MED-SURG
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MED-SURG
BURNS
Damage to the skin's integrity by some kind of energy source
Types of Burns
• Thermal - Most common - as a result of a flame, flash, scald, or contact with hot things (liquid, steam, fire); e.g.
from cooking, burning leaves, smoking
• Chemical - as a result of contact with acids, alkalis, or organic substances - no heat needed
- acids (e.g. hydrochloric, oxalic, hydrofluoric)
- alkali (e.g. cement, oven/drain cleaners, heavy industrial cleaners); Because it attaches to tissue, it is more
difficult to treat.
- organic compounds (e.g. phenols and petroleum products)
• Electrical - caused by extreme heat produced by an electric current passing through the body and
damaging tissue
- Because the majority of the injury occurs beneath the skin, determining the level of damage is difficult. 'iceberg effect'
• Cold - caused by skin cold exposure; frostbite
• Radiation - as a result of sun exposure or cancer therapy
• Friction - induced by skin abrasion
- rope bur
- road rash (car accident)
SUPERFICIAL PARTIAL
EPIDERMIS
DERMIS
FAT
HYPODERMIS
DEEP PARTIAL
THICKNESS
FULL
THICKNESS
MUSCLE
SKIN STRUCTURE AND DEGREE OF BURN
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MED-SURG
BURNS
Burn Severity Depends on:
• Patientrisk factors
• Location of Burn
- Calculated in % of TBSA
- Use Rule of 9s (see next page)
• Extent of Burn
• Depth of Burn
• If they experienced an inhalationinjury or not
Depth of Burn
1 st
Degree
- Superficial partialthickness
- Only the epidermis
- The least severe
- Heals in seven days
- Dermatitis
- Pressure blanching
- Pain and slight swelling
- Pink/red skin
- Pleasant to the touch
- There are no blisters.
- There is usually no scarring.
2 nd
Degree
- Deep partialthickness
- The epidermis and the dermis
- Excruciatingly painful
- Blemishes
- Bleaching redness
- Inflammation (mild - moderate)
- Red/pink, shiny, and wet
- If the condition is severe, skin grafting may
be required.
3 rd
Degree
- Fullthickness
- All layers are harmed
- Not painful due to damage to nerves
- Skin will not heal; skin grafting is required.
- Healing will take months.
- Dry, leathery, tough skin (eschar)
- It might be black, yellow, red, or waxy white.
Eschar- dead tissue - dangerous if
around torso or extremity; will need
to be removed via escharotomy
4 thDegree
- Deep fullthickness
- All layers are damaged, including muscles,
bone, and ligaments.
- NO SENSE OF PAIN
- Black with eschar charring
- Months to recover
- Skin grafts will be required.
In Full Thickness, watch for acute
tubular necrosis (ATN), due to the
release of myoglobin and hemoglobin
that block kidney tubules.
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MED-SURG
BURNS
Extent of Burn
• To estimate the extent of the burn, utilize the Rule of Nines to calculate the
TBSA burned and then the Parkland Formula to calculate the fluids required.
4.5%
4.5%
Rule of Nines
4.5%
18%
Front
Purpose:
4.5%
4.5%
18%
Back
4.5%
1%
• Determine the total body surface area burnt (TBSA%) for second, third,
9%
and fourth degree burns.
9%
9%
• Using the Parkland Formula, determine the amount of fluid treatment required.
• Determine whether the patient satisfies the criteria for the burn unit.
Add the percent of each body
part burned.
This number equals the
TBSA%.
Use for 2nd
degree burns
or greater
Parkland Formula
Purpose:
To determine the total volume of
fluids (mL) required by a patient
24 hours after a burn.
Make sure TBSA is NOT a decimal!
Forinstance, if a patient has a TBSA% =
45%, use 45 in the equation, NOT 4
.5
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 overthe
next16 hours
Location of Burn - potential problems
• Respiratory - face, mouth, neck, and trunk (due to edema or eschar)
• Disability - Eyes, hands, feet, and joints (due to damage to nerves)
• Infection - Perineum (due to infection from urine/feces) and ears, nose (thin skin)
• Trouble Healing - Ears and nose (due to thin skin and poor blood supply)
• Compartment syndrome - Fullthickness circumferential burns
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MED-SURG
BURNS
Patient Risk Factors
• Previous heart, lung, or kidney disease (body already taxed)
• Diabetes mellitus
• Vascular Disease of the Periphery
• Any long-term illness that causes weakness
Inhalation Injury
Damage to respiratory system due to
breathing in toxic substances
Affects: Upper & lower airways
Signs:
• If the burn patient suffers fractures, head injuries, or other trauma.
• Age - whether children or the elderly
- Facial burns
- Soot in the spit, mouth, and nose
- Hair charring (head & nose)
- Brigntred's skin
- Hoarseness of voice
Pre-Hospital and Emergency Care
• At scene -
- Remove from the source of the fire
- Put an end to the burning process.
• Small thermal burns (10% orless TBSA)
- Cover with a cool, clean, tap-water-soaked cloth.
• If >10% TBSA or electrical/inhalation burn and patient unresponsive:
- Focus on CAB
• C - Circulation - Examine the pulse and raise the burned limb (s)
• A - Airway - Examine for patency, soot around the nose and on the
tongue, charred nasal hair, and blackened oral or nasal membranes.
• B - Breathing - check for ventilation
• If the patient is responding, do A B C
• Cool large burns no longerthan 10 minutes
- Do not submerge in cold water.
- Do not use ice to cover.
- Remove as much of the burned garments as possible.
- Wrap in a sheet or blanket.
• Chemical burns: remove all chemicals from the skin; remove any
chemical-containing clothing; and then cleanse the skin with water.
•Monitor patient with inhalation injury for signs of respiratory distress
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MED-SURG
BURNS
Phases of Burn Management
Emergent Phase
Onset of burn until
24 - 48 hours post
• Time required to address immediate, life-threatening issues
• Primary concerns: the start of hypovolemic shock and the production
of edema
• Hypovolemic shock is the most serious initial hazard to a large burn patient.
• The phase comes to a conclusion when fluid mobilization and diuresis
commence.
Pathos:
Increased capillary permeability causes:
• Plasma fluid will exit the intravascular area.
• Then come Na+ and Albumin.
• Fluids migrate to interstitial tissue
• Edema develops
• The blood thickens.
•
•
Intervention:
• IV accessibility (2)
• Using the formula, calculate fluids (lactated Ringer's).
• Electrical burns necessitate more fluids and
potentially osmotic diuretics (mannitol)
• Catheter to track urine output
- Check every hour monitor
- Target >30cc/hr
• Albumin injections are possible.
• Test urine for Hg and Mb (ATN)
• Raise the extremities above the level of the heart.
• Initially, pain medications were administered by
IV; opioids were prescribed.
• Intubation may be required (esp for face/neck burns)
• Wound treatment can begin if normal airway,
circulation, and fluid replacement are obtained
Hct, K+, Na+, WBC
Fluid may lead to hypovolemic shock:
- HR
- CO
- BP
Monitor for:
• Acute hypovolemic shock
• Imbalances in electrolytes
• Renal insufficiency
• Digestive issues
Wound Care:
• 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- removal of necrotic tissue
• Positioning - no cushions (especially if you have neck/ear burns); roll a cloth
under your shoulders
• Elevate the extremities to avoid edema and contractures.
• Do not allow two burn sites to come into contact (to prevent webbing)
• Range of motion/splints to prevent contractures
• Use pain relievers before dressing changes or debridement!
• Graft kinds include autograft (self), allograft (cadaver), CEA (grown from the patient's
own skin), and artificial skin.
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MED-SURG
BURNS
Phases of Burn Management
Acute Phase
48 - 72 hours after
burn until wound heals
Monitor:
• Normal urine output
• GI distress (pain, vomiting, blood in stool - this could
be a Curlings ulcer; constipation)
• Bowel noises (no sounds may be paralytic ulcer)
• Suctioning may necessitate the use of an NG tube
(to remove fluids, gas)
• Compartment syndrome if circumferential burns
- Distal extremity pulse absent/weak, coolto touch,
abnormal color
• Respiratory condition, particularly in cases of burn or
inhalation injury to the chest, face, or neck
• Imbalances in electrolytes:
- Potassium and sodium
• Infection signs ( HR, RR, BP, UO,
confusion, chills, appetite)
- Will need systemic abx
• Neurology: keep an eye out for signs of delirium.
• The fluid has been mobilized, and diuresis has
begun ( urine production)
• It could linger for several weeks or months.
• Infection prevention, pain management, nutrition,
and wound care are among the top priorities.
Intervention:
• NPO until bowel sounds + orderto eat:
- Will need Cal/Pro/Carb diet
- May need enteral
- Watch for hyperglycemia
- Early nutrition will complications and
mortality and healing
• Tetanus injection, antibiotics, and ulcer medication
• Sedatives, hypnotics, and antidepressants may also
be required.
• Pain relievers- IV is the best approach because the
skin layer and muscle may be injured.
• To avoid infection, use sterile sheets, gowns, gloves,
and isolate yourself.
• To avoid contractures, stretch ROM and move as
much as possible.
• Maintain a room temperature of at least 85F.
Rehabilitative Phase
wound closure to patient's optimal level
• The burn has healed, and the patient is back to work (physically and mentally)
• It can happen as soon as two weeks after the burn to 7-8 months afterwards.
• Primary areas of focus: psychosocial, ADLs, PT, OT, and cosmetic correction.
Goals:
• Avoid scarring/contractures (ROM & splints)
• Daily living activities (ADLs)
• Psychosocial aspects
• Physical/Occupational/Cosmetic Consultations
Educate:
• Scar management moisturizing
• Sun protection
• The significance of PT and OT
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MED-SURG
HEMATOLOGICAL
Components of Blood
Plasma
White Blood Cells
• Blood's liquid component
• A location where RBCs, WBCs, and platelets are
suspended
• Also known as leukocytes
• Less than RBCs
• Protect against infection
• When blood counts are low, this is referred
to as leukopenia.
- Infections are becoming more common.
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
Platelets
AKA
thrombocytes
•
• Aid in the clotting process
• When it is low, it is referred to as
thrombocytopenia.
- Bruising and abnormal bleeding
When
high called thrombocythemia
•
- Blood clotting may cause transient
ischemic attack
Thrombocytopenia
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
Cause
PLT <150,000
Signs
• Anemia
• Prolonged bleeding time
• Leukemia
• Platelet disorders
• Enlarged spleen
• Toxins
• Petechiae on lower legs
• Purpura (bruising)
• Bleeding gums
• Blood in stool/urine
• Cirrhosis
• Heavy menstrual cycles
• Infections
• RBC transfusions
• INR, PT/PTT
Treatment:
Pathology:
platelets
clotting bruising
and abnormal bleeding
• Address the root problem
• There is no aspirin.
• Preventing injuries
• Make use of electric razors.
• Possible:
- Platelet transfusion
- BMT
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MED-SURG
HEMATOLOGICAL
Vitamin B12 Deficiency Anemia
Anemia
In this condition, the number of RBCs is minimal.
Blood cannot get enough oxygen!
Cause
Signs
• Gastric Bypass
• Weak, pale
• PPI use
Iron-Deficiency Anemia
Signs
• Abnormal bleeding
• Weak
• Alcohol
• Low dietary intake
- Tingling
Treatment:
• Stop the hemorrhage
• Iron supplementation
- Usually PO, large
amounts by IV
- Side effects: stool
dark, constipation
- Take 30 min b4
breakfast with Vit C
Diagnosis:
• Blood test: Fe,
Pathology:
• B12 injection/nose spray/tablet
• High-B12 foods (eggs, chicken,
•
red meat, milk)
• Tiredness
• Reduced Fe absorption
- Loss of sensation
Treatment:
• Pale
• An insufficient dietary intake
B12, MCV>100
• Nerve malfunction
- Muscle weakness
• Breathing difficulties
(GI tract, menstrual)
• Blood test:
• SOB
(esp. vegans)
Cause
Diagnosis:
levels of B12
• Pica
Pathology:
Aplastic Anemia
Iron reserves that are low
or depleted (needed to
produce RBCs)
Iron-rich foods:
Cause
Signs
Diagnosis:
• Autoimmune
• Tiredness
• Blood test ( RBCs, WBCs, PLT)
disease
• Egg whites
• Weakness
• An infection
• Lettuce
• Whiteness
• Bone marrow exam
Pathology:
• Toxicity
• Dark flesh
• Chemotherapy
• Beans
• Fish and seafood
• Raisins and apricots
• Maternity
• Viral Hepatitis
Treatment:
• Transplantation of
stem cells
• Blood transfusion
Hct, Hgb
• Bone marrow failure
is caused by damage
to bone marrow cells.
• Bone marrow regeneration
medications
Folate Deficiency Anemia
Sickle Cell Disease
Cause
Signs
Diagnosis:
Signs
Treatment:
• Alcoholism
• Pale
• Blood test:
• Transplantation of stem cells
• Malabsorption
• SOB
• Anemia (chronic)
• Chrohn's/Celiac
• Dizzy
• Pregnancy
• Irritable
folate, MCV>100
• Folate tablet PO
• High-folate foods (oranges,
peanuts, lentils, leafy greens)
• Oxygen treatment
• Tiredness/weakness
• Exertion-induced pain
• Weight loss
Treatment:
• Yellowness
Diagnosis:
• Blood test- electrophoresis
Pathology:
• levels of folate
Pathology:
• Inherited genetic abnormality
of Hgb
sickle- shaped RBCs
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MED-SURG
FRACTURES
MUSCULOSKELETAL
WHAT IS A FRACTURE?
A fracture is a total or partial interruption in the progression of bone structure.
TYPES OF FRACTURES
STAGES OF BONE HEALING
stage 1
Transverse
Comminuted
The bone has a straight
The bone is crushed,
across fracture.
resulting in numerous
little fragments.
HEMATOMA FORMATION
• The first 1-2 days after a fracture
• There is bleeding into the damaged area
stage 2
Greenstick
The bone is twisted on one
Oblique
side and shattered on
The fracture cuts the
the other.
bone at an angle.
Spiral
The broken bone is pushed
into another bone.
• Granulation tissue formation
• Bone reconstruction begins.
• Still insufficient strength to support weight
commonly seen in children
Impacted
FIBROCARTILAGINOUS CALLUS FORMATION
The fracture partially
surrounds the bone.
stage 3
BONY CALLUS FORMATION (OSSIFICATION)
• The 3rd and 4th weeks of fracture healing
• The callus is being replaced by mature bone.
stage 4
Open/Compound
REMODELING
A fracture in which the
• This could take months or years!
bone penetrates the skin.
• Compact bone takes the place of porous bone.
increased risk for infection
• X-rays are used to track the mending of bones.
COMPARTMENT SYNDROME
Cause
Pressure
Increased pressure and build-up, causes
tissue impairment leading to cell death!
SIGNS & SYMPTOMS
• Excruciating, throbbing pain
• Medication does not ease pain
• Out of proportion to the injury
• Increases intensity with passive ROM
TREATMENT
• Position the extremities at the
heart level (not above heart level)
• Remove the cast or splint.
Blood flow cut off
NURSING ASSESSMENT
Post-Fracture
Neurovascular assessments
Tissue damage due to HYPOXIA
(lack of oxygen)
Compartment Syndrome
Muscle swelling
causing compression
of nerves and vessels
Signs
5 P's
Pain
Pallor
Pulselessness
Paresthesia
Paralysis
burning
or tingling
sensation
fasciotomy
Fascia is cut to relieve
tension & pressure
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MED-SURG
MUSCULOSKELETAL
GOUT
HYPERURICEMIA
PATHOLOGY
Gout is a kind of arthritis
"high" "uric acid" "in the blood"
WHAT IS
URIC ACID?
Purine breakdown produces
marked by elevated
uric acid during digestion. It is
uric acid levels.
Expected range:
F: 2.5 - 8 mg/dL
M: 19. - 7.5 mg/dL
created by the liver and is primarily
eliminated by the kidneys.
This results in uric acid crystal
accumulation in the joints.
SIGNS & SYMPTOMS
TOPHI
Accumulation of sodium urate
crystals in joints such as the big
Tophi think Toe
toe and hands, or other areas
• Gouty arthritis, acute
• Deformity of bones
• Pain (severe)
• Joint injury
• Inflammation
• Tophi
• Temperature at the site • Kidney calculi
such as the ears.
Can be acute or chronic
EDUCATION
CAUSES
- Educate on avoiding:
• Stay hydrated: 2-3 liters per day
• Foods high in purines
• Uric acid deposits can cause kidney
• Medications (aspirin)
stones, fluids help prevent this!
• Alcohol
• Weight loss program if overweight
• Dehydration
Foods high in purines:
Organ
meats
(liver, kidney)
Red
meats
Seafood
Alcohol
(beer)
• Purine-rich diet
• Specific drugs
• Laxatives (causes dehydration)
• Ibuprofen
• The antibiotic cyclosporine
• Purine metabolism disorder
• Kidney issues
• Inadequate uric acid excretion
by the kidneys
MEDICATIONS
Generic
Trade name
Generic
Trade name
allopurinol
Aloprim, Zyloprim,
colchicine
Mitigare, Colcrys
Lopurin
Allopurinol
prevents gout
Colchicine
for aCute gout attacks
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MED-SURG
MUSCULOSKELETAL
OSTEOPOROSIS
PATHOLOGY
DIAGNOSTIC
Osteoporosis
essentially means:
having porous
bones
OsteoPorosis
"porous"
"relating to bone"
• Bone density test:
Dual-energy x-ray absorptiometry (DEXA)
This procedure uses X-ray images to
determinecthe amount of calcium and other
The rate of bone resorption (osteoCLASTS) is greater
minerals in the bones.
than the rate of bone formation (osteoBLASTS)
=
decreased total bone mass
Normal bone marrow has small holes in it,
but osteoporosis causes much larger holes
SIGNS & SYMPTOMS
• There may be no symptoms until a
fracture occurs.
• Broken bones (hips, spine, wrist)
RISK FACTORS
• Pain in the low back, neck, or hips
Calcium & vitamin intake is LOW
Age: women after menopause (the decrease in estrogen at
• The back will be rounded (hunch back),
resulting in a loss of height.
menopausecauses increase bone resorption)
Lifestyle (smoking, excessive alcohol intake, sedentary lifestyle, immobility)
Caucasian or Asian women
Inherited (family history)
Underweight/malabsorption disorder (Celiac disease, bariatric surgery,
FRACTURES
Clients often think they
fell and broke something,
BUT bones may break
first causing them to fall.
eating disorders)
Medications: long-term use of corticosteroids, anticonvulsants, levothyroxine,
long-term use of proton pump inhibitors, etc.
AT HOSPITAL
• Use call light
NURSING INTERVENTIONS
Assessing for
risk factors
Educate on stopping
Educate on ways
to prevent
osteoporosis
• Non-slip socks
Teaching about
preventing injury
• Communicate falls risk
• Clutter-free environment
smoking & limiting alcohol
AT HOME
MEDICATIONS
Calcium supplements with
Vitamin D Bisphosphonates
(ends in "dronate")
PREVENTION
• No area rugs
(risk for falling)
• Weight-bearing exercises
• Watch out for pets
(weights, hiking, etc).
• Keep glasses near by
• Consume foods rich in
calcium & vitamin D
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MED-SURG
MUSCULOSKELETAL
Osteoarthritis (OA)
OSTEOARTHRITIS (OA) & RHEUMATOID ARTHRITIS (RA)
PATHOLOGY
TREATMENT
Distal
OA is a non-inflammatory degenerative joint condition. It is
• Orthotics (splints, braces,
interphalangeal
articular cartilage deteriorates, causing bone injury.
• Assistance with walking (canes)
caused by cartilage degradation between the joints. The
(DIP) called
and knee braces)
Heberden’s nodes
• Workout
Proximal
• Loss of weight
Proximal
• Occupational and physical
SIGNS & SYMPTOMS
interphalangeal
therapy (OT/PT) (PT)
(PIP) called
• Anesthetics
• Pain
Bouchard's nodes
• Post-activity stiffness (subsiding within 30 min)
• Impairment of function
RISK FACTORS
• Enlargements of the bones
Movement / Exercise
rest
Aggravated / symptoms worsen
Symptoms are relieved
PATHOLOGY
• Obesity
• Older age
• Female gender
Occurring mostly at the weight-bearing joints (hips, knees)
Exact mechanism is unknown
RA is a kind of arthritis that is persistent and inflammatory.
Rheumatoid Arthritis (RA)
Distal
It is considered an autoimmune disease.
swollen, inflamed
synovial membrane
• Certain occupations (heavy labor)
• Genetics
DIAGNOSIS
• Hard to diagnose because symptoms are very ,
similar to other diseases
• (+) Rheumatoid factor
• Increase erythrocyte sedimentation
• C-reactive protein (indicates inflammation in the body)
• X-ray shows joint deterioration
SIGNS & SYMPTOMS
• Pain in symmetrical joints
• Fingernail deformity
• Typically, symptoms are
• It can affect all joints
bilateral and symmetric.
(fingers, wrists, neck, s
houlders, and so on).
• Morning stiffness
(lasting more than an hour)
• Systemic affects include
• Inflammation, warmth, and
the heart, lungs, and skin.
redness
RISK FACTORS
May cause an
inflammatory response
& destructive
synovial fluid
• Environmental factors (smoking, pollution)
• Bacterial or viral illness
• Cigarette smoking
• Family history
TREATMENT
GOAL: Decrease joint pain & swelling.
Decrease changes of joint deformity & minimize disability.
• Medications
• Surgery
NSAIDS
Corticosteroids
• Synovectomy: removal of synovium
• Joint replacement
DMARDS
• Arthrodesis: "joint fusion"
• Joint support
• Splints & assistive devices
• Range of motion (ROM) exercise
• Low impact exercise (walking, water aerobics, etc).
• Occupational therapy (OT) & physical therapy (PT)
• Heat or cold? heat For stiffness cold For
pain/inflammation
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MED-SURG
NEUROLOGICAL ASSESSMENTS
MENTAL STATUS
LEVEL OF CONSCIOUSNESS (LOC)
Are they aware of their surroundings?
Level of CONSCIOUSNESS (LOC)
is always #1 with neurological assessment
Are they oriented to person, place, time, & situation?
Do they have their short term & long term memory?
A change in LOC may be the only sign that there is a PROBLEM!
• What is your name?
PUPILLARY CHANGES
Ask these types of
questions to assess
mental status:
• Do you know where you are?
• Do you know what month it is?
PERRLA
• Who is the current U.S. president?
• What are you doing here?
Pupils, Equal, Round, Reactive to Light & Accommodation
Normal Pupil size: 2 - 6 mm
DEEP TENDON REFLEX (DTR) RESPONSES
GLASGOW COMA SCALE
0
1+
2+
3+
4+
Tool for assessing a client's response to stimuli
EYE
OPENING
RESPONSE
Spontaneous
To speech
To pain
No response
Oriented
VERBAL
RESPONSE
Confused
Inappropriate words
Unclear sounds
No response
Obeys command
Moves to localized pain
MOTOR
RESPONSE
Flex to withdraw from pain
Abnormal fl exion
Abnormal extension
No response
TOTAL
4
3
2
1
= No response ABSENT
= Present, but sluggish or diminished
= Active or expected response NORMAL
= More brisk than excited; hyperactive
= Brisk, hyperactive, with intermittent, or transient clonus
BABINSKI REFLEX (PLANTAR REFLEX)
5
4
3
2
1
Elicited by stroking the lateral side of the foot
Intact CNS
The toes contract and draw together as the
lateral sole of the foot is stroked.
6
5
4
3
2
1
brain dysfunction
When stroked, the toes fan out.
Remember that this is only natural
in newborns and infants up to the
babinski think normal
in babies & the big
toe fans out
age of 2, but it is abnormal in adults!
3 - 15
WORST
INTERPRETATION
BEST
3
<8
15
Severe impairment of neurological
function, coma, or brain death
Unconscious patient
Fully alert & oriented
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MED-SURG
NEUROLOGICAL
SEIZURES
causes
Abnormal & sudden
What is a
seizure?
electrical activity of the brain
Chronic seizure activity
What is
EPILEPSY?
• fever
• Hypoxia
(Febrile seizure in child)
• Tumor of the brain
• Infection of the CNS
• Low blood sugar
• Withdrawal from drugs
• Head injury
or alcohol
due to a chronic condition
• Hypertension
• Imbalance in ABG
stages of a seizure
Prodromal
When symptoms start
Warning sign right before
(can be days before
• Weird smell or taste
before the actual seizure
the seizure happens)
the seizure happens:
• Altered vision
• Dizzy
Generalized Seizures
TONIC-CLONIC
MYOCLONIC
Ictus
SEIZURE!
Aura
post -Ictus
Recovery after the seizure
Status Epilepticus:
a seizure that lasts >5 minutes
without any consciousness
during the seizure
"Used to be called grand-mal" May begin with an aura.
Stiffening (tonic) and/or rigidity (clonic) of the muscles.
Sudden jerking or stiffening of the extremities
(arms or legs).
• Possible injury
• Confusion
• Very tired
Not all patients
experience an aura
THE ENTIRE BRAIN IS AFFECTED
• Headache
Care during the seizure
Seizure Precautions
• maintain a patent airway
• loosened clothing
• bed in lowest position
• privacy provided as soon as possible
• side rails up and padded
ABSENCE
ATONIC
Usually looks like a blank stare that lasts seconds.
• have oxygen & suction available
Often goes unnoticed
• client in side-lying position
Sudden loss of muscle tone. May lead to sudden
• pillow under head
(immediately post-seizure)
falls or dropping things.
• Note the time & duration of the seizure
Don't
Partial (focal) Seizures
THE ENTIRE BRAIN IS AFFECTED
Sensory symptoms with motor
SIMPLE PARTIAL
symptoms and stays aware.
• Restrain the client
• Force the jaw open
• Place anything in their mouths
• Leave the client
They may report an aura.
COMPLEX PARTIAL
Altered behavior/awareness and
loses consciousness for a few seconds.
76
MED-SURG
NEUROLOGICAL
CEREBROVASCULAR ACCIDENT (CVA) "STROKE"
Ischemic stroke
PATHOLOGY
The brain's blood supply is
suddenly cut off. The
pathophysiology of a stroke varies
according to the type of stroke.
BLOCKAGE
"Thrombotic or embolic"
• Fibrinolytic therapy
• Thrombosis:
("clot buster")
A blood clot that formed on the artery wall
Suffix: -ase
• Embolism:
Examples: alteplase,
A blood clot that has left part of the body
Blood flow is cut off which leads to ischemia
F Face drooping
• Uneven smile
A Arm weakness
• Arm numbness;
can't lift arm
Left brain
• Issues with language
(dysphagia)
• RIGHT-sided hemiparesis
S Speech diffi culty
• Slurred speech
T Time to call 911
(1-sided weakness)
left think languages
Right brain
• Behavioral changes
• Lack of impulse control
• LEFT-sided hemiparesis
(1-sided weakness)
Hemorrhagic stroke BLEEDING
• Ruptured artery
Right think Reckless
Receptive: Unable to comprehend speech
(Wernicke's area)
Expressive: Can comprehend speech, but
can't respond back with speech (Broca's area)
NURSING CONSIDERATIONS
Positioning of the client
Assist with safe feeding
• Raise the head of the bed to ICP
• Do not feed until the gag reflex
under the affected arm.
• Break down pharmaceuticals
Preventative dvt measures
• Compression stockings
Diet modifications
• Frequent position change
• Following a stroke, a patient
Non-Modifiable
• Hypertension
• Family history
• Obesity
• Stress
• Oral contraceptives
will begin on a liquid diet
and gradually proceed to
of motion every 2 hours
Modifiable
of strokes
• Older age
• Male gender
• Black
• Hispanic
has returned.
• Possibilities of aspiration
• Keep suction near the bed.
• Encourage passive range
RISK FACTORS
• Diabetes mellitus
• Prevent ICP
ischemia & increased ICP
• Mobilization
• Anticoagulation therapy
• Stop the bleeding
• Uncontrolled hypertension Blood
• Place a pillow in a neutral position
Types of aphasia:
• Atherosclerosis
TREATMENT:
• Aneurysmal (weakening of the vessel)
accumulation in the brain causes
Remember:
If the stroke occurs in
the left side of the brain,
the right side of the body
will be affected
streptokinase
Must be given within
4.5 hours from onset
of symptoms
Transient Ischemic Attacks (TIAs)
"Mini strokes" • No cerebral infarction occurs
SIGNS & SYMPTOMS
MEDICATIONS:
Assist with
communication skills
• Be patient
• Make clear statements
• Ask simple questions
• Don't rush!
a regular diet.
Liquid
• Thin
• Nectar-like
• Honey-like
• Spoon-thick
Food
• Pureed
• Mechanically altered
• Mechanically softened
• Regular
77
MED-SURG
NEUROLOGICAL
What are
Cranial nerves?
CRANIAL NERVES
XII: Hypoglossal
Function:
Nerves that originate from the brain stem.
They send information to & from various parts of the body.
Mnemonics
Glosso means tongue!
Tongue movement (swallowing & speech)
Test:
Inspect tongue & ask to stick tongue out
Ooh,
Olfactory
Ooh,
Optic
Ooh
Oculomotor
To
Sensory
Say
Sensory
Marry
Motor
Money
Motor
Trigeminal
But
Both
And
Abducens
My
Motor
Feel
Facial
Very
Vestibulocochlear / Acoustic
Velvet.
M
Trochlear
Some
Touch
Good
Such
Heaven!
Brother
Says
Both
Sensory
Big
Both
Vagus
Brains
Both
Spinal Accessory
Matter
Motor
More
Motor
Glossopharyngeal
Hypoglossal
Function:
Controls strength of neck & shoulder muscles
VII: Facial
Test:
Ask the client to rotate their head & shrug
their shoulders
X: Vagus
SE
I: Olfactory
Function:
Sense of smell
Test:
Smell substance with eyes closed
(test each nostril separately)
II: Optic
SE
Function:
B
Vision
Function:
Test:
MOTOR - Facial expression
• Snellen chart
SENSORY - Taste (sweet & salty)
B
• Ophthalmoscopic exam
• Confrontation to check peripheral vision
Test:
• Ask client to do different facial expression
Function:
Tongue movement (swallowing & speech)
(Frown, smile, raise eyebrows, close eyes, blow etc)
• Test tongue by giving client sour, sweet, bitter, and
salty substances.
Test:
VI: Abducens
B
M
Function:
Controls parallel eye movement
Function:
MOTOR - Tongue movement & swallowing
SENSORY - Taste (sour & bitter)
III: Oculomotor
M
Function:
Inspect tongue & ask to stick tongue out
IX: Glossopharyngeal
B BOTH
Start
M
XI: Spinal Accessory
SE SENSORY
M MOTOR
Abduction - moving laterally
AKA away from midline
Ocular (eye) motor (movement)
Controls most eye movements,
pupil constriction, & upper-eyelid rise
Test:
• Look up, down, & inward
• Ask the client to follow your fi nger
as you move it towards their face
Test:
Test:
• Look up, down, & inward
Test tongue by giving client sour, bitter, &
• Ask the client to follow your fi nger
salty substance.
IV: Trochlear
M
as you move it towards their face
Function:
VIII: Vestibulocochlear
/ Acoustic
Function:
Balance & hearing
SE
V: Trigeminal
B
Function:
MOTOR - Mastication (biting & chewing)
SENSORY - Facial sensation
Test:
Test:
• Stand with eyes closed
• Pressure on the forehead cheek & jaw
• Otoscopic exam
• Rinne & Weber Tests
with a cotton swab to check sensation
• Ask client to open mouth & then bite down
Controls downward & inward eye movement
Test:
• Look up, down, & inward
• Ask the client to follow your fi nger
as you move it towards their face
78
MED-SURG
NEUROLOGICAL
What are
Cranial nerves?
CRANIAL NERVES
Nerves that originate from the brain stem.
They send information to & from various parts of the body.
Mnemonics
Some
S
O
Say
S
O
Marry
M
To
T
Money
M
Touch
T
But
B
And
A
My
M
Feel
F
Brother
B
Very
V
Says
S
Function:
XI:
B BOTH
Start
XII:
Test:
SE SENSORY
M MOTOR
Ooh,
O
Ooh,
Ooh
/A
Good
G
Big
B
Velvet.
V
Brains
B
Such
S
Matter
M
Heaven!
H
More
M
I:
Function:
Test:
II:
Function:
Test:
X:
VII:
Function:
Function:
Test:
Test:
Function:
III:
Test:
Function:
VI:
IX:
Function:
Test:
Function:
Test:
Test:
IV:
Function:
VIII:
Function:
Test:
V:
Test:
Function:
Test:
79
MED-SURG
CARDIAC
HEART FAILURE
PATHOLOGY
The heart cannot supply enough blood to meet o demands.
Superior
Vena Cava
Left Sided HF
Aorta
Pulmonary Artery
- Diastolic HF (Filling) property: the ventricle does not fill
- Systolic HF (ejection) occurs when the ventricle fails to
Pulmonary Vein
Left Atrium
Right Atrium
expel correctly.
Left Ventricle
Right Sided HF
• Failure of the right ventricle
inferior
Vena Cava
- fluid accumulates in the venous system
Right
Cardiac Muscle
Ventricle
Can be caused by any alteration to cardiac output (co)
Preload
RISK FACTORS
Associated Diseases
• HTN
• CAD
=
Afterload
volume in the ventricle at the end of diastole
=
pressure the heart must eject blood against during Systole (contraction)
Cardiac output
Stroke volume
• MI
=
=
Volume of blood pumped by the heart in one minute (in L)
volume ejected with each heartbeat
SIGNS & SYMPTOMS (Chronic HF)
INTERVENTIONS
• Hypertensive Crisis
• Fatigue • Anxiety • hepatomegaly
R
• CAD /MI
• Pulmonary HTN
• weakness • fatigue • dyspnea
• Cardiomyopathy
• Vaivular disorders
• Myocarditis
• Anorexia + • G1 bloating edema • Ascites
• Murmurs • JVD • HR
• Rheumatic HD
• Hyperthyroidism
• Depression •Bilateral edema
• Shallow respirations • nocturia
L
• dry, hacking cough • orthopnea
• Change in mental status
• Crackles • PMI displaced
• S5 + S4 heart Sounds
80
MED-SURG
CARDIAC / HEART FAILURE
NURSING MANAGEMENT
RULE OUT or Assess
ASSESSMENT
• previous health issues • current medications • elimination behaviors
• sadness anxiety • Nutrition • Paller • edema • Chest pain • dyspnea • lung sounds
• PMI • Ascites • Jugular veins • murmurs • stomach distension
• hepatocellular carcinoma
INTERVENTIONS
• educate client on meds • educate patient
on the necessity of fluid restriction
• gradually increase activity level
• train pt to report weight gain of -316 in
2 days or 4-6 lbs in a week
• Ensure that the patient contacts
LABS
BNP, BUN, Creatine,
electrolytes, CBC, EF
the HCP if they experience dizziness,
DIET
exhaustion, swelling, or SDB.
• Low Salt
- up to 1800 mg / day
• Increase Vegetables, Seafood
• trans/ Saturated fat
• Sugar intake
• Caffeine
PHARMOLOGY
DIURETICS
VASODILATORS
RAAS Inhib.
• Loop. Thiazide& K+ sparing
• afterload
• dilate venuies + arterioles
• Fluid volume
• Cardiac Output
• renal blood flow
• Preload
• dilate renal art.
• relieve Sx of HF.
• PVP
- ( perfusion fluid loss)
• Relieve edema
• Blood Pressure
• Ex) -captopril -benazepril
-enalapril -Valsartan -losartan
• Relieve dyspnea
ANTICOAGULANTS
• Prevent thromboembolism
MORPHINE
INOTROPES
B BLOCKERS
• afterload
•
• Inhibit SNS
• cardiac output HR +SV
• promote reverse remodeling
• Promote vasodilation
• ex) metoprolol
• ex) digoxin , mirione ,dobutamine
• anxiety
• afterload
• Preload
81
MED-SURG
CARDIAC
CORONARY ARTERY DISEASE
PATHOPHYSIOLOGY
Lipid deposits accumulate in the artery's intima, triggering endothelial irritation
(inner layer of vessel). Fat accumulation occurs gradually over time.
Stages of atherosclerosis development
NORMAL FUNCTIONS
1) Fatty streak
- reversible
2) Fibrous plague
- can happen by 30 years
3) Complicated lesion
- occlusion can occur
ENDOTHELIAL DISFUNCTION
PLAQUE FORMATION
PLAQUE RUPTURE THROMBOSIS
RISK FACTORS
Modifiable they
can change
Non Modifiable can't change
• Aging
• hyperlipidemia > 200mg/dL
• The gender (men are more at risk)
• hypertension BP 140/90
• Genetic proclivity
• Diabetes mellitus
• Family history of heart disease
• Smoking
• Race (white men are more likely to be affected than
• Sedentary lifestyle
African Americans) (african americans have oun earlier onset)
• obesity -waist circ. >40’’ (m) >35" (w)
• psychosocial risk factors
• depression + anxiety
DIAGNOSIS
• homocysteine
Dx not made until advanced disease but risk
factors can be identified through screening
NUTRITIONAL THERAPY
increase omega-3 fatty acid intake
• Saturated fats <7 %.
• Healthy Cholesterol
- bacon, butter, egg yolks, lard
• Trans fats
- margarine, shortening + veg. oil
• Monounsaturated Fat
- olive. Canola, and peanut oil
• Polyunsaturated fat
- Sunflower, Soy, corn, safflower,
- nuts, seeds, egg yolks
20 30 y
Of daily kcal.
• Fiber 10-25,1 day
- beans, wheat, bran, fruit
• Sodium
- canned/frozen food, dairy,
deli meat, olives, Cheese
82
MED-SURG
CARDIAC / CORONARY ARTERY
DISEASE
NURSING MANAGEMENT
ASSESSMENT
INTERVENTIONS
Assessment It's important to identify those at risk before Symptoms are evident.
Screen for modifiable risk Factors like
BP,
lipids,
Blood sugar.
The goal is to decrease disease
weight. Ask
progression by lowering or eliminating
about family he of heart disease. Determine eating habits, stress levels, amount
risk factors.
of exercise,
Education
Teach them about health promotion to risk factors
HTN
OBESITY
SMOKING
• Monitor BP at home and report any rises
• cut back on calories.
• Begin a smoking cessation program.
• lose weight • cut back on salt intake
• stay away from fad / crash diets
• quit smoking • exercise
• Avoid eating large, heavy meals.
• Activities to replace smoking
• Enlist the help of family and friends
• consume smaller, more frequent meals
ELEVATED LIPIDS
to quit.
PHYSICAL INACTIVITY
• reduce total + saturated fat intake;
use lipid-lowering medications as directed
• moderate activity for at least 30 minutes
5 days per week
• Increase your consumption of complex
carbohydrates.
DRUG THERAPY
Statins
Side effect
• Atorvastatin
• Rash • GI disturbances
• Pravactatin
•
• Simvastatin
• rhabdomyolysis
Niacin
Bile-Acid
Sequestrants
PCSK9 Inhibitors
liver enzymes •myopathy
• Flushing • pruritis
• Gl disturbance • hypotension
•
homocystesne
• bad taste • GI disturbances
• Indigestion • bloating
Nursing
• monitor liver enzymes and
creatinine kinase if muscle
weakness or pain occurs
• aspirin 20 mins before can
• folic acid will
flushing
homocysteine
• Interfere w/ absorption of many drugs
• injection. • reactions
• used with max statin therapy
• limb pain • fatigue • muscle pain
• given by injection Q 2-4
83
MED-SURG
CARDIAC
CHRONIC STABLE ANGINA
PATHOPHYSIOLOGY
Chronic steady chest discomfort is one of the symptoms of advanced CAD. This is due to the heart
using less oxygen than is required. When the heart lacks 02,
(ischemia) Chest pain occurs --> angina
Enology
ASSESSMENT
The mismatch between Supply and demand is caused by:
Decreased 02 Supply
Increased 02 demand
- atherosclerosis
- aortic Stenosis
- coronary arter spasm
- thrombosis
- heart faiwre
- Valve disorders
- anemia
- asthma
- COPD
- Pneumonia
- Cocaine | amphetamines
Precipitating Factors
Quality of Pain
Region and Location
Severity
Timing / onset
- cardiomyopathy
- dysrhythmias
- left ventricular hypertrophy
- tachycardia
- anxiety
SIGNS & SYMPTOMS
- hypertension
- hyperthyroidism
• Chest pain that spreads to the jaw,
- exertion
back, neck, and shoulders
- Cocaine | amphetamines
• The pain is only felt for a few minutes.
• alleviated by relaxation
Cardiac Output
LABS
(NORMAL RANGE)
HR
SV
Preload
Contractility
• Troponin I (0-0.099 oglml)
• CK-MB (< Gng /m2 )
• Myoglobin (0-85 ng / mL)
After load
• CRP (<3.0mg/L)
• CBC
• homocysteine levers
• Lipids
• Basic metabolic panel
Diastolic filling
Force or contraction
Ventricular ejection
84
MED-SURG
CARDIAC
CHRONIC STABLE ANGINA
DIAGNOSTIC STuDIES
DRUG THERAPY
• X-ray of the chest 12 lead ECG
Antiplatelets
(to view ColciFications)
• Stress examination
• Electrocardiogram
• Cardiac Catheterization (aids in
determining the severity and location
of the blockage)
• EBCT - electron beam CT (identifies
and quantifies coronary calcification).
• Platelet aggregation inhibition in arteria circulation
Glucoprotein Ilb /llla Inhibitors
• Inhibit platelet aggregation -->ex) tirofiban + abciximab
Anticoagulants
• Prevent formation of blood Clots Heparin, Warfarin, apikaban
Direct Thrombin Inhiloitors
They bind directly to thrombin and are used in place of Heparin.
Nitrates
Treatment
A
- antiplatelet
- antianginals
- ACE Inhibitors
B
- Beta blockers
C
- cessation of Smoking
- Blood pressure control
- Cholestero management
- cat ++ Channel blockers
- Cardiac rehab
D
- diet modification
- diabetes control
- depression screening
- dilate peripheral /coronary blood vessels
- instruct pt to take one dose + if Sx not relieved take
another in 5 mins+ call 911
ACE Inhibitors
- Vasodilation
- for those w/ EF <40%.
Angiotensin 2 receptor blockers
(ARBs) - Biock Angiotensin 2 thus causing Vasodilation
Beta - Blockers
HR+BP -->Take vitals before giving
Calcium Channel Blockers
- Only iven if B-blockers are not indicated or are ineffective
Morphine
E
- education
- exercise
Analgesic that also helps
F
- flu vaccine
Thrombolytic
HR +BP and reduces myocardial 02 demand
Helps "dissolve" Clots that May be blocking Blood Flow
Lipid Lowering Agents
Nitroglycerin Fast Facts
- Should be taken in conjunction with a low-fat diet.
• Should always be easily accessible.
• Can result in orthostatic hypotension
• Prophylactic lasing is possible.
• Keep out of direct sunlight.
85
MED-SURG
CARDIAC
ENDOCARDITIS
Pathophysiology :
Risk Factors:
IV drug use, heart valve replacement history, altered immunity, or structural cardiac abnormalities.
Possible Ports of entry
Assessment :
The endocardium is infected by a microbe (virus, bacterium, or fungi).
• Oral cavity • IV placement • GI/GU infection • abcess
Positive blood cultures, murmurs, S3 or S4 heart sounds, fever, chills, night sweats, anorexioa,
petechiae, osler's nodes, petechiae, anorexioa, petechiae, anorexioa, petechiae, anorexioa, petechi
Diagnostics:
positive blood cultures and echocardiography evidence
Complications:
Treatment:
Valvular insufficiency, emboli development, heart failure, and sepsis are all symptoms of valvular insufficiency.
Antibiotics that target the specific bacteria that infects the tissue. Iv is generally given. Rest to avoid the
onset of heart failure If antibiotics are ineffective, surgical intervention, such as:
- removing contaminated valve
- eliminating congenital shunts | chordae tendineae repair of injured valve
- removing abscesses from the heart
* Safety Alert:
tell the patient that they must notify all health care professionals, including dentists, about their endocarditis
PERICARDITIS
Pathophysiology:
Risk Factors:
Assessment :
Pericardial inflammation | pericardial change
Recent myocardial infarction, upper respiratory infection, and pericardial effusions
Breathing causes substernal precordial pain that spreads to the neck. Supine position exacerbates pain.
It is possible to hear pericardial friction rub. ST elevation in an Exg lead
Diagnostics:
WBCs, EKGs, biood cultures, and echocardiograms are all examples of tests.
Nursing Interventions:
Auscultate blood pressure to look for paradoxical blood pressure, which is a symptom
of tamponade. Assist the patient in finding a comfortable position, which is usually upright or leaning forward.
Treatment:
Bacterial pericarditis --> AntibioticS + drainage Masignant pericarditis - chema /radiation, NSAIds for pain
Avoid anticoaguLants + aspirin as these increase risk of cardiac tamponade.
Tamponade is a medical emergency that may necessitate pericardiocentesis or a pericardial window to drain and
alleviate pressure from the fluid that surrounds the heart.
86
MED-SURG
CARDIAC
VALVULLAR HEART DISEASE
Aortic Stenosis
Pathophysiology :
The most prevalent type of valve malfunction. During systole, the aortic valve opening narrows and
obstructs left ventricular outflow. As stenosis develops, the left ventricle fails and causes pulmonary congestion.
Signs & Symptoms:
On exercise, dyspnea, angina, and synlope Narrow pulse pressure, peripheral cyanosis, and
severe exhaustion
Systolic crescendo- decrecendo murmur
Aortic Regurgitation (Insufficiency )
Pathophysiology :
During diastole, the aortic valve leaflets do not shut adequately, resulting in backflow into the left ventricle.
The ventricle progressively enlarges.
Signs & Symptoms:
Left ventricular failure produces exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea,
nocturnal angina with sweating, and palpations after being asymptomatic for many years (esp. when lying on left side).
DRUG THERAPY
Diurectics
•
vascular fluid
ACE Inhibitors
• prevent peripheral
volume, CO & BP
vasoconstriction which
through diuresis
BP and strain on the heart
Beta Blockers
•
release of epi, norepi which
HR, BP and oxygen demands
Digoxin
• increases ca++ which
causes heart muscles
to contract more efficiently
Heart VAlve Repair
These operations do not fully restore the valve, but they are a safer alternative to typical valve replacement surgeries.
Balloon valvuloplasty - To increase the aperture, a balloon catheter is introduced from the femoral vein to either the
mitral or aortic valve.
TAVR - Transcatheter aortic valve replacement involves the implantation of a prosthetic valve following balloon
valvuloplasty. The valve is implanted through the femoral artery while the heart is paced at around Z00 bpm.
87
MED-SURG
CARDIAC
VALVULLAR HEART DISEASE
Focused Assessment
• Obtain vitals and a health history, especially a
Mitral Regurgitation
history of rheumatic fever or endocarditis; inspect for
edema; and auscultate the heart and lungs for
(insufficiency)
murmurs and congestion.
Pathophysiology :
Calcific changes prevent the
mitral valve from completely shutting during Systae,
Diagnosis
resulting in backfow into the left atrium during
Echocardiography - Transthoracic (tte) or
left atrium, causing hypertrophy.
contraction. Backflow adds volume and strain to the
Signs & Symptoms:
transesophageal (tee) ultrasound is used to view neart
valve function and detect vegetation.
Exercise tolerance testing (ETT) -
To test symptomatic
response and functional capacity, physical exercise
or drugs are used.
Chest x-Ray -
Fatigue, chronic weakness,
anxiety, and, if HF develops, dyspnea on exertion,
EKG reveals ventvicular and atrial enlargement,
palpitations, neck vein distension, and other symptoms.
High pitched Systolic murmur at apex.
Severe regurgitation = S3 heart Sound
as well as aortic/mitral regurgitation and L ventricle enlargement
Mitral Stenosis
Pathophysiology : Mitral valve tissue hardens and calcifies,
causing the valve to constrict and preventing proper function.
Flow From the Left Atrium --> Left Ventricle
Signs & Symptoms: Right H F ofthopnea, hemoptysis,
Valve of pulmonary trunk
Aortic valve
Double-leaf mitral valve
paroxysmal nocturnal dyspnea, pitting edema, atrial fibrillation,
nepatomegaly, neck vein distension, and exertional dyspnea
Rumbling, apical diastolic Murmur
Tricuspid
Mitral Valve Prolapse
Pathophysiology :
In systole, the vaLve leaflets grow and prolapse into the L atrium.
Signs & Symptoms:
Asymptomatic until it advances, causing mitral regurgitation.
Some patients describe palpitations or exercise intolerance.
Midsystolic click and late systolic murmur at the apex
88
MED-SURG
CARDIAC
ACUTE CORONARY SYNDROMES
CAD
Chronic Stabe Angina
&
Acute coronary Syndromes
=
=
unstable Angina
or
Myocardial Infarction
(atherosclerotic plaque ruptures
Causing clotting or vasoconstriction)
SIGNS & SYMPTOMS
Risk Factors
• Substernal Chest pain/pressure
Myocardial Infarction
lasting > 30 mins
• Pain onty relieved w/ opiates
- Ischemia occurs when myocardial tissue is deprived of oxygen.
• nousea / Vomiting
ST-Elevation - ST elevation > Imm on 2 contigous leads on 12-lead ExG
• Hyperlipidemia • Hypertension
• smoking • Obesity •
age
• Diabetes • Sedentary lifestyle
• CAD & Atherosclerosis
Unstable Angina
• Chest pain at rest or during exercise that lasts
more than 15 minutes and is not
• anxiety • Palpitations
• dizziness • disorientation
Non ST-Elevation - ST may be inverted, or T waves may vary.
Risk Factors
• Fatigue • diaphoresis
• Shortness of breath
Emergent Care of Chest Pain
• Assess Airway, Breathing & Circulation
• Obtain vital signS + 12-lead EKG
• Administer O2 to maintain >90% O2 saturation
• Administer Nitro Q5 mins/per orders for NSTEMI
• for STEMI
• for NSTEMI
If an emergent cath is
Obtain cardiac biomarkers
available, prepare for it or
and repeat EkG, then schedule
begin Fibrolytics within
a cath within 24 hours.
30 minutes.
alleviated by nitro
• Having an unpredictable onset that is
unrelated to activity or emotions
Stable Angina
• Nitroglycerin relieves chest pain caused by effort or intense emotions.tt
89
MED-SURG
CARDIAC
HYPERTENSION
Pathophysiology
Chronic high blood pressure: > 140 mmHg Systolic , > 90mmHg diastolic
Blood Pressure :
The measuring of force on blood vessel walls. Adequate blood pressure is required to sustain adequate
perfusion of the body's tissues. However, elevated blood pressure can have long-term detrimental consequences.
Baroreceptors :
Are in charge of sensing stretching and sending signals to
vasomolor centers to vasodilate. When blood pressure is low, baroreceptors
Category
SBP
DBP
Normal
< 120
< 80
Pre-HTN
120-139
80-89
Stage 1
140-159
90-99
Stage 2
>- 160
>- 100
activate the SNS.
Systemic Vascular Resistance :
Is the opposing force that
prevents blood movement in valley vessels. As SVR + Cardiac output increase,
so does blood pressure.
Renal System :
The kidneys are in charge of salt retention and elimination. They secrete Renin, which, coupled with
angiotensin, helps regulate blood pressure. Prostaglandins derived from the rena (medulla). have a circulatory vasodilator effect
Endocrine System :
The adrenal medulla releases Epinephrine, which is controlled by the endocrine system. This raises
the heart rate and cardiac output. When there is a larger amount of salt in the blood (high Osmolality), ADH is released from the
hypothalamus, causing the kidneys to reabsorb water.
Nervous System :
The sympathetic nervous system immediately responds to dips in blood pressure by increasing HR and
causing widespread vasoconstriction: BP can be lowered by inactivation of the SNS --> vasodilation
Risk Factors
Primary Hypertension
also called essential or idiopathic. Bp without an identified cause
Secondary Hypertension
Occurs as a result of other disorders or conditions such as :
• The male gender
• Cirrhosis of the liver
• oral contraceptives
• excessive alcohol intake
• elevated triglyceride and cholesterol levels
t• Aortic constriction
• corticosteroids
•
• Age + SBP
w/ age
• a family tree
• Thyroid disorder
• use of Stimulants
• obesity
• African and American ancestry
• Cushing's disease
• Cox -2 inhibitors + NSAIDs
• diabetes mellitus
• Lower Socioeconomic Status
• Kidney disease
• hign estrogen Levels
• tobacco use
• High levels of stress,
• Obstructive sleep apnea
sodium intake
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MED-SURG
CARDIAC
HYPERTENSION
Education
Lab Values Of
• Assure that the patient continues to take their prescriptions
even if they are not experiencing any symptoms.
• Show the patient or caregiver how to take their blood pressure
and keep track of it.
• Teach the patient that the only true cures for hypertension are
lifestyle changes and exercise.
• Provide both verbal and written medication instructions to
ensure adherence.
• In order to relax, encourage the client to try yoga or meditation.
• If applicable, assist with smoking cessation.
Nutrition
they can be used to evaluate potential risk factors or
consequences associated with hypertension.
• BuN /Creatinine- increased = Kidney -function
Electrolytes - Can be
or
d/t medications
Cholesterol - high Cholesterol can contribute
to vessel disease or stenosis
• Glucose - Diabetes is a risk factor for HTN
Uric Acid - can
with diuretic use
Potassium - helps detect hyperaldosteronism
Evaluation & Amplumantation
* Dietary Approaches to Stop Hypertension (DASH)
Fruits, vegetables + lows fat dairy
• Avoid Foods high in Sodium and Fat
• Limit Salt intake to < 2g / day
• Provide support to limit alcoholand caffeine intake
* If taking potassiumwasting diuretics, increase
potassium intake
• Salt Substitutes can be higin in K+ So monitor for
signs of hyperkalemia
• Include Sources of omega -3 fatty acids which
have been shown to
• Although there are no labs that detect hypertension,
triglycerides
• Anchovies
• tuna
• Salmon
• whitefish
• trout
• Walnuts
• flax seed
• Edamame
• Make sure the BP cuff is properly placed to minimize false
high / low readings.
• If the upper arm is unavailable due to IV lines or fistulas, place the
cuff on the forearm.
• Reposition the arm so that it is at heart level.
• Check for orthostatic hypotension and instruct patients to rise
and stand up steadily.
• Arrange for regular check-ups to ensure the patient's blood
pressure is under control.
• Regularly check vital signs, weight, and urine output.
• Immediately report any critical blood pressure readings to your
doctor, ensuring an accurate reading and an assessment
of your symptoms.
• Check for cardiovascular adverse effects such as neck vein
distension, tachycardia, dysrhythmias, and extremities edema.
• Make sure the patient understands how to report issues such as
vision changes, dizziness, weariness, headaches, and palpations.
Nursing Diognosis
• Inadequate health management
• Anxiety r/t Management Complexity
• Possibility of reduced cardiac tissue
• the risk of ineffective renou perfusion
Complications
• Heart Attack
• Loss of vision due to heart failure
• Renal disease
• Heart disease
• Sexual impotence
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MED-SURG
CARDIAC
EKG WAVEFORMS
QRS Complex
P wave ............. Atrial contraction (DEpolarization)
R
PR segment ..... Movement of electrical activity from atria to ventricles
ST
segment
PR
interval
T
P
QRS Complex ... Ventricle contraction (DEpolarization)
TP
interval
St segment ..... Time between ventricular depolarization & repolarization
T wave ............. Ventricle relaxing (REpolarization)
P
TP Interval ..... Ventricle are relaxing & filling
Q
S
PR
segment
Heart Rhythm
Measurements
QT interval
Basic Rhythms
Normal Sinus
60 - 100 bpm
Sinus Tachycardia > 100 bpm
Sinus Bradycardia < 60 bpm
PR Interval
0.12 - 0.2
QRS Complex
0.06 - 0.12
QT Interval
< 0.40 seconds
REpolarization think...
RElaxing
REpolarizing
REfilling with blood
DEpolarization think...
DEcompressing
SICK DAY MANAGEMENT
PR INTERVAL
ST SEGMENT
QT INTERVAL
Electrical activity is transferred
The time elapsed between ventricular
The time required for ventricles
from the atria to the ventricles.
depolarization and repolarization
to depolarize, contract, and
(ventricular contraction)
then repolarize.
5-LEAD PLACEMENT
SMOKE OVER...
WHITE ON RIGHT
LA
RA
CHOCOLATE
IN MY HEART
V
FIRE
RL
GREEN GOES LAST
LL
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MED-SURG
CARDIAC
6 STEPS TO INTERPRETING EKGs
1
BASIC RHYTHMS
P-WAVE
NORMAL SINUS 60 - 100 bpm
Identify and investigate the P-waves
• Must be present and upright
SINUS TACHYCARDIA > 100 bpm
• It comes before the QRS complex.
SINUS BRADYCARDIA < 60 bpm
• Each QRS complex has one P-wave.tt
1 sec.
2
3
PR INTERVAL
PR interval measurement
Normal PR interval:
0.12 - 0.2 seconds
QRS COMPLEX
Normal QRS complex:
0.06 - 0.12
Is every P-wave
followed by a
QRS complex?
• Should not be widened or shortened
– this may indicate problems!
Widen is often seen in PVCs,
Electrolyte imbalances
& drug toxicity!
0.04
sec.
0.20 sec.
4
R-R
1 large box = 0.20 seconds
Are the R-R intervals consistent?
5 large boxes = 1 second
• Regular or irregular?
5
1 small box = 0.04 seconds
DETERMINE THE HEART RATE
6 SECOND METHOD
Count the number of R’s in between
the 6 second strips & multiply by 10
Be sure and check that
the strip is 6 seconds!
Count the boxes
BIG BOX METHOD
300 divided by the number
of big boxes between 2 R’s
1
6 R’s X 10 = 60 beats per minutes
6
IDENTIFY THE EKG FINDING!
2
3 4 5
300 / 5 = 60 BPM
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MED-SURG
CARDIAC
EKGs
NORMAL SINUS RHYTHM
RATE
60 - 100 bpm
RHYTHM
Regular
P-WAVE
Upright & uniform
before each QRS
PR INTERVAL
Normal
QRS COMPLEX
Normal
SINUS BRADY
The sinus node creates an impulse at a slower-than-normal rate
CAUSES
R
T
P
Q S
RATE
< 60 bpm
RHYTHM
Regular
P-WAVE
Upright & uniform before each QRS
PR INTERVAL
Normal
QRS COMPLEX
Normal
TREATMENT
• Lower metabolic needs
• Correct the underlying cause!
• Sleep, athletic training, hypothyroidism
•
• Vagal stimulation
the heart rate to normal
• Medications
• Calcium channel blockers, beta blockers, Amiodarone
SINUS TACHY
The sinus node creates an impulse at a faster-than-normal rate
RATE
> 100 bpm
RHYTHM
Regular
P-WAVE
Upright & uniform before each QRS
PR INTERVAL
Normal
QRS COMPLEX
Normal
CAUSES
• Physical or psychological strain
• Loss of blood, fever, exercise, and dehydration
• Specific drugs
• Stimulants such as coffee and nicotine
• Illicit drugs such as cocaine and
amphetamines
TREATMENT
• Epinephrine stimulates the
sympathetic nervous system.
• Heart disease
• Tamponade of the heart
• Thyroid hyperthyroidism
• Identify the underlying cause!
•
the heart rate to normal
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MED-SURG
CARDIAC
EKGs
VENTRICULAR TACHYCARDIA (VT)
Irregular, coarse waveforms of different shapes.
looks like
tombstones
The ventricles are quivering and there is no
contractions or cardiac output which may be fatal!
RATE
100 - 250 bpm
RHYTHM
Regular
P-WAVE
Not visible
PR INTERVAL
None
QRS COMPLEX
Wide (like tombstones) > 0.12 seconds
CAUSES
MANIFESTATIONS
• Myocardial ischemia / infarction
• Patient is usually awake (unlike V-fi b)
• Electrolyte imbalances
• Chest pain
• Digoxin toxicity
• Lethargy
• Stimulants: caffeine & methamphetamine
• Anxiety
• Syncope
• Palpitations
No Cardiac Output
=
Low Oxygen
TREATMENT
STABLE CLIENT WITH A PULSE
UNSTABLE CLIENTS WITHOUT A PULSE
• Oxygen
Also called PULSELESS V-TACH
• Antidysrhythmics (ex. Amiodarone...stabilizes the rhythm)
• CPR
• Synchronized Cardioversion
• Follow ACLS protocol for defibrillation
SHOCK!
• Possible intubation
• Drug therapy
• Synchronized administration of shock
• Epinephrine, vasopressin, amiodarone
(delivery in sync with the QRS wave).
• Cardioversion is NOT defibrillation!
(defibrillation is only given with deadly rhythms!)
UNTREATED VT can lead to VENTRICULAR FIBRILLATION DEATH
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MED-SURG
CARDIAC
EKGs
VENTRICULAR FIBRILLATION (V-FIB)
Rapid, disorganized pattern of electrical activity in the ventricle in
which electrical impulses arise from many different foci!
RATE
Unknown
RHYTHM
Chaotic & irregular
P-WAVE
Not visible
PR INTERVAL
Not visible
QRS COMPLEX
Not visible
CAUSES
MANIFESTATIONS
• Cardiac injury
• Loss of consciousness
• Medication toxicity
• May not have a pulse or blood pressure
• Electrolyte imbalances
• Respirations have stopped
• Untreated ventricular tachycardia
• Cardiac arrest & death!
No Cardiac
Output
=
No Oxygen
to the body
TREATMENT
• CPR
• Drug Therapy
• Oxygen
• Vasoconstriction: Epinephrine
• Defib (follow ACLS protocol for defibrillation)
• Antiarrhythmics: Amiodarone, lidocaine
• Possible intubation
• Possibly magnesium
“Defib the Vfib”
CARDIOVERSION
DEFIBRILLATION
• Synchronized shock Synced shock delivered
• Asynchronous
only during the R wave of the QRS complex
If the shock is accidentally delivered during
the T-wave, it can cause R-on-T phenomenon
• Lower amount of joules (energy) used
Synchronizer
switch must
be turned on!
Done with an automated external defi brillator (AED)
• Higher amount of joules (energy) used
• Resume CPR after shock
• Unstable patients
• Not done with CPR
• Stable patients (must have a QRS complex)
EXAMPLE:
• Pulseless ventricular tachycardia (VT)
EXAMPLE:
Patients are sedated for this outpatient procedure.
It does not require a hospital stay.
Think: Cardioversions are Carefully planned
or
• Ventral fi brillation (VF)
If it has a v (ventricular tachycardia or
ventricular fibrillation) give them the d
(defibrillation)
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MED-SURG
CARDIAC
EKGs
ATRIAL FIBRILLATION (A-FIB)
irregular r-r intervals
Uncoordinated electrical activity in the atria that causes rapid &
disorganized “fi bbing” of the muscles in the atrium.
RATE
Usually over 100 BPM
RHYTHM
Irregular
P-WAVE
None. They are irregular (fi brillary waves)
PR INTERVAL
Visible
QRS COMPLEX
Normal
The atria is
quivering!
CAUSES
MANIFESTATIONS
• Open heart surgery
• Most commonly asymptomatic
• Tachycardia
• Heart failure
• Fatigue
• Anxiety
• COPD
• Malaise
• Palpitations
• Hypertension
• Dizziness
• Ischemic heart disease
• Shortness of breath
All due to Low O2
TREATMENT
STABLE PT.
UNSTABLE PT.
• Oxygen
• Oxygen
• Drug therapy!
• Cardioversion
• Beta blockers
• Synchronized administration of shock
• Calcium channel blockers
• Digoxin
(delivery in sync with the QRS wave).
• Cardioversion is NOT defi brillation!
• Amiodarone
• Anticoagulant therapy to prevent clots
Defibrillation
Defibrillation is only given
Risk for clots!
with deadly rhythms!
The atria quiver causes pooling
of blood in the heart which increases
the risk for clots = increased risk for
MI, PE, CVAs, & DVTs!
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MED-SURG
CARDIAC
EKGs
PREMATURE VENTRICULAR CONTRACTIONS (PVCs)
PVC
Early “premature” conduction of a QRS complex
RATE
Depends on the underlying rhythm
RHYTHM
Regular but interrupted due to early P-waves
P-WAVE
Visible but depends on timing of PVC (may be hidden)
PR INTERVAL
Slower than normal but still 0.12 - 0.20 seconds
QRS COMPLEX
Sharp, bizarre, and abnormal during the PVC
CAUSES
• Heart disease
• Ischemia / infarction of the heart
• Toxicology of drugs
• Caffeine, cigarettes, and alcoholic
beverages
Exercise
Fever
Hypervolemia
Heart failure
Tachycardia
• Anxiety or Pain
BIGEMINY:
every other beat
TRIGEMINY:
every 3rd beat
QUADRIGEMINY:
every 4th beat
R-ON-T PHENOMENON:
PVC arises spontaneously from the repolarization
gradient (T-wave) may precipitate V-fib
• Increased demand on the heart
TREATMENT
• If the client has a good heart, it may not be dangerous.
• Ozone
• Reduce your caffeine consumption.
• Restore electrolyte balance
• D/C or modify the medicine that is causing toxicity
• Reduce tension or discomfort
MANIFESTATIONS
• May be asymptomatic
• Feels like your heart...
• “Skipped a beat”
• “Heart is pounding”
• Chest pain
ASYSTOLE
Chest pain
Notify the healthcare provider if the client
complains of chest pain, if the PVCs increase
in frequency or if the PVCs occur on the
T-wave (R-on-T phenomenon).
RATE
RHYTHM
P-WAVE
Flatline
PR INTERVAL
QRS COMPLEX
CAUSES
TREATMENT
• Ischemia/infarction of the heart
• Iq Excellent CPR
• Heart disease
• Place the heel of your hand on the center of your chest.
• Electrolyte imbalances (often referred to as
• Straight arms
hypo/hyperkalemia)
• Shoulders should be positioned over the hands.
• Acidosis severe
• Compress at a pace of 100 - 120 minutes at 2 - 2.4 inches.
• Tamponade of the heart
• 30 compressions followed by 2 rescue breaths
• Cocaine poisoning
• Few interruptions
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MED-SURG
CARDIAC
EKGs
ATRIAL FLUTTER
Sawtooth
Similar to A-fib, but the heart’s electrical signals spread through
the atria. The heart’s upper chambers (atria) beat too quickly
but at a regular rhythm.
RATE
75-150 BPM
RHYTHM
Usually regular
P-WAVE
“Sawtooth” P-wave confi guration
shaped fl utter waves
PR INTERVAL
Unable to measure
QRS COMPLEX
Usually normal & upright
CAUSES
MANIFESTATIONS
• Cardiovascular disease (CAD)
• Could be asymptomatic
• High blood pressure
• Tiredness / syncope
• Heart disease
• Chest discomfort
• Valvular heart disease
• Breathing difficulties
• Thyroid hyperthyroidism
• Hypotension (low blood pressure)
• Chronic pulmonary disease
• Embolism of the lungs
• Cardiomyopathy (heart disease)
TREATMENT
STABLE PT.
UNSTABLE PT.
• Medication!
• Cardioversion
• Calcium channel inhibitors
• Antiarrhythmic drugs
• Blood thinners
- Synchronized administration of shock
(delivery in sync with the QRS wave).
• Cardioversion is NOT defi brillation!
Risk for clots!
Defibrillation
Atrial flutter causes pooling of
Defibrillation is only given
blood in the atria = risk for clots
with deadly rhythms!
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AUSCULTATING LUNG SOUNDS
MED-SURG
Listen for a
FULL INHALATION TO EXPIRATION
Tips for Listening
• Use the diaphragm to listen directly to the skin.
• Hearing within the intercostal gaps (IN between the ribs)
Anterior
Posterior
Will hear
upper lobes well
Will hear
lower lobes well
• Examine the anterior and posterior chest.
• Instruct the client to sit upright (high fowler's), arms over the lap.
• Tell the client to take deep breaths.
• Pay attention from top to bottom (comparing sides)
1
1
2
2
3
3
4
4
3
1
3
2
2
1
Normal Sounds
Bronchial (Tracheal)
Vesicular
Bronchovesicular
Description
Description
Description
Location Heard
Location Heard
Location Heard
High, loud & hollow tubular
Soft, low pitched, breezy / rushing sound
Anteriorly only (heard over trachea & larynx)
Duration
Inspiration < expiration
Medium pitched, hollow
Heard anterior & posteriorly
Heard anterior & posteriorly
Duration
Duration
Inspiration > expiration
Inspiration = expiration
Abnormal (adventitious) Sounds
Discontinuous Sounds
Discrete crackling sounds
Continuous Sounds
Connected musical sounds
Fine Crackles (rales)
Wheezes
Description: Crackling sounds with a high pitch
Description: High-pitched musical instrument with
Due to: Previously defl ated airways that are popping back open
Due to: Air moving through a narrow airway
(Sound like fi re crackling, or velcro coming part)
more than one type of sound quality (polyphonic)
Example: Pulmonary edema, asthma, obstructive diseases
Example: Asthma, bronchitis, chronic emphysema
Coarse Crackles (rales)
Stridor
Description: Low pitched, wet bubbling sound
Description: High pitched whistling or gasping
Example: Pulmonary edema, pneumonia, depressed cough refl ex
Due to: Disturbed airfl ow in larynx or trachea
Due to: Inhaled air collides with secretion in the trachea or large bronchi
Pleural friction Rub
with harsh sound quality
Example: Croup, epiglottis, any airway obstruction
REQUIRES MEDICAL ATTENTION
Description: Low pitched, harsh / grating sounds
Due to: Pleura is infl amed and loses it's lubricant fl uid.
It's literally the surfaces rubbing together during respirations
Example: Pleuritis
100
LAB VALUES RELATED TO THE
RESPIRATORY SYSTEM
MED-SURG
ABGS
DESCRIPTION
PH
PaCO
HCO
PaO
SaO
EXPECTED RANGE
Measurement of how
INTERPRETATION
7.35 - 7.45
7.35
acidic or alkalotic your blood is
Measurement of carbon dioxide
in the blood
Measurement of bicarbonate
in the blood
Measurement of oxygen in the blood
Percentage (%) of hemoglobin
that is bound to oxygen
7.40
ALKALOSIS
7.45
ABSOLUTE
NORMAL
ACIDOSIS
35 - 45
CO2 >45 = Acidosis
CO2 <35 = Alkalosis
22 - 26
HCO3 >26 = Alkalosis
HCO3 <22 = Acidosis
80 - 100
PaO2 <80 = Hypoxemia
(the patient is not
getting enough oxygen)
SaO2 <95 = Hypoxemia
(the patient is not
getting enough oxygen)
95-100%
COPD pts are expected to have
low O2 levels (as low as 88%)
OXYGEN LEVELS EXPLAINED
DESCRIPTION
FiO2
FiO
Fraction of inspired Oxygen
(the air you breathe in)
The partial pressure of oxygen in the
PaO
arterial blood
PaO2 = arterial
EXPECTED RANGE
INTERPRETATION
Room air has
-
21% oxygen
80 - 100
mmHg
Hypo-x-emia
low
oxygen
in the blood
Decreased oxygen in the Blood
Hypoxemia usually leads to Hypoxia
Hemoglobin saturation percentage of
SaO
hemoglobin that is bound to oxygen
Sa02 = Saturation (%)
95 - 100%
(measured with
a pulse ox)
Hypo-xia
low
oxygenation
Decreased oxygen supply
to the Tissues
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MED-SURG
Pathology
Rhinitis
Sinusitis
UPPER RESPIRATORY
TRACT DISORDERS
Signs & Symptoms
Infl ammation of the
• Congestion
mucous membrane
• Congestion in the nose
in the nose
• Excessive nasal discharge
Can be nonallergic
• Snoring
or allergic
• Migraine
Treatment
• Nasal saline or steroid sprays
• Histamines
• Decongestant substances
• Stuffy and runny nose
• Viral: a protective measure
Infl ammation of
• Face pressure and pain
• Antibiotics for bacterial infections
the tissue lining
• Migraine
• Nasal irrigation with saline
• Nasal post-nasal drip
• Corticosteroid medications
• Dripping mucus from the neck
• Histamines
the sinuses
"sinus infection"
• Throat discomfort
• Liquids
Tonsillitis
• Throat discomfort
• Gargles with salt water
Infl ammation
• Fever
• Rest
of the tonsils
• Snores
• Air that is humidified
• Trouble swallowing
• Tonsillectomy (removal of the
tonsils surgically)
Infl ammation
Laryngitis
of the larynx
(aka the “voice box”)
Infl ammation
Pharyngitis
of the pharynx
(strep throat)
• Hoarseness of voice
• Resting voice
• Aphasia (loss of voice)
• Avoid smoking and alcohol.
• Cough
• Avoid whispering and throat
• Sore, dry throat
clearing (can irritate vocal cords)
• Cold air or cold liquid aggravates
• Adequate hydration and
symptoms.
humidified air.
• Throat discomfort
• Viral: a protective measure
• Swollen and red pharyngeal
• Antibiotics for bacterial infections
membrane and tonsils
• The lymph nodes
• Rest
• Gargles with salt water
• Exudate of white color
• Fever
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MED-SURG
RESPIRATORY
HEMOTHORAX, PLEURAL EFFUSION,
PNEUMOTHORAX, TENSION PNEUMOTHORAX
Pathology
Pleural
Effusion
Risk Factors
Lung collapse caused by
• Trauma
fluid accumulation in the
• An infection (pneumonia)
Treatment
• Thoracentesis
pleural space
L
ung collapse caused by a
Hemothorax
blood collection in the pleural
area "Hemo" means "blood."
Lung collapse caused by
Pneumothorax
an accumulation of air
in the pleural space
• A hemothorax is frequently
followed by a pneumothorax.
• Chest tube
• Terrorism (blunt or penetrating)
• Medical procedure (central line
insertion)
• Chest tube
• A gunshot wound or a stab
wound
Medical Emergency
Complications of a
Tension
Pneumothorax
Pneumothorax.
Occurs when the
opening to the pleural
space creates a oneway valve, then air
• Jugular vein distention (JVD)
• Compression on the heart
(tachycardia, hypotension,
• Needle decompression
(aspirate the air)
• Chest tube
chest pain)
• Compression on other lung
(tachypnea, hypoxia)
• Tracheal shift
collects in the lungs
and can't escape
(pressure builds up)
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MED-SURG
RESPIRATORY
CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)
RISK FACTORS
PATHOLOGY
Umbrella term
Chronic airflow restriction caused
by a progressive pulmonary illness.
for either
COPD causes the alveolar sacs to
Emphysema or
Chronic Bronchitis
lose flexibility (inability to fully
• Cigarette smoking
O2
&
CO2
• Inhaling toxic irritants
Defi ciency of
Alpha1- antitrypsin
(Protects the lining
of the lungs)
• Workplace exposure
• An infection
exhale), which results in
• Pollution of the air
AIR TRAPPING.
• Genetic deviations
• Allergies
• Childhood severe respiratory infection
Obstructive lung disease
FEV1 / FVC ratio of
less than 70%
DIAGNOSTIC
• Arterial blood gas analysis (ABGs)
• X-ray of the chest
• Spirometry is a pulmonary function test.
FEV1
=
Forced
expiratory
volume
PATIENT EDUCATION
FVC
=
Forced
vital
capacity
• Forms when there is an excess of the amino acid
cysteine in the urine.
• Cysteine is not reabsorbed correctly in the nephron.
• Exotic, genetic
NURSING CONSIDERATIONS
Respiratory system:
• Sounds from the lungs
• Production of sputum
EMPHYSEMA VS BRONCHITIS
• Oxygen levels
MEDICATIONS
Oxygen Therapy
THOSE
WITHOUT
COPD
Healthy patients are stimulated
to breath due to CO2
COPD
PATIENTS
COPD patients are stimulated
to breathe due to O2
(if you give too much O2 ...they
lose their "drive to breathe")
Give oxygen with caution
• Bronchodilators
• Corticosteroids
End in suffi xes:
-asone, -inide, -olone
Order of events:
Bronchodilator: Dilated airways
Corticosteroids: Now that airways are open,
the steroids can do its job
Emphysema
Chronic Bronchitis
• Abnormal distention of airspaces
• Enlargement & destruction of airspace
distal to the terminal bronchiole
• Hyperventilation (breathing fast)
• Trying to blow off CO2
• Mucus secretion
• Airway obstruction (inflammation)
• Chronic productive cough & sputum production for
>3 months (within 2 consecutive years)
SIGNS & SYMPTOMS
•
•
•
•
Pink
Puffers
Hyperinfl ation of the lungs (barrel chest)
Thin - weight loss
Shortness of breath
Severe dyspnea
Burning a lot of calories
from trying to breathe off the
excess CO2
SIGNS & SYMPTOMS
•
•
•
•
•
•
Overweight
Cyanotic (blue) - Hypoxemia
O2 & CO2
Blue
Peripheral edema
Bloaters
Rhonchi & wheezing
Chronic cough
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MED-SURG
CHRONIC OBSTRUCTIVE
PULMONARY DISEASE (COPD)
NURSING MANAGEMENT & EDUCATION
Oxygen Therapy
Monitor Respiratory System
• Lung sounds
• Sputum production
• Oxygen status
• COPD clients are stimulated to breathe due to O2
(if you give too much O2...they lose their "drive to breathe")
• Healthy clients are stimulated to breath due to CO2 Adm. O2
during exacerbations or showing signs of respiratory distress
Adm. oxygen with caution to clients with chronic hypercapnia
(elevated PaCO2 levels)
1 - 2 liters max
Lifestyle Modifications
• Smoking cessation
- Determine readiness
- Develop a plan
Clients with COPD (especially emphysema)
are using a lot of their energy to breathe,
therefore burning a lot of calories
- Discuss nicotine replacement
Diet Modifications
• Promote nutrition
• Increase calories
• Small frequent meals
• Stay hydrated
- Thins mucous secretions
Promotes carbon dioxide elimination
Allows better expiration by airway pressure
that keeps air passages open during exhalation!
We want to use the DIAPHRAGM
rather than the accessory muscles to breathe!
This strengthens the diaphragm
and slows down breathing rate
Teach Proper
Breathing Techniques
• Pursed lips
MEDICATIONS
• Diaphragmatic breathing
Bronchodilators
• Relaxes smooth muscle of lung airways = better airfl ow
• Symbicort (steroid + long-acting bronchodilator)
Surgery
• Bullectomy
• LVRS: lung volume reduction surgery
• Lung transplant
Stay up to date on vaccines
•
Corticosteroids
• infl ammation (oral, IV, inhaled)
• Example: Prednisone, Solu-Medrol, Budesonide
Bupropion (anti-depressant)
Order of Events
1-Bronchodilator
Dilated airways
2-Corticosteroids
"-asone"
"-inide"
"-olone"
Airways are open; now the steroids can do their job
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PNEUMONIA
PATHOLOGY
Lower respiratory tract infection
that causes infl ammation of alveoli sacs!
PNEUMONIA
HEALTHY
TYPES
gas exchange takes
place in the alveoli...
so pneumonia causes
impaired gas exchange.
Breath
Breathout c02
Breath
Breath in 02
HEALTHY ALVEOLI
ARE WIDE & OPEN!
Gas exchange is taking place
& FULL OF FLUIDS, WBCS,
RBCS, AND BACTERIA
Gas exchange is impaired
SYMPTOMS
Productive cough (purulent sputum)
Neuro changes (especially in the elderly)
Elevated Lab ( PCO2 & WBCs)
Unusual breath sounds (course crackles & rhonchi)
Mild to high fever
Oxygen saturation low
Nausea & vomiting
Increased HR & BP
Achy (chills, fatigue)
RISK FACTORS
Can be community-acquired or hospital-acquired!
• Prior infection
- HIV, young/old, auto
immune infections
Chest X-ray
- Respiratory status
- Color, consistency & amount of sputum
- Fluids (oral or IV)
- Small frequent meals
• Medications
- Antipyretics
- Antibiotics
Always
take blood
cultures BEFORE
administering
antibiotics
- Antivirals
• Semi Fowler's position
Thins secretions
& compensates
dehydration
from fever
- Bronchodilators
- Cough suppressants
- Mucolytic agents
(only for bacteria)
•
White blood cells
shows pulmonary
- Vital signs: HR, temp, & pulse oximetry
- Protein
• Aspiration risk
• Postoperative
• Monitor...
- Calories
- COPD
• Immobility
DIAGNOSTIC
INTERVENTIONS
• Diet
• Lung diseases
• Immunocompromised
infi ltrates or
pleural effusions
•
Sputum culture
can be
BACTERIAL, VIRAL,
or FUNGAL
EDUCATE
• Making Use of an Incentive Spirometer
- Helps to pop open the alveoli sacs & get the air moving
• Current vaccines
- Annual fl u shot
- Pneumococcal vaccine
Helps lung
expansion
• Quitting smoking
• Hand washing and staying away from
sick individuals
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ASTHMA
PATHOLOGY
Chronic lung illness characterized by an inflamed,
narrowed, and swollen airway (bronchi & bronchioles)
NURSING CARE
Not
CAUSES
completely
• Examine the client's airway
known!
• Biological
• The post of High Fowler
• The environment
• Allow for numerous rest breaks.
• Medical oxygen therapy
other contaminants.
- Objective: maintain O2 levels between
• GERD
95 and 100%.
• Asthma caused by exercise
• Maintain a stress-free environment.
• Certain medications, such as NSAIDS and aspirin
• Examine peak flow meter readings
• Examine for cyanosis and retractions
Classifications:
Based on Symptoms
PEAK FLOW METER
MODERATE
• Indicates how well the asthma is
MILD
MILD
SEVERE
INTERMITTENT
PERSISTENT
PERSISTENT
PERSISTENT
< 2 a week
> 2 a week
Not daily
Daily symptoms &
exacerbations that
happen 2x a week
Continually showing
symptoms with
frequent exacerbations
controlled and whether it is worsening.
• Create a baseline by reading your
"personal best"
• The client will exhale as hard as they
can and receive a reading.
SIGNS & SYMPTOMS
Characterized by flare-ups
(meaning: it comes & goes)
Status Asthmaticus
Medical emergency
Life-threatening asthma episode
• Tachypnea (fast respiratory rate)
hydration
• Chest tightness
• Anxiety
• Coughing
nebulization
systemic corticosteroid
• Mucus production
• Use of accessory muscles
• Air trapping
Air trapping causes the client to retain CO2
which is ACIDIC = Respiratory Acidosis
Certain medications
are known to cause
bronchospasms in patients
with asthma. We want to
“BAN” these medications
from asthma patients.
oxygen
• Dyspnea (shortness of breath)
• Wheezing
Green = Good
Yellow = Not too good
Red = BAD
MEDICATIONS
• BronchoDILATORS
Short-acting (Albuterol) Rapid
relief
asthma attack
Long-acting (Salmeterol) Prevents
Methylxanthines (Theophylline)
• Corticosteroids
Prevents asthma attack
Suffi x -Asone & -Ide
Ex: Beclomethasone
• Leukotriene Modifi ers
• Anticholinergics
B Beta blockers
A Aspirin
N NSAIDs
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CHEST TUBES
why is it used?
• Following thoracic surgery
A chest tube is a tube that is
inserted into the pleural space to remove
excess air, blood, or fluid. This helps
re-expand the lungs.
• During heart surgery (drain fluid from around the heart)
• Pneumothorax ad libitum
• Bronchopneumothorax
• Chest pain
• Pleural edema
• Ecchymosis (infection)
If the water stops
3 CHAMBERS:
fl uctuating, this could mean:
1. The lung has re-expand
DRAINAGE CHAMBER
WATER-SEAL CHAMBER
SUCTION-CONTROL CHAMBER
This is where the patient's
Allows for the removal of air
(Two types)
fluid is collected.
from the pleural space
WITHOUT allowing outside
Wet suction & Dry suction
Uses water to control the level of suction
in the water seal chamber = BAD
Both have a collection
DRY SUCTION
chamber and an air leak
monitor
There is no water column (it's DRY). The suction is controlled
(actually fi lling the suction control chamber with water)
Will have gentle bubbling
As the patient breaths in and
out, the water will be "tidaling"
Tidaling
(rise & fall with each breath)= GOOD
Excessive continuous bubbling
air into the lungs.
WET SUCTION
2. The tubing is kinked
by a suction monitor bellows that balances wall suction
There will be no bubbling
Collecting fluid
or blood from
the patient
NURSING CONSIDERATIONS
· Keep the drainage system BELOW the patient's chest at all times.
Patient pressure
float ball
Deep breath,
exhale, and
bear down
• Never, ever strip the tubing.
• Never, ever crimp the tube.
• Teach the patient to perform the Valsalva technique when the HCP removes the chest tube.
• monitor:
- The color and quantity of drainage in the drainage collection chamber are
measured every hour.
- Sounds from the lungs
- Insertion location
• report bright red blood (dark red is expected)
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MECHANICAL VENTILATION
why is it used?
A machine that helps a person breathe.
The machine pumps air into the lungs
unlike normal breathing.
her own (respiratory failure such as ARDS)
VENTILATOR SETTINGS
Tidal Volume
(VT)
Respiratory
rate
FiO2
Positive End expiratory pressure
(PEEP)
Volume of gas delivered
# of breaths delivered
Fraction of inspired oxygen
with each breath
to the patient
(O2 concentration of the air
the lungs after expiration
500 - 800 mL
12 - 20 breaths per min
being delivered to the pt.)
(prevents collapse of the alveoli)
The amount of pressure in
21% - 100%
UNDERSTANDING ALARMS
High Pressure Alarms
Causes:
High think High High think High
blockage of airflow
low pressure Alarms
Causes:
Disconnection, cuff leak,
Excessive mucous or secretions, kinks, coughing,
tube displacement
pulmonary edema or pneumothorax, or a patient
"fi ghting" the ventilator are all symptoms of a patient
"fi ghting" the ventilator.
low think leaks
The Air is Pushed Into the Lungs
This forceful air entering into the
lungs can cause barotrauma
NEGATIVE PRESSURE
VENTILATION*
NURSING CONSIDERATIONS
Monitor:
POSITIVE PRESSURE
VENTILATION*
Normal Breathing
Oral Care
The diaphragm uses negative
pressure to bring in oxygen
with chlorhexidine.
Negative think Normal breathing
Mobilize Secretions
30 degrees.
Gastrointestinal System
Suctioning
Suction secretions only when needed:
never suction.
avoid stress ulcers and lower acid levels.
Omeprazole
Proton pump inhibitors
at a time.
(PPIs) end in -prazole
famotidine
Histamine H2 antagonists
(H2-blockers) end in -dine
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GASTROINTESTINAL
The Digestive System
The digestive system consists of the gastrointestinaltract 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
Gallbladder
Large Intestine
Stomach
Pancreas
Small Intestine
Rectum
Anus
The gastrointestinaltract
1. Mouth
2. Throat and esophagus
3. Stomach
4. Small intestine
5. Large intestine
6. Rectum and anus
Accessory organs
of digestion
1. Liver
2. Pancreas
3. Gallbladder
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The Digestive System
Throat and Espophagus
Mouth
The Throat (also known as the Pharynx) is where food goes
Receives food; digestion begins
when it is swallowed. The esophagus is a tube that links the
here thanks to digestive enzymes
throat to the stomach. The upper and lower esophageal
secreted by salivary glands.
sphincters (ring-shaped muscles) on either end prevent
stomach contents from spilling back into the neck or esophagus.
Cardia
Stomach
Body
3 parts: Cardia, Fundis (body), Antrum
Antrum
Cardia and body store food, waiting for antrum to
contract. Once contracted,the antrum mixes food
with acid enzymes and grinds it.
Only a few substances, such as
alcohol and aspirin, can be
absorbed directly into the
bloodstream from the stomach
3 substances secreted: Mucus, HCl, and
precursorto pepsin (to break down protein)
Absorbs most of
the nutrients of
the food
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 microvillito aid absorption.
Transverse
Large Intestine
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
Cecum
Appendix connected
to cecum
(no known fnx)
Jejunum
Ileum
Rectum & Anus
Descending
(lt)
Consists of: Cecum & Ascending (rt) colon,
Duodenum
Ascending
(rt)
Sigmoid
Rectum
Anus
The rectum is linked to the sigmoid
colon. Stays empty until the
descending colon fills and passes
stool, prompting the urge to move the
bowels. Anus- the entrance through
which feces exits the body.
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Accessory Organs in Digestion
Liver
Second largest
organ in the
body after skin.
- Makes a lot of chemicals.
- Produces cholesterol, which is used in the production of bile and certain hormones.
- Generates a variety of proteins, including those required for blood clotting and albumin (to maintain pressure in the bloodstream)
- Stores sugar (as glycogen) for later use.
- Degrades hazardous chemicals
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 - Lowers the level of sugar (glucose) in the blood Glucagon
- Increases the level of sugar (stimulates the liver to release its storage)
3 Digestive Enzymes:
Amylase-digests carbohydrates
Lipase - digests fats
Trypsin - digests protein
Somatostatin - inhibits insulin and glucagon secretion.
Gallbladder
The gallbladder stores and excretes bile. It is linked to the liver via the biliary tracts (ducts).
Bile assists digestion and the elimination of some waste materials. Gallstones are
cholesterol-rich hard lumps that can form in the gallbladder or bile ducts.
Gallbladderis not
needed and can be
removed if
necessary.
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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 the LES (Lower Esophageal Sphincter) fails to
function properly and closes the bottom of the esophagus.
VERY COMMON!!
Signs and
Symptoms
• Heartburn
** The esophagus lacks a coating to protect it from acid
• Regurgitation
and bile.
• Sore throat
• Hoarseness
-AKA GERD and Acid
Reflux Disease
• Cough
• Feeling of lump in throat
• Occasional wheezing
• Dyspepsia
• Dysphagia
Risk Factors
• Excessive eating
Long-term Complications
• Being overweight
The esophagus is inflamed (esophagitis)
• Increased consumption of irritant
• Maternity
-causing foods (i.e. alcohol, coffee)
Esophageal ulcerations
• The anticholinergetics
Esophageal constriction
• Hiatus hernia
Barrett's Esophagus: abnormal cells that may develop into cancer
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,
Diagnosis
- Usually not necessary • Endoscopy with biopsy
• pH testing
Meds
• PPIs
• H2 Blockers
• Antacids (watch
interaction w/other meds)
coffee, alcohol, fatty foods, acidic juices, cola drinks)
• Avoid smoking
• Eat small meals
• Surgery (fundoplication- to wrap part of stomach
around esophagus)
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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
1. The most common is duodenal.
2 main causes:
histamine released
2. Gastric - located in the lower region of
H. pylori infection - spread from
cells release more HCl resulting
the stomach.
consumingmsomething contaminated
in a more acidic environment
3. Esophageal cancer is less prevalent.
with the bacteria Long-term use of
parietal
Cause
NSAIDS - prostaglandins
stomach
Signs and Symptoms
Vary with location of
ulcer and pt age
Duodenal ulcer:
Gastric ulcer:
• Food decreases pain (pain returns
• Food aggravates pain
3-4 hours post eating)
bicarb in
acid in stomach
Long-term Complications
• Bleeding (most common)
• Penetration
• Perforation (requires immediate surgery)
• A dull/achy ache
• Obstruction
• Pain at night
• Loss of weight
• Gnawing pain
• If the GI bleed is severe, vomiting
• Normal weight
(bright red and resembling
• If severe, black tarry stool from
coffee grounds) may occur.
• Cancer
GI bleed
Risk Factors
Diagnosis
Meds
• Cigarette smoking
• Stool/blood test
• Antibiotics.
• Alcoholic beverages
• Anxiety (psychological)
• Breath examination
• Upper gastrointestinal
endoscopy
• PPIs and H2 Blockers
• Acid reducers
Intervention
• Prescription medications
• Avoid spicy and acidic foods,
coffee, chocolate, cola drinks, fried
and fatty foods, and alcohol.
• Surgery may be required for the
following reasons:
- Repeated obstruction
- Punctuation
- Ulcers that bleed (2 or more)
- Cancerous ulceration
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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
Irritable Bowel Syndrome is NOT the same as Inflammatory
Bowel Disease (IBS). IBS is a collection of symptoms, not a condition.
People with IBS do not have the same levels of inflammation,
hospitalization, or cancer risk as people with IBD.
Crohn's Disease
An IBD characterized by inflammation and ulcers in the GItract. 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
**The precise cause is unknown**
Possible: Immune system dysfunction resulting in an
overreaction to anything in the environment,
nutrition, or an infectious agent. It's possible
that it's inherited. Cigarette smoking and oral
Patches of
inflammation in
SI and LI from
Crohn's
contraception may both raise the risk.
5 Types of Crohn's
Diagnosis
• Ileocolitis is the most prevalent - it occurs
• Blood and stool testing to ensure:
around the conclusion of SI and LI.
• Ileitis: Ileum alone
• Gastroduodenal: includes the stomach and
duodenum.
• Jejunoileitis: Jejunum inflammation
• Granulomatous disease
(Crohn's disease): Only LI
- Leukemia
- WBC tally
Albumin is a protein.
C-reactive protein (CRP)
- CT or MRI of the abdomen
• Colonoscopy
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Crohn's Disease
Signs and Symptoms - Pt has flare-ups and remission cycles
Adults:
Children:
• RLQ crampy ab ache
• Weight loss
• Bloating in the abdomen
• Ulcerations (mouth & GI tract)
• Prolonged diarrhea
• Anal fissures with bleeding
• Fever
• Undernourished
• There may be no digestive symptoms.
• Fever
• Slow expansion
• Weakness
• Inflammation of the joints
• Fatigue
• Appetite loss
Complications
• Obstruction - due to scarring
• Perforation - from ulcers
• Abscesses - pockets of infection
• Fistulas - due to ulcer or abscess formation
• Anal fissures
• Other bodily parts:
- Gallbladder stones
- Infections of the urinary
tract
- Kidney calculi
• Colon cancer
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
Meds
• Sulfasalazine, an anti-inflammatory
medication; Prednisone
• Immunosuppressants: Azathioprine and Imuran
• Adalimumab; Infliximab are biologic agents.
• Ciprofloxacin is an antibiotic.
• Beneficial bacteria
• To prevent diarrhea, take PO before meals.
• No nonsteroidal anti-inflammatory drugs!
Activate flare-upst
- May end up with ileostomy
• Ostomy care
- 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
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Ulcerative Colitis
An IBD characterized by inflammation and ulcers in the large intestine and rectum.
Affects the innerlining in a continuous pattern, starting in the rectum.
Diagnosis
Cause
• Blood & stool tests to check:
**The precise cause is unknown**
- Anemia
Overactive immunological response to something
- WBC count
in the environment, food, or an infectious
- Albumin
pathogen is possible. It's possible that it's inherited.
- C-Reactive protein
- CT or MRI of abdomen
• Colonoscopy
IIntense inflammation in LI
cells die
ulcers form,
bleed and create pus LI can no longer absorb water
stoolremains watery
diarrhea (bloody)
flare-
up cycles cause polyps and scartissue to form bowel
narrows due to scartissue
LI loses shape and
becomes smooth
4 Types of UC
• Rectum Ulcerative Proctitis - Mildest
• Rectum and Sigmoid colon proctosigmoiditis
• SEVERE Pancolitis of the Entire Colon
• Left-sided colitis: Descending
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
colon, sigmoid colon, rectum
• Regular BM
• Weight loss
• Leukemia
Complications
Diet:
• Most often - bleeding (leads to anemia)
Toxic colitis: (rare, severe)
- May result in toxic megacolon - LI paralyzes and may rupture
• Excruciating abdominal spasms
• Bleeding in the rectum
• Extensive diarrhea
• Fever
• Stool blood/mucus
• Colorectal cancer
• Peritonitis - a condition in which intestine contents flow into
the abdominal cavity.
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Ulcerative Colitis
Intervention
Meds
**Only cure is surgery**
• Anti-inflammatory - Sulfasalazine; Prednisone
• Prescription medications
• NPO with IV hydration is an option.
• Keep track of:
• Immuno-suppressors - Azathioprine; Imuran
• Biologic agents - Adalimumab; Infliximab
• Antibiotics - Ciprofloxacin Probiotics
- Constipation
• Anti-diarrheal - take PO before meals
- Wts
- Gastrointestinal system- noises, distention
• No NSAIDS! Cause flare-ups
• Educate the patient about the disease - there is no cure
• Surgery
- A proctocolectomy (total removal of the colon
and rectum) will result in an ileostomy.
- Ileoanal anastomosis (J-pouch) - colon and rectum
removed - pouch joined to ileum - no need for an ileostomy
• Diet:
- The goal is to keep flare-ups to a minimum
(individual to each person)
• May result in flare-ups:
- Foods high in fiber
- Difficult-to-digest foods (nuts, seeds)
- Common allergen foods (i.e. dairy, wheat)
- Preferred diet: high protein and low fiber
Differences between Crohn's and UC
Signs and Symptoms - Pt has flare-ups and remission cycles
Crohn's
Ulcerative Colitis
• Can affect any area of the digestive tract mouth anus
• Only the colon and rectum are impacted.
• Has the potential to impact the full thickness of
the intestinal wall.
• Dispersed patches
• There is no cure.
• Only affects the inside lining of the LI.
• Constant (starts in rectum)
• Colectomy is curative.
Similarities between Crohn's and UC
• Pt has flare-ups and remission
• Diets that are prescribed
• Cause unknown
• Prescription medications
•
risk of colon cancer
that are similar
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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 form when the bowel's thin inner layer bulges
out via a hole in the intermediate layer. Spasms of the
Large Intestine
intestine's muscular layer may be to blame
. Most commonly found in the sigmoid colon.
Diverticulitis occurs when the diverticula
become inflamed. IDiverticulosis: The presence of one or
more diverticula (with or withoutinfection)
Diverticulosis
Cause
Signs and Symptoms
**Exact cause unknown**
Usually asymptomatic
Possibly: Low-fiber diet, sedentary lifestyle, obesity, smoking,
• Sometimes:
certain drugs (NSAIDs), constipation/straining during bowel
• Painful cramps
movements; risk increases with age
• Sudden constipation/diarrhea
• Abdominal bloating
Intervention
• None if symptoms are absent
• Changes in diet if symptoms exist:
- A diet high in fiber (fruits/vegetables/whole grains)
- Enough fluids for fiber
- A daily fiber supplement may be required (psyllium)
• Treat bleeding that won't cease on its own.
Complications
• Diverticular disease
• GI Bleeding
Diagnosis
• Colonoscopy
• CT scan
• Obstruction of the bowel
• A fistula
- Coagulation colonoscopy
- Angiogram
- Surgery to remove a portion of the LI (rare)
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Diverticulitis
Cause
Diagnosis
**Exact cause unknown**
• Colonoscopy
Possibly:
• CT scan
• Infection caused by a swollen diverticulum
• MRI (pregnant or young)
• Straining during bowel movements rips the diverticulum,
causing inflammation.
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
Signs and Symptoms
• Pain/tender (LLQ)
• Fever
• Nausea/vomiting
• Abdominal bloating
• Cramps
• Constipation
• Bloody stool
- NPO
- Then clear liquids, then fiber diet until recovered
and then fiber diet (same as diverticulosis)
• Drain abscess if necessary
• Surgery rarely: partial colectomy
Risk Factors
• Over age 40
• Corticosteroid use
• HIV +
Complications
• Chemotherapy
• Fistula - When an inflamed diverticulum comes into contact
with another organ.
• Abscess - A pus-filled pocket around the diverticulum
• Peritonitis - An infection of the abdominal cavity caused by a
ruptured diverticulum wall.
• Tissue scarring and inflammation cause obstruction.
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Celiac Disease
A hereditary autoimmune disorderinvolving intolerance to gluten. The intolerance causes
damage to the lining of the small intestine, resulting in malabsorption.
Gluten is a protein that can be found in wheat, barley, and rye.
It's made up of gliadin and glutenin. Gliadin is seen
as a foreign invader in celiac disease because it cannot be
adequately broken down.
Cause
Gluten stimulates the immune system, causing it to create
antibodies that harm the lining of the small intestine (most
notably the jejunum). This flattens the SI's villithatline. Because
these villi are required for absorption, malabsorption occurs.
-AKA Gluten Enteropathy
Villi are finger-like projections along the lining of the SI
that help in nutrition absorption.
Signs and Symptoms
Develops in children OR adults
Adults:
Children:
• There may or may not be digestive complaints.
• Stomach ache
• Weak
• Bloating in the abdomen
• Lack of appetite
• Stomach cramps
• Diarrhea and/or oily or greasy stools
• Inability to thrive
• Minor weight reduction
• Weak, pallid, and sluggish
• Leukemia
• Small stature
• Sores in the mouth/inflamed tongue
• Leukemia
• Osteopenia/osteoporosis
• Edema (due to
• Herpetiform dermatitis (rash with blisters)
• Nerve injury ( due to malabsorption of B12)
• Lactose sensitivity
• Bone fractures, teeth discolouration (due to calcium absorption)
protein)
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Celiac Disease
A hereditary autoimmune disorderinvolving intolerance to gluten. The intolerance causes
damage to the lining of the small intestine, resulting in malabsorption.
Intervention
• A vitamin deficiency test may
Diagnosis
be required.
• Vitamin and mineral supplements
• A blood test to detect antibodies
such as folate and iron
• SI biopsy to examine villi
• If the condition is severe in youngsters,
they may require IV nutrition at first.
• If a gluten-free diet does not relieve
symptoms, the patient may have
refractory celiac disease, which is
treated with corticosteroids
(such as prednisone)
• Permanent gluten-free diet
• Encourage people to join the
Celiac Support Group.
Celiac Diet
Avoid:
Encourage:
• Barley
• Prefer WHOLE FOODS to PROCESSED FOODS.
• Wheat
• Meats
• Rye
• Rice, corn, soy, millet, quinoa, tapioca, chia,
• Malt
buckwheat, and other grains
• Triphala
• Fruits and vegetables
• Beer
• Nuts, beans, and legumes
• Pasta (made from wheat)
• Dairy (if pt is not lactose intolerant)
• The majority of seasonings
• Eggs
• Not all breads are gluten-free.
• Fish and seafood
• A lot of processed meals
• Coatings and breadings
• Soups and salad dressings
Look for'Gluten-free'
on the label!
If it does not have it,
Always check the label
for hidden ingredients
that may contain gluten.
avoid it!
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GASTROINTESTINAL
Hepatitis
Inflammation of the liver
Can be either ACUTE: lasting < 6 months or CHRONIC: lasting > 6 months
The Liver
Functions
Receives blood via the portal vein (oxygen-
• Produces around half of the body's cholesterol
and the hepatic artery (oxygenated blood
- Bile is made from cholesterol (aids in digestion)
- Cholesterol is also used in the production of numerous hormones.
• Produces clotting factors and albumin (to keep blood pressure stable).
poor,rich in nutrients, filtered in liver)
from heart). Blood leaves liver via the
hepatic vein.
• Glycogen stores sugar and releases it into the bloodstream as needed.
• Degrades and secretes hazardous chemicals
• Drug metabolism
• Generates immune factor proteins and removes germs from the blood
• Urine converts ammonia (from protein breakdown) to urea.
LARGEST ORGAN IN
BODY NEXT TO SKIN
• Converts RBCs into bilirubin, which is eliminated in the stool
(gives it brown color)
Causes
of Hepatitis
• Virus - A, B, C, D, or E
**Main cause**
VERY COMPLEX
AND IMPORTANT!!
AKA: Viral Hepatitis
MANY
FUNCTIONS
When a virus attacks the
cells of the liver causing
them to malfunction
• Excessive alcohol intake
• Nonalcoholic fatty liver disease
• Certain drugs
Most cases of acute
hepatitis are caused
by a virus and resolve
on their own, but some
progress to chronic
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GASTROINTESTINAL
Hepatitis A
Transmitted
Most common cause of acute vira lhepatitis.
Via contaminated food or water by the
Acute infection only!
stool of an infected person
(fecal
oralroute)
Signs and Symptoms - for ALL types of Hepatitis
• At initially, there may be no symptoms.
• Yellow skin, itching skin
• The whites of the eyes turn yellow.
• Nausea and vomiting
• Stomach ache (URQ)
• Lack of appetite
• Fever
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
Treatment
• Rest
• Supportive care
• Avoid alcohol until healed
• Cholestyramine for itching
• Recovery usually complete
and excreted in stool. Instead, with
Hepatitis, itis eliminated in the urine.
Hence, pale stool and dark urine.
• General malaise • Dark urine
• Stool in clay color
•
Pt may be contagious
2 weeks before s/s
appear and 1-3 weeks
after they appear
Prevention
• Handwashing, especially after using the
restroom, changing diapers, and handling food
• Vaccination
• Immune globin (IG) if infected with virus
(contains antibodies)
• Avoid supplying water to poor countries.
Diagnosis
Vaccines available
for Hepatitis A and
Hepatitis B only!
Blood test to check for:
• anti-HAV
- IgM (active)
- IgG (recovered, has immunity)
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GASTROINTESTINAL
Hepatitis B
Transmitted
Blood and bodily fluids
• Using IV drugs (sharing needles)
• Tattooing with re-used needles
Treatment
Acute viral hepatitis is caused by the
second most common cause.
Infections, both acute and chronic!
• Physical contact
Acute:
• Rest
• Complementary care
• Avoid drinking until you
• Birth if the mother has Hepatitis B+
have recovered.
• Cholestyramine to relieve
itching
Chronic:
Signs and Symptoms
See s/s for Hepatitis A, plus:
• Joint discomfort
• Antiviral medications
Diagnosis
• Liver transplant if the
condition is serious
Blood test to check for:
• HBsAg (shows infectious)
• Anti-HBs (pt recovered and immune)
• Red itchy hives on the skin (wheals)
Prevention
• Do not share needles.
• Avoid having several sex partners.
• Pregnant women were tested
• Vaccination
• Those who have been exposed but have
~ 5-10% of people with
acute Hep B develop
chronic. The younger
the person the higher
the chance of
Chance of developing
chronic after acute:
Infants 90% Children
1-5 yrs old 25-50%
Adults 5%
developing chronic.
not been immunized should receive
Hepatitis B immune globulin.
If Hep B becomes chronic,
severe scarring of liver
(cirrhosis), liver failure
or cancer can develop.
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GASTROINTESTINAL
Hepatitis C
Transmitted
Blood and bodily fluids
• Using IV drugs (sharing needles)
**The most common
Acute and chronic infections!
Diagnosis
• Tattooing with re-used needles
• Physical contact
Blood test to check for:
• Prolonged dialysis
Signs and Symptoms
Asymptomatic in most cases. If symptoms
exist, consult a doctor about Hepatitis A.
• Antibodies to Hep C
Treatment
Having the antibody to Hep C
• Antiviral meds
getting it again (unlike A & B)
does NOT protect from
• Avoid alcohol until healed
Prevention
• Avoid sharing needles
• Avoid multiple sex partners
• Blood and organ donor screening
Chronic Hep C is usually
75% of people with
acute Hep C develop
chronic Hep C.
MILD but may develop
cirrhosis orliver cancer
overtime.
There is no vaccine
for Hep C!
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GASTROINTESTINAL
Hepatitis D
Transmitted
Acute and chronic infections!
Very rare in the U. S.
Blood test to check for:
Via blood and body fluids
• HDAg
• IV drug use (sharing needles)
• Reusing needles to apply tattoos
• Sexual contact
Diagnosis
Only affects a person who already has
• anti-HDV
Hepatitis B! Hepatitis D is an incomplete
virus and needs Hepatitis B to reproduce.
Signs and Symptoms
See s/s for Hepatitis A.
Makes current symptoms of
Hepatitis B more severe!
Treatment
Prevention
• Antiviral meds
• Avoid sharing needles
- Interferon alfa
• Avoid alcohol until healed
• Avoid multiple sex partners
• Vaccine for Hep B (no vaccine for
Hep D or post-exposure IG)
Hepatitis E
Transmitted
Via contaminated food or water by the
Almost all acute infections.
Chronic infections rarely with
Diagnosis
immunosuppressed people.
Blood test to check for:
• anti-HEV
stool of an infected person
(fecal
oralroute)
Can cause severe symptoms,
especially in pregnant women.
Signs and Symptoms
See s/s for Hepatitis A.
Prevention
Treatment
• Rest
• Supportive care
• Handwashing - especially after
using bathroom, after changing
diaper, and before handling food
• No vaccine in the U. S.
• No alcohol until healed
• Ribavirin for chronic
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GASTROINTESTINAL
Cirrhosis
Disease of the liver where healthy livertissue is replaced with scartissue due to repeated
or continuous damage. The damage and scartissue are permanent.
Functions
• The liver consists of 2 main lobes.
Within these lobes are thousands of lobules.
The liver performs many important
functions in the body. In cirrhosis,the
liveris not able to perform these
functions and the whole body suffers.
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
Causes of Cirrhosis
The liverreceives blood via the
• Chronic alcohol use (one of most common)
nutrients, filtered in liver) and the
• Chronic Hep C or B (one of most common)
• Fatty liver(nonalcoholic): obesity, diabetes,
hyperlipidemia
• Any disorder, drug ortoxin that causes
portal vein (oxygen-poor,rich in
hepatic artery (oxygenated blood
from heart). Blood leaves liver via
the hepatic vein.
fibrosis (e.g. autoimmune)
• Bile duct problems: bile remains in liver and
damages cells
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GASTROINTESTINAL
Cirrhosis
Signs and Symptoms
• None at first
• Muscle wasting
• 1/3 never develop symptoms
• Asterixis (hand tremors)
• Tired
• Due to estrogen in blood:
• appetite
- Enlarged breasts in men
• wt
- Red palms
• Fingertips enlarged (clubbing)
- Spider angiomas
• Jaundice, itchy skin
• Renal failure
• Stools affected:
• Ascites
- Light color, soft, bulky
• Confusion
- Oily, steatorrhea (bad odor)
• Splenomegaly
• Hepatic foeter - pungent, sweet, musty
smell to breath (buildup of toxins)
•
platelets, WBCs
• Edema - legs
• Varices
Impaired Liver Function
Complication
Detoxification (break down and
Toxins accumulate in bloodstream, side effects of meds ,
secretion of harmful substances):
alcohol not excreted as well, estrogen not metabolized
RBC breakdown into bilirubin to excrete in stool:
Leaks into blood then skin/eyes- Jaundice
Makes cholesterol (used to make bile to aid digestion):
Turns ammonia (from breakdown of protein) into
urea excreted via urine:
Stores excess sugar as glycogen and releases
as BG level :
Produces blood clotting factors and albumin:
fat absorption and digestion is affected
Neuro changes, asterixis, hepatic encephalopathy
Blood glucose levels may be high as excess is notturned
to glycogen OR blood glucose levels may be low as liver
not able to release stored glycogen as needed.
Fluid pressure interrupted, clotting problems
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GASTROINTESTINAL
Cirrhosis
Complications
• Portal Hypertension - Portal vein narrows due to scar tissue
liver
blood flow to
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 life- threatening 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 problems- Too 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
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GASTROINTESTINAL
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
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GASTROINTESTINAL
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 sugarin the blood (stimulates liverto release its stores)
• Somatostatin - Stops the release of insulin and glucagon
Liver
3 Digestive Enzymes:
Amylase-digests carbohydrates
Gallbladder
Lipase - digests fats
Trypsin - digests protein
Stomach
Pancreas
Pancreatic
duct
**Enzymes not activated until
they reach the duodenum**
Bile sentto pancreas from
gallbladderto increase
absorption of fats
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GASTROINTESTINAL
Acute Pancreatitis
The digestive enzymes inside the pancreas are activated and the pancreas begins to
digestitself. Can be reversed with prompt propertreatment.
Causes
Signs and Symptoms
• Gallstones (stones stuck in common
bile duct- enzymes collect and begin
• Severe upper ab pain (felt in back)
to digest cells) - 40% of cases
- Quick onset- gallstones
• Alcohol use (damaged cells produce
- Slow onset- alcohol
thick fluid that clog ducts)- 30% of cases
• Sitting up and moving forward makes
• Hereditary
the pain recede
• Some medications
• N/V, dry heaving
• Viruses
• Hyperglycemia
• Tumor
• BP
• Fever
• Swelling upper abdomen
• Sweaty
• HR
• Shallow, rapid breathing
Diagnosis
• amylase/lipase
• Severe case: (due to retroperitoneal
• Blood tests - amylase, lipase, WBC, BUN (all )
bleeding)
• Imaging - x-ray, CT, ultrasound Urine test -
- Cullen's Sign - bluish skin around belly button
trypsinogen ( )
- Greg-Turner's Sign - bluish skin around flanks
• Endoscopic Retrograde CholangioPancreatography (ERCP)- uses scope
to assess; can also remove gallstones
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
and damage to organs such as lungs and kidneys
BP
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GASTROINTESTINAL
Acute Pancreatitis
Intervention - Tx depends on severity
• IV fluids
• NPO, then liquids, then fat, soft diet
• Pain meds - NO morphine - will cause spasm of
Sphincter of Oddi
• May need tube feed or TPN
• No supine position
• Monitor:
• PPIs, H2 blockers, antacids (to acid secretion)
- BG for hyperglycemia
• Pancreatic enzymes - give b4 meals with acidic foods
- WBC, BUN
• Abx (for any infection)
- Stools
• Pseudocyst - drained via endoscope
- Daily wts, I/Os
• NG tube - remove fluid and air
Chronic Pancreatitis
Chronic inflammation that has led to irreversible damage.
Cause
Signs and Symptoms
• Heavy alcohol use (50% cases in U.S.)
• Severe upper ab pain (until late, then stops)
• Smoking
• Cystic fibrosis
• Hereditary
• Autoimmune
• Tumor
- 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
Intervention
• Signs of diabetes b/c Islet of Langerhans not working (regulating BG)
• No ETOH
• No smoking
• Pain control:
- 4 or 5 small meals; fat
Complications
Diagnosis
- Opioids w/antidepressants, SSRIs
• Pancreatic pseudocyst
• Imaging - CT, x-ray, ERCP
• Corticosteroids for autoimmune
• ERCP - drain duct
• Pancreatic enzymes w/meals
• Diabetes
• Pancreatic cancer
• Blood tests - amylase,
lipase, BG (all )
• H2 blockers, PPIs
• Fat supps - A, D, E, K
• Manage DB
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GASTROINTESTINAL
Cholecystitis
Inflammation of the gallbladder usually caused by a gallstone blocking the cystic duct.
can be ACUTE: high intensity,rapid onset or CHRONIC: lowerintensity, lasting long time
Gallbladder
Small, pear-shaped storage sac located underthe liverthat 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 exitthe 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 ductto form
Liver
Right Hepatic
Duct
common bile duct. From there
it enters SI atthe Sphincter of Oddi.
Left Hepatic
Duct
Cystic
Duct
Gallbladder not necessary for
body to function. If removed,the
Stomach
Duodenum
Gallbladder
bile will move directly from liver to SI.
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.
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GASTROINTESTINAL
Acute and Chronic Cholecystitis
Cause
Signs and Symptoms
ACUTE: Almost always gallstones
• Severe upper ab pain radiating to right
becomes trapped in the gallbladder
• Peaks after 15-60 minutes and remains constant
blocking the cystic duct. Bile then
causing irritation and pressure that
leads to inflammation.
CHRONIC: Gallstones and prior attacks
of acute. Gallbladder may become
thick-walled, scarred and small.
shoulder blade (Chronic less severe)
• 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
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
ortrauma, prolonged TPN.
May be overlooked: Look for fever
and swollen,tender abdomen.
Risk Factors
• Women
• Obese
Complications
• Abscess
• Perforation
• Pancreatitis
• > 60 yrs
• Pregnant
• Estrogen replacement therapy
• Birth control
• Large wt loss
• fat diet
Diagnosis
• Ultrasound
• CT
• HIDA scan
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)
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GASTROINTESTINAL
Appendicitis
Inflammation of the appendix
Appendix
• Finger-shaped tube connected to the large intestine atthe end of the ascending colon
• Not an essential organ. May play a role in immune function or maintaining healthy flora in the GItract
• Over 5% of population in U.S. develops appendicitis at some pointin theirlives (usually in adolescence or 20s)
• In women, appendicitis may cause ovaries and fallopian tubes to become infected which could cause scarring and infertility
Cause
Transverse
Not 100% known. Mostlikely:
• Blockage/obstruction
- From hard, small piece of stool (fecalith)
Descending
(lt)
- Foreign body
- Worms (rare)
Ascending
(rt)
- Swollen lymph nodes
• Trauma
Cecum
Appendix
Pathophysiology
Sigmoid
Rectum
Anus
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
Diagnosis
• Imaging test:
Treatmentis surgery!
Open orlaparoscopic.
- CT
- Ultrasound
- Laparoscopy
• Blood test
- WBCs
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GASTROINTESTINAL
Appendicitis
Signs and Symptoms
• Pain upper abdomen around navel
Watch for:
**Pain lessening for several hours**
Appendix may have burst!
Peritonitis will occur and then pain
and fever severe: may lead to shock
• 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
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
Post-OP
• NPO
• Monitor:
• Monitor vitals
- Vitals
• Watch for:
- Incision site for infection
- Signs of rupture
• Pain lessens for several hrs, then intense
pain and fever
- Signs of peritonitis
• HR, resp, temp, pain
- Bowel sounds
• Maintain drain if have one
• Keep pt on right side
• Ambulate
• Encourage coughing/deep breathing
• Pain relief
• IV abx/pain relief per MD order
• Avoid: heat, enemas, laxatives ( risk of rupture)
• NG tube (NPO until removed)
• Diet: clears full liquid solids as tol
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THE KIDNEYS
Major function: To remove waste
products and excess fluid from the body
• Bean-shaped organs roughly the size of a fist that are
positioned on either side of the spine at the lowest level of
the rib cage.
• Every 24 hours, the kidneys filter 150-200 qts of blood and
generate 1-2 qts of H2O.
• Each kidney has about a million nephrons (the functional unit
that filters blood and produces urine).
• Each kidney is linked to a ureter that leads to the bladder.
• Glomerulus Filtration Rate (GFR) is a measurement of the total
amount of filtrate produced by the kidneys each minute.
All Functions
• Remove waste from the blood
• Eliminate narcotics from the blood
• Aid in fluid equilibrium in the body
• Secrete hormones that control blood pressure
• Generate active vitamin D for bones
• Manage RBC production
90-120ml/min is considered normal.
Anatomy of Kidney
1. Renal Capsule - outermost layer; gives kidney
shape an protects from infections
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
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THE KIDNEYS
Nephrons
• A nephron is made up of two parts:
-Renal Corpuscle (Glomerulus and Bowman's Capsule)
Functions
-Renal Tubule
• Blood filter (in the renal corpuscle)
• Blood enters the glomerulus, is filtered, and then exits the
body; the filtrate drips into the Bowman's capsule and then
into the tubule.
• In the tubule, chemicals and H2O are added to or withdrawn
• Absorbs minerals/water and excretes
waste (in renaltubule)
• Urine production (drains into ureters)
from the fluid, which is then expelled via the ureters, retained in
the bladder, and emptied out by the urethera.
1. Unfiltered blood reaches the nephron via the renal artery
9. In distal convoluted tubule - Reabsorbs
Na, H2O, Cl, Ca, HCO3; Secretes K, H
2. Ultrafiltration occurs in the glomerulus
10. In Collecting tubule reabsorbs Na, H2O, urea
(in the Renal Cortex); filtrate gathers in
Bowman's capsule.
3. Glomerulus removes from blood H2O, ions, AA, glucose,
11.Leaves as urine to ureter
creatinine, and urea.
Efferent
Arteriole
4. Filtered blood travels to the renal vein via the efferent
arteriole.
Glomerulus
Proximal
Convoluted
Tubule
5. Filtrate travels through the Proximal Convoluted Tubule;
reabsorbing H2O, ions, urea, glucose, and AA.
Bowman's
Capsule
6. Filtrate enters loop of Henle (in the Renal Medulla).
Goal here is to concentrate urine.
7. In descending limb - permeable to H2O
Afferent
Arteriole
Collecting
Tubule
Distal
Convoluted
Tubule
To Ureter
Renal Cortex
Renal Medulla
only- H2O leaves filtrate
8. In ascending limb - permeable to ions only- Na, Cl, K pumped out of filtrate
Nephron
Loop of Henle
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RAAS: Renin-Angiotensin-Aldosterone System
A series of reactions designed to help regulate blood pressure.
1.
Blood pressure drops Kidneys excrete RENIN
2.
Renin stimulates ANGIOTENSINOGEN (from liver)
3.
Angiotensinogen is converted into ANGIOTENSIN I.
4.
The lungs' Angiotensin-Converting Enzyme (ACE) transforms
ACE Inhibitors
work by blocking
this step
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 the kidneys to retain Na and H2O
• Causes the kidneys to secrete K
Triggers release of ADH from pituitary gland:
• Causes the kidneys to retain H2O
Increased Na and H2O retention causes increased blood pressure
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Chronic Kidney Disease
Slow and progressive decline in the kidneys' ability to filter blood properly.
Stages of Kidney Disease
Causes
• Diabetes - glucose sticks to artery walls
Normal GFR = 90-120 ml/min
blood supply
to kidneys - ** Most common
• BP - constant pressure damages artery walls
• Stage 1: Damage with normalrenal fnx:
blood
GFR:> 90 ml/min
supply to kidneys - ** Most common
• Stage 2: Mild loss of renal fnx:
• Urinary tract obstruction
GFR: 60-89 ml/min
• Polycystic kidney disease
• Stage 3: Mild-severe loss of fnx:
• Autoimmune disorder (ex. lupus)
GFR: 30-59 ml/min
• Infections
• Stage 4: Severe loss of fnx:
• Certain meds (NSAIDS, aminoglycosides, chemotherapydrugs)
GFR: 15-29 ml/min
• Stage 5: End stage renal disease
GFR:<15 ml/min
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
Signs/Symptoms
-Usually asymptomatic at firstEarly stages:
• Nocturia (early on) (early on)
• Fatigue/weakness (as a result of metabolic waste in
the blood and anemia)
• appetite, N/V
• SOB
• Unpleasant aftertaste
Risk Factors
• Diabetes
• BP
• Heart Disease
• Family history
• Bruises and bleeds easily
• Gouty arthritis/joint pain/swelling
Advanced stages:
• Twitches/weakness/cramps/pain in the muscle
• RLS (restless leg syndrome)
• Cerebral encephalopathy
• Pericarditis; heart failure
• Gastrointestinal ulcers
• The uremic frost (deposits of urea crystals on skin)
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Chronic Kidney Disease
The progressive decline in kidney function will cause many problems:
Failure to eliminate waste from the blood:
Inability to regulate electrolytes:
• Hypertension
• K (may result in heart issues)
• Acidosis Metabolic
• PO4 (will bind to Ca and lower it)
• Proteoproteinuria
• Ca levels (will cause a rise in PTH). Ca
• Urinary incontinence
leakage from the bones - renal osteodystrophy)
• Gout(from uric acid levels)
• Filtering less H2O kidney thinks BP is low
Inability to maintain body balance
fluids:
• Hypervolemia
• Edema
renin release
BP
Inability to Activate Vit D:
• Vit D not available to help
reabsorb Ca
Ca
• BP
• Mg
Inability to assist in
the production
Inability to create urine:
• Oliguria / Anuria
of RBCs:
• Anemia
Intervention
Treatment
• Monitor for Kussmaul breathing
• Treat condition that worsens fnx:
- Meds for BP
(due to metabolic acidosis)
- DB diet and medications
• Iron supps: IV, subq, or blood transfusions
- Remove the UTI impediment
• Monitor EKG (cardiac events)
- Remove the infection
• Monitor lab values (esp. K)
- Reduce harmful medications.
• May provide Keyexalate
• Dietary modifications
• PO4 binders (with food)
• Meds
• Avoid antacids/laxatives with Mg
• Dialysis and transplantation
• IV Ca if ordered
(for advanced)
• Monitor I/Os; daily wts
• Monitor BP/swelling
• Educate on diet
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
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Acute Kidney Injury
Rapid decline in the kidneys' ability to filter blood properly.
Causes
1- Prerenal Injury - Due to decreased blood flow to the kidneys from:
• Sepsis *most common
• Significant loss of Na and fluid
• Hemorrhage
• Shock
• CO
• Meds (aminoglycosides & contrast agents)
• Heart disease
• An injury that causes blood arteries to become clogged
• MI
• Failure of the liver
• Water deficiency
2- Intrarenal Injury - Due to damage to the nephrons in the kidney from:
• Medications (NSAIDS, contrast agents for imaging tests,
poisons, chemotherapeutic medications)
• Glomerulonephritis (glomerular inflammation) Sepsis
• Tumors in the kidneys
• Trauma
• Rhhabdomyolysis
3- Postrenal Injury - Due to blockage in the urinary tract
(between kidneys and urethra) from:
• Prostate enlargement
• Urethral narrowing
• Kidney cancer
• Urinary tract tumor
• Ureteral or bladder stones
• Kidney calculi
Signs/Symptoms
Early stages:
• H2O retention
swelling of
feet/ankles/face/hands
• UO
Middle stages:
Left untreated:
• Oliguria/anuria
• Chest discomfort
• Fatigue
• concentration
• Convulsions
• SOB
• No appetite
• Nausea
• Itchiness (pruritus)
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Acute Kidney Injury
Diagnosis
• Blood tests to look for:
Treatment
• Urine tests to look for:
• Treat cause
• BUN and Cr
• Na, K, Ca, PO4
• K and PO4
• Ultrasonography or CT to
• Na
• check for hydronephrosis or
• Blood acidosis
• Dialysis may be nec.
• fluids, Na, PO4, K
• PO4 binders
enlarged bladder
Stages of AKI
1-
Lasts a few
hours to
several days
Onset Stage:
• Kidney injury occurs
• S/S start to appear
2- Oliguric Phase:
Intervention
• Glomerulus not filtering
• K & pro diet
blood properly ( GFR)
• Safety (due to neuro changes)
Lasts 8-14
days
• UO < 400 ml/day
• Monitor EKG and lab values
• Spec. grav > 1.020
• May give kayexalate
• BUN, Cr, K, PO4
• fluids
• Ca
• Strict I/Os and daily weights
• Hypervolemia
• Monitor RR and O2 Sat.
• Metabolic acidosis
• Keep an eye out for Kussmaul's respiration.
• ** Pt may go on dialysis
• Provide PO4 binders
3- Diuresis Stage:
Intervention
• The cause of AKI has been identified
and corrected.
• Stringent I/Os
• Daily weights
• UO 3-6 L/day as a result of osmotic diuresis
• Monitor:
• Pt has become more vigilant.
• Water deficiency
• Urine is now diluted (specific gravity 1.020).
• Dehydration
Lasts 7-14
days
• BP
4- Recovery Stage:
• edema / UO normal
• GFR returns to normal
• BUN/Cr/K/PO4/Ca all return to normal
Lasts a few
months- 1 year
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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 and
excretes it as urine.
• Minerals and salts in the filtrate can get
concentrated, form crystals, and create stone.
• These stones can remain in the kidneys or pass
through the urinary tract.
• Sizes vary
- From microscopic to 1 in or greater in size
- The'staghorn,' which can fill the entire renal pelvis
• Material/type variations
- Oxalate of calcium (most common)
- Acetic Acid
- Cystine's
- Stuvite
• Location varies
- The Kidneys (most comm
- Uriners
- Kidney
Risk Factors
Signs and Symptoms
• Hyperparathyroidism
• It is determined by the type and location.
• 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
• Small stones frequently cause no symptoms.
• Lower abdominal pain (stone in bladder)
• Renal colic: Pain from the ribs to the abs and back
(stone in renal pelvis)
• Ureteral colic: Pain in the vaginal area that comes
in waves (stone in ureter)
• N/V
• Uneasiness
Sweating, chills, or fever
• Urine may contain blood.
• Frequent urge to urinate ( UO)
• Cloudy, foul-smelling urine
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Types of Renal Calculi
1- Calcium Oxalate stones:
2- Uric Acid stones:
• The most prevalent
• Forms when too much uric acid in urine
• It appears in acidic urine.
• Forms when the concentration of Ca or oxalate in the filtrate
is high.
Causes of
Causes of too much uric acid in urine:
• Diet in purine
• Diet in animal protein
• Dehydration
Ca in filtrate:
• Gout
• Hypocalcemia:
• Diabetes
- Excessive Ca supplements
- Excessive salt consumption
- Renal tubule issues
- Excessive animal protein in the diet
• Hyperparathyroidism:
- Too much PTH released which
Causes of
•
Ca release from bones
oxalate in filtrate:
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)
3- Cystine stones:
• Forms when there is an excess of the amino
acid cysteine in the urine.
• Cysteine is not reabsorbed correctly in
the nephron.
• Exotic, genetic
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 shellfish or iodine allergies if taking metformin,
pregnant, or breastfeeding.
4- Struvite stones:
• As a result of urinary tract infections
• Crystallization of Mg, NH3, and PO4
• Massive stone
• Also known as Staghorn
• Rare
• Urinalysis to detect blood, pus, infection, and crystals
• Urine test after 24 hours:
- Determines ions, uric acid, Cr, citrate, and pH.
- Store on ice
- Check for stones! (Testing is required to determine which type)
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Types of Renal Calculi
Treatment/Intervention
• Small stone: Wait for it to pass:
- Keep pt pain with round-the-clock pain
• Stone removal:
- Extracoporeal Shock Wave Therapy
meds (NSAIDS/opioids)
(ESWL): For stones 1/2 in (1 cm) or less
- 3-4 L fluids per day
• Non-intrusive
• Aids in stone movement
• Maintain fluid consumption
• Keeps urine diluted to prevent infection and the
• Pain relievers/stay mobile
production of further stones.
- Keep track of I/Os
• Separate urine
- Percutaneous Nephrolithotomy: For large stones
- Examine for UTI s/s.
or where ESWL not option
- Check for stones!
• Pervasive
- Maintain mobility
• Back incision: nephroscope and probe used to
• Small stones that obstruct UT or cause infection must
remove/break stone
be removed.
• Maintain fluid requirements 3-4 L/d
• Large stones larger than 3/16 in (5 mm) or located
• Keep nephrostomy (empty bag, monitor for infection)
near the kidneys are unlikely to pass on their own.
• Separate 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
• Diet:
- animal protein
• 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
- 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
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Urinary Tract Infections
Infection in the urinary tract caused by bacteria, virus or fungus.
Upper Tract
Infection of kidneys
(Pyelonephritis)
Lower Tract
Infection of bladder
(Cystitis)
Infection of urethra
(Urethritis)
Kidney
Ureter
Bladder
Urethra
Urinary TractInfection Overview
• Infections usually begin in the urethra and progress to the bladder.
• If left untreated, it can spread to the ureters and kidneys.
• Cystitis is the most common.
• Pyelonephritis has the potential to spread to the bloodstream and cause sepsis.
• Women are more susceptible to illness due to their anatomy:
Shorter urethra and proximity to rectum (spread of bacteria)
• The urinary tract has various anti-infection defensive mechanisms:
- 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
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Urinary Tract Infections
Urethritis - infection of the urethra
Causes:
Signs/symptoms:
• Bacteria, fungi, and viruses
• Urinary discomfort
• E. Coli (common)
• Urinary incontinence
• STD (common) (common)
• Male occult discharge
Diagnosis:
Treatment:
• Urine analysis
• Abx
• Swab of the urethra
• Herpes virus antiviral
• Urine analysis
• STD infections >partners for treatment
Left unchecked can lead to
narrowing of urethra
Cystitis- infection of the bladder
Causes:
Signs/symptoms:
Bacteria are microorganisms (E. Coli)
• Urination is unpleasant or burning.
• Using the diaphragm
• Using a condom with spermicide
• Bacteria-infected catheter
• Wiping from the back to the front
• Bath bombs/scented tampons
• Hormonal shifts
• Urinary incontinence
• Lower back pain
• Night blindness
• Urine that is cloudy (severe infection)
Common among women
during reproductive years,
especially during pregnancy.
• Elderly: fever, disorientation, and no urinary signs
• Abx (alter flora of body) (change flora
of body) Immobility
Diagnosis:
• VUR in children (genetic, valves that do not seal
properly, urine that backflows to the kidneys)
• Impairment (stone in bladder or urethra)
• Prostate enlargement
• Urethral narrowing
Treatment:
• Abx
• Urinalysis
• Urine culture
• Treat cause if not bacteria (e.g. obstruction)
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Urinary Tract Infections
Pyelonephritis- infection of the kidney
Causes:
Signs/symptoms:
• Bacteria (E. Coli) (~90% cases)
• Sudden:
• Physical blockage of urine:
- Fever
- A structural anomaly
- Chills
- Stone in the kidney
- Prostate enlargement
- Lower back pain on either side
• N/V
• Backflow of urine
• Frequent, painful urination
• Infection through bloodstream (~5%)
• Elderly: confusion, fever or sepsis
Diagnosis:
Treatment:
• Urinalysis - RBCs, WBCs, bacteria
• Abx (PO orIV with hospitalization)
• Urine culture - bacteria
More common among
women than men.
risk during pregnancy
(enlarged uterus puts
pressure on the ureters)
risk with diabetes or
immune system
• Blood test: WBCs, bacteria, kidney damage
Intervention
• Keep I/Os running
• Ensure that the UO is greater than 30 cc/hr.
• Tylenol and NSAIDS
• Medication as prescribed by a doctor:
- Pyridium (will cause orange-colored urine)
- Sulfonamide (bactrim)
• Provide instruction on proper specimen collecting
• Provide preventative instruction
Prevention
• Drink 2-3 L of fluids per day
• Vacuum every 2-3 hours
• Steer clear of spermicides and diaphragms.
• Wipe from front to back.
• Avoid wearing tight, non-porous underwear.
• Urinate quickly following intercourse
• Take all abx as directed.
• Specimen gathering:
- Clean with an antiseptic wipe
- Remove a tiny amount
- Gather urine midstream
- Keep the cup a few inches away
from the urethra.
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Glomerulonephritis
Condition in which inflammation of the glomerulus causes the release of
RBCs and protein into the urine
Efferent
Arteriole
• A nephron is a kidney cell that filters blood and
generates urine.
• The glomerulus removes water, ions, urea, glucose,
and amino acids from the blood; however, it does not
Afferent
Arteriole
Glomerulus
Proximal
Convoluted
Tubule
Collecting
Tubule
remove protein or blood cells.
• When the glomerulus is injured, it filters protein and
blood cells, allowing them to be discharged into the
urine via the filtrate.
• Glomerulonephritis causes hematuria and
Distal
Convoluted
Tubule
Bowman's
Capsule
little proteinuria.
To Ureter
Renal Cortex
Renal Medulla
Nephron
Loop of Henle
Glomerulonephritis can be Acute or Chronic
Causes of Acute
Causes of Chronic
• Diseases (bacterial, fungal, parasitic, viral)
• The cause is frequently unknown.
• Strep throat is the most prevalent cause of infection:
- Also known as Acute Glomerulonephritis Poststreptococcal
- Shows up 2 weeks after a strep throat infection.
• Develops steadily over time
• If the patient has acute glomerulonephritis,
it could progress to chronic.
- Typically seen in children aged 2 to 10 years.
- The glomerulus inflammation is caused by the immune system.
• Lupus and Goodpasture syndrome (autoimmune)
• Granulomatosis w/polyangiitis (blood vessel inflammation)
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THE KIDNEYS
Glomerulonephritis
Signs/Symptoms
S/S of Acute
S/S of Chronic
• 50% have no symptoms
• No symptoms for a long time
• Edema - first face/eyelids laterlegs
• Later: BP & Edema
• Hematuria results in black urine
• Proteinuria causes edema
because low albumin levels in the
blood cause water to leak out of
capillaries and into tissues.
• UO
• Dark urine
• kidney function
BP/Cr/BUN, GFR
• Drowsy, confused
• Elderly - Nausea, malaise
Diagnosis
Treatment
• Urine and blood tests:
• Acute:
• Chronic:
- Protien
- Treat the disorder/infection
- ACE Inhibitors or ARBs
- Red blood cells
- Diet: protein & Na
- Na diet
- GFR
- Diuretics
- BUN/Cr
- Hypertension medications
• A biopsy is performed to confirm
- Abx or corticosteroids could be used
glomerulonephritis.
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:
- K, BUN, Cr, BP
• Provide meds per MD order:
- Diuretics
• Monitor for swelling and lung sounds
- Antihypertensives
• fluids; diet: protein & Na
- Abx
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THE KIDNEYS
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 (albumin) in blood
Signs/Symptoms
protein in blood
edema (waterleaves capillaries into tissues)
• Liver senses hypoalbuminemia and makes more albumin and atthe same time
makes cholesterol and TG
• Loss of appetite; malaise
hyperlipidemia
• Proteinuria (more than 3 gm/day)
• Also lose
- Immunoglobulins from blood
• **Frothy pee (from protein)
increase risk forinfections
- Proteins that prevent clot formation
• Ascites, puffy face/hands/legs
increase risk of clot formation
Causes
• Primary - (originates in kidneys):
- Minimal Change Disease - most common
cause in children
- Focal Segmental Glomerulosclerosis - most
common cause in adults - scartissue forms
in part of glomeruli
• Back pain
Treatment
• If the reason is known, treat it.
• Medications include ACE inhibitors, ARBs, statins, and
maybe corticosteroids, immunosuppressants,
and anticoags.
• Laxatives
• Diet: sat fat/chol/Na
• Secondary (>50% of adult NS cases are secondary):
- Usually a systemic disease like lupus or DB
- NSAIDS
- Glomerulonephritis
- Certain allergies
Intervention
• Monitor fluid status:
- I/Os - Weights per day
- Adults: 30 cc/hr or 1 ml/kg/hr
Diagnosis
• In older persons, it may be misdiagnosed as heart
failure
• Urine and blood testing for Cr, albumin, and lipids
• Watch for infection ( immune system)
• Keep an eye out for blood clots, which can
cause swelling and pain in the
legs and arms (DVT)
• Monitor pulmonary status
• Diet:
sat fat/cholesterol/Na
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THE KIDNEYS
Dialysis
Artificial process forremoving 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:
• Extremely high amounts of K or Ca
• Uremic encephalopathy
• Cardiomyopathy
• Acidosis (acidification)
• Heart disease
Goal of Dialysis
• waste in blood
• Correct acidosis
• Reverse electrolyte imbalances
• Remove excess fluid
• Excess fluid in the body
• Edema of the lungs
• Renal failure symptoms
• GFR 10-15 ml/min
Two other options to filter blood:
• Hemofiltration - a continuous technique performed in the intensive care unit that can
filter enormous volumes of blood
• Hemoperfusion - utilized in the treatment of poisoning; a charcoal filter absorbs the poison
Hemodialysis
• Blood is taken from the body and pumped into a
dialyzer, which filters metabolic waste, electrolytes,
and fluids. Blood was cleansed and returned.
• The total amount of fluid returned can be changed.
• The total time required is around 3-5 hours three
times each week.
Complications
• BP (most common)
• Infection of graft or fistula
• Fever
• Anaphylaxis (allergy to
substance in dialyzer or tubing)
• Arrhythmias
• Embolism of the lungs
• Bleeding in the colon, brain,
eyes, or abdomen caused by an
excess of heparin in the dialyzer
• Can be performed at home or at a dialysis center.
• The most common dialysis procedure
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THE KIDNEYS
Dialysis
Peritoneal Dialysis
Complications
• Makes use of the peritoneum (the membrane that lines the abdominal
• BP (most common)
cavity) as a natural filter.
• Bleeding (irritation of peritoneum)
• Fluid (dialysate) is administered into the peritoneal cavity via catheter.
• Infection (atinsertion site)
• Dialysate sits for a while, absorbing waste products and electrolytes before
• Hypoalbuminemia
being drained and discarded. Repeat 4-5 times each day.
• Scarring of peritoneum
• Osmosis is used: dialysate has a high concentration of glucose that attracts
• Hernias (ab or groin)
liquids (more fluid is drained than was instilled)
• Constipation - interferes with
• Less efficient than hemo, but can be run for extended periods of time
dialysate flow
• Completed at home; machine or manual
Prevention
• External shunt/catheterCannula inserted into a major
vein and a large artery close to
each other; for immediate use; usually
short-term. Infection, clotting, and skin
erosion are all possibilities.
• Arteriovenous fistulas -
• Arteriovenous graft- A synthetic connector
Large artery and vein sewed together
is used to join an artery and a vein (this
beneath the skin's surface (creates
also provides a single blood channel for
one blood vessel for both withdraw
both withdrawal and return). Surgery and
and return) Surgery and recovery
recovery time are required (up to 2 mos)
time are required (up to 6 wks)
Intervention
• Wts are crucial
• Monitor for complications:
- Excessive fluid lost= BP or shock
- N/V
- Fluid retention = BP or edema
- Signs of bleeding (clotting time)
• Monitor vitals during dialysis!
- Fistula/graft site
• Peritoneal- keep in Semi-Fowler's position
- Agitation/disorientation/convulsions
(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
- Peritoneal: Color of fluid removed
(bloody effluent may be bleeding inside)
- Peritoneal: Cloudy discharge may mean infection
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THE KIDNEYS
Diuretics
Medications used to remove extra fluid volume from blood through
increased urination. They work by altering the processes in the nephrons.
Efferent
Arteriole
Glomerulus
4 main types of diuretics
Proximal
Convoluted
Tubule
• 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
Afferent
Arteriole
Osmotic
part of distal convoluted tubule
and collecting duct
Bowman's
Capsule
Collecting
Tubule
Distal
Convoluted
Tubule
• Osmotic - work in the proximal
convoluted tubule and descending
K-sparing
To Ureter
Thiazide
Loop
limb of loop of Henle
Nephron
Location of action in the nephron
Diuretics Overview
• Loop diuretics are the most potent.
• Thiazide is the greatest HTN medication.
• K LOSS is caused by both Loop and Thiazide.
• Because K-Sparing is fairly weak, it is used with Loop and Thiazide to assist spare K.
• Keep in mind that waterloves Na and will follow it!
• Because all diuretics increase urine, dehydration is the primary issue for usage, coupled with electrolyte balance.
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THE KIDNEYS
Loop Diuretics
(Most powerful diuretic)
Names
Action
• Most end with NIDE or MIDE
• Blocks reabsorption of Na, Cl and K in
• Bumetanide (Bumex)
loop of Henle (where 25% of Na is
• Furosemide (Lasix)
absorbed from filtrate)
• Torsemide (Demadex)
filtrate
• Ethacrynic acid
(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)
Side Effects
• Ca, K, Na and Mg levels
• BP
Na in
• uric acid levels gout
H2O excreted as urine
• Ototoxicity
Used for
• Pulmonary edema
• HTN (Thiazides work better)
• Ca levels
• Edema
• Heart failure
• Liverimpairment w/ascites
• Monitorlabs:
- Hypokalemia (will need to supplementif <3.5 mEq/L)
(if on digoxin, monitorlevel)
- Hypocalcemia
- Hyponatremia (if on lithium, monitorlevel)
- Hypomagnesemia
• Educate:
- Dehydration S/S
- Blood pressure and heart rate monitoring
Interactions
• NSAIDS: blood flow to kidneys
• Lithium: Na
• Digoxin: K
diuretic effects
lithium
digoxin
- Weigh yourself everyday and contact your doctor
if you gain 3 pounds in one day.
- Encourage K foods
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THE KIDNEYS
Thiazide Diuretics
Names
• Hydrochlorothiazide (HCTZ) (HCTZ)
• Indapamide (Indapamide)
• Hydrochlorothiazide
• Metolazone
• Chlorthalidone is a medication.
(Not as powerful as Loop)
Action
Side Effects
• Blocks reabsorption of Na and Cl in
•
Na levels
•
Ca (helps with preventing
the first part of the distal convoluted
tubule (where 5-7% of Na is absorbed
from filtrate)
Na in filtrate
renal stones and
bone density)
H2O
•
K and loss of H+ions
excreted as urine (H2O loves Na and
•
BP
will follow it)
• Hyperglycemia
•
uric acid levels (gout)
Nursing Considerations
• Monitor:
- Dehydration
- Hypotension
• I/Os
• Vitals
• Daily weights
Used for
• HTN (best) (best)
• Heart disease
• Renal calculi caused by Ca
• Keep an eye out for gout symptoms.
• Monitor glucose levels in DB patients.
• Give with meals to GI upset
• Monitorlabs:
- Hypokalemia (will need to supplementif <3.5 mEq/L)
(if on digoxin, monitorlevel)
- Hypercalcemia
- Hyponatremia (if on lithium, monitorlevel)
Contraindications
• Renal dysfunction
• Maternity
• Educate:
- S/S of dehydration
- Diet in K
- Wt daily & notify MD if +3 lbs in 1 day
- Monitor BG if DB
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THE KIDNEYS
Potassium-sparing Diuretics
(Keeps K in blood)
Names
Side Effects
Used for
• Spirolactone (Aldactone)
• Hypokalemia
• HTN
*The most prevalent
• Eclerenone
• Triamterene (Triamterene)
• Amiodarone
• Edema due to
• Spironolactone may have
- Heart failure
antiandrogenic properties:
- Liverimpairment
- Gynecomastia
- Nephrotic syndrome
- Inconsistent menstruation
• Hypokalemia (due to other diuretics)
- Sexual impotence
Nursing Considerations
• Monitor:
- Dehydration
• Vitals
• I/Os
• Daily wts
• Give with meals to GI upset
• Monitorlabs:
- Hyperkalemia (EKG changes - Tall peaked T waves)
• Hyperaldosteronism
Action
• It functions in 2 ways:
- Directly block Na channels (in DCT and CD), preventing
Na from passing through and being excreted.
- By competing with aldosterone (the most common);
aldosterone causes nephrons to reabsorb more Na and
H20 into the circulation.
• Does not lower K levels like other diuretics.
• Loop orthiazide is frequently recommended to save K.
• Educate:
- S/S of dehydration
- Diet in K and no salt substitutes
- Wt daily & notify MD if +3 lbs in 1 day
Interactions
• May increase K:
- ACE inhibitors
- ARBs
- NSAIDS
• If on lithium, monitorlevel
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THE KIDNEYS
Osmotic Diuretics
(Least common)
Names
Action
• Mannitol (Osmitrol) -
• Has osmotic pressure in the renal tubules,
*Most common
which slows fluid reabsorption (particularly
in the proximal tubule and the initial section
of the Henle loop)
Side Effects
• Heart disease
• Respiratory congestion
Nursing Considerations
• Hyponatremic state
• Administer via IV
• Edema of the lungs
• Monitor:
- Vitals
- I/Os
- Daily wts
• Instruct ptto report changed in LOC
Used for
• Manage cerebral edema
• To intraocular pressure
• Treating or avoiding Dialysis Disequilibrium Syndrome
is a dialysis-related neurological disorder (rare)
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ENDOCRINE
ENDOCRINE SYSTEM OVERVIEW
FUNCTION OF THE
ENDOCRINE SYSTEM:
The endocrine system is comprised of glands and organs that secrete
hormones (chemical messengers). These chemical messengers transport
data and instructions from one cell to the next.
HORMONES RELEASED by the endocrine organs/glands
1-THYROID GLAND
• Thyroxine (T4)
• Triiodothyronine (T3)
• Calcitonin
3- ADRENAL GLAND
• Adrenal medulla
• Aldosterone
• Cortisol levels
• Adrenal cortex
• Adrenaline
• Noradrenaline
5- PITUITARY GLAND
2- PARATHYROID GLAND
• Parathyroid hormone (PTH)
4- HYPOTHALAMUS
• Hormone producing growth hormone (GHRH)
• Thyrotropin-releasing hormone (TRH) (TRH)
• Gender-specific gonadotropin-releasing
hormone (GnRH)
• Corticotropin-releasing hormone (CRH) (CRH)
6- TESTES
• Testosterone
• Luteinizing hormone (LH) (LH)
7- OVARIES
• Estrogen
• Progesterone
• Follicle-stimulating hormone (FSH) (FSH)
• Prolactin levels
• Thyroid-stimulating hormone (TSH) (TSH)
• Human growth hormone (GH)
• Adrenocorticotropin-releasing hormone (ACTH)
• Lateral
• ADH (antidiuretic hormone) (Vasopressin)
• Oxytocin
8- PANCREAS
• Insulin
• Glucagon
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ENDOCRINE
ENDOCRINE HORMONES
Thyroxine (T4)
Triiodothyronine (T3)
Calcitonin
The thyroid produces and stores these hormones. Maintains a constant
condition of body metabolism.
Thyroid gland secretes it.
CALcitonin think CALcium
Calcium regulation in the body.
Thyroid-Stimulating
Hormone (TSH)
TSH stimulates the thyroid, causing T3 & T4 to be released
Oxytocin
Muscle contractions to aid in the removal of the infant
Prolactin
After childbirth, it stimulates milk production
Insulin
Glucagon
Epinephrine &
Norepinephrine
Cortisol
It works to lower blood glucose levels. Insulin transports sugar and potassium
into cells to be used as energy later.
Works to INCREASE blood glucose levels.
Breaks down stored glucose (glycogen) in the liver
Hormones of stress When blood pressure lowers, catecholamines are released.
Aids at times of EXTREME stress
Glucocorticoid. Helps regulate metabolism,
blood glucose levels,
and has anti-infl ammatory properties. Helps in times of CHRONIC stress
Antidiuretic Hormone (ADH)
Aids in the regulation of your body's water content
Aldosterone
Mineralocorticoid that promotes fluid equilibrium
Parathyroid Hormone (PTH)
Aids in the rise of serum calcium in the blood
Estrogen
Progesterone
Aids in the regulation of the menstrual cycle and the expansion of the uterus
during pregnancy.
It aids in the regulation of the menstrual cycle and
encourages the growth of maternal tissues and fetal
organs during pregnancy.
Progesterone think
Pregnancy hormone
Contributes to the development of male sex organs
Testosterone
and reproductive tissue, is essential for sperm
production, and promotes secondary sex traits.
( bone mass, muscle mass, growth of body hair)
TESTosterone
think TESTes
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ENDOCRINE
LAB VALUES RELATED TO THE ENDOCRINE SYSTEM
THYROID PANEL
T3 & T4 are always opposite of TSH
(negative feedback mechanism)
EXPECTED RANGE
T3
(TRIIODOTHYRONINE)
80 - 220 ng/dL
T4
(THYROXINE)
4 - 12 mcg/dL
Hyperthyroidism:
T3 & T4 TSH
O.5 - 5 mU/L
Hypothyroidism:
T3 & T4 TSH
THYROID STIMULATING HORMONE
(TSH)
Thyroxine
hormone (T4)
Hypothalamus
Thyroid gland
TRH
TRH
Pituitary gland
Thyroid Stimulating
Hormone (TSH)
Triiodothyronine
hormone (T3)
Calcitonin
BLOOD GLUCOSE
EXPECTED RANGE
Blood glucose goal
Fasting blood sugar
(FBS)
2-hr oral glucose
tolerance test
70 - 110 mg/dL
< 100 mg/dL
< 140 mg/dL
DESCRIPTION
Any time of day
(regardless of when the last meal was)
For at least 8 hours, no caloric intake
Consume a glucose drink
(75g of glucose dissolved in water)
The most frequent
technique for persons
with diabetes to check
their blood glucose
levels is using a finger
stick blood sugar test.
A blood test that determines the average
HbA1c
< 5.7%
blood glucose (sugar) levels during the
previous 2-3 months
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ENDOCRINE
DIABETES TYPE 1 & 2
TYPE 1 - DIABETES MELLITUS (T1DM)
Type One
we have nOne
PATHOLOGY
no insulin production
• As a result of an autoimmune response
• Because there is no insulin to carry glucose into the
cells, the cells are starved of glucose.
• The cells convert protein and fat into energy, causing
ketones to accumulate = acidosis!
• Typically diagnosed throughout childhood
TYPE 2 - DIABETES MELLITUS (T2DM)
does not produce enough insulin, or produces
bad insulin that does not work properly
• Insulin sensitivity
• Insulin receptors are worn out and dysfunctional!
• Usually diagnosed as an adult
(due to a poor diet, sedentary lifestyle, and obesity)
RISK
FACTORS
Easy to remember because childhood comes 1st in life and adulthood comes 2nd
• Hypertension • Obesity
• Family history
• Inactivity • High cholesterol
• Genetics
• Family history of smoking
S&S
Onset: ABRUPT
3 P'S
Polyuria refers to profuse peeing.
Polydipsia refers to extreme thirst.
Polyphagia refers to extreme appetite.
Onset: ABRUPT
3 P'S
Polyuria refers to profuse peeing.
Polydipsia refers to extreme thirst.
Polyphagia refers to extreme appetite.
DIAGNOSTIC CRITERIA
TREATMENT
Has 2+ treatments:
Only has 1 treatment:
INSULIN
Oral hypoglycemic agents will not work for
this pt. Insulin dependent for life!
Casual
Any time of the day
(doesn't matter when
the last meal was)
> 200 mg/dL
Fasting blood
sugar (FBS)
No caloric intake for
at least 8 hours
> 126 mg/dL
1. Diet and physical activity
2. Hypoglycemic agents used orally Metformin, for example.
3. Insulin, maybe.
Insulin is not administered routinely in a type 2
diabetic patient. Only in times of stress, surgery,
or sickness will insulin need to be administered.
Glucose Tolerance Test
HbA1c
Drink a glucose drink
(75g of glucose
dissolved in water)
> 200 mg/dL
Blood test that measures the
average blood glucose (sugar)
levels for the last 2-3 months
> 6.5%
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ENDOCRINE
DIABETES TYPE 1 & 2 CONTINUED
Ulcer
DIABETIC FOOT CARE
• Wash your feet every day.
• Use warm water (test the temperature first) and mild soap
• Gently pat dry your feet.
• Examine your feet daily with a mirror (look for cuts, blisters, or sores)
• Avoid using over-the-counter products (callus remover, alcohol, etc)
• Trim toe nails straight across
• Avoid crossing legs
• Inform the HCP of any infection symptoms.
SICK DAY MANAGEMENT
Monitor
• Checking blood glucose
levels frequently
• Check the temperature
frequently
Report to the hcp if:
• Ketones can be found in urine.
• If your blood sugar level is higher
than 250 mg/dL
• Stay hydrated (avoid dehydration)
When you are unwell, do not skip insulin
• If the temperature exceeds 101oF
• Ketones in urine
Diabetes can negatively affect almost every organ system
Organ
Affected
This is because high blood sugar levels harm the blood vessel walls and nerves
Kidneys
NEPHROPATHY
Kidney damage
Complications
Excess blood glucose
levels can harm the
small blood vessels in
the filtering system
(glomeruli).
This leads to renal
failure and, in severe
cases, end-stage
kidney disease.
Nerves
Eyes
Heart
Brain
PERIPHERAL
NEUROPATHY
Diabetic
RETINOPATHY
Cardiovascular
disease
stroke
Eye damage
Damage to the heart &
major coronary arteries
Nerve damage outside of the brain
and spinal cord. Excessive
blood glucose levels might
harm the nerves.
This causes tingling, numbness,
and eventually loss of sensation.
Foot nerve injury can lead to serious
problems such as acute infections in s
crapes and blisters.
All of this sugar in the blood also
causes delayed wound healing, which
increases the risk of infection.
Excessive
blood sugars
damage the retinal
blood vessels.
This results in blindness,
cataracts, and glaucoma.
Excess blood
glucose harms the
blood vessels
and nerves that
Excess blood
glucose damages and
stiffens the blood
vessels. It can also l
ead to the formation
of fatty deposits.
govern the heart.
This contributes to
coronary artery disease,
hypertension, and
atherosclerosis.
This may result
in a blood clot that
travels to the brain
and causes a stroke.
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ENDOCRINE
DKA VS. HHNS
HYPERGLYCEMIC HYPEROSMOLAR
DIABETIC KETOACIDOSIS (DKA)
NONKETOTIC SYNDROME (HHNS)
Happens mostly in Type 1 Diabetic patients
Happens mostly in Type 2 Diabetic patients
PATHOLOGY
Not enough insulin
Body can't allow blood sugar
into the cells for energy
Ketones
are a
byproduct of
metabolism
There is NO acidity!
Simply put, high levels
of glucose in the blood
Blood sugar becomes VERY high
Cells break down protein & fat into energy
acidosis
ketones
RISK
FACTORS
Ketones build up = Acidosis!
4 S's
• Nervousness (surgery)
• Inadequate fluid intake
• Sepsis (infection) (infection)
• kidney function
• Neglecting insulin
• Infection
• Stomach (virus causing nausea and vomiting)
• Stress
• Undiagnosed diabetes
• Older adults
Onset: ABRUPT
• Hyperglycemia (300 - 500 mg/dL)
Onset: ABRUPT
S&S
• Acidosis and ketosis
Remember:
cO2
is an acid
• Water deficiency
• Acidosis metabolica
• Kussmaul breathing (trying to
No
metabolic
acidosis
• Hyperglycemia (more than 600 mg/dL)
• 3 P's (Polyuria, Polydipsia, Polyphagia)
• Water deficiency (hypovolemia)
• Neurovascular alterations (confusion,
blow off CO2)
loss of locomotion, headache)
• Acid breath, sometimes known
as "fruity breath"
TREATMENT
• IV insulin with potassium (K+)
• Fluid replacement
NOTE FOR BOTH:
• Correction of electrolyte imbalance
Regular insulin is the
only insulin given IV
• Administer bicarbonate for metabolic acidosis
insulin causes sugar & K+ to go in the
cells, causing hypokalemia unless we
administer K+ with IV insulin
DKA remember to monitor K levels
regular goes right
into the vein
• Replacement of fluids
• Electrolyte imbalance correction
• Insulin administration
• Intravenous insulin with potassium (K+)
• Insulin subcutaneous
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ENDOCRINE
HYPERGLYCEMIA VS. HYPOGLYCEMIA
HYPERGLYCEMIA
HYPOGLYCEMIA
BLOOD
GLUCOSE GOAL:
BLOOD SUGAR
70 - 110 mg/dL
> 200 mg/dL
Gradual (hours to days)
The brain
needs glucose...
no glucose
causes
BRAIN DEATH!
BLOOD SUGAR
< 70 mg/dL
Happens suddenly
SIGNS & SYMPTOMS
SIGNS & SYMPTOMS
• Urinary incontinence
• Fresh fruity breath
• Skin that is cool, clammy
• Migraine
• Polydipsia (excessive thirst)
• Quick, deep breathes
• Perspiring (Diaphoresis)
• Unsteadiness
• Heart palpitations
• Inability to awaken from a
(air hunger)
• Polyphagy
• Excessively hot and dry skin
• Tingling and numbness
• Tiredness and weakness
• Mouth dryness (dehydration)
• Sluggish wound healing
• Perplexity
• Vision shifts
• Can result in coma
Cool and clammy requires some sweets
Hot & dry = Sugars high
CAUSES
CAUSES
• Workout
• Sepsis (infection)
4 S's
deep slumber
• Swimming, cycling, college athletes,
• Anxiety
and so forth.
• Anabolic steroids
• Failure to take insulin or oral diabetic medicine
• Failure to follow a diabetic diet
• Alcoholic beverages
Rapid insulin
has the
highest risk for
hypoglycemia
• Insulin peak times
TREATMENT
DIABETIC DIET
Complex carbohydrates
Fiber-rich foods
Heart-healthy fish
"Good fats"
Sugar-free fluids
Saturated fats
Trans fats
Cholesterol
Sodium
CONSCIOUS PATIENTS
15 x 15 x 15
15 grams of carbs consumed
Check blood
If necessary,
orally Juice, soda, and
glucose levels
add another
low-fat milk NOT
again in 15 minutes.
15 grams of carbs.
PEANUT BUTTER OR HEAVY MILK
TREATMENT
• Give insulin as needed
• Check your urine for ketones
Rapid
Short
Intermediate
Long
Generic
names
Lispro
Aspart
Glulisine
Regular
nph
Glargine
Detemir
Brand
names
Humalog
Novolog
Apidra
Humulin R
Novolin R
Humulin N
Novolin N
Lantus
Levemir
UNCONSCIOUS PATIENTS
Do not put anything in the mouth of an
Emergency
call a rapid response
unconscious client; they may aspirate!
Administer IV 50% dextrose (D50)
or Glucagon (IM, IV, SubQ)
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ENDOCRINE
FUNCTION
THYROID DISORDERS
-The thyroid gland secretes three hormones (T3, T4, & Calcitonin)
• Iodine is required for the production of these hormones
- Thyroid gives you ENERGY!
HYPERTHYROIDISM
HYPOTHYROIDISM
PATHOLOGY
PATHOLOGY
Excessive production of thyroid hormone
Low production of thyroid hormone
Too much ENERGY!
Not enough ENERGY!
• Graves syndrome
• Excessive iodine (helps produce T3 and T4)
• Nodular Toxic Goiter
• Hashimoto's thyroiditis
• Inadequate iodine levels • Hypothalamic hormone
• Affects women more frequently
• Thyroid surgery
• Thyroid replacement therapy (Toxicity)
than men
LAB VALUES
LAB VALUES
T3 & T4
• Thyroid hormone replacement therapy
T3 & T4
TSH
TSH
SIGNS & SYMPTOMS
SIGNS & SYMPTOMS
• Hyper-excitable
• Goiter (enlarged thyroid)
• Nervous/tremors
• Hot
• Irritable
• Exophthalmos
• Attention span
• Increased:
• Increased appetite
• Blood pressure
• Weight loss
• Pulse
• Hair loss
• GI function
Bulging eyes
caused by fluid
accumulation
behind the eyes
• No power
• Flustered speaking
• Tiredness
• Skin that is dry
• There are no expressions
• Thick hair
• Increased weight
• Decreased:
• Cold
• HR
• Menorrhagia
• GI function (constipation)
• Blood sugar (Hypoglycemia)
LIFE-THREATENING COMPLICATIONS
LIFE-THREATENING COMPLICATIONS
Thyroid Storm!
Myxedema Coma!
Acute / life threatening emergency!
TREATMENT
TREATMENT
• Thyroid Medications
• PTU or methimazole
• Beta Blockers ( HR & BP)
• Compounds containing iodine
• Radioactive Iodine Treatment
• Thyroid surgery
• Hormone replacement therapy (replacing levothyroxine)
• Levothyroxine synthesized
• Levothroid or Synthroid
• Will be on this drug indefinitely
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ENDOCRINE
PARATHYROID GLAND DISORDERS
FUNCTION
The parathyroid gland generates and secretes PTH (parathyroid hormone), which regulates calcium levels in the blood
PTH
PTH
HYPERPARATHYROIDISM
HYPOPARATHYROIDISM
Calcium Phosphorus
Calcium Phosphorus
CAUSES
CAUSES
• Can arise as a result of an unintentional removal of the parathyroid.
Primary cause:
• Thyroidectomy, parathyroidectomy, or major neck dissection
Parathyroid tumor
are all options.
or hyperplasia
• Genetic proclivity
Secondary cause:
• Radiation exposure
Chronic kidney failure
• Magnesium deficiency
SIGNS & SYMPTOMS
SIGNS & SYMPTOMS
• Stones: Kidney stones ( calcium)
• Tingling and numbness
• Bones:
CHVOSTEK’S SIGNS:
• Muscle spasms
- Skeletal pain
Facial muscle contraction
• Tanya
- Pathological fractures from bone deformities
with a gentle tap on the
• High blood pressure
facial nerve
• Abdominal MOANS
• Nervousness, irritation, and
- Vomiting, nausea, and abdominal pain
- Obesity / anorexia
- Indigestion
• Psychic GROANS
- Mental irritability
- Confusion
Think “C” for Cheesy smile
sadness
POSITIVE TROUSSEAU SIGN:
Stones,
Bones,
moans, &
groans
Carpal spasm caused by inflating
a blood pressure cuff
Same S&S of
hypocalcemia!
TREATMENT
TREATMENT
• IV Calcium
• Subthyroidectomy
• Phosphorus binding drugs
• Removal of several glands
• DIET: Calcium Phosphorus
• Implement:
- Phosphates, calcitonin, & IV or
oral bisphosphonates
• DIET: fiber & moderate calcium
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ADRENAL CORTEX DISORDERS
RETAINS:
NA+ & H2O
LOSES:
K+
ENDOCRINE
Each kidney has
an adrenal gland
on top of it.
Adrenal cortex hormones:
Glucocorticoids • Mineralocorticoids • Sex hormones
CUSHING'S
ADDISON'S
Disorder of the adrenal cortex
Disorder of the adrenal cortex
Too many steroids
Not enough steroids
They "have a cushion "
We need to "Add" some
CAUSES
CAUSES
• Ladies
• Surgery to remove both adrenal glands
• Excessive usage of cortisol medicines
• Adrenaline gland infection
• Adrenal gland tumor that secretes
• Tuberculosis, CMV, and bacterial infections
cortisol
• Muscle atrophy
• Moon expression
• The buffalo hump
• Truncal obesity with narrow limbs
• Fat pads supraclavicular
• Increased weight
• Prostatitis (masculine characteristics)
• Glucose NA+
• K+ CA+
• Hypertension
TREATMENT
SIGNS & SYMPTOMS
• Tiredness
ADDISONIAN CRISIS
• Vomiting, nausea, and diarrhea
• Obesity
• Low blood pressure, hypovolemia
• Perplexity
• Blood sugar
• Na & H20 K+
• Hyperpigmentation of the skin
• Vitiligo: white areas of
depigmentation
SIGNS & SYMPTOMS
SIGNS & SYMPTOMS
∙ Profound fatigue
Think SHOCK!
∙ Dehydration
• Hypotension
∙ Renal failure
∙ Rapid respiration
∙ Hyponatremia
∙ Hypokalemia
∙ Cyanosis
∙ Fever
• Weak rapid pulse
Treatment:
Fluid resuscitation
& high-dose
hydrocortisone
∙ Nausea/vomiting
TREATMENT
• Adrenoplasties
• Glucocorticoid and/or mineralocorticoid administration
• Requires glucocorticoid replacement
• Protein and carbohydrate-rich diet
for the rest of one's life
• Prevent infection
• If an adrenal tumor is present,
chemotherapy drugs should be adm.
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ENDOCRINE
PITUITARY GLAND DISORDERS
Antidiuretic Hormone (ADH):
ADH is found in the
PITUITARY
GLAND!
ADH regulates & balances
the amount of water in your blood
SYNDROME OF INAPPROPRIATE
ANTIDIURETIC HORMONE (SIADH)
sIADH think soaked Inside
DIABETES INSIPIDUS (DI)
SIADH is often of non-endocrine origin
DI think Dry Inside
Retains Water
Too much ADH
INCREASED ICP
CAUSES
• Respiratory disease
• TB
• Serious pneumonia
• Central Nervous System
Disorders
• Trauma to the head
• Neurosurgery
• Pharmaceuticals
can lead to an
ADH problem
• Vitamin C
• Phenothiazoles
• Antidepressants
• Thiazide diuretics
• Anticonvulsants
CAUSES
• Trauma to the head, brain tumor
• Central nervous system
infections (CNS)
• Pituitary gland manipulation
• Meningitis, encephalitis, or
- Surgical ablation,
craniotomy, sinus surgery,
tuberculosis
• Renal tubule failure to react
hypophysectomy
to ADH
• Diabetes medications
• Tumor
Loses Water
Not enough ADH
• Nicotine is a stimulant
• HIV
SIGNS & SYMPTOMS
• excretes a lot of diluted urine
• Muscle ache and weakness
• Polydipsia (excessive thirst)
• Migraine
• High blood pressure
• Urinary incontinence
• Hypotension due to posture
production of
• Hypertension
• Water deficiency
• Hypertension
concentrated urine
• Vomiting and nausea
• Reduced skin turgor
• Urinary specific gravity is low.
• Hyponatremic state
• Mucous membranes that are dry
SIGNS & SYMPTOMS
• Insufficient urinary
• Excessive fluid volume
• Increased weight without edema
Normal specific gravity:
1.005 - 1.030
TREATMENT
TREATMENT
• Put seizure safeguards in place.
• Raise the HOB to encourage venous return.
• Adequate fluids
• Vasopressin or desmopressin
• Limit fluid intake
• IV hypotonic saline
• Monitor
• Loop diuretics for administration
• ADH replacement
• Intake & output
• Vasopressin antagonists in administration
(replace the missing hormone!)
• Weight
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ENDOCRINE
ADRENAL MEDULLA DISORDER
Adrenal medulla hormones:
Epinephrine • Norepinephrine
"fight or flight"
response
PHEOCHROMOCYTOMA
RARE adrenal gland tumor that secretes high
quantities of epinephrine and norepinephrine
Healthy
Pheochromocytoma
Adrenal gland
Too much
adrenaline is
released from
adrenal gland
Kidney
CAUSES
• They have a family history of developing the tumor
SIGNS & SYMPTOMS
• High blood pressure (severe)
H'S
• Migraine
• Heat (excessive sweating)
TREATMENT
Avoid
Stimuli!
It may cause a
hypertensive crisis!
• Adrenoplasties (if a tumor is present)
• Inform the client not to smoke, use coffee,
or shift positions abruptly.
• Hyperthyroidism
• Prescription antihypertensives
• Diabetes mellitus
• Encourage relaxation, a tranquil environment
• Diet: abundant in calories, vitamins, minerals
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FMAF serulal &
Reproductive Health
MED-SURG
Signs & Symptoms
That necessitate additional investigation
• Unusual vaginal bleeding
Pelvic Inflammatory
Disease
Recommended Screenings
Breast Self- Exam
P: cervicitis is caused by STls
1 week following the commencement of menstruation
trichomoniasis + gonorrhea this
• Lie fiat - use finger pads
spreads to endometrium, fallopian
• palpate the entire breast
• inexplicable postmenopausal symptoms tubes + pelvic cavity
S|Sx: Pelvic pain, Fever, irreqular
• bruising
bleeding or asymptomatic
Abnormal Findings
•soft
• hard
• bidirectional
• atypical discharge
Tx: IV antibiotics or surgery to repair
• chronic itching
any abscesses Encourage pt. to return for
• stools with blood
Nocmai Findings
follow ups and continue to practice sex.
• Easily moveable
• unidirectional
• Fixed
Mammography
Sexually Transmitted Infections
Starting at the age of 40, this should be done
on a yearly basis.
Trichomoniasis
S|Sx: purulent thin + frothy discharge, pH, itching.
Tx: Flagyl, abstaining from sex until cured
• performed in conjunction with ultrasound
• employs low-dose x-ray or HRI
Vulvar Seif- Exam
Bacterial Vaginosis
S|Sx: thin grayish vaginal discharge + fishy odor. Flagyl or clindamycin
should be done once a month
• ocular examination of the external genitalia
Chlamydia & Gonormea
• Make use of a hand-held mirror
SISx: can be asymptomatic or yellow vaginal discharge + painful urination
Tx: azithromycin or doxycycline ıf left untreated, can cause uterine scarring
Pelvic examination + Pap Test
This should be done every year
Syphilis
SISx: Primary - pairness chancre; Secondary- Splenomegaly
• 2 weeks following menstruation
Menopause
hepatomegaly headache, anorexia + Skin rash
Latent - left untreated can Last for Years
Fallopian Tubes
Tertiary- Paralysis - psychosis can occur.
Uterus
Tx: penicillin G
Menstruation's end and the changes that
occur at the end of reproduction
• happens between the ages of 45 and 55
• Menstruation is erratic, and then it stops
Herpes
SISx: vesicles appear in a cluster + burst in about
Ovary
Ovary
Cervix
1-7 days, "The virus remains dormant forever
Tx: Antivirals to reduce symptoms
Vagina
• LDLS & HDLS which increases CAD risk.
• Hot flashes develop as a result of
vasomotor instability.
• Uterine hyperplasia is treated with
estrogen/progesterone treatment.
Pharmacology
Birth Control
Progesterones
• inhibit conception by interfering with ovulation
Contribute to the creation of favorable conditions
Complications:
Thromboembolic events like stroke, MI, PE
• Hypertension – keep an eye on your blood pressure
• Instruct the women not to smoke.
Administration:
• should be taken every day at the same time
· Use alternative contraception if a pin is missing
for Petal growth. To counteract the negative
effects of estrogen therapy
comprications:
• Mammary cancer (post-menopausai women)
• Stroke, MI, PE • Edema
• Breast tenderness • Migraines
174
MALE Sexual &
Reproductive Health
MED-SURG
Benign Prostatic Hyperplasia
Erectile Dysfunction
Hypogonadism
The prostate gland grows larger.
inability to obtain or keep
Gradual reduction in androgen secretion
This interferes with urine flow.
an erection
R: Atheroscuerosis, hypertension,
S|Sx: difficulty starting a urine stream,
PVD, Alcohol, Diabetes mellitus,
urine flow, urinary frequency,dysuria,
obesity, renal -Failure, stress
bladder pain, incontinence
Tx: Modify reversible couses,
Dx: digital rectal exam, urinalysis, PSA,
Sexual counseling, Vacuum
Cystoscopy, uroflowmetry
erection device, penile implants,
Tx: caffeine, spicy +acidic foods
androgen replacement,
Finasteride (5a- Reductase inhibitor)
Erectogenic drugs
Flomax (a-Adrenergic receptor blocker)
depression, mood swings, sleep
disturbances, loss of muscle mass
and Strength
Dx: Serum biood ievels and physical exam
Tx: Testosterone replacement therapy to
Maintain levels of 280 - 1100 ng /dl
Risks of TRT:
Bladder
contraindicated in patients w/ BPH
Male Infertility
Prostate tissue is removed to clear
a blockage in the urethra.
E: can be caused by disorders of the testes,
Penis
N: Administer Abx pre- procedure,
hemorrhage post-op, maintain CBI +
S|SX: decreased libido, fatigue, ED,
• HDL , Hct , Sleep apnea
Transurethral resection
of the prostate
encourage o high fluid intake, monitor for
that begins as early as 40 years of age
hypothalamic- pituitary system or with
abnormalities ejaculating
Urethra
Epididymis
ensure drainage is pink + without clots.
Teach kegel exercises after cath removal
Testis
Scrotum
Dx: Semen analysis, hormone studies
Tx: lifestyle changes (alcohol/stress),
infertility drugs
Pharmacology
Androgens
Development of sex traits in men
Increase in skeletal muscle
Tx of delayed puberty + muscle wasting
Benign Prostatic Hyperplasia
5- Alpha Reductase Inhibitors
decreases usable testosterone causing a
Complications:
reduction of the prostate size + also
• Immature height in boys
helps slow male-pattem baldness
• male features in women as well as acne
• jaundice • cholesterol • hypercalcemia .
complications:
libido, gynecomastia, volume of ejaculate
Contraindications:
Nursing:
• can affect anticoagulants - monitor PT- INR
Effects con take 6 months to be therapeutic
Erectile Dysfunction
decrease mechanical obstruction
Alpha 1 Adrenergic Antagonists
Phosphodiesterase Type 5 inhibitors
Enhances blood flow to the corpus cavernosum
to cause penile erection
Complications:
Myocardial infarction, priapism, hearing Loss,
contraindications:
Nitroglycerine , QT prolongation, CV disease
of the urethra as wen os decreasing bood pressure.
Complications:
hypotension, dizziness, decreased volume of ejaculate,
congestion, sleepiness
Nursing:
Monitor blood pressure Closely at start of therapy
and advise the patient to rise slowly.
175
MED-SURG
CRITICAL CARE
SHOCK
Reduced tissue perfusion and poor cellular metabolism characterize this condition.
Shock in a nutshell
• Shock happens when blood pressure falls so low that
the body's cells do not receive enough blood and thus
do not receive adequate oxygen.
• Organ cells cease to function normally because to a
lack of oxygen.
• The cells are irrevocably injured and die, causing the
organ to fail.
• Multiple Organ Dysfunction Syndrome occurs when
Types of Shock
• Cardiovascular
• Hypovolemic state
• Distributor
- Septic
- Neurogenic
- Anaphylactic
two or more organs fail (MODS)
• MODS = high risk of death
Causes
• Cardiogenic - Caused by insufficient heart pumping
- MI complications include pulmonary embolism, heart valve malfunction, arrhythmia, myocarditis,
endocarditis, and cardiac tamponade.
• Hypovolemic - characterized by a low blood volume
- External (injury) or internal severe bleeding (ulcer, GI bleed,ruptured blood vessel)
- Excessive fluid loss resulting from a significant burn, severe diarrhea/vomiting, pancreatitis, or
uncontrolled diabetes
• Distributive - As a result of excessive blood vessel dilatation (vasodilation)
- Septic infection is a severe bacterial illness
- Neurogenic - spinal cord damage (or occasionally to brain)
- Anaphylactic shock is a severe allergic reaction.
176
MED-SURG
CRITICAL CARE
STAGES OF SHOCK
1- Initial Stage- Not clinically apparent
• Cardiac Output(CO) very low and cell hypoxia occurs
• Cells switch from aerobic to anaerobic (oxygen-free) metabolism
• Lactic acid is produced by anaerobic metabolism.
• Because the liver isn't getting enough oxygen, it can't process the lactic acid
• Buildup of lactic acid in blood pH drops
• Lactic acidosis is defined as serum lactate levels more than 4 mmol/L
2- Compensatory Stage - Body tries to recover
• The goal is to raise CO or Blood Volume (BV) in order to aid tissue perfusion:
• The SNS is stimulated by baroreceptors to release epinephrine and norepinephrine
• This will cause vasoconstriction
BP and HR
perfusion to vital organs and to non-vital organs
(puts atrisk for paralytic ileus)
• The body moves fluid from the interstitial compartment to the intravascular
• Kidneys activate the RAS
CO & BP compartment.
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
• Kidneys retaining Na
BV
serum osmolality this tells pituitary gland to release ADH
keeps H2O in kidneys
BV
• If the cause of the shock is treated at this point, the patient can recover
3- Progressive Stage- All major organs begin to die
• If the patient reaches this level, the compensatory stage has failed and the patient is being transferred to MODS
• Cells swelling now and capillary permeability is
• Fluids and protein drawn into interstitial space
• BV
edema and BV
CO and tissue perfusion
• Changes in mental status / ARDS / GI bleeding / Ulcers / Toxic waste buildup
• Cardiac dysrhythmias that cause the CV system to fail completely
• DIC (disseminated intravascular coagulation) causes severe bleeding
4- Refractory Stage - Cannot be reversed.
All organs begin to shut down.
177
MED-SURG
CRITICAL CARE / SHOCK
Treatment/Intervention
HYPOVOLEMIC
CARDIOGENIC
Signs and Symptoms
• EKG
• Capillary refill
• Monitor your heart rate, rhythm, BP and CO levels.
• BP, CO, HR, UO
• Keep an eye out for fluid excess.
• Tachypnea and Crackles
• Cyanosis and pallid, clammy skin
• Peripheral pulse is weak
• Medications: nitrates, inotropes, and diuretics
• N/V
• UO beginning to
• A sluggish peripheral pulse
• Stop fluid loss and restore volume
• SV, CO, BP, HR
• Dry, clammy skin
• Extra oxygen
• Capillary refill
• Concerned, perplexed
• Keep an eye for fluid excess and UO
• No specific medications
• Tachypnea
SEPTIC
• Vasoconstriction
• Warm/flushed skin in the beginning, then cool/clammy later
• At first, the pulse is powerful (bounding).
• BP, HR, UO
• Gastrointestinal bleeding/paralytic ileus
• Confusion, hyperventilation
• Respiratory failure, crackles
NEUROGENIC
• Extra oxygen
• If necessary, intubate/mech vent.
• Concerned, perplexed
• There may be no indicators at first.
ANAPHYLACTIC
• Evaluate heart and lung sounds
• First, refill the fluid.
• Then there are vasopressors (norepinephrine)
• The inotropes (dobutamine)
• Abx -Begin within the 1st hour! (Obtain culture before to beginning)
• Closely monitor glucose levels.
• Extra oxygen
• If necessary, intubate/mech vent.
• Vasoconstriction
• Keep the pt airway open
• BP, HR
• Extra oxygen
• Inability to control body temperature
• If necessary, intubate/mech vent.
• First, warm, dry skin
• Vasopressors:
• Later on, cool, dry skin
• Irritable bowel syndrome
• Reflex activity loss
• Apomorphine (for bradycardia)
• Maintain spine stability
• Monitor temperature and UO
• Vasoconstriction
• Keep the pt airway open.
• HR, BP
• Extra oxygen
• Dizziness and chest discomfort occur suddenly
• Fluid resuscitation utilizing colloids
• Incontinence
• Medications: epinephrine (IM or IV), antihistamines,
• Lip and tongue swelling
• Zantac, albuterol, and corticosteroids if hypotension persists
• Flushing, stridor, and wheezing
• Anxious and confused,
LOC
• Cramping/abdominal pain/N/V/D
for more than 2 hours
• * Preventive measures
• * Keep an epipen handy.
178
MED-SURG
ABGs
4 MUST-KNOW COMPONENTS
PH
Analyzes how acidic or
Regulated by both
alkaline your blood is
lungs & kidneys
Regulated
measurement of carbon
Bicarbonate levels in
the blood are measured
arterial circulation.
*also a measure of gases
such as O2 & Co2
Regulated
blood are measured.
GAS
ABGS measure how
Acidic or Alkalotic
22 - 26
by the kidneys
Oxygen levels in the
BLOOD
the blood is in the
Regulated
Base consider bicarbonate
PAO2
35 - 45
by the lungs
dioxide in the blood
HCO3
A B G
ARTERIAL
CO2 thought acid
PACO2
7.35 - 7.45
80 - 100
by the lungs
There is no need to interpret alkalosis or acidosis with this value.It simply indicates whether or not the patient is hypoxic.
TIC-TAC-TOE METHOD
2- RESPIRATORY OR A METABOLIC
1- KNOW YOUR LAB VALUES!
Acidosis
Normal
Alkalosis
PH
C02
Alkalosis
Opposite
PH
C02
Acidosis
Metabolic
PH
HC02
Alkalosis
Equal
PH
HC02
Acidosis
Acidosis
Normal
Alkalosis
PH
< 7.35
7.35 - 7.45
> 7.45
Respiratory
CO2
> 45
35 - 45
< 35
HCO3
< 22
22 - 26
> 26
Acid
Base
Normal
There are 2 ways
to analyze the
information
3- UNCOMPENSATED, PARTIALLY COMPENSATED, OR FULLY COMPENSATED?
If the pH is out of range &
CO2 or hCO3 is in range
=
UNCOMPENSATED
If CO2, hCO3 & PH
are ALL out of range
=
PARTIALLY
COMPENSATED
If PH is in range
(7.35 - 7.45)
=
FULLY
COMPENSATED
7.35
7.40
Acidosis
Absolute
Normal
7.45
Alkalosis
PH in range?
Even if the PH is "normal," it might still be on the acidotic or alkaline side.
KIDNEYS
How do the
organs
Compensate?
Excreting excess
LUNGS
acid & bicarb (HCO3)
OR
Retaining
Bicarb
Hydrogen
hydrogen & bicarb (HCO3 B)
Hours - days to compensate
CO2
CO2
think
ACID
Hyperventilation
=
CO2 = Alkalosis
Hypoventilation
=
CO2 = Acidosis
Compensates FAST!
179
MED-SURG
ABGs
ABG PRACTICE QUESTION EXAMPLE
The patient labs are the following;
Ph 7.50
PaCO2 50 mm Hg
PaO2 90 mm Hg
HCO3 32 mEq/L
QUESTION
A client with a bowel obstruction has been treated with gastric suctioning for 4 days.
The nurse notices an increase in nasogastric drainage. Which Acid-base imbalance
does that nurse correctly identify?
TIC-TAC-TOE METHOD
1
What does the problem give you?
2
PH
7.50
ACIDIC
ALKALOTIC
Acid
Base
Normal
NORMAL
CO2
CO2
50
ACIDIC
ALKALOTIC
NORMAL
HCO3
32
ACIDIC
ALKALOTIC
NORMAL
PH
HCO3
RESPIRATORY ACIDOSIS
RESPIRATORY ALKALOSIS
3
METABOLIC ACIDOSIS
METABOLIC ALKALOSIS
UNCOMPENSATED, PARTIALLY COMPENSATED, or FULLY COMPENSATED?
YES
Is the pH in range?
1
NO
YES
NO
PARTIALLY COMPENSATED
Is the HCO3 in range?
YES
NO
FULLY COMPENSATED
ACIDIC
ALKALOTIC
Which of the four scenarios from the ROME
method matches the information given in your problem?
Acidosis
NORMAL
CO2
50
ACIDIC
ALKALOTIC
NORMAL
HCO3
32
ACIDIC
ALKALOTIC
NORMAL
3 UNCOMPENSATED, PARTIALLY COMPENSATED, or FULLY COMPENSATED?
Metabolic Alkalosis,
partially compensated
If CO2,
hCO3 & PH
are ALL
out of range
2
What does the problem give you?
7.50
FINAL ANSWER:
UNCOMPENSATED
Is the CO2 in range?
PH
ROME METHOD
There is no need to interpret alkalosis or
acidosis with this value. It simply indicates
whether or not the patient is hypoxic.
YES
NO
UNCOMPENSATED
Is the CO2 in range?
YES
NO
PARTIALLY COMPENSATED
Is the HCO3 in range?
YES
NO
FULLY COMPENSATED
Alkalosis
Respiratory
PH
C02
Alkalosis
Opposite
PH
C02
Acidosis
Metabolic
PH
HC02
Alkalosis
Equal
PH
HC02
Acidosis
RESPIRATORY ACIDOSIS
RESPIRATORY ALKALOSIS
Is the pH in range?
Normal
METABOLIC ACIDOSIS
METABOLIC ALKALOSIS
If CO2, hCO3 & PH
are ALL out of range
FINAL ANSWER:
Metabolic Alkalosis,
partially compensated
180
MED-SURG
ABGs
RESPIRATORY ACIDOSIS VS. RESPIRATORY ALKALOSIS
RESPIRATORY ACIDOSIS
RESPIRATORY ALKALOSIS
LUNG PROBLEM
KIDNEYS COMPENSATE
LUNG PROBLEM
KIDNEYS COMPENSATE
The lungs are
The kidneys excrete excess
The lungs are
The kidneys excrete excess
retaining
hydrogen & retain
losing
bicarb (HCO3) & retain
too much CO2
bicarb (HCO3)
too much CO2
hydrogen
PH
< 7.35
PH
> 7.4 5
CO2
> 45
SIGNS & SYMPTOMS
SIGNS & SYMPTOMS
• Hypertension (BP)
• Perplexity
• Heart rate
• Respiration rate
• Migraine (Headache)
• Bewildered, exhausted
• Heart rate
• Sleepiness / coma
• Tetany
• Uneasiness
CO2
< 35
• EKG variations
Facial muscle twitching
in reaction to
hypocalcemia when tapping
the facial nerve
• (+) Chvostek's symbol
CAUSES
CAUSES
DEPRESS
RETAINING CO2 : "Depress" breathing
LOSING CO2 : "Tachypnea"
rugs (opioids & sedatives)
Temperature
dema (fluid in the lungs)
neumonia (excess mucus in the lungs)
Hyperventilation
Aspirin toxicity
espiratory center of the brain is damaged
mboli (pulmonary emboli)
pasms of the bronchial (asthma)
ac elasticity damage (COPD & emphysema)
All these things cause impaired gas exchange
INTERVENTIONS
• Offer emotional support
• Resolve the breathing issue!
• Promote healthy breathing patterns
INTERVENTIONS
• O2 administration
• Respiration into a paper bag
• Give anti-anxiety medications or sedatives to breathing rate
• Monitor K+ & Ca- levels
• Semi-Role Fowler's
• Turn, cough, and take a deep breath (TCDB)
Normal CA9 - 11 mg/dL
• Pneumonia: fl uids to thin secretions
& administer antibiotics
• If CO2 >50, they may need an endotracheal tube
• Monitor potassium levels
Normal K+
3.5 - 5.0 mmol/L
181
MED-SURG
ABGs
METABOLIC ACIDOSIS VS. METABOLIC ALKALOSIS
METABOLIC ACIDOSIS
LUNGS COMPENSATE
METABOLIC ALKALOSIS
KIDNEY PROBLEM
LUNGS COMPENSATE
KIDNEY PROBLEM
Too much hydrogen
The lungs will retain CO2
Too much bicarb (HCO3)
The lungs will blow off CO2
Too little bicarb (HCO3)
PH
< 7.35
Too little Hydrogen
PH
> 7.4 5
HCO3
< 22
SIGNS & SYMPTOMS
• Respiratory rate
• Hyperkalemia
- Twitching of muscles
- Weakness
Kussmaul's breathing
Deep rapid breathing
> 20 breaths per minute
-Arrhythmias
•
Blood pressure
• Confusion
SIGNS & SYMPTOMS
Hypoventilation
< 12 breaths per minute
• Respiratory rate
• Potassium (K+)
- Dysrhythmias
- Tremors
- Vomiting
- Tetany
- Muscle cramps/weakness
- EKG variations
Metabolic Acidosis = serum potassium
Metabolic Alkalosis = serum potassium
• Diabetic ketoacidosis
• Acute/chronic kidney injury
• Malnutrition
• Severe diarrhea
CAUSES
• Too many antacids
CAUSES
Not enough insulin
= fat metabolism
= excess ketones (acid)
HCO3
> 26
• Hyperaldosteronism
• Excess vomiting
• Diuretics
Breaking down of fats
= excess ketones (acid)
Remember Bicarb
comes out of your Base
Too much
sodium bicarbonate (BASE)
Excess loss of
hydrochloric acid (HCL)
from the stomach
INTERVENTIONS
• Keep an eye on the K+ and Ca- levels
Normal K+
3.5 - 5.0 mmol/L
INTERVENTIONS
• Administer IV solution of sodium bicarb to bases & acids
• Start seizure precautions
• Keep track of K+ levels
• Give insulin (this prevents fat
respiratory distress
Normal CA9 - 11 mg/dL
• Diet
• Dialysis to remove toxins
ketones from being created)
• Calories
due to polyuria
• Keep an eye out for indicators of
KIDNEY DISEASE
breakdown, which prevents
• Monitor for hypovolemia
• Substitute K+
· Treat vomiting with antiemetics (Zofran or Phenergan)
• Monitor intake and outflow.
DIABETIC KETOACIDOSIS (DKA)
• Give IV fluids to help the kidneys eliminate bicarbonate
• Protein
182
MED-SURG
CANCER
Carcinoma
General Nursing Interventions
P: Any cancer originating in the epithelium
S|Sx: a swelling with a crusty surface, a
• Treat Nausea + educate about Carbohydrate
slow-growing, flat area of redness
Risk Factors:
Sunburn, repeated invitation, qenetic
for prevention
• Maintain rigorous infection control. Take charge of yourself,
the patient, and any guests.
• Non-pharmacological and pharmacological
pain control
tendency, lighter skin, older
than 60 years
Treatments
Sarcoma
P: cancer originating in the connective tissues
S|Sx: apparent soft tissue bulge or mass
Risk Factors:
Surgery - tumor is removed or destroyed
Radiation - localized destruction of cancer cells
- can cause local irritation + fatigue
Chemotnerapy - Kills + stops the reproduction
of neoplastic cells
- Skin, hair, nail, GI cells also impacted
-Genetic predisposition
-Von Willebrand disease
- Lymphedema
WARNING SIGNS
Melanoma
P: a cancer originating in melanocytes Any
which are located in the basal layer of epithelium
S|Sx: new skin markings, moles that alter shape
or size, new skin pigments
Change in bowel /bladder
Any sore that doesnt heal
Unusual bleeding | discharge
Indigestion
Thickening or Lumps
Obvious Skin Changes
Nagging cough /hoarseness
Leukemia
P: a cancer of blood- forming cells.
Either acute or Chronic
N: Avoid invasive procedures such as
catheterizations and injections
to avoid infection.
Prevent excessive bleeding caused by
low platelet count.
183
NOTES