Ca if ordered
Monitor I/Os; daily wts
Monitor BP/swelling
Educate on diet
Inability to regulate electrolytes:
K (can cause heart problems)
PO4 (will bind to Ca and
decrease it)
Ca levels (will increase PTH cause Ca to leak from bones renal osteodystrophy)
Mg
↑
↑
↓
↑
Inability to help
produce RBCs:
Anemia
Inability to
create urine:
Oliguria/
Anuria
Treatment
Treat condition that worsens fnx:
Meds for ↑ BP
Diet and meds for DB
Remove UTI obstruction
Clear infection
Reduce meds that cause damage
Dietary changes
Meds
Dialysis/Transplant (for advanced)
Diet
↓ Protein; consume sufficient carbs
to offset calories
↓ K (avoid: potatoes, avocadoes,
strawberries, tomatoes, oranges,
bananas)
↓ PO4 (avoid: poultry, fish, dairy,
nuts, sodas)
↓ Mg (avoid: pumpkin seeds,
almonds, spinach, cashews)
↓ Na
lOMoARcPSD|22650627
Acute Kidney Injury
Rapid decline in the kidneys' ability to filter blood properly.
Causes
Prerenal Injury - Due to decreased blood flow to the kidneys from:
Sepsis *most common
Hemorrhage
↓ CO
Heart failure
MI
Dehydration
Loss of large amounts of Na and fluid
Shock
Meds (aminoglycosides & contrast agents)
Injury that blocks blood vessels
Liver failure
Intrarenal Injury - Due to damage to the nephrons in the kidney from:
Meds (NSAIDS, contrast agents
used in imagery tests, poisons,
chemotherapy drugs)
Trauma
Rhabdomyolysis
Glomerulonephritis
(inflammation of glomeruli)
Sepsis
Tumors within kidneys
Postrenal Injury - Due to blockage in the urinary tract (between
kidneys and urethra) from:
Enlarged prostate
Narrowing of urethra
Bladder cancer
Tumor in urinary tract
Stones in ureters or bladder
Renal calculi
Signs/Symptoms
Early stages:
Middle stages:
Left untreated:
H2O retention →
swelling of
feet/ankles/face/hands
↓ UO
Oliguria/anuria
Fatigue
↓ concentration
No appetite
Nausea
Itchiness (pruritus)
Chest pain
Seizures
SOB
lOMoARcPSD|22650627
Diagnosis
Blood tests to look for:
↑ BUN and Cr
↑ K and PO4
↓ Na
Blood acidosis
Treatment
Urine tests to look for:
Na, K, Ca, PO4
Ultrasonography or CT to
check for hydronephrosis
or enlarged bladder
Treat cause
Dialysis may be nec.
↓ fluids, Na, PO4, K
PO4 binders
Stages of AKI
Lasts a few
hours to
several days
Onset Stage:
Kidney injury occurs
S/S start to appear
Oliguric Phase:
Glomerulus not filtering
blood properly (↓ GFR)
UO < 400 ml/day
Spec. grav > 1.020
↑ BUN, Cr, K, PO4
↓ Ca
Hypervolemia
Metabolic acidosis
** Pt may go on dialysis
Diuresis Stage:
Cause of AKI has been
corrected
UO 3-6 L/day due to
osmotic diuresis
Pt now more alert
Urine now diluted (spec.
grav. < 1.020)
Intervention
↓ K & ↓ pro diet
Safety (due to neuro changes)
Monitor EKG and lab values
May give kayexalate
↓ fluids
Strict I/Os / Daily wts
Monitor RR & O2 Sat
Watch for Kussmaul breathing
Give PO4 binders
Intervention
Strict I/Os
Daily wts
Monitor:
Dehydration
Hypovolemia
↓ BP
Recovery Stage:
↓ edema / UO normal
GFR returns to normal
Lasts 8-14
days
BUN/Cr/K/PO4/Ca all
return to normal
Lasts 7-14
days
Lasts a few
months- 1 year
lOMoARcPSD|22650627
Renal Calculi (Kidney Stones)
Hard deposits of minerals and salts that form out of the filtrate produced
by the nephron.
The nephron filters waste from the blood into
a filtrate that is excreted in urine
Sometimes the minerals and salts in the
filtrate become concentrated, form crystals
and turn into stone
These stones either stay in kidney or travel
through the urinary tract
Vary in size
From microscopic to 1 in or more
Largest is the 'staghorn' which can fill
entire renal pelvis
Vary in material/type
Calcium Oxalate (most common)
Uric Acid
Cystine
Struvite
Vary in location
Kidneys (most common)
Ureters
Bladder
Risk Factors
Hyperparathyroidism
Dehydration
Renal tubular acidosis
Diets low in Ca or high in:
Animal protein
Vit C (increases oxalate in urine)
Family history
Bariatric surgery
Decreased mobility
Hypocitraturia - citrate helps stop stone
formation & keeps urine alkaline
Staghorn
Stones in
kidneys
Stone in
ureter
Stone in
bladder
Signs and Symptoms
Depends on type and location
Small stones often no symptoms
Pain in lower abs (stone in bladder)
Renal colic: Pain in between ribs
and hips to abs and back (stone in
renal pelvis)
Ureteral colic: Pain in waves in
genital area (stone in ureter)
N/V
Restlessness
Sweating/chills/fever
Blood may be in urine
Frequent urge to urinate (↓ UO)
Cloudy, foul-smelling urine
lOMoARcPSD|22650627
Types of Renal Calculi
Calcium Oxalate stones:
Causes of
↑Ca in filtrate:
Causes of
↑oxalate in filtrate:
Hypercalcemia:
Excessive Ca supps
Eating too much salt
Renal tubule problems
Too much animal protein in diet
Hyperparathyroidism:
Too much PTH released which ↑
Ca release from bones
Most common
Forms in acidic urine
Forms when concentration
of Ca or oxalate in filtrate
↑
Uric Acid stones:
Forms when too much uric acid in
urine
Causes of too much uric acid in urine:
Diet ↑ in purine
Diet ↑ in animal protein
Dehydration
Gout
Diabetes
↑ intake of high-oxalate foods
GI disorders (UC, Crohn's)
Fats aren't digested so they
bind with Ca and leave oxalate
behind (oxalate normally
binds with Ca)
Struvite stones:
Cystine stones:
Forms when too much amino acid
cysteine in urine
Cysteine not properly reabsorbed
in nephron
Rare, genetic
Due to urinary tract infections
Mg, NH3 and PO4 crystallize
Very large stone
AKA Staghorn
Rare
Diagnosis
Renal colic- good
indication of stones
Hard to dx otherwise;
need to eliminate other
causes of pain
CT; Ultrasound
KUB xrays
IVP (Intravenous Pyelogram)
Check for allergies to
shellfish or iodine, if on
metformin, pregnant or
breast feeding
Urinalysis to show:
blood/pus/infection/crystals
24-hr urine test:
Measures ions, uric
acid, Cr, Citrate, Ph
Keep on ice
Strain for stones!
(need to test to
determine what type)
lOMoARcPSD|22650627
Treatment/Intervention
Small stone: Wait for it to
pass:
Keep pt pain ↓ with
round-the-clock pain
meds (NSAIDS/opioids)
3-4 L/day fluids
Helps move stone
Keeps urine diluted to
prevent infection and
add'l stone formation
Monitor I/Os
Check for s/s of UTI
Strain for stones!
Keep mobile
Small stones that block UT or
w/infection will need to be
removed
Large stone > 3/16 in (5 mm)
or close to kidneys probably
won't pass on own
Stone removal:
Extracoporeal Shock Wave Therapy
(ESWL): For stones 1/2 in (1 cm) or less
Noninvasive
Maintain fluid intake
Pain medication/Keep mobile
Strain urine
Percutaneous Nephrolithotomy: For
large stones or where ESWL not option
Invasive
Incision in back: nephroscope &
probe used to remove/break stone
Maintain fluid needs 3-4 L/d
Maintain nephrostomy (empty bag,
monitor for infection)
Strain urine (if stone not removed)
Uteroscopy: to remove stones in lower
part of ureter
Scope inserted from urethra to
kidneys to remove or break stone
Maintain fluids
Pain medication/Keep mobile
Strain urine (if stone not removed)
Prevention
Maintain hydration 2L/d
Alluprinol - to ↓ uric acid
levels
HCTZ (hydrocholorthiazide) to ↓ Ca in urine
ABx to prevent UTIs
Do not ↓ intake of Ca other
than in med form
Diet:
↓ animal protein
↓ food high in purine
Bacon, liver, sardines, anchovies, dried
peas, beans, beer
↓ foods high in oxalate
Rhubarb, spinach, cocoa, nuts, pepper,
tea
Instruct on how to strain urine and keep stone
lOMoARcPSD|22650627
Urinary Tract Infections
Infection in the urinary tract caused by bacteria, virus or fungus.
Upper Tract
Kidneys
Infection of kidneys
(Pyelonephritis)
Ureters
Lower Tract
Infection of bladder
(Cystitis)
Infection of urethra
(Urethritis)
Bladder
Urethra
Urinary Tract Infection Overview
Infections usually start in urethra and spread to bladder
If unchecked, can spread to ureters and kidneys
Cystitis most common
Pyelonephritis can spread to bloodstream and lead to sepsis
Women at greater risk of infection due to anatomy: Shorter urethra and closeness
to rectum (spread of bacteria)
Urinary tract has several defense mechanisms against infection:
Valves - at ureters and bladder (one-way)
Muscles of bladder - squeeze urine out
Pressure in bladder - pushes urine out
Urine is sterile with antiseptic qualities
Lining of urinary system has immune cells
Male prostate glands secrete fluid with antimicrobial properties
Bacteria in vagina - lactobacilli - keeps area acidic
lOMoARcPSD|22650627
Urethritis - infection of the urethra
Causes:
Bacteria, fungus, virus
E. Coli (common)
STD (common)
Diagnosis:
Urinalysis
Urethral swab
Urine culture
Causes:
Signs/symptoms:
Pain during urination
Frequent need to urinate
Occ discharge in men
Treatment:
Abx
Antiviral for herpes
STD infections > treat partners
Left
unchecked
can lead to
narrowing
of urethra
Cystitis- infection of the bladder
Bacteria (E. Coli)
Common among women during
Diaphragm use
reproductive years, especially
Condom w/spermicide use
during pregnancy.
Catheter infected w/bacteria
Wiping back to front
Signs/symptoms:
Bubble baths/scented tampons
Burning/painful during urination
Hormonal changes
Frequent need to urinate
Abx (change flora of body)
Pain lower back
Immobility
Nocturia
VUR in children (genetic, valves don't
Cloudy urine (severe infection)
close properly, urine backflows to
Elderly: fever, confusion, no
kidneys)
symptoms related to urination
Obstruction (stone in bladder or
urethra)
Enlarged prostate
Narrowing of urethra
Diagnosis:
Treatment:
Urinalysis
Urine culture
Abx
Treat cause if not bacteria (e.g. obstruction)
lOMoARcPSD|22650627
Pyelonephritis- infection of the kidney
Causes:
Bacteria (E. Coli) (~90% cases)
Physical blockage of urine:
Structural abnormality
Kidney stone
Enlarged prostate
Backflow of urine
Infection through bloodstream (~5%)
Signs/symptoms:
Sudden:
Chills
Fever
Pain in lower back on either
side
N/V
Frequent, painful urination
Elderly: confusion, fever or sepsis
Intervention
Maintain I/Os
Make sure UO >30 cc/hr
Tylenol/NSAIDS
Meds per MD order:
Pyridium (will cause
orange-colored urine)
Sulfonamide (bactrim)
Instruct on proper specimen
collection
Instruct on prevention
More common among
women than men.
risk during pregnancy
(enlarged uterus puts
pressure on the ureters)
risk with diabetes or
immune system
↑
↑
↓
Diagnosis:
Urinalysis - RBCs, WBCs,
bacteria
Urine culture - bacteria
Blood test: WBCs, bacteria,
kidney damage
Treatment:
Abx (PO or IV with
hospitalization)
Prevention
Drink 2-3 L fluids/day
Void every 2-3 hours
Avoid spermicides and diaphragms
Wipe front to back
Avoid tight, non-porous underwear
Urinate immediately after intercourse
Take all abx as prescribed
Specimen collection:
Wipe w/antiseptic wipe
Void small amount
Collect urine midstream
Keep cup few inches from urethra
lOMoARcPSD|22650627
Glomerulonephritis
Condition in which inflammation of the glomerulus causes the release of
RBCs and protein into the urine
Glomerulus
The nephron is the part of the kidney that
filters blood and produces urine
The glomerulus filters out water, ions, urea,
glucose and amino acids from the blood
It does NOT filter out protein and blood
cells
However, when the glomerulus is damaged it
will filter protein and blood cells allowing
them to be excreted via the filtrate into the
urine
Glomerulonephritis leads to hematuria and
small amounts of proteinuria
Proximal
Convoluted
Tubule
Efferent
Arteriole Afferent
Arteriole
Distal
Convoluted
Tubule
Bowman's
Capsule
Collecting
Tubule
Renal Cortex
Loop of
Henle
Renal Medulla
To Ureter
Nephron
Glomerulonephritis can be Acute or Chronic
Causes of Acute
Infections (bacterial, fungal, parasitic, viral)
Most common infection is from Strep throat:
Called Acute Glomerulonephritis
Poststreptococcal
Appears 2 weeks after strep throat infection
Usually in pediatric population 2-10 yrs
Immune system actually causes the
inflammation of the glomerulus
Lupus and Goodpasture syndrome (autoimmune)
Granulomatosis w/polyangiitis (blood vessel
inflammation)
Causes of Chronic
Cause often unclear
Develops very slowly over years
If pt had acute glomerulonephritis
it may develop into chronic
lOMoARcPSD|22650627
Signs and Symptoms
S/S of Acute
50% have no symptoms
Edema - first face/eyelids later legs
UO
Dark urine
kidney function
BP/Cr/BUN,
Drowsy, confused
Elderly - Nausea, malaise
↓
↓
→↑
↓GFR
Hematuria leads to dark urine
Proteinuria leads to edema b/c
low albumin in blood causes
water to move out of capillaries
into tissues
S/S of Chronic
No symptoms for a long time
Later: BP & Edema
↑
Diagnosis
Blood and urine tests:
Protein
Blood cells
GFR
BUN/Cr
Biopsy to confirm
glomerulonephritis
Treatment
Acute:
Treat the
disorder/infection
Diet: ↓ protein & Na
Diuretics
HTN meds
Possibly Abx or
corticosteroids
Chronic:
ACE
Inhibitors
or ARBs
↓ Na diet
Acute poststreptococcal glomerulonephritis resolves completely in most
cases, especially in children.
1% in children and 10% in adults develop chronic kidney disease.
Intervention
Monitor fluid status
I/Os
Daily wts
Void 30 cc/hr or 1 m/kg/hr (kids)
Monitor for swelling and lung sounds
↓ fluids; diet: ↓ protein & Na
Monitor:
K, BUN, Cr, BP
Provide meds per MD order:
Diuretics
Antihypertensives
Abx
lOMoARcPSD|22650627
Nephrotic Syndrome
Condition in which damage to the glomerulus causes excessive amounts of
protein to be excreted into the urine.
↑ protein in urine (>3 gm/day) → ↓ protein in blood
↓ protein (albumin) in blood → edema (water leaves capillaries into tissues)
Liver senses hypoalbuminemia and makes more albumin and at the same time
makes cholesterol and TG → hyperlipidemia
Also lose
Immunoglobulins from blood → increase risk for infections
Proteins that prevent clot formation → increase risk of clot formation
Causes
Signs and Symptoms
Primary - (originates in kidneys):
Minimal Change Disease - most common cause
in children
Focal Segmental Glomerulosclerosis - most
common cause in adults - scar tissue forms in
part of glomeruli
Secondary (>50% of adult NS cases are secondary):
Usually a systemic disease like lupus or DB
NSAIDS
Glomerulonephritis
Certain allergies
Treatment
Treat cause if known
Meds: ACE Inhibitors, ARBs,
statins, possibly:
corticosteroids,
immunosuppressants, anticoags
Diuretics
Diet: ↓ sat fat/chol/Na
No appetite; malaise
Proteinuria (>3 gm/day)
**Frothy urine (from protein)
Puffy face/hands/legs, ascites
Ab pain
Diagnosis
May be mistaken for heart
failure in older adults
Urine/blood tests: Cr,
albumin, lipids
Intervention
Monitor fluid status:
I/Os
Daily wts
Void 30 cc/hr adults or 1 ml/kg/hr
Watch for infection (↓ immune system)
Watch for blood clots: swelling, pain in
legs, arms (DVT)
Monitor pulmonary status
Diet: ↓ sat fat/chol/Na
lOMoARcPSD|22650627
Dialysis
Artificial process for removing waste products and excess fluids from the
body when kidneys are not functioning properly.
Two types of dialysis: Hemodialysis and Peritoneal Dialysis
Patient with kidney failure may need to go
on dialysis when:
Very high levels of K or Ca
Uremic encephalopathy
Pericarditis
Acidosis
Heart failure
Excessive fluid in body
Pulmonary edema
Symptoms of renal failure
GFR < 10-15 ml/min
Goal of Dialysis
↓ waste in blood
Correct acidosis
Reverse electrolyte
imbalances
Remove excess fluid
Two other options to filter blood:
Hemofiltration - done in ICU as a
continuous procedure; can filter large
amounts of blood
Hemoperfusion - used to treat
poisoning; charcoal filter absorbs poison
Hemodialysis
Blood removed from body and
pumped into a dialyzer (artificial
kidney) which filters metabolic
waste, electrolytes and fluids. Blood
returned purified.
Total amount of fluid returned can be
adjusted
Total time is about 3-5 hours 3 times
per week
Can be done at home or dialysis
center
Most common dialysis
Complications
↓ BP (most common)
Infection of graft or
fistula
Fever
Anaphylaxis (allergy to
substance in dialyzer or
tubing)
Dysrhythmias
Air embolus
Bleeding in the
intestine, brain,
eyes or abdomen
from too much
heparin in dialyzer
lOMoARcPSD|22650627
Peritoneal Dialysis
Uses the peritoneum (membrane that lines the
abdominal cavity) to act as a natural filter
Fluid (dialysate) infused through catheter into
peritoneal space
Dialysate sits for a period of time, absorbs waste
products, electrolytes and then is drained and
discarded. Repeated 4-5 times/day.
Uses osmosis: dialysate has concentration of
glucose attracting fluid (more fluid is drained
than was instilled)
Less efficient than hemo, but can be run for
longer times
Done at home; can use machine or manually
↑
Complications
↓ BP (most common)
Bleeding (irritation of peritoneum)
Infection (at insertion site)
Hypoalbuminemia
Scarring of peritoneum
Hernias (ab or groin)
Constipation - interferes with
dialysate flow
Venous Access
External shunt/catheter Cannula placed in large vein
and large artery near each
other; for immediate use;
usually short-term. Prone
to infection, clotting, skin
erosion
Arteriovenous fistulas Large artery and vein sewn
together below surface of
skin (creates one blood
vessel for both withdraw
and return)
Requires surgery and
healing time (up to 6 wks)
Arteriovenous graft - Uses a
synthetic connector to
connect artery and vein
(also creates one blood
vessel for both withdraw
and return)
Requires surgery and
healing time (up to 2 mos)
Intervention
Wts are crucial
Excessive fluid lost = BP or shock
Fluid retention = BP or edema
Monitor vitals during dialysis!
Peritoneal- keep in Semi-Fowler's position
(to take advantage of gravity)
Diet peritoneal: adequate pro & cal; low to
no salt (table or K-containing)
Diet hemo: Na and K restricted, phosphorus
limited
↑
↓
Monitor for complications:
N/V
Signs of bleeding (clotting time)
Fistula/graft site
Agitation/disorientation/convulsions
Peritoneal: Color of fluid removed
(bloody effluent may be bleeding inside)
Peritoneal: Cloudy discharge may mean
infection
lOMoARcPSD|22650627
Diuretics
Medications used to remove extra fluid volume from blood through
increased urination. They work by altering the processes in the nephrons.
Glomerulus
4 main types of diuretics
Loop - work in the loop of Henle mainly the thick ascending limb
Thiazide - work in the first part
of the distal convoluted tubule
Potassium-sparing - work in last
part of distal convoluted tubule
and collecting duct
Osmotic - work in the proximal
convoluted tubule and descending
limb of loop of Henle
Proximal
Convoluted
Tubule
Osmotic
Bowman's
Capsule
Efferent
Arteriole Afferent
Arteriole
Distal
Convoluted
Tubule
Thiazide
K-sparing
Collecting
Duct
Loop
Loop of
Henle
To Ureter
Nephron
Location of action in the nephron
Diuretics Overview
Loop are the most powerful diuretics
Thiazide best for HTN
Both Loop and Thiazide cause K LOSS
K-Sparing are rather weak, so used w/Loop and Thiazide to help spare K
Remember water loves Na and will follow it!
All diuretics increase urination, so dehydration main concern for use
along with maintaining electrolyte balance
lOMoARcPSD|22650627
Loop Diuretics
Names
Most end with NIDE or MIDE
Bumetanide (Bumex)
Furosemide (Lasix)
Torsemide (Demadex)
Ethacrynic acid
Used for
Pulmonary edema
HTN (Thiazides work better)
Ca levels
Edema
Heart failure
Liver impairment w/ascites
↑
Side Effects
↓Ca, K, Na and Mg levels
↓ BP
↑ uric acid levels → gout
Ototoxicity
Interactions
↓ blood flow to
→ ↓diuretic effects
↓Na →↑lithium
↓K → ↑digoxin
NSAIDS:
kidneys
Lithium:
Digoxin:
**Most powerful diuretic**
Action
Blocks reabsorption of Na, Cl and K in
loop of Henle (where 25% of Na is
absorbed from filtrate)
Na in
filtrate
H2O excreted as urine
(H2O loves Na and will follow it)
→↑
→↑
Nursing Considerations
Monitor:
Dehydration
Hypotension
Vitals
I/Os and Daily wts
Look for signs of gout
Slow IV route for furosemide to avoid
damaging inner ear (ototoxicity)
Monitor labs:
Hypokalemia (will need to
supplement if <3.5 mEq/L) (if on
digoxin, monitor level)
Hypocalcemia
Hyponatremia (if on lithium,
monitor level)
Hypomagnesemia
Educate:
S/S of dehydration
BP and HR mmnt
Wt daily & notify MD if +3 lbs in 1
day
Encourage K foods
↑
lOMoARcPSD|22650627
Thiazide Diuretics
Names
Hydrochlorothiazide (HCTZ)
Indapamide
Chlorothiazide
Metolazone
Chlorthalidone
Used for
HTN (best)
Heart failure
Renal calculi from Ca
Side Effects
↓Na levels
↑ Ca (helps with
preventing renal stones and
↑ bone density)
↓K and loss of H+ ions
↓BP
Hyperglycemia
↑uric acid levels (gout)
Contraindications
Renal impairment
Pregnancy
Not as powerful as Loop
Action
Blocks reabsorption of Na and Cl in
the first part of the distal convoluted
tubule (where 5-7% of Na is absorbed
from filtrate)
Na in filtrate
H2O excreted as urine (H2O loves
Na and will follow it)
→↑
↑
→
Nursing Considerations
Monitor:
Dehydration
Hypotension
Vitals
I/Os
Daily wts
Look for signs of gout
Monitor glucose in DB pt
Give with meals to GI upset
Monitor labs:
Hypokalemia (will need to
supplement if <3.5 mEq/L) (if on
digoxin, monitor level)
Hypercalcemia
Hyponatremia (if on lithium,
monitor level)
Educate:
S/S of dehydration
Diet in K
Wt daily & notify MD if +3 lbs in 1
day
Monitor BG if DB
↓
↑
lOMoARcPSD|22650627
Potassium-sparing Diuretics
Names
Spironolactone (Aldactone)
*Most common
Eplerenone
Triamterene
Amiloride
Side Effects
Hyperkalemia
Spironolactone may cause
antiandrogen effects:
Gynecomastia
Menstrual irregularity
Sexual dysfunction
Nursing Considerations
Monitor:
Dehydration
Vitals
I/Os
Daily wts
Give with meals to GI upset
Monitor labs:
Hyperkalemia (EKG changes Tall peaked T waves)
Educate:
S/S of dehydration
Diet in K and no salt
substitutes
Wt daily & notify MD if +3 lbs
in 1 day
↓
↓
Keeps K in blood
Action
Works in 2 ways:
Directly inhibit Na channels (in DCT
and CD) so Na can't go thru and is
therefore excreted
By working against aldosterone
(most common); Aldosterone's role
is to cause nephron to reabsorb
more Na & H20 into blood
Does NOT decrease K levels like the
other diuretics do
Often prescribed with loop or thiazide
to spare K
Used for
HTN
Edema due to
Heart failure
Liver impairment
Nephrotic syndrome
Hypokalemia (due to other diuretics)
Hyperaldosteronism
Interactions
May increase K:
ACE inhibitors
ARBs
NSAIDS
If on lithium, monitor level
lOMoARcPSD|22650627
Osmotic Diuretics
Names
Mannitol (Osmitrol) *Most common
Nursing Considerations
Administer via IV
Monitor:
Vitals
I/Os
Daily wts
Instruct pt to report changed in
LOC
Least common
Action
Exhibits osmotic pressure in renal
tubules that inhibits fluid reabsorption
(specifically in the proximal tubule and
first part of loop of Henle)
Used for
Treat cerebral edema
To intraocular pressure
Treat or avoid Dialysis Disequilibrium
Syndrome - neurological condition
from dialysis (rare)
↓
Side Effects
Heart failure
Pulmonary congestion
Pulmonary edema
Hyponatremia
lOMoARcPSD|22650627
Respiratory Disorders
Lung Anatomy and Physiology
Right Lung
*Has three lobes
Trachea
Carina
Primary
Bronchi
Left Lung
*Has two lobes
Secondary
Bronchi
Tertiary
Bronchi
Bronchioles
Notch for heart
Alveolar Sacs
Physiology of Gas Exchange
Inhaled air moves down the trachea to the carina where it splits into the right and
left primary bronchi. The primary bronchi break down into the secondary and
tertiary bronchi then into the bronchioles. From there into the alveolar sacs for gas
exchange.
RBCs from
heart
(deoxygenated)
RBCs to body
(oxygenated)
Air
Alveolus wall
CO2 O2
Capillary wall
Alveolus
lOMoARcPSD|22650627
Pneumonia
Respiratory tract infection that causes inflammation of the alveoli sacs.
Causes- Microorganism
**May involve more than one**
Bacteria - **Very common
Virus - **Very common
Mycobacteria
Fungi
Parasites
Usually the body can fight off these
microorganisms, but sometimes it
can't and pneumonia results.
Signs and Symptoms
Cough (produces sputum)
Chest pain (pleuritic)
Chills
Fever, aching
SOB
Rhonchi/Wheezes
Oxygen sat <90%
Nausea/vomiting
Medications
Antibiotics
Antivirals
Bronchodilator
Mucolytic (thins mucus)
The inflamed alveoli sacs lose their ability to inflate
and deflate and perform gas exchange. The pt then
starts to experience hypoxemia (low oxygen in the
blood) which leads to respiratory acidosis.
Risk Factors
65+ years of age
Diabetes
Lung cancer
Smoking
Immobile (e.g. stroke)
Post abdominal
surgery
Prior infection
Heart failure
COPD, asthma
Impaired immune
system
AIDS
Infants
Elderly
Two main types of pneumonia:
Community-acquired (contracted outside the
healthcare community)
Hospital-acquired (contracted in hospital- developed
48-72 hrs after admission)
Diagnosis
Chest x-ray
Abnormal lung sounds
Sputum culture
Intervention
Monitor:
Respiratory system
for lung sounds
Oxygen sat. should
be >95%
Suction as needed
Oxygen therapy
Encourage:
Coughing
Deep breathing
Fluids
Educate:
Stop smoking
Vaccinations
lOMoARcPSD|22650627
COPD
Chronic obstructive pulmonary disease is the persistent narrowing (blocking or obstruction) of
the airways. This occurs with emphysema, chronic obstructive bronchitis, or both.
Emphysema
Chronic Bronchitis
**Pink Puffers**
**Blue Bloaters**
Alveoli sacs are inflamed and cannot inflate
and deflate. Inhaled air is stuck in sac, causing
hyperinflation → diaphragm flattens → unable
to fully exhale → hyperventilation
'Pink Puffers' nickname comes from pink skin
color (vs blue) and hyperventilating
Bronchioles become damaged → increased
sputum production → hard to exhale →
increased air volume → hyperinflation along
with ↓ O2 levels and ↑ CO2 levels in blood
'Blue Bloaters' nickname comes from
cyanosis from hypoxia and bloating from
right-sided heart failure
Signs and Symptoms- Takes years to develop and show symptoms
Decreased energy
SOB
Weight loss
Respiratory acidosis
PCO2>45, PO2<90
Risk Factors
Smoking!!
Environmental pollution
Occupational (chemicals, dust)
Medications
Inhaled bronchodilators
Inhaled corticosteroids
Take bronchdilators 1st!!
Rinse mouth after use to
avoid thrush
Cough (dry or productive)
Coarse crackles or
wheezing
Barrel chest (emphysema)
May cough up blood
Pursed lip breathing
Breathing with tripod
stance
Cyanosis (bronchitis)
Diagnosis
Spirometry (pulmonary function test)
Chest Xrays
ABGs
Intervention
Smoking cessation!!
Supplemental oxygen
(keep oxygen at 8893%)
Educate:
Avoid sick people
Avoid extreme
temperatures
Educate:
Vaccines
Pursed-lip
breathing
Diaphragm
breathing
High-cal diet in
small meals
lOMoARcPSD|22650627
ASTHMA
Chronic lung disease that causes narrowing and inflammation of the airways
Causes:
Unknown (May be genetic or environmental)
Pathology
Asthma Attack
Bronchi and bronchioles are
chronically inflamed
Smooth muscles surround the airway and
help with dilating and constricting. These
muscles constrict during asthma attack.
Chest tightness and difficulty breathing
result. Then goblet cells produce excess
amounts of mucous. Air becomes trapped in
alveoli inhibiting proper gas exchange
respiratory acidosis.
May lead to Asthma attack
Asthma attack triggers
Allergens (pollens, dust mites, animal
dander)
Infections (colds, bronchitis)
Irritants (tobacco, fumes, air pollution)
Exercise
Stress/anxiety
NSAIDS, aspirin, sulfites
Signs and Symptoms
Early
SOB
Fatigue
Wheezing
Coughing at night
Incresed resp rate
↓ Peak flow best
Active
Tight chest
Wheezing
Difficulty
breathing
Increased RR
Needs Medical Intervention!
Inhaler won't work
Can't talk
Diagnosis
Dr eval s/s
Spirometry
X-Ray
Cyanosis
Sweaty
Medications
Bronchodilators
Corticosteroids
→
Asthma categories
Intermittent
Symptoms 2 days/week or less
No interference w/daily life
Mild persistent
Symptoms >2 days/week
Slightly interfere w/daily life
Moderate persistent
Symptoms occur daily
Interfere w/daily life
Severe persistent
Occur often throughout day
Greatly interfere w/daily life
Intervention
Keep pt calm
Monitor vitals
Position in high Fowler's
Bronchodilators/
oxygen/corticosteroids
Monitor skin color
Monitor lungs
Educate:
Avoiding triggers
lOMoARcPSD|22650627
ACUTE RESPIRATORY DISTRESS SYNDROME
(ARDS)
Respiratory failure when the capillary membrane surrounding the alveoli sac is damaged.
Pathology
Fast onset!
→
Capillary membrane is damaged fluid
leaks into the alveoli sac collapse of sac
lungs become stiff decreased gas
exchange hypoxemia organs suffer
→
→
→
→
→
Occurs often in people already hospitalized
who develop a complication.
High mortality rate
Cause- Indirect or Direct
Indirect
Sepsis **Most common
Burns
Blood transfusion
Pancreatitis
Drug overdose
Direct
Diagnosis
Pneumonia
Aspiration
Inhalation of toxic
substance
Embolism
Drowning
Chest injury
Pulse oximetry
(measures O2 levels)
Chest x-ray
Signs and Symptoms
Usually develop within 24-48 hrs post-injury or disease
SOB
Rapid, shallow breaths
Crackles
Wheezing
Medications
Corticosteroids
Antibiotics
Cyanosis
Increased heart rate
Confusion
Sleepiness
Intervention
Usually mechanical intervention w/PEEP
Pressure kept at 10-20 cm H2O
Prone position (so heart does not compress
lungs)
Monitor:
Urine output
BP
CO
Mental status
lOMoARcPSD|22650627
PLEURAL EFFUSION
Abnormal collection of fluid in pleural space
Cause
Heart failure
Tumors
Pneumonia
Pulmonary embolus
Coronary artery bypass
surgery
Chest injury
Cirrhosis
Kidney failure
Pleural space is the area between the two
layers of the membrane that covers the
lungs
Diagnosis
Chest x-ray
Ultrasonography
Lab tests on fluid
(will determine cause)
Signs and Symptoms
Fluid is either:
** Rich in protein (exudate)
OR
** Watery (transudate)
Medications
**Usually no symptoms**
IV Antibiotics if caused by
pneumonia
SOB
Chest pain (pleuritic)
Decreased chest sounds
Intervention
Will need to treat the disorder causing PE
Small effusions may not need treatment
Large effusions may require drainage via
thoracentesis
Lung Terminology
Tidal volume: Amount of air moved
in and out of lungs with each
respiratory cycle
Residual volume: Amount of air in
lungs after forced expiration
Peak Flow Meter: Measures how well air
moves out of lungs
Personal Best is the highest number
over a 2-week period (when asthma is
controlled)
Spirometry- test to evaluate
respiratory function and assess
pulmonary disorders
Forced expiratory volume
(FEV)- measures how much
air a person can exhale
during a forced breath
Forced vital capacity (FVC)total amount of air exhaled
during the FEV test. Normal
is 80-120%
lOMoARcPSD|22650627
Shock
Condition characterized by decreased tissue perfusion and impaired
cellular metabolism.
Shock in a nutshell
Shock occurs when the blood pressure
becomes so low that the body's cells do not
receive enough blood and therefore not
enough oxygen
Organ cells stop functioning normally due to
the low oxygen supply
The cells become irreversibly damaged and
die and the organ begins to fail
When 2 or more organs fail = Multiple Organ
Dysfunction Syndrome (MODS)
MODS = high likelihood of death
Types of Shock
Cardiogenic
Hypovolemic
Distributive
Septic
Neurogenic
Anaphylactic
Causes
Cardiogenic - Due to inadequate pumping of the heart
Complications of MI, pulmonary embolism, malfunction of a heart valve,
arrhythmia, myocarditis, endocarditis, cardiac tamponade
Hypovolemic - Due to low blood volume
Severe bleeding - External (injury) or Internal (ulcer, GI bleed, ruptured
blood vessel)
Excessive loss of body fluids - major burn, severe diarrhea/vomiting,
pancreatitis, untreated diabetes
Distributive - Due to excessive dilation of blood vessels (vasodilation)
Septic - severe bacterial infection
Neurogenic - injury to spinal cord (or occasionally to brain)
Anaphylactic - serious allergic reaction
lOMoARcPSD|22650627
Stages of Shock
Initial Stage- Not clinically apparent
Cardiac Output (CO) very low and cell hypoxia occurs
Cells change from aerobic to anaerobic (without oxygen) metabolism
Anaerobic metabolism creates lactic acid
Liver not receiving enough oxygen so can't metabolize the lactic acid
Buildup of lactic acid in blood pH drops
Serum lactate > 4 mmol/L = lactic acidosis
→
Compensatory Stage - Body tries to recover
Goal is to increase CO or Blood Volume (BV) to help tissue perfusion:
Baroreceptors stimulate the SNS to release epinephrine and norepinephrine
This will cause vasoconstriction
BP and HR
perfusion to vital
organs and to non-vital organs (puts at risk for paralytic ileus)
Body shifts fluid from interstitial compartment to intravascular
CO & BP
Kidneys activate the RAS produces Angiotensin II (a vasoconstrictor)
more blood to heart and BP
tissue perfusion and cells more oxygen
Aldosterone released due to Angiotensin II kidneys keep Na & H2O
BV
Kidneys retaining Na
serum osmolality
this tells pituitary gland to
release ADH keeps H2O in kidneys
BV
At this stage if cause of shock is corrected patient can recover
→↑
↓
→
→
↑ →↑
→↑
↑ →↑
→↑
→↑
→
→↑
→
→
Progressive Stage- All major organs begin to die
If patient hits this stage, the compensatory stage has failed and patient
moving to MODS
Cells swelling now and capillary permeability is
Fluids and protein drawn into interstitial space edema and BV
BV
CO and tissue perfusion
Mental status changes /ARDS / GI bleeding / Ulcers / Toxic waste buildup
Cardiac dysrhythmias leading to complete deterioration of CV system
DIC - (disseminated intravascular coagulation) - leads to massive bleeding
↓ →↓
↓
↑
→
↓
Refractory Stage - Cannot be reversed. All organs begin to shut down.
lOMoARcPSD|22650627
↓Capillary refill
↓BP, ↓CO, ↑HR, ↓UO
Crackles, tachypnea
Cyanosis & cool, pale, clammy skin
Weak peripheral pulse
Anxious, confused
N/V
EKG
Monitor - HR, rhythm, BP, CO
Watch for fluid overload
Asses heart sounds, lung sounds
Supplemental O2
Intubate/mech vent if necessary
Meds:
Nitrates, inotropes, diuretics
UO beginning to
SV, CO, BP, HR
Capillary refill
Tachypnea
Weak peripheral pulse
Cool, clammy skin
Anxious, confused
↓ ↓ ↓ ↑
↓
Stop loss of fluids, restore volume
Supplemental O2
Monitor fluid overload & UO
No specific meds
May not have signs at 1st
Vasodilation
Warm/flushed skin early, then
cool/clammy later
Pulse strong (bounding) at 1st
BP, HR, UO
GI bleeding/paralytic ileus
Hyperventilation, confused
Crackles, respiratory failure
Fluid replacement 1st
Then vasopressors (norepinephrine)
Inotropes (dobutamine)
Abx - Start within 1st hour! (obtain culture
right before start)
Monitor glucose closely
Supplemental O2
Intubate/mech vent if necessary
Anaphylactic
Neurogenic
Hypovolemic
↓
Treatment/Intervention
Septic
Cardiogenic
Signs and Symptoms
↓ ↑ ↓
Vasodilation
BP, HR
Unable to regulate body temp
Warm, dry skin at 1st
Cool, dry skin later on
Bowel dysfunction
Loss of reflex activity
↓ ↓
Maintain pt airway
Supplemental O2
Intubate/mech vent if necessary
Vasopressors
Atropine (for bradycardia)
Stabilize spine
Monitor temp and UO
Vasodilation
HR, BP
Sudden dizziness, chest pain
Incontinence
Swelling of lips and tongue
Wheezing, SOB, stridor, flushing
Anxious and confused, LOC
Cramping/ab pain/N/V/D
Maintain pt airway
Supplemental O2
Fluid resuscitation w/colloids
Meds: epinephrine 1st tx (IM or IV),
antihistamines, zantac, albuterol,
corticosteroids if hypotension persists > 2 hr
* Prevention
* Carry epipen
↑ ↓
↓