lOMoARcPSD|22650627

Med-Surg Study Guide

Table of Contents
Burns 2 Hematologic Disorders 87
Cancer 8 Musculoskeletal 89
Cardiac 12 Musculoskeletal System 89
Cardiac Basics 12 Fracture 92
Heart Failure 14 Osteoarthritis 95
Coronary Artery Disease 16 Rheumatoid Arthritis 97
Angina Pectoris 18 Osteoporosis 100
Myocardial Infarction 20 Gout 103
Electrolyte Imbalances 22 Neurology 105
Sodium 22 Brain Anatomy and Physiology 105
Potassium 23 Stroke 108
Calcium 24 Seizure 114
Magnesium 25 Increased Intracranial Pressure 118
Phosphorus 26 Multiple Sclerosis 123
Chloride 27 Parkinson's Disease 126
Relationships 28 Myasthenia Gravis 130
Endocrine 29 Guillain-Barre Syndrome 133
Endocrine System 29 Renal 136
Thyroid Gland and Disorders 32 Kidneys, Nephrons and RAAS 136
Hyper- and Hypoparathyroidism 37 Chronic Kidney Disease 139
Adrenal Glands and Disorders 40 Acute Kidney Injury 141
DI vs SIADH 45 Renal Calculi 143
Diabetes Mellitus 48 Urinary Tract Infections 146
Gastrointestinal 58 Glomerulonephritis 149
The Digestive System 58 Nephrotic Syndrome 151
Gastroesophageal Reflux Disease 61 Dialysis 152
Peptic Ulcer Disease 62 Diuretics 154
Inflammatory Bowel Disease 63 Respiratory Disorders 159
Diverticulosis and -itis 67 Lung Anatomy and Physiology 159
Celiac Disease 69 Pneumonia 160
Hepatitis 71 COPD 161
Cirrhosis 77 Asthma 162
Pancreatitis 80 ARDS 163
Cholecystitis 83 Pleural Effusion 164
Appendicitis 85 Shock 165
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BURNS
Damage to the skin's integrity by some kind of energy source

Types of Burns
Thermal - Most common - caused by flame, flash, scald or contact with hot
objects (liquid, steam, fire); e.g. from cooking, burning leaves, smoking
Chemical - caused by contact with acids, alkali or organic compounds - no heat
needed
acids (e.g. hydrochloric, oxalic, hydrofluoric)
alkali (e.g. cement, oven/drain cleaners, heavy industrial cleaners); harder
to treat because adheres to tissue
organic compounds (e.g. phenols and petroleum products)
Electrical - caused by intense heat generated from an electric current that
passes through the body and damages tissue
hard to determine extent of damage because most of damage is below the
skin - 'iceberg effect'
Cold - caused by cold exposure to skin; frostbite
Radiation - caused by sun or cancer treatment
Friction - caused by abrasion to skin
road rash (car accident)
rope burn

Superficial partial Epidermis

thickness (1st degree)
Sweat
Deep partial gland Dermis
thickness Hair
(2nd degree) Follicle

Fat
Full
thickness
(3rd & 4th Muscle
degree)
Bone
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Burn Severity Depends on:

Depth of Burn Location of Burn
Extent of Burn Patient risk factors
Calculated in % of TBSA If they experienced an inhalation
Use Rule of 9s (see next page) injury or not

Depth of Burn

st Degree rd Degree
Superficial partial thickness Full thickness
Epidermis only All layers are damaged
Least severe Not painful due to damage to nerves
Heals in 7 days Skin will NOT heal - needs skin
Erythema grafting
Blanching on pressure Will take months to heal
Pain/mild swelling Dry, leathery hard skin (eschar)
Skin pink/red May be black, yellow, red, waxy
Warm to touch white
No blisters Eschar - dead tissue - dangerous if
Usually no scarring around torso or extremity; will need
to be removed via escharotomy
th Degree
nd Degree
Deep full thickness
Deep partial thickness
All layers destroyed and extends to
Epidermis and dermis
muscles, bone, ligaments
Very painful
NO pain sensation
Blisters
Black, charred with eschar
Redness that blanches
Months to heal
Swelling (mild - moderate)
Will need skin grafts
Shiny red/pink and moist
If severe, may need skin In Full Thickness, watch for acute
grafting tubular necrosis (ATN), due to the
release of myoglobin and hemoglobin
that block kidney tubules.
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Extent of Burn
To determine the extent of burn, calculate the TBSA burned using the Rule
of Nines and then use the Parkland Formula to calculate the fluids needed

Rule of Nines
Purpose:
4.5%
To calculate the total body surface area burned 4.5%
(TBSA%) for 2nd, 3rd and 4th degree burns
To determine the amount of fluid therapy needed 18%
18%
using the Parkland Formula 4.5% Front 4.5%
Back
4.5%
4.5%
To determine if the patient meets criteria for
burn unit
1%
Add the percent of each body 9% 9% 9% 9%
Use for 2nd part burned.
degree burns This number equals the
or greater TBSA%.

Parkland Formula
Purpose: To calculate the total volume
4 mL X TBSA (%) X Body weight (kg) =
of fluids (mL) that a patient needs
total mL of fluid (lactated Ringer's) needed
24 hours after experiencing a burn.
Make sure TBSA is NOT a decimal!
Give first half of Give second half of
For instance, if a patient has a TBSA% =
the solution in the solution over the
45%, use 45 in the equation, NOT .45
the first 8 hours next 16 hours

Location of Burn - potential problems

Respiratory - face, mouth, neck, trunk (due to edema or eschar)
Disability - Eyes, hands, feet, joints (due to damage to nerves)
Infection - Perineum (due to infection from urine/feces) and ears, nose (thin skin)
Trouble Healing - Ears, nose (due to thin skin and poor blood supply)
Compartment syndrome - Full thickness circumferential burns
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Patient Risk Factors Inhalation Injury

Damage to respiratory system due to
Preexisting heart, lung, kidney breathing in toxic substances
disease (body already taxed)
Affects: Upper & lower airways
Diabetes
Peripheral Vascular Disease Signs: Burned in enclosed space
Any chronic disease that causes Burned on face
weakness Spit, mouth, nose have soot
If burn patient also has fractures, Hair singeing (head & nose)
head injuries, other trauma Brignt red skin
Age - children or elderly Hoarse voice

Pre-Hospital and Emergency Care

At scene -
Remove from source of burn
Stop the burning process
Small thermal burns (10% or less TBSA)
Cover with cool, clean, tap water-dampened towel
If >10% TBSA or electrical/inhalation burn and patient unresponsive:
Focus on CAB
C - Circulation - check for pulse and elevate burned limb(s)
A - Airway - check for patency, soot around nose and on tongue,
singed nasal hair, darkened oral or nasal membranes
B - Breathing - check for ventilation
If patient is responsive, do A B C → →
Cool large burns no longer than 10 minutes
Do not immerse in cool water
Do not cover with ice
Do remove as much burned clothing as possible
Do wrap in sheet/blanket
Chemical burns - remove all chemicals from skin; remove clothing containing
chemical and then flush skin with water
Monitor patient with inhalation injury for signs of respiratory distress
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Phases of Burn Management

Emergent Phase Onset of burn until 24 - 48 hours post

Time required to resolve the immediate, life-threatening problems
Main concerns: onset of hypovolemic shock and edema formation
Hypovolemic shock is the greatest initial threat to a patient with a major burn
Phase ends when fluid mobilization and diuresis begin

Monitor for:
Hypovolemic shock
Pathos: Electrolyte imbalances
Increased capillary permeability causes: Renal failure
GI problems
Plasma fluid to leave intravascular Intervention:
space IV access (2)
Na+ & Albumin follow Calculate fluids (lactated Ringer's) using
Fluids shift to interstitial tissue formula
Edema results Electrical burns need higher fluids and
Blood thickens possibly osmotic diuretic (mannitol)
↑ ↑ ↓ ↓
Hct, K+, Na+, WBC Catheter to monitor urinary output
↓ Fluid may lead to hypovolemic Monitor every hr
shock: Goal >30cc/hr
↑ HR Albumin may be administered
↓ CO Monitor urine for Hg and Mb (ATN)
↓ BP Elevate extremities above heart level
Pain meds via IV initially; opioids
May need intubation (esp face/neck burn)
Wound Care: Wound care can begin once proper airway,
Open or Closed circulation and fluid replacement achieved
Open: open to air with topical antimicrobial - often limited to facial burns
Closed: topical antimicrobial and area covered with sterile dressing
Debridement - necrotic tissue removed
Positioning - no pillows (esp with neck/ear burns); rolled towel under shoulders
Elevate extremities - helps prevent edema and contractures
Do not let 2 burn areas touch (to prevent webbing)
ROM/splints to prevent contractures
Premedicate w/pain meds before dressing changes or debridement!
Graft types: autograft (self), allograft (cadaver), CEA (grown from pt own skin), artificial skin
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Acute Phase 48 - 72 hours after burn until wound heals

Fluid has mobilized and subsequent diuresis has begun ( urine production) ↑
May last weeks to months
Focus: prevent infection, pain management, nutrition, wound care
Monitor: Interventions:
Proper urine output NPO until bowel sounds + order to eat:
Signs of GI distress (pain, vomiting, blood ↑
Will need Cal/Pro/Carb diet
in stool - may be Curlings ulcer; May need enteral
constipation) Watch for hyperglycemia
Bowel sounds (no sounds may be ↓
Early nutrition will complications
paralytic ulcer) ↑
and mortality and healing
May need NG tube for suctioning (to Tetanus shot, antibiotics, ulcer meds
remove fluids, gas) May also need: sedative, hypnotics,
Compartment syndrome if antidepressants
circumferential burns Pain meds- IV best route b/c skin layer
Distal extremity pulse absent/weak, may be damaged as well as muscle
cool to touch, abnormal color Avoid infection: sterile linens, gowns,
Respiratory status esp with chest, face, gloves, protective isolation
neck burn or inhalation injury Stretch ROM and move as much as
Electrolyte imbalances: possible to avoid contractures
sodium and potassium Keep room temp at least 85F
↑ ↑ ↓
Infection signs ( HR, RR, BP,
↓ ↓
UO, confusion, chills, appetite)
Will need systemic abx
Neurology: watch for signs of delirium

Rehabilitative Phase wound closure to patient's optimal level

Burn has healed and patient functioning again (physically and mentally)
May happen as early as two weeks post-burn to 7-8 months after
Focus: psychosocial, ADLs, PT, OT, cosmetic correction

Goals: Educate:
Prevent scars/contractures (ROM & splints) Moisturizing for scar
Activities of daily living (ADLs) management
Psychosocial Sun management
PT/OT/Cosmetic consults PT and OT importance
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Cancer
Disease characterized by uncontrolled and unregulated growth of cells

Pathophysiology Cancer
1. Defective cell proliferation: Occurs in all ages,
Normal cells proliferate only at cell higher in men than
death or when physiologically necessary women
(such as infection) and exhibit contact The second most
inhibition (respect cell boundaries) common cause of
Cancer cells proliferate indiscriminately death in U.S
and have no contact inhibition; form 1/3 of all cancer-
tumor related deaths in U.S.
2. Defective cell differentiation: due to tobacco use,
Normal cells mature and perform one unhealthy diet,
specific function physical inactivity
Cancer cells have a defect and perform and/or obesity
more than one function

3 Stages of Cancer
Initiation - mutation/change in DNA occurs (exposure to carcinogen)
Most cancers not due to inherited genes, but to damage during lifetime
Carcinogens (cancer-causing agents)
Chemical - e.g. benzene, arsenic, formaldehyde
Radiation - e.g. UV radiation
Viral - e.g. Epstein-Barr virus, HIV, Hep B
Promotion - proliferation of ALTERED cells by promoters (e.g. dietary fat,
obesity, cigarette smoke, alcohol consumption); Reversible at this stage
Latent period - 1-40 yrs between initial genetic alteration and clinical
evidence
Progression - Increased growth rate of tumor, increased invasiveness, metastasis
(spread of cancer to a distant site). Most frequent sites of metastasis are lungs,
liver, bone, brain and adrenal glands
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Types of Cancer
Leukemias and lymphomas - cancers of the blood and blood-forming tissues
Carcinomas - cancers of the cells that line the skin, lungs, digestive tract, and
internal organs
Sarcomas - cancers of the mesodermal cells (e.g. muscles, blood vessels, bone)

Anatomic Site
Cancer Classification Based on:
Histology (grading) - I, II, III, IV, X (better prognosis worse) →
Anatomic extent of disease (varies widely per cancer type)

Prevention ** KEY
↓exposure to carcinogens (smoking, tanning beds, sun)
Diet - ↑veggies/fruits/whole grains, ↓dietary fat and preservatives
Limit alcohol intake
Regular exercise C hange in bowel or bladder habits
Healthy weight A sore that does not heal
6-8 hrs sleep/night
U nusual bleeding or discharge
↓ stress
Regular physical exam Thickening or a lump in the breast/body
Follow cancer screening guidelines I ndigestion or difficulty swallowing
Self-exam O bvious change in a wart or mole
Know 7 warning signs
N agging cough or hoarseness
Diagnosis - ** Depends on the suspected site of cancer **
Pathologic evaluation of a tissue sample is the only definitive
means to diagnose cancer
Cytology studies (e.g. Pap) Radiographic studies (mammogram,
Tissue biopsy ultrasound, CT scan, MRI)
Chest x-ray Radioisotope scans (e.g. bone, hair, lung, brain)
CBC PET scan
Liver function studies Tumor markers
Endoscopic exam (upper GI, Genetic markers
sigmoidoscopy, colonoscopy) Bone marrow examination
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Treatment
Surgery - to eliminate or reduce the risk of cancer development; includes prophylactic removal of non-vital
organs (e.g. mastectomy, thyroidectomy, hysterectomy)
Chemotherapy (antineoplastic therapy); a systemic therapy and a mainstay of cancer tx for most solid
tumors and hematologic malignancies (e.g. leukemia, lymphomas)
Goal is to eliminate or reduce the number of cancer cells in the primary tumor and metastatic tumor site
Methods: oral or IV (most common; may cause local tissue breakdown/necrosis)
Regional chemotherapy - delivery of drug directly to the tumor site; reduced systemic toxicity
Chemotherapy agents cannot distinguish between normal cells and cancer cells
Side effects are result of destruction of normal cells, especially rapidly proliferating ones (e.g. bone
marrow, lining of GI system, skin/hair/nails)
Long-term side effects: damage to heart, lungs, liver, kidneys
Radiation therapy - local therapy; high-energy beams delivered into tissue to break the chemical bonds in
DNA; only has effect on tissues within tx field
Teletherapy - exposed to radiation via machine
Brachytherapy - implanting radioactive material directly into tumor
Immunotherapy (biologic therapy); uses the immune system to fight cancer; e.g. cytokines, vaccines,
monoclonal antibodies (most successful)
Targeted therapy - acts on specific targets associated with cancer; does less damage to normal cells than
chemo; e.g. tyrosine kinase inhibitors
Hormone therapy - can block the effects of certain hormones that enhance the growth of cancer (e.g.
corticosteroids, estrogen receptor blockers, androgen receptor blockers)
Hematopoietic stem cell transplantation (HSCT)- originally called BMT or PSCT
Goal is to eradicate diseased tumor cells and/or clear the bone marrow of its components to make way
for engraftment of transplanted, healthy stem cells; used for pt w/tumors resistant to chemo or rad tx
Uses high levels of chemo and/or radiation to clear the bone marrow; healthy stem cells are infused
afterwards
Intensive procedure with high risks
Complications: bacterial, viral, fungal infections; graft-vs-host disease

Complications of Cancer
Malnutrition - Seen as fat/muscle depletion ↑
Cancer cachexia - Wasting syndrome ( morbidity risk)
↑ ↑
Small meals/ cal/ pro Anorexia, unintended weight loss and appetite
Encourage nutrition supplements (Ensure); Tissue wasting, skeletal muscle atrophy, immune
↑ ↓
cal/ density foods (e.g. oils, butter) dysfunction
Weigh at least 2x/wk Cannot be reversed nutritionally
Oncologic emergencies - life-threatening ↑
Best management is to treat cancer; nutrition
Obstructive - tumor obstruction of an organ intake; Megace may help
or blood vessel (e.g. superior vena cava Infection - a primary cause of death in pt with cancer
syndrome, spinal cord compression) Instruct - call HCP if temp is 100.4 F or higher
Metabolic - hypercalcemia, SIADH, tumor Dysgeusia - altered taste sensation
lysis syndrome Encourage experimenting with different foods and
Infiltrative - Cardiac tamponade spices
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Potential Side Effects of Chemotherapy or Radiation and Management

Mucositis/Stomatitis/Esophagitis Fatigue (universal symptom) look for any
Assess oral mucosa daily reversible cause:
Instruct to avoid hot/spicy foods Anemia
Saline oral rinse Hypothyroidism; Dehydration
Artificial saliva Depression; Anxiety
No tobacco or alcohol Encourage rest/exercise as tolerated
Topical anesthetics (e.g. viscous lidocaine) Anorexia
Nausea/Vomiting Small, frequent meals high pro/cal
Antiemetics (Zofran, Reglan) Monitor wt and look for dehydration
Before chemo and as needed Nutr supplement drinks (Ensure, etc)
Monitor for dehydration If severe- parenteral or enteral nutrition
Diarrhea Bone Marrow suppression (one of most common
Antidiarrheal drugs →
symptoms) anemia
At least 3 L fluid/day Monitor: neutrophils, PLT, RBC
Constipation Iron supps/erythropoetin
Stool softeners Leukopenia
↑ fiber foods Monitor WBC (esp. neutrophils)
↑ fluids Monitor body temp/signs of infection
Activity if tolerated May need WBC growth factors
Thrombocytopenia Hepatotoxicity
Watch for bleeding (e.g. petechiae) Monitor liver fnx tests
Monitor PLT Nephrotoxicity
Neutropenia Monitor BUN/CR
Prevent infection! Hand washing May need Sodium Bicarbonate and allopurinol
Monitor temp Cardiotoxicity
Intracranial Pressure Monitor EKG
Monitor neurologic status; may need Hyperuricemia
corticosteroids ↑
Monitor UA levels; fluids
Pneumonitis Allopurinol prophylactically
Monitor for dry, hacking cough; fever Skin changes
Pericarditis/Myocarditis Erythema (patches of red skin)
Monitor for CV symptoms (e.g. dyspnea) Protect from temp extremes, tight
Alopecia garments, harsh chemicals
Avoid excessive brushing, shampooing, hair Lubricate dry skin, aloe vera gel
drying, curling, etc Photosensitivity/hyperpigmentation
Suggest hair pieces, scarves, wigs Avoid sun exposure
Cognitive changes (brain fog) - Encourage: Pain management - moderate to severe in 50% pt
Exercise brain (word puzzles, etc) NSAIDs, opioids, morphine, fentanyl
Use detailed planner; no multitasking Monitor for constipation
Sleep/rest
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The Heart
To body

Flow of Blood
Aorta
Superior
Vena Pulmonary
Cava Artery
Pulmonary

through
Pulmonary
Veins
Veins
Left
Atrium

the heart
Right
Pulmonary Mitral Valve
Atrium
Valve
Aortic
Valve Left
Tricuspid Valve Ventricle

Inferior
Right
Vena
Ventricle
Cava

Right Side - Deoxygenated blood Left Side - Oxygenated blood

1. Superior/Inferior Vena Cava (from body) 7. Pulmonary Veins (from lungs)
2. Right Atrium 8. Left Atrium
3. Tricuspid Valve 9. Mitral Valve
4. Right Ventricle 10. Left Ventricle
5. Pulmonary Valve 11. Aortic Valve
6. Pulmonary Artery (to lungs) 12. Aorta (supplies body)

Heart Sounds
S1 Closing of the atrioventricular valves; high-pitched, use diaphragm. NORMAL

S2 Closing of the semilunar valves; high-pitched, use diaphragm. NORMAL

S3 Heart may be in fluid overload or failure; low-pitched, use bell. MAY BE ABNORMAL

S4 Ventricle resistance; low-pitched, use bell. ABNORMAL

Murmurs May indicate wall defect or valve problem; low-pitched, use bell. MAY BE ABNORMAL
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The Heart
Cardiac Terms
Preload: Volume of blood in the ventricles at end
of diastole
The resistance the left ventricle must
Afterload: afterload= cardiac workload
overcome during systole

The amount of blood pumped out of the

Stroke Volume: Normal = 60-100 ml/beat
ventricles with each beat

Cardiac Output:
The amount of blood the heart pumps in CO = HR X SV
1 minute (in liters) (Normal = 4-8L/min)

Volume of blood expelled with every

Ejection Fraction: Normal = 50-70%
contraction

Cardiac Biomarkers
Normal
Cardiac Troponin: 0-0.4 ng/mL Protein released into the bloodstream when the heart
(cTnT) >1.5 = critical muscle is damaged. BEST INDICATOR OF ACUTE MI!

Creatine Kinase: Enzyme released into the bloodstream when heart, brain
0-5 ng/mL
(CK-MB) or skeletal muscle damaged.

Brain Natriuretic Peptide released into the bloodstream when ventricles fill
<100 pg/mL
Peptide (BNP): with too much fluid and STRETCH.

Found in heart and skeletal muscles; released into

Myoglobin:
5-70 ng/mL bloodstream with MI or severe muscle damage. Not a
(MB)
specific indicator of MI, but good to rule out.

Cardiac Index: Cardiac Output adjusted for body surface area. More
2.5 -4.0 L/min/m2
(CI) accurate measure of cardiac function.

Central Venous 2 - 8 mmHg Measures right ventricular preload. Indicates fluid

Pressure (CVP): volume status.

Mean Arterial Average arterial pressure. Indicates perfusion of organs

70 - 100 mmHg
Pressure (MAP): and tissues.

Pulmonary Artery
Measures left ventricular preload. Indicates left-sided
Wedge Pressure: 6-12 mmHg
heart function.
(PAWP)
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Heart Failure
When the heart is not able to supply enough blood to meet the body's need for blood and oxygen.
Two types: Left-sided and Right-sided

Left-sided
Systolic: Weakened heart
muscle can't squeeze blood
to the body

Right-sided Left-sided
Inability to pump blood Diastolic: Stiff heart muscle
from body to lungs can't relax and fill with
blood

Left-sided
Right-sided Two types: Diastolic and Systolic
Right chamber has lost Diastolic Systolic
its ability to PUMP.
Left ventricle doesn't Left ventricle doesn't
Fluid backs up
FILL properly EJECT properly
peripherally
STIFF heart muscle WEAK heart muscle
Often occurs due to
Normal EF Decreased EF
left-sided heart failure

Causes and Risk Factors Signs and Symptoms

CAD
Left-sided Right-sided
MI Dyspnea Swelling of legs and hands
HTN Shallow respirations Fatigue
Damaged valves Weakness/fatigue Weight gain
Myocarditis Dry, hacking cough Ascites
Congenital heart defects Orthopnea JVD
Heart arrhythmias Crackles Edema
Family history S3 + S4 heart sounds Anorexia
PMI displaced
 lOMoARcPSD|22650627

Diagnosis
Blood test for BNP-
BNP Levels
secreted when there is increase pressure in the ventricles
level is high in heart failure <100 pg/mL
X-ray - check for enlarged heart and pulmonary infiltrates No failure
Echocardiogram - 100-300 pg/mL
to look at ejection fraction, back flow and valve problems Present
ejection fraction is decreased in most heart failure 300 pg/mL Mild
Heart cath 600 pg/mL Moderate
Nuclear stress test 900 pg/mL Severe

Heart failure can be High salt intake or fluids

acute or chronic Infection Uncontrolled atrial fib
Renal failure
and exacerbated by:

Interventions
Monitor Instruct Diet
Heart rate (Digoxin) Restrict fluids Low sodium
Respiratory status Increase activity 2-3 gm/day
Blood pressure (vasodilators) gradually (balance with Low fat (trans/sat)
Diuretics rest) Low sugar
strict I/Os Monitor wt and report No caffeine
daily weights gain of 3 lbs in 2 days <2 L fluids/day
monitor electrolytes (esp K+) Monitor for edema Spread fluids out
Labs: Flu vaccine over day
BNP Smoking cessation
BUN/Creatinine Limit alcohol
Troponin
Edema
Medications
Diuretics (Loop, Thiazide, K+ Sparing)
ACE inhibitors
Angiotensin II receptor blockers
Beta Blockers
Anticoagulants
Vasodilators
Digoxin
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Coronary Artery Disease

Build up of fatty plaques due to atherosclerosis in the coronary artery.
Can lead to restriction of blood flow to the heart and heart damage or death.

Coronary Arteries

Left coronary
artery

Right coronary Left circumflex

artery artery

Right marginal Left anterior

artery descending artery
Posterior descending
artery

Normal Atherosclerosis Atherosclerosis

coronary artery (Plaque buildup) with blood clot

Risk Factors
Not Modifiable Modifiable Possible Factors
Age Diabetes Sleep apnea
Gender HTN (>140/90) High hs-CRP levels (high-
Men > 45 yrs High LDL cholesterol sensitivity C-reactive
Women > 55 yrs Smoking protein)
Race (African American) Sedentary lifestyle High TG levels
Family history Obesity High homocysteine levels
Metabolic syndrome Preeclampsia
High stress Heavy alcohol use
Unhealthy diet Autoimmune diseases
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Coronary Artery Disease

Early on most are
Signs and Symptoms ASYMPTOMATIC

Chest pain during activity Sweating

Women's symptoms often
(angina) Weakness
include:
Heaviness Dizziness
Nausea/vomiting
Tightness Nausea/vomiting
Back pain
Burning Racing heartrate
Jaw pain
Squeezing Palpitations
SOB with no chest pain
SOB Pain in the arms or
Very tired shoulders

Coronary Artery Angina

Heart failure
Heart attack
Disease can lead to: Arrhythmia

Diagnosis Interventions
Blood test (TC, LDL, HDL,
Goal is to prevent further progression of CAD by reducing
TG) or eliminating risk factors.
EKG- to assess if MI or not Goal: HDL >40mg/dL and LDL<100 mg/dL
Stress test- for any EKG
changes during exercise Instruct Diet
Nuclear stress test- to
Smoking cessation Low fat
assess blood flow
Exercise Cholesterol <200 mg/day
Heart cath- to identify any
Weight loss Adequate fiber
blockages
Stress management Monitor sodium
Heart CT scan- to check
Lowering BP Add in healthy fat (omega-3)
for calcium deposits
Lowering cholesterol Encourage fruits, vegetables
Managing DB and whole grains
Decrease alcohol intake
Monitor s/s

Medications
Statins Niacin
Beta Blockers Aspirin/Plavix
ACE Inhibitors Nitrates
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Angina Pectoris
Chest pain caused by reduced blood flow to the heart.
Three types: Stable, Unstable and Variant

Stable Unstable Variant

** Most common ** ** Most dangerous ** ** Rare **
Predictable Unpredictable Pain at rest
Occurs with exertion or Occurs at rest, exertion Caused by spasm in
stress or stress coronary artery
Short duration Symptoms unrelieved Reversible ST
Symptoms relieved by by rest or meds elevation
rest or nitroglycerin

Atherosclerosis
(Plaque buildup)

Causes Risk Factors

**Atherosclerosis Main Cause ** Obesity
Age
Sedentary lifestyle
Atherosclerosis Men > 45 yrs
Smoking
Coronary artery spasm Women >55 yrs
Poor DB management
Thrombosis Emotional stress
High cholesterol/TG
Heart failure Weather extremes
High BP
Valve disorders Heavy meals
Family history
Aortic stenosis
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Angina Pectoris
Signs and Symptoms
Chest pain that may radiate SOB Feeling of gas, indigestion
to jaw, neck, shoulders, back Diaphoresis Women:
Pressure Weakness/fatigue Nausea
Squeezing Pallor SOB
Burning Dizziness Abdominal pain
Fullness Nausea/vomiting Discomfort in neck, jaw, back

Diagnosis Interventions
EKG
Instruct Diet
Stress test
Echocardiogram BP control Low fat
Coronary angiography Smoking cessation Cholesterol <200
Chest x-ray Diet modification mg/day
Blood tests (troponin, lipids) Control DB Adequate fiber
Cardiac catherization Exercise Monitor sodium
Cardiac MRI Flu vaccine Add in healthy fat
Decrease chol levels (omega-3)
Flu vaccine Encourage fruits,
vegetables and whole
Surgery grains
(if necessary)
PCI: stent in artery OR
CABG: reroute around artery
Medications
Immediate relief: Nitroglycerin to
dilate heart arteries
Store pills out of light
Patch for unstable
Ca channel blockers
Beta Blockers
Antiplatelet/Anticoagulant
Statins
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Myocardial Infarction
(AKA Heart Attack)
Decreased blood flow in a coronary artery leads to decreased oxygen to the heart muscle
which causes damage to the heart

Heart changes after MI

Early signs of 24-36 hrs 10 days 2 months

MI post MI post MI post MI

Heart muscle not Inflammation sets in Macrophages

Scarring occurs
physically Neutrophils arrive arrive to clean
Heart size and
changed yet Heart fails to pump up dead cells
functionality
Enzymes released: efficiently New tissue is
changed due to
Myoglobin 1 hr post Arrhythmias may weak
increased collagen
Troponin 2-4 hrs post develop
CK-MB 4-6 hrs post

Risk Factors Signs and Symptoms

Diabetes Chest pain (left Women present with
HTN substernal) with no relief different symptoms:
Obesity with rest or meds Fatigue
High cholesterol levels Jaw and/or left arm pain Shoulder blade
Smoking Heart burn discomfort
Gender (male) Increased HR SOB
Sedentary lifestyle SOB Silent MI
Stress Nausea/vomiting No chest pain
Age (45+ men, 55+ women) Diaphoresis Occurs mainly in DB
Family history Anxious, scared due to neuropathy
Race- African American

When a coronary artery Cell death is

becomes 100% blocked, irreversible
the muscle cells die after 30 minutes
 lOMoARcPSD|22650627

Myocardial Infarction

ST Elevation (STEMI) ST Depression

Normal EKG
Full blockage (No O2) Partial Blockage (Low O2)

Diagnosis
EKG
ST elevation - full blockage (no O2), worst type of MI b/c most damage
ST depression - partial blockage (low O2)
Blood tests: Troponin, CK-MB, myoglobin
Echocardiogram - to check for damage
Heart cath - to check for blockages and muscle damage
Stress test

Interventions
Immediate Instruct Potential Complications
12-lead EKG of MI
Low salt and fluid
Monitor BP/HR
Decrease stress, Cardiogenic shock
Oxygen
alcohol, caffeine Dysrhythmias
Bed rest
Smoking cessation Heart failure
Collect enzymes
Increase exercise Cardiac tamponade
Administer meds
Weigh daily
Monitor lungs for
'crackles'

Surgery Medications
Nitrates
If necessary Antiplatelets
ARBs
PCI or Morphine
Statins
CABG Beta Blockers
Calcium channel blockers
ACE Inhibitors
Anti-thrombotic agents
 lOMoARcPSD|22650627

Sodium
Major Extracellular Fluid (ECF) cation. Helps maintain stable blood pressure levels.
Assists in acid-base balance and fluid balance. Inverse to Potassium
Helps regulate nerve function and muscle Normal: 135-145 mEq/L
contraction

Hyponatremia <135 mEq/L Hypernatremia >145 mEq/L

Signs and Symptoms Signs and Symptoms

Fatigue Thirst
Nausea/vomiting Agitation
Confusion Confusion
Seizures Irritability
Weakness Restlessness
Muscle cramps HTN and fluid retention
Tachycardia Low Decreased urine output High
Causes Causes
Increased Na+ excretion:
Excess oral/IV Na+ intake
Vomiting/Diarrhea
Na+ intake Excess hypertonic IV fluids
Sweating
insufficient: Fever
Diuretics
Fasting Watery diarrhea
NG suction
NPO Dehydration
Fluid overload:
ADH Overproduction of aldosterone (Cushing's)
CHF
oversecretion GI tube feedings
Hypotonic fluids
(SIADH) Impaired thirst
Liver failure
Management Management

Increase oral Na+ intake

Decrease oral Na+ intake
Decrease fluids
If due to fluid loss, administer IV
Diuretics if due to hypervolemia
infusions slowly to avoid cerebral edema
ADH antagonist (for SIADH)
If due to decreased excretion of Na+,
If due to hypovolemia, IV NaCl infusions
provide diuretics that increase Na+ loss
at low rate (only in critical situations-hard
on veins, risk of fluid overload)

Encourage! High Sodium Foods Avoid!

Soups, canned foods Most processed foods Pizza, hot dogs
Ham, bacon, sausage Cheese, dressings Cold cuts
 lOMoARcPSD|22650627

Potassium
Major Intracellular Fluid (ICF) cation. Inverse to Sodium
Helps regulate fluid balance, muscle Similar to Magnesium
contractions and blood pressure. Normal: 3.5-5.0 mEq/L
Assists in sending nerve impulses.

Hypokalemia <3.5 mEq/L Hyperkalemia >5.0 mEq/L

Signs and Symptoms Signs and Symptoms
Irregular heartbeat
Weakness
Nausea and diarrhea
Thready pulse
Abdominal cramping
Muscle leg cramps
Tall peaked T wave
Shallow respirations
Tingling in hands, feet
Hypoactive bowel sounds
and mouth
Constipation
Weakness
Inverted T wave Low Muscle cramps
High
Causes Causes
Diuretics
Tissue damage, burns, trauma
Vomiting
Kidney disease
Diarrhea
Adrenal insufficiency (Addison's disease)
Drains (NG tubes)
K-retaining diuretics
Corticosteroids
Acidosis
Long-term laxative use
ACE inhibitors
Fasting, NPO
Uncontrolled diabetes
IV therapy with K- deficient solutions
Excessive K intake
Magnesium deficiency
Management Management

Oral K- supplements (given with food) Discontinue IV and PO K

Liquid potassium chloride Initiate K-restricted diet
K-retaining diuretic K-excreting diuretics
Hold K-wasting diuretics IV Calcium
In very low levels (<2.5), potassium IV IV Insulin
infusion (SLOWLY) Albuterol
Dialysis

Encourage! High Potassium Foods Avoid!

Baked potato Banana, avocado Spinach
Sweet potato Watermelon Canned clams
 lOMoARcPSD|22650627

Calcium
Assists in formation of bones and teeth, muscle Regulated by PTH and calcitonin
contraction, normal functioning of many Inverse to Phosphorus
enzymes, blood clotting and normal heart Similar to Vitamin D and Magnesium
rhythm Normal: 9-11 mg/dL

Hypocalcemia <9 mg/dL Hypercalcemia >11 mg/dL

Signs and Symptoms Signs and Symptoms

Muscle weakness
Tingling fingers, face and
Decreased DTR
limbs
Arrhythmias
Muscle spasms
Bone pain
Arrhythmias
Nausea and vomiting
Tetany
Anorexia
Muscle cramps
Laryngospasms Low Excessive urination
Thirst
High
Causes Causes

Decreased Mg levels Hyperparathyroidism

Insufficient Ca or Vit D intake Malignancy (bone destruction from
Increased serum phosphorus metastatic tumor)
Hypoparathyroidism Thiazide diuretics
Pancreatitis Kidney disease
Kidney disease Antacids with calcium
Diarrhea Severe dehydration
Phenytoin Inactivity (e.g. paralysis)

Management Management
Discontinue:
Encourage foods high in Ca
Vit D supplements
Supplements PO or IV: Ca, Mg, Vit D as
IV or PO calcium
prescribed
Thiazide diuretics
Calcium IV must be administered
Administer calcitonin and/or
SLOWLY
biphosphonates
Move clients carefully as they are at risk
Avoid foods high in calcium
for fractures
Last resort: dialysis

Encourage! High Calcium Foods Avoid!

Dairy foods Green leafy vegetables like Brazil nuts
Sardines curly kale, okra, spinach Canned salmon
 lOMoARcPSD|22650627

Magnesium
Regulates: Helps make protein, bone and DNA
Muscle contraction and nerve function Similar to Calcium
Blood sugar levels Normal: 1.5-2.5 mg/dL
Blood pressure

Hypomagnesemia <1.5 mg/dL Hypermagnesemia >2.5 mg/dL

Signs and Symptoms Signs and Symptoms

Hyperreflexia (increased DTR)

Hypotension
Seizures
Decreased DTR
Lethargy
Bradypnea (Low RR)
Tachycardia
Vomiting
Disrhythmias
Nausea
Hypertension
Coma (severe)
Nausea/vomiting Low High
Weakness

Causes Causes

Diuretics
Kidney failure (decreased renal excretion
Chronic alcoholism
of Mg)
Diarrhea
Large intake of Mg-containing antacids
Malnutrition
Excessive Mg-containing laxative use
Crohn's disease
Hyperkalemia from Addison's disease
Celiac disease
Hypothyroidism
Fluid loss via NG suction

Management Management

Magnesium sulfate IV (slowly) Diuretics

Oral magnesium salts IV Calcium Gluconate
Encourage high-magnesium foods Dialysis
Decrease Mg-containing foods
Avoid laxatives and antacids containing
Mg

Encourage! High Magnesium Foods Avoid!

Pumpkin seeds Almonds and cashews Brazil nuts
Dark chocolate Spinach and avocados Salmon
 lOMoARcPSD|22650627

Phosphorus
Builds and repairs bones and teeth 85% of the body's phosphorus located in bones
Helps nerve function Inverse to Calcium
Assists in energy production in cells Vit D and Phosphorus assist in each other's absorption
Makes muscles contract Normal: 2.5-4.5 mg/dL

Hypophosphatemia <2.5 mg/dL Hyperphosphatemia >4.5 mg/dL

Signs and Symptoms Signs and Symptoms

Confusion
Most are asymptomatic
Irritability
Bone pain
Muscle weakness
Muscle spasms (calves
Lethargy
and feet)
Bone pain and fractures
Itchy skin
Numbness
Increased DTR
Loss of appetite
Decreased ability to breathe
Low High
Causes Causes

Hyperparathyroidism
Hypoparathyroidism
Malabsorption from long-term antacid use
Overuse of Vit D
Vitamin D deficiency
Diabetic ketoacidosis
Chronic diarrhea
Severe kidney disfunction
Long-term diuretic use
Chemotherapy
Severe malnutrition
Excessive alcohol use
Burns

Management Management

Oral phosphorus Calcium carbonate or calcium acetate

Oral vitamin D given with food
Encourage high-phosphorus foods Avoid phosphate enemas
IV phosphate- monitor kidney fx, Ca level, Decrease high-phosphorus foods in diet
EKG Last resort= dialysis

Encourage! High Phosphorus Foods Avoid!

Milk and cheese Chocolate Fish, beef, chicken
Egg yolks Soft drinks and beer Nuts and beans
 lOMoARcPSD|22650627

Chloride
Helps keep the ICF and ECF in balance Level controlled by the kidneys
Helps maintain blood volume, blood pressure Normal: 95-105 mEq/L
and pH of body fluids

Hypochloremia <95 mEq/L Hyperchloremia >105 mEq/L

Signs and Symptoms Signs and Symptoms

Difficulty breathing Muscle weakness

Muscle spasms Excessive thirst
Dehydration Hypertension
Weakness Fatigue
Fatigue Fluid retention
Diarrhea Irregular heartbeat
Vomiting Low High
Causes Causes

Renal failure
Severe diarrhea
Prolonged diarrhea and vomiting
Extremely high ingestion of dietary salt
Diuretic therapy
Renal or metabolic acidosis
NG tube suctioning
Respiratory alkalosis
Chronic lung disease
CKD
CHF
Diabetes insipidus or diabetic coma
Metabolic alkalosis
Chemotherapy
Chemotherapy

Management Management

Treat underlying cause Meds to curb nausea, vomiting, diarrhea

IV fluids (like normal saline) Hydration if dehydrated
Encourage more sodium chloride in diet Decrease saline IV
Maintain blood glucose levels
Stop meds if they are contributing to the
problem

Encourage! High Chloride Foods Avoid!

Table salt Rye Lettuce and celery
Seaweed Tomatoes Olives
 lOMoARcPSD|22650627

Electrolyte Relationships
Sodium / Potassium = INVERSE

+
Na = K+

Calcium / Phosphorus = INVERSE

+
Ca = PO4

Calcium / Vitamin D = SIMILAR

+
Ca = Vit. D

Calcium / Magnesium = SIMILAR

+
Ca = Mg

Magnesium / Potassium = SIMILAR

Mg = K+
Magnesium / Phosphorus = INVERSE

Mg = PO4
 lOMoARcPSD|22650627

The Endocrine System

A network of glands and organs that regulate and control various body
functions by producing and secreting hormones.

Pineal Hypothalamus
Pituitary

Parathyroid
Thyroid

Thymus

Adrenal

Pancreas

Ovaries
(female)
Testes
(male)

Major Endocrine Glands

1. Hypothalamus 6. Thymus
2. Pituitary 7. Adrenal
3. Pineal 8. Pancreas
4. Parathyroid 9. Ovaries
5. Thyroid 10. Testes
 lOMoARcPSD|22650627

Hypothalamus Gland
Location: Base of brain
Function: Major role in endocrine system; maintains body's homeostasis; releases hormones
that stimulate the pituitary gland
Main Hormones: Oxytocin, Anti-Diuretic Hormone (ADH/Vasopressin)

Pituitary Gland - AKA 'Master' gland

Location: Connected to hypothalamus in brain
Function: Secretes hormones that send signals to other endocrine glands to release or inhibit
their own hormone production
Main Hormones and target organ:
Growth hormone - Bones, muscles, organs
Prolactin - Breasts (mammary glands) to stimulate milk production
Luteinizing hormone (LH) -
ovaries to produce estrogen/progesterone
testes to produce testosterone
Follicle-stimulating hormone (FSH) - same as LH
Adrenocorticotropic hormone (ACTH) - adrenal glands to produce
corticosteroids
Thyroid-stimulating hormone (TSH) - thyroid to produce thyroid
hormones
ADH (made in hypothalamus but stored in pituitary) - kidneys to ↑
water absorption in blood
Oxytocin (made in hypothalamus but stored in pituitary) - breasts
(for milk production) and uterus (for contractions)

Pineal Gland Thyroid Gland

Location: Between two hemispheres in brain Location: Lies just below the Adam's
Function: Regulates circadian rhythm and apple in the neck
reproductive hormones Function: Regulates the body's
Main Hormone: Melatonin metabolism
Main Hormones: T3 (Triiodothyronine),
Parathyroid Glands T4 (Thyroxine- converts to T3),
Location: Four glands in the neck BEHIND the thyroid Calcitonin
Function: Regulate calcium and phosphate levels No relation other
Main Hormone: Parathyroid hormone (PTH) than name
 lOMoARcPSD|22650627

Thymus Gland
Location: Behind sternum between lungs
Function: Stimulates the development of T cells which are sent to lymph nodes to help fight
disease. Only active until puberty then shrinks and becomes fat!
Main Hormone: Thymosin

Adrenal Glands - AKA Suprarenal

Location: Two glands located one on top of each kidney
Function: Two parts to each gland (Medulla and Cortex), each with its own function.
Medulla: Secretes epinephrine and norepinephrine to help control activities of
sympathetic nervous system (blood pressure, heart rate, sweating)
Cortex: Secretes two types of corticosteroid hormones:
1. Glucocorticoids:
a. Hydrocortisone (cortisol) - helps convert food to energy
b. Corticosterone - regulate immune response
2. Mineralcorticoids: The main one is aldosterone - maintains balance of salt and
water to control blood pressure
Main Hormones: Epinephrine, Norepinephrine, Hydrocortisone, Corticosterone, Aldosterone

Pancreas - belongs to both endocrine and digestive systems

Location: Next to stomach, connected to duodenum
Function: Main endocrine function is to regulate blood glucose levels; only 5% of pancreas is
endocrine cells (Islets of Langerhans)
Main Hormones:
1. Gastrin - stimulates cells in stomach to produce acid for digestion
2. Glucagon - stimulates cells to release glucose to raise blood glucose levels
3. Insulin - regulates blood glucose levels by allowing cells to absorb & use glucose (thus
lowering blood glucose levels)
4. Somatostatin - released when insulin and glucagon get too high
5. Vasoactive intestinal peptide (VIP)- controls H2O secretion/absorption from intestines

Ovaries Testes
Location: On either side of uterus Location: Within the scrotum
Function: For proper physical development Function: For proper phys. development of
of girls and to ensure fertility boys, then libido, muscle strength, bone dens.
Main Hormones: Estrogen, Progesterone Main Hormone: Testosterone
 lOMoARcPSD|22650627

The Thyroid Gland

Location: Lies just below the Adam's apple in the neck
Function: Regulates the body's metabolism
Main Hormones: T3 (Triiodothyronine), T4 (Thyroxine- converts to T3), Calcitonin

Thyroid uses iodine in food we eat Hypothalamus releases

to make the 2 main hormones (T3 Thyrotropin-releasing
and T4) →
Hormone (TRH) Pituitary
T3 & T4 function: releases Thyroid-stimulating
Regulate metabolism →
Hormone (TSH) thyroid
Affect: produces T3 & T4
Heart rate Too much T3 & T4 in blood
SNS stimulates pituitary to stop
Growth/development releasing TSH (negative
Body temperature feedback loop)
Fertility
Digestion/burning calories If thyroid is enlarged, a goiter may
Muscle contraction appear below or to the sides of the
Calcitonin helps incorporate Adam's apple
calcium into bone

Thyroid Function Tests

Blood tests:
TSH - Best indicator of thyroid function
Need to test along with T4 & T3 to see if problem lies with thyroid or
pituitary
T4 & T3
TRH
Thyroid Binding Globulin (TBG) (carries T3 & T4 in blood)
Antibodies (to check for autoimmune disease)
Biopsy (if cancer suspected)
Ultrasonography (if growths are detected)
Radioactive iodine uptake test (to measure thyroid activity)
 lOMoARcPSD|22650627

Hyperthyroidism
Condition that occurs when there is a high level of thyroid hormones
in the blood - AKA Overactive Thyroid

Causes: Signs and Symptoms - think FAST

Graves Disease (see Graves
Enlarged thyroid gland (goiter)
Disease section) - most common Sped up body functions
Toxic multinodular goiter - ↑ HR/BP
Plummer Disease - many nodules Palpitations due to arrhythmias
that secrete excess thyroid Excess sweating/hot
hormones Shaky hands
Thyroiditis - Inflammation caused Nervous/anxious/irritable
by: Insomnia
Wt loss/ ↑ appetite
Virus
Frequent BM/diarrhea
Autoimmune
Change in menstrual cycles
Single toxic nodule - abnormal Elderly - 'Masked' hyperthyroidism
tissue within the thyroid produces Weak
excess thyroid hormones Confused
Certain meds Withdrawn
Iodine (too much) Depressed
Other s/s if caused by Graves (see
Overactive pituitary gland - rare
Graves Disease section)

Treatment Meds
Will depend on cause Antithyroid meds:
Iodine - not used long-term; given Methimazole - most common
when tx needed fast (i.e. thyroid Propylthiouracil (PTU) - watch
storm - see Thyroid Storm section) for liver damage
Radioactive iodine - destroys part or Stop the production of T3 & T4
all of thyroid gland; may need HRT Educate pt:
for rest of life Do not abruptly stop
Thyroidectomy - removal; will need Same time each day
HRT for rest of life Avoid iodine-rich foods
Beta-blockers - ↓ HR, tremors and No aspirin/salicylates
anxiety Watch for thyroid storm and
Meds hypothyroidism
 lOMoARcPSD|22650627

Intervention
Cool, calm environment If thyroidectomy:
Daily wts Monitor for possible parathyroid issues
Monitor EKG, HR, BP and thyroid storm
Monitor for thyroid storm Watch Ca levels
Educate on: Keep pt in Semi-Fowler's position
Radioactive iodine therapy Keep trach kit, oxygen nearby
Thyroidectomy

Graves Disease
Autoimmune disorder where the antibody (Thyroid Stimulating
Immunoglobulin - TSI) stimulates the thyroid to produce and secrete excess
thyroid hormones into the blood; often hereditary
Signs/Symptoms include those for hyperthyroidism PLUS :
Protruding eye balls/puffy eyes
Double vision; sensitive to light
Pretibial Myxedema - red, swelling on the skin, lower legs and feet (has
an orange peel texture)
TX- same as for hyperthyroidism, PLUS
For eyes: Elevate HOB, eye drops, selenium, diuretics
Corticosteroid cream for itchy skin

Thyroid Storm- a life-threatening emergency!

Sudden, extreme overactivity of the thyroid gland
Cause: Pt w/hyperthyroidism that is unmanaged/ill-treated or is ill (sepsis;
DKA; surgery); post-thyroidectomy; taking salicylates; pregnant, or exposed to
radioactive iodine therapy
S/S: Typical hyperthyroidism s/s to the EXTREME! Fever, HTN and
↑
tachycardia (may lead to CHF or MI), RR (may lead to resp failure), restless
and confused (may lead to seizures, delirium, come)
Interventions: Monitor HR, BP, RR, EKG, temperature; sedatives, no iodine
Meds: Antithyroids (Methimazole, PTU) - block synthesis; Iodide solution -
blocks secretion; Tylenol (no salicylates), Beta Blockers (Inderal) - block
conversion; Glucocorticoids (Dexamethasone) - suppresses immune system
 lOMoARcPSD|22650627

Hypothyroidism
Condition that occurs when there is a low level of thyroid hormones in the blood

Causes: Signs and Symptoms- think SLOW

Primary
Possible enlarged thyroid gland
Hashimoto's thyroiditis - most (goiter)- usually w/Hashimoto's
common- autoimmune disorder Slowed down body functions
where body attacks thyroid Fatigued- usually 1st sign
Thyroiditis - usually temp Eyelids droop
Tx for hyperthyroidism or Eyes/face puffy (myxedema)
thyroid cancer Voice hoarse/speech slow
Low iodine in diet (rare in U.S.) Hair sparse, coarse, dry
Skin coarse, dry, scaly
Radiation to head & neck
Wt gain
Genetic disorder
Constipated
Secondary- rare Muscle cramps
When pituitary gland fails to No tolerance to cold
secrete enough TSH ↓ HR
Change in menstrual cycles
**Affects mainly women Elderly may appear depressed,
middle to older aged** confused, forgetful, demented

Treatment - Meds
Thyroid hormone replacement
Synthroid
Thyrolar
Cytomel
NO sedatives/narcotics - increase
risk for myxedema coma (see
Myxedema Coma section)
 lOMoARcPSD|22650627

Intervention
Monitor for myxedema coma Monitor for hyperthyroidism
(see next section) NO sedatives or narcotics
Administer meds as prescribed Educate pt:
Don't take within 4 hrs: Don't abruptly stop taking
Carafate meds
Aluminum Hydroxide Take same time every day
Simethicone Medication interactions
Multivitamin

Myxedema Coma - a life-threatening emergency!

Sudden, extreme underactivity of the thyroid gland
Cause: Pt w/hypothyroidism that is unmanaged/ill-treated or is ill, abruptly
stops taking thyroid replacement meds, takes sedatives or lithium, or thyroid
gland is removed
S/S: Typical hypothyroidism s/s to the EXTREME!
↓ ↓HR, BP
↓ Temp RARE-
↓ BG Occurs mainly in
↓ Na elderly women
Resp failure
Myxedema (swelling of eyes/face)
Drowsy
May lead to confusion, stupor, coma
Interventions:
Monitor HR, BP, EKG, Wt
Monitor resp status (may need mech vent)
Keep warm
IV solutions as prescribed:
Normal saline and glucose
Synthroid (monitor for toxicity)
Glucose
No sedatives or narcotics
 lOMoARcPSD|22650627

Hyper- and Hypoparathyroidism

Two disorders caused by too much or too little parathyroid hormone.

The main purpose of the parathyroid glands is to control blood calcium levels.

It's all Parathyroid glands monitor

Role of Calcium in body about the the Ca level 24 hrs/day.
Nerve impulse calcium!
↓
When the level , the glands
make and release parathyroid
transmission
hormone (PTH).
Muscle contraction
Bone health
↑
When the level , the glands
make less PTH or stop the
Blood clotting
release altogether. (PTH
negative feedback loop)

When Ca level is low, PTH is sent to:

Bones to release Ca into blood
Normal Ca levels =
Intestine to ↑ absorption of Ca from diet
Kidneys to: 8.6 - 10.0 mg/dL
Reabsorb Ca (and stop the release into urine)
Stimulate the production of active Vit D (needed to absorb Ca)
Block phosphate form being reabsorbed (excretes in urine instead)

Hyperparathyroidism
Disorder caused by over-production of PTH by a parathyroid gland.
Leads to Hypercalcemia and Hypophosphatemia
2 types:
Primary - Caused by enlarged PT gland(s)
Noncancerous growth - ** Most common
Enlargement (hyperplasia)
Cancerous tumor (very rare)
Secondary - Caused by another condition that causes ↓Ca levels in the body
Severe Ca deficiency
Severe Vit D deficiency
Chronic kidney failure (kidneys can't covert Vit D so SI can't absorb Ca)
 lOMoARcPSD|22650627

Complications
Risk Factors Osteoporosis
Diagnosis
Kidney stones Blood tests:
Radiation tx for cancer in
CVD Ca
neck area
In pregnant women may PO4
Lithium (bipolar disorder)
cause neonatal Mg
hypoparathyroidism PTH
Sometimes:
Urine for Ca
Signs and Symptoms EKG
Osteoporosis Bone density
Kidney stones (↑ Ca levels cause kidney to reabsorb Ca)
Excess urination (↑ Ca levels cause ↑ urine production)
N/V
No appetite Surgery
Ab pain (↑ stomach acid)
Constipation (parathyroidectomy)
Feeling ill in general
is the main treatment
Tired/weak
Bone and joint pain for Primary
Depressed/forgetful
Hyperparathyroidism
Intervention
Admin meds per MD order
Monitor:
Vitals
EKG
Meds
Ca/PO4 levels Calcimimetics 'Senispar' - mimics role
Renal status of Ca in blood to ↓ PTH levels - used in
I/Os, encourage fluids pt w/secondary hyperparathyroidism-
Diet: ↓ Ca, ↑ PO4 take w/food to avoid GI distress
Calcitonin - injected or nose spray - ↓
Post-op: osteoclasts and ↑ kidney excretion of
Monitor respiratory status
Ca
Keep in Semi-Fowler's position
Loop diuretics 'Lasix' - ↓ Ca
Keep trach kit, oxygen, suction on hand
reabsorption in renal tubules- monitor
Watch for ↓ Ca levels:
K+ levels
Tingling
Bisphosphonates 'Aredia' or 'Fosomax'
Twitching
- slows down osteoclasts
+ Trousseau's Sign
+ Chvostek Sign
Laryngeal nerve damage (voice changes,
trouble swallowing or speaking)
 lOMoARcPSD|22650627

Hypoparathyroidism
Disorder caused by decreased production of PTH by the parathyroid glands.
Leads to Hypocalcemia and Hyperphosphatemia

Causes: Very
Following thyroid or PT surgery RARE
Accidental removal during thyroid surgery
Parathyroidectomy (usually transient)
Signs and Symptoms
Inability of kidneys and bones to respond to
PTH (pseudo-hypoparathyroidism) Parathesia - tingling,
numb skin
Congenital (Neonatal hypoparathyroidism- +Trousseau's Sign
due to pregnant mom with +Chvostek Sign
hyperparathyroidism) Severe tetany -
bronchospasm,
Immune system develops antibodies against laryngospasm,
PT tissue hand/feet spasm,
Hypomagnesemia seizures, EKG changes
↓ Ca, ↑ PO4
Usually caused by chronic alcoholism

Intervention
Monitor Ca and PO4 levels
Have trach kit, oxygen and suction at
Meds bedside
IV calcium - slowly, can cause tissue Diet - ↑ Ca, ↓ PO4
sloughing, watch if pt on Digoxin (risk Meds per MD order
of toxicity)
Oral Ca w/Vit D - give separate times Diet
than Fe and thyroid hormone
Encourage:
PO4-binders - Aluminum carbonate -
Beans
given after meals to ↑ excretion of PO4
Almonds
by GI system
Dark green, leafy veges
PTH replacement - Natpara - Monitor
Dairy
Ca levels; watch for GI distress,
Fortified cereals, OJ
paresthesia
Avoid:
Soft drinks, coffee
Eggs, red meat
Alcohol, tobacco
 lOMoARcPSD|22650627

The Adrenal Glands

Location: Two glands located one on top of each kidney
Function: Two parts to each gland (Medulla- inner layer and Cortex- outer layer),
each with its own function.
Medulla: Secretes epinephrine and norepinephrine to help control activities
of sympathetic nervous system (blood pressure, heart rate, sweating)
Cortex: Secretes two types of corticosteroid hormones:
Glucocorticoids:
Hydrocortisone (cortisol) - regulates metabolism
Corticosterone - regulate immune response
Mineralcorticoids: The main one is aldosterone - maintains balance of
salt and water to control blood pressure
Main Hormones: Epinephrine, Norepinephrine, Hydrocortisone, Corticosterone,
Aldosterone

Adrenal glands

Hypothalamus releases Corticotropin-

releasing Hormone (CRH) → Pituitary
releases Corticotropin (ACTH) →
adrenal glands release glucocorticoids
In response to stress, the hypothalamus
stimulates the medulla to release
Kidneys
epinephrine and norepinephrine
Adrenal Adrenal The renin-angiotensin-aldosterone
Cortex Medulla system (regulated by kidneys)
stimulates adrenal glands to produce
more or less aldosterone

Kidney
 lOMoARcPSD|22650627

Cushing's Syndrome
Condition due to very high level of cortisol released from adrenal glands

Causes: Signs and Symptoms

Large doses of corticosteroids (ex.
Excessive fat on torso & top of back
Prednisone, Dexamethasone) (known as buffalo hump)
Asthma, rheumatoid arthritis, Large round face (moon face)
lupus Weak muscles
Tumor in adrenal glands Thin skin, bruise easily
Tumor outside the pituitary glands- Striae on abdomen/chest
producing corticotropin (ACTH) Fatigue, depression
↑ BP
↑ BG
Cushing's Disease
↓K
Very high level of cortisol due to Osteoporosis
pituitary gland producing too Irregular menstrual cycles in women
much ACTH. Usually caused by a ED in men
tumor in the pituitary. The adrenal ↑ body and facial hair, women balding
glands are normal. Hirsutism in women
Children: grow slowly, short stature
Treatment
Will depend on cause Diagnosis
↓ corticosteroids if possible (weigh Measure cortisol in
benefits) urine/saliva/blood for 24 hr pd
↑ pro, ↑ K diet (will be ↑ all day in Cushing's)
Meds to ↓ cortisol and its effects: CT, MRI, chest x-ray to look for
Metyrapone tumors
Ketoconazole
Mifepristone Intervention
Radiation tx
Surgery Prep for surgeries
Remove tumors Monitor for infection/skin
Adrenalectomy (may need breakdown
corticosteroids for life) Monitor BG, K, Na, Ca
 lOMoARcPSD|22650627

Addison's Disease
Deficiency of cortisol and aldosterone due to underactive adrenal glands

AKA Primary Adrenal

Insufficiency Signs and Symptoms
(See next page for Secondary Develop slowly over time, vary/person
Adrenal Insufficiency) Weak, tired, dizzy
Dark patches of skin (knuckles, scars,
Causes: creases, gums)
Autoimmune reactions - body Black freckles
attacks adrenal cortex Wt loss/No appetite
Cancer Muscle aches
Tuberculosis/infections N/V/Ab pain/Diarrhea
Trauma to adrenal cortex No tolerance to cold
↓ BP, dehydration
In infants/children: genetic
Crave salt
Depression
Diagnosis ↓ Na, ↓ BG, ↑ K, ↑ Ca
S/S slow to show, no definitive Irregular menstruation in women
blood test so difficult to dx ED in men
Blood tests may show ↓ Na, ↑ K,
↓ cortisol, ↑ ACTH Intervention
Monitor BG and K
Treatment
Administer meds as prescribed
Goal is to replace cortisol & Educate:
aldosterone with meds- will Don't abruptly stop meds
need for life Report ↑ stress levels (may
need adjustment)
Meds
Carry injection of cortisol for
Cortisol replacement: emergency
Hydrocortisone (divided Wear med alert bracelet
doses each day) Diet ↑ Prot/carbs, include Na
Prednisone Avoid undue stress and
Dexamethasone strenuous exercise
Aldosterone replacement: Watch for Addisonian Crisis (see
Fludrocortisone next page)
 lOMoARcPSD|22650627

Secondary Adrenal Insufficiency

Decrease in cortisol due to lack of ACTH from pituitary gland

Causes: S/S:
Chronic steroid use *Most common Similar to Addison's Disease, except:
Pituitary tumor No dark patches of skin
Removal of pituitary gland No dehydration
Head injury Na & K levels normal
Corticotropin level is LOW
Treatment: Prednisone or hydrocortisone

Addisonian Crisis (Adrenal Crisis)

Extremely low cortisol levels. Life-threatening emergency!

Causes: S/S:
Pt has Addison's Dz and: Severe Ab/low back/leg pain
Not treated properly Sudden, extreme weakness
Experiencing extreme stress,
accident, injury, surgery, severe
↓
Extremely BP
Dehydration
infection Severe vomiting/diarrhea
Adrenalectomy May lead to
Pituitary gland not producing ACTH Kidney failure
Treatment: Shock
IV Solu-Cortef/IV fluids (D5NS) Loss of consciousness
**STAT!**

Intervention:
Monitor for:
Infection
Neuro status
Electrolyte status (Na, K, BG)
 lOMoARcPSD|22650627

Pheochromocytoma
Tumor in the adrenal medulla that produces excessive amounts of catecholamines

Normally, the adrenal medulla secretes Tumors are mostly benign

catecholamines (epinephrine, Usually in one gland
norepinephrine, dopamine) in response Affect mostly adults (20-40 yrs)
to stress. They cause:
↑ ↑ ↑ ↑
HR, BP, BG, BMR
Signs and Symptoms
↑ Fat metabolism
↑ Thermogenesis Severe HTN, ↑ BG
Severe headaches
Feelings of anxiety/fear
Tachycardia
However, in pheochromocytoma, the
Excess sweating
tumor causes these reactions without
N/V
stress. Back/Ab/chest pain
Tremors in hands
Anxiety/fear
Diagnosis Heat intolerance
24 hr urinary catecholamines & Flush face
metanephrines (breakdown products)
Serum catecholamines Intervention
MRI/CT to look for tumor
Monitor:
BP, HR, BG
Treatment
Look for hypertensive crisis:
Tumor removal or complete >180 systolic or >120 diastolic
adrenalectomy S/S: Headache, changes in
Until surgery, ↓ catecholamines vision or neuro, seizures, SOB
and BP with meds Chest pain
EKG changes
Meds Meds as ordered
Educate pt:
Alpha-adrenergic blockers: High cal diet
Cardura, Minipress, Hyrtin No stimulants
Beta-adrenergic blockers: Hormone therapy post-surgery
Labetalol or Inderal
 lOMoARcPSD|22650627

DI vs SIADH
Diabetes Insipidus vs Syndrome of Inappropriate Antidiuretic Hormone

ADH is produced in hypothalamus and

It's all about
stored/secreted in pituitary gland.
Antidiuretic
ADH secreted or withheld due to changes
Hormone
in hydration status
(ADH)!
ADH function: to cause the body to retain
ADH water and constrict blood vessels.
aka How? By causing the renal tubules to
Vasopressin retain water.

Diabetes Insipidus SIADH

D = DRY S = Soaked
Too little ADH Too much ADH

↓ADH ↑ADH
Cannot retain water Retains too much water
↑urine output ↓ urine output
↑Na ↓Na
Dehydrated Overhydrated
 lOMoARcPSD|22650627

Diabetes Insipidus
Condition in which the kidneys are unable to retain water.

Types/Causes:
Central DI - Pituitary gland does not secrete ADH - Most common
Damage to hypothalamus or pituitary gland
Brain damage: Head trauma, stroke
Brain tumor
Too little ADH
Aneurysm ↓ADH
Certain drugs: Declomycin (tx. for SIADH) Cannot retain water
Nephrogenic DI - Kidneys do not respond to ADH ↑urine output
Hereditary
Acquired
↑Na
Dehydrated
Certain drugs: Lithium, Declomycin
Polycystic Kidney Disease, Sickle Cell Disease
Gestational - Rare
Placenta produces vasopressinase which can cause ADH to breakdown

Signs and Symptoms Diagnosis

Water deprivation test - 12 hours no fluid
Polyuria - LOTS of urine - 4-24L/day Measure urine , electrolytes, wts regularly
Polydipsia - crave water/ice Then inject ADH after 12 hrs
Dehydrated - dry mucous If ↓ urination, urine concentrated, BP rises,
membranes/skin; ↓ skin turgor HR normal = Central DI
Urine diluted (↓ spec gravity) If not = Nephrogenic DI
↑ Na - due to ↓ water levels
Hypotension - due to severe dehydration
and vessels dilated
Treatment
Extreme fatigue No cure ↓ Na diet
Muscle pain/weakness Give adequate water Meds

Intervention Meds
Chlorpropamide (Diabinese)
Strict I/Os, daily wts
↑ ADH hormone
Monitor electrolytes (Na, K)
May cause ↓ BG, photosensitivity
Meds as prescribed
Desmopression (DDAVP, Stimate)
↓ Na diet
Nasal spray/tablet/injection/or IV
Avoid caffeine: tea, coffee,
May cause ↓ Na
energy drinks
Thiazide diuretics
 lOMoARcPSD|22650627

SIADH
Condition in which the body makes too much ADH

Causes:
Lung cancer (ADH produced outside the pituitary)
Damage to hypothalamus or pituitary gland
Infection/germs Too much ADH
Pneumonia ↑ADH
CNS disorder - stroke, hemorrhage, trauma Retains too much water
HIV ↓urine output
Certain drugs ↓Na
Carbamazepine Overhydrated
Chlorpropamide (tx. for DI)

Signs and Symptoms Diagnosis

Blood and urine tests
↑ fluid retention (wt gain)
(Na & K)
↓ Na - causes most of outward symptoms
Difficult to diagnose - need to rule
Sluggish, confused
out other conditions
Muscle cramps, fatigue
↑ HR
↓ Urine output; concentrated (↑ spec gravity) Treatment
↑ HTN Treat cause
Seizures (later on) Restrict fluids
Meds

Intervention
Meds
Daily wts/monitor wt gain
Strict I/Os IV Hypertonic Saline - slowly
Restrict fluids Loop diuretics - monitor K
Safety due to confusion Demeclocycline or lithium
Admin meds per MD order ↓ effect of ADH on kidneys
Conivaptan or tolvaptan
Block ADH receptors and prevent kidneys
from responding to ADH
 lOMoARcPSD|22650627

Diabetes Mellitus
Disorder in which the amount of glucose in the blood is elevated.

What happens in diabetes mellitus?

The food we eat is broken down into glucose and absorbed

into our blood.

Simple carbs are broken down fastest, followed by complex

carbs and then protein and fats.
Important!!

Once the glucose is in the blood, the pancreas releases insulin

to move the glucose out of the blood and into our cells.

From the cells, the glucose is either used by the body

immediately or stored in the liver and muscles as glycogen or in
our body as fat (if liver and muscle glycogen stores are full).

In diabetes, the pancreas either doesn't release enough

insulin, doesn't release any at all OR the cells do not respond
to the insulin.

All situations lead to high levels of glucose in the blood

(hyperglycemia).
 lOMoARcPSD|22650627

Insulin/Glucagon Feedback Loop

Blood glucose ↑→ →
Pancreas releases INSULIN glucose
enters cells to be used or saved as glycogen or fat Blood→
glucose ↓
Blood glucose ↓→ Pancreas releases GLUCAGON liver →
releases stored glycogen (converts to glucose in blood) →
Blood glucose ↑

Types of Diabetes
Prediabetes
Type I
Type II
Gestational

Prediabetes
Blood glucose levels too high to be considered normal but not high
enough to be labeled Diabetes
Fasting blood glucose levels are 100-125 mg/dL
Decreasing body weight by 5-10% can usually return BG levels back to
normal and decrease risk of developing DB in future
 lOMoARcPSD|22650627

Type I Diabetes
Pancreas produces LITTLE TO NO INSULIN because the insulin-producing
cells have been destroyed
Usually diagnosed at a young age
Happens suddenly
Pt MUST take insulin each day for life
Causes: Genetic, auto-immune (virus)

Signs and Symptoms

Pt usually young and thin
Experiencing the 3 Ps:
↑
Polyuria - When BG levels (above 160-180 mg/dL), glucose spills
→
into urine kidneys will excrete add'l H2O to dilute glucose
Polydipsia - Excess urination will trigger thirst response
Polyphagia - Calories (glucose) will be lost in urine causing hunger
Breath smells of acetone - due to DKA (see Complications section)
Blurred vision
Drowsiness
Nausea
Decrease endurance during exercise
Wounds heal slowly
Rashes
Yeast infections
 lOMoARcPSD|22650627

Type II Diabetes
Pancreas produces insulin, however, the cells do not respond to it
(Known as Insulin Resistance)
Glucose can't get into cells
Pancreas continues to produce insulin; leads to Hyperinsulinemia
Hyperinsulinemia leads to Metabolic Syndrome
Causes: Obesity, sedentary lifestyle,
poor diet (lots of refined carbs), stress, Metabolic Syndrome
plus a genetic component BP, BG, TG ↑ ↑ ↑
Pt usually overweight adult HDL ↓
Excess fat around waist

Signs and Symptoms

May take years before diagnosed - Symptoms subtle at first

↑ urination Slow wound healing

↑ thirst Rashes
Fatigue Yeast infections
Blurred vision Glycosuria
Dehydrated

Gestational Diabetes
Similar to Type II Diabetes
Cells not receptive to insulin
May need to take insulin during pregnancy
Must monitor BG levels and diet throughout pregnancy
Goes away after birth
 lOMoARcPSD|22650627

Treatment/Intervention of DB
Diet

BG
Monitoring
Exercise Medication

DB Management Triad
Patients with DB need to monitor their BG throughout the day
Diet, exercise and meds all work together to help maintain proper BG
levels
The nurse's goal is to educate the pt on all 3 parts of the triad: Diet,
Exercise and Meds

Diet
Each diet will vary per pt as each individual's 4
BG responds differently to different foods Water or 0
2 calorie drink
Begin with the Diabetes Plate Method:
1 Carbohydrate
1 = Nonstarchy vegetables: Broccoli, Nonstarchy foods
vegetables
tomatoes, lettuce, etc 3
Protein
2 = Carbohydrate foods: breads, pasta, etc
Foods
3 = Lean beef, chicken, eggs, beans, etc

Exercise
Pt should test BG prior to exercising
If < 100 mg/dL, eat small carb snack before exercise and monitor for
hypoglycemic symptoms while exercising (have simple carb on hand)
↓
If glucose >300 mg/dL wait until glucose before exercising
If exercise for extended pd of time, monitor BG during exercise
Add'l food may be needed as intensity and duration rises
 lOMoARcPSD|22650627

Medications
Oral meds may be necessary for Type II pt when diet and exercise aren't
enough to control BG
↓ ↑
Biguanides (Metformin) - liver stores of glycogen, body's
sensitivity to insulin; side effects: N/Ab pain/Bloating/Diarrhea
Sulfonylureas (Glyburide, Glipizide, Glimepiride) - helps body secrete
insulin; avoid with ETOH; side effects: hypoglycemia, wt gain
Meglitinides (Repaglinide) - helps body secrete insulin (fast-acting);
side effects: hypoglycemia, wt gain
Thiazolidinediones (Avandia, Actos) - makes tissues more sensitive
↓ ↑
to insulin, glucose production in liver; side effects: risk for heart
↑
failure, bladder cancer, bone fractures, chol, wt gain
Alpha-glucoside Inhibitors (Precose, Glyset) - block the breakdown of
starchy foods; take with first bite of each meal; side effects: gas,
diarrhea, stomachache
Instruct pt:
Watch for hypoglycemia with:
Beta blockers; ASA, MAO inhibitors, Bactrim, ETOH
Watch for hyperglycemia with:
Thiazide diuretics, glucocorticoids, estrogen therapy
Type I pt (and some Type II) will need to take insulin daily

Insulin
Important points to remember:
4 types: Rapid-Acting, Short-Acting (Regular), Intermediate-Acting
(NPH), Long-Acting
Regular is the only insulin given IV
If Regular given at same time as NPH, can be in same syringe
If Regular given with long-acting, must be in a different syringe
NPH: If mixed, clear-to-cloudy (Regular is clear; NPH is cloudy)
Long-acting: Do NOT mix
Rotate injection site and do not massage area
 lOMoARcPSD|22650627

Rapid-Acting Take with meal

Aspart Onset: 15 minutes
Lispro Peak: 1 hour
Glulisine Duration: 3 hours
To remember: Ralph Rapidly Ate Lots of Grapes: 15 Red, 1 green, 3 seedless

Take 30-40
Short-Acting (aka Regular) minutes
Onset: 30 minutes before
Peak: 2 hour eating
Duration: 8 hours
To remember: Steelers came up short against the Ravens 30 to (2) 8

Covers
Intermediate-Acting (aka NPH) insulin
Onset: 2 hours needs for
Peak: 8 hours 1/2 day
Duration: 16 hours
To remember: In the Night, Paul Had 2 8-oz glasses of water and peed 16 times.

Covers
Long-Acting insulin
Detemir Onset: 2 hours needs for
Lantus Peak: None FULL day
Glargine Duration: 24 hours
Do NOT mix
To remember: During the Long Game: 2 goals, No penalties, 24 min on ice.
No mixups!
Watch for:
Somogyi Effect: Drop in BG in middle of night causes rebound hyperglycemia in
a.m.; treat with bedtime snack of carbs and/or change in bedtime insulin
Dawn Phenomenon: Natural increase in BG right before waking; in DB there is
no insulin to deal with BG leading to hyperglycemia; treat with bedtime insulin
change
 lOMoARcPSD|22650627

Complications of Diabetes
Diabetic Ketoacidosis (DKA) - mostly affects Type I
Hyperglycemia (exceeding 300 mg/dL)
→
No insulin body burns fats for energy produces ketones →
→ →
(byproduct) excess acid in body acid/base imbalance (metabolic
acidosis)
Kidneys attempt to reabsorb glucose but there is too much glucose →
→ →
leaks into urine osmotic diuresis polyuria and excretion of
→
electrolytes (Na, K, Cl) dehydration
Pt usually young; will lead to coma and death if not treated
Causes: Type I diabetics: undiagnosed, not taking appropriate insulin, not
eating, or experiencing sepsis/illness/extreme stress

Signs and Symptoms

Polyuria/Polydipsia ↓ HTN
Dehydration Kussmaul breathing (to correct
Wt loss the blood's acidity)
Fatigue Ab pain in kids
Fruity smell to breath (ketones) Blood ph < 7.35
Tachycardia HCO3 <15 mEq/L

Intervention - Needs tx STAT

Goal is to↑ hydration, ↓ BG and correct acid-base imbalance.
Treat hydration first: Treat BG:
0.9% NS then progress to IV regular insulin (make sure K
0.45% NS is normal > 3.3)
D5W added to 0.45% NS once Monitor BG hourly
BG 250-300 mg/dL Monitor K levels; add K to IV if
needed
Monitor for cerebral edema
 lOMoARcPSD|22650627

Hyperosmolar Hyperglycemic State (HHS) - mostly affects Type II

BG extremely high (exceeding 600 mg/dL)
→
Passing large amounts of urine severe dehydration blood →
abnormally concentrated (hyperosmolar)
Differs from DKA in that pt has some insulin, so there is no breakdown of
fats (no ketosis or metabolic acidosis)
Kidneys attempt to reabsorb glucose but there is too much glucose →
→ →
leaks into urine osmotic diuresis polyuria and excretion of
→
electrolytes (Na, K, Cl) dehydration
Causes: Type II DB with illness or infection or taking corticosteroids or
diuretics; usually older adults

Signs and Symptoms

Mental change Polyuria
Main outward symptom Polydipsia
Confusion to drowsiness to Dehydration
coma Fever
Hyperglycemia: >600 mg/dL Fatigue

Intervention
↑
Goal is to hydration and BG ↓
Hydrating patient will help solve BG problem so focus on that 1st.

Treat hydration first: Treat BG:

0.9% NS then progress to IV regular insulin (make sure K
0.45% NS is normal > 3.3)
D5W added to 0.45% NS once Monitor BG hourly
BG 250-300 mg/dL Monitor K levels; add K to IV if
needed
Monitor for cerebral edema
 lOMoARcPSD|22650627

Hypoglycemia: Other Complications

BG < 60 mg/dL or drops rapidly Atherosclerosis which can lead to:
Angina
Signs/Symptoms: Heart failure
Sweating Lightheaded Stroke
Clammy Double vision Diabetic retinopathy
Confused Tremors Neuropathy
Treatment: HTN
Simple carbs PO (fruit juice, honey, hard
Chronic Kidney Disease
candy, glucose tablets or gel packs) Fatty liver disease
IVD50 if unconscious Yeast infections
Ulcers/infections of feet/hands
 lOMoARcPSD|22650627

The Digestive System

The digestive system consists of the gastrointestinal tract and accessory
organs of digestion. The system is responsible for breaking food down into
nutrients, absorbing nutrients into the bloodstream and eliminating the
indigestible parts of food from the body.

Mouth
Throat

Esophagus

Liver
Stomach

Gallbladder
Pancreas

Small Intestine
Large Intestine

Rectum
Anus

The gastrointestinal tract Accessory organs of digestion

1. Mouth 1. Liver
2. Throat and esophagus 2. Pancreas
3. Stomach 3. Gallbladder
4. Small intestine
5. Large intestine
6. Rectum and anus
 lOMoARcPSD|22650627

Mouth Throat and Espophagus

Receives food; process of Throat (AKA Pharynx) is where food goes after it is
digestion begins here via swallowed.
digestive enzymes released by Esophagus: channel that connects the throat with the
salivary glands stomach. Either end has ring-shaped muscles (Upper and
Lower Esophageal Sphincters) to prevent stomach
Cardia contents from flowing back into throat or esophagus
Body
Stomach
Antrum
3 parts: Cardia, Fundis (body), Antrum
Cardia and body store food, waiting for antrum to Only a few substances, such as
contract. Once contracted, the antrum mixes food with alcohol and aspirin, can be
acid enzymes and grinds it. absorbed directly into the
3 substances secreted: Mucus, HCl, and bloodstream from the stomach
precursor to pepsin (to break down protein)
Duodenum
Jejunum Small Intestine
Ileum 3 segments: Duodenum, Jejunum, Ileum
Duodenum- receives food from the stomach via pyloric sphincter.
Absorbs most of
Pancreas sends pancreatic enzymes. Liver and gallbladder send bile.
the nutrients of
Jejunum and Ileum- Absorb fat and other nutrients
the food
The entire surface area of the jejunum and ileum and most of the
duodenum are covered in villi and microvilli to aid absorption.
Transverse
Large Intestine
Ascending Consists of: Cecum & Ascending (rt) colon,
Descending Has lots of
Cecum (rt)
(lt) Transverse colon, Descending (lt) colon and bacteria for
Sigmoid colon digestion,
Sigmoid
Rectum Secretes mucous and is largely responsible for creating gas
Anus absorption of water from the stool

Appendix
Rectum & Anus
connected Rectum connects to sigmoid colon. Stays empty until the descending
to cecum colon becomes full and passes stool, causing urge to move bowels.
(no known fnx) Anus- opening through which stool leaves the body
 lOMoARcPSD|22650627

Accessory Organs in Digestion

Liver

- Produces many chemicals.

- Produces cholesterol which is used to make bile and some
hormones Second largest
- Produces many proteins, such as those needed to clot organ in the
blood and albumin (to maintain pressure in the body after skin.
bloodstream)
- Stores sugar (as glycogen) to use when needed
- Breaks down harmful substances

Pancreas

Has 2 types of tissue: Pancreatic acini and Islets of Langerhans

3 Digestive
Pancreatic acini cells- Produce the digestive enzymes and secrete them
Enzymes:
into the duodenum. Also secrete large amounts of sodium bicarbonate
Amylase-digests
which neutralizes acid from the stomach.
carbohydrates
The Islets of Langerhans- Produce hormones which are secreted into
Lipase - digests
the blood. The hormones are:
fats
Insulin - Decreases the level of sugar (glucose) in the blood Trypsin - digests
Glucagon - Raises the level of sugar in the blood (stimulates liver to protein
release its stores)
Somatostatin - Stops the release of insulin and glucagon

Gallbladder

The gallbladder holds and releases bile. It is connected to the liver via
Gallbladder is not
biliary tracts (ducts). Bile aids in digestion and eliminating some waste
needed and can be
products.
removed if
Gallstones are hard masses made of cholesterol that may form in
necessary.
gallbladder or bile ducts.
 lOMoARcPSD|22650627

Gastroesophageal Reflux Disease

Contents of stomach flow backward from the stomach into the esophagus. The acid and
bile cause inflammation in the esophagus and pain in the bottom of the chest.
-AKA -
Cause
GERD and
** Occurs when LES (Lower esophageal sphincter) does not Acid Reflux Disease
function properly and hold bottom of esophagus closed.
** Esophagus has no lining to protect against acid and bile VERY COMMON!!

LES
Long-term Complications
Inflammation of the esophagus
(esophagitis)
Ulcers of the esophagus
Narrowing of the esophagus
Abnormal cells that may become cancer
Signs and Symptoms (Barrett's Esophagus)
Heartburn
Regurgitation
Sore throat
Risk Factors
Hoarseness Overeating
Cough Overweight
Feeling of lump in throat Pregnancy
Occasional wheezing Increased intake of foods that irritate (i.e.
Dyspepsia alcohol, coffee)
Dysphagia Anticholinergetics
Hiatal hernia
Diagnosis
- Usually not necessary - Intervention
Endoscopy with biopsy Meds as prescribed
pH testing Raise HOB after eating +/or while sleeping
Refrain from eating 2-3 hrs before bed
Lose wt if needed
Meds Avoid foods that irritate (peppermint,
PPIs coffee, alcohol, fatty foods, acidic juices,
H2 Blockers cola drinks) Surgery (fundoplication-
Antacids (watch interaction Avoid smoking to wrap part of stomach
w/other meds) Eat small meals around esophagus)
 lOMoARcPSD|22650627

Peptic Ulcer Disease (PUD)

A sore in the lining of the stomach or duodenum caused by stomach acid and digestive juices.

Pathophysiology 3 Types of Peptic Ulcers

→
Acid penetrates the lining histamine 1. Duodenal - Most common
→
released parietal cells release more HCl 2. Gastric - usually in lower part of
resulting in a more acidic environment stomach
3. Esophageal - not as common
Cause
2 main causes:
Long-term Complications
Bleeding (most common)
1. H. pylori infection - spread from consuming Penetration
something contaminated with the bacteria Perforation (requires immediate
2. Long-term use of NSAIDS - surgery)
↓ prostaglandins →↓ bicarb in stomach→ Obstruction
↑ acid in stomach Cancer

Signs and Symptoms Vary with location of ulcer and pt age

Duodenal ulcer: Gastric ulcer:

Food decreases pain (pain returns Food increases pain
3-4 hours post eating) Dull/achy pain
Pain at night Weight loss
Gnawing pain If severe, vomiting (bright red and
Normal weight looks like coffee grounds) from GI
If severe, black tarry stool from bleed
GI bleed

Risk Factors Diagnosis Meds

Smoking Blood/stool test Antibiotics
Alcohol Breath test PPIs/H2 Blockers
Stress (psychological) Upper endoscopy Antacids

Intervention
Meds as prescribed Surgery may be needed for:
Diet: Low fiber and avoid: spicy Obstruction that recurs
and acidic foods, caffeine, Perforation
chocolate, cola drinks, fried and Bleeding ulcers (2 or more)
fatty foods, alcohol Cancerous ulcer
 lOMoARcPSD|22650627

Inflammatory Bowel Disease (IBD)

Disease where the intestine is inflamed, causing recurring abdominal pain and diarrhea.
2 main types of IBD: Crohn's and Ulcerative Colitis

Inflammatory Bowel Disease is NOT the same as Irritable Bowel Syndrome

(IBS). IBS is a group of symptoms, not a disease. People with IBS do not
experience increased inflammation, hospitalization or increased risk of
cancer as people with IBD experience.

Crohn's Disease
An IBD characterized by inflammation and ulcers in the GI tract. May affect ANY part of
the digestive tract, but most commonly occurs in the last part of the small intestine
(ileum) and the large intestine. Affects the entire bowel wall (through the layers) in a
scattered pattern (not continuous) giving it a cobblestone appearance.

Cause
**Exact cause unknown** Patches of
Possibly: Dysfunction of the immune system inflammation in
causing an overreaction to something in the SI and LI from
environment, diet or an infectious agent. May be Crohn's
hereditary. Cigarette smoking and oral
contraceptives may increase risk.

5 Types of Crohn's
Ileocolitis: Most common - end
Diagnosis
of SI and LI Blood & stool tests to check:
Ileitis: Only ileum Anemia
Gastroduodenal: stomach and WBC count
duodenum Albumin
Jejunoileitis: Jejunum C-Reactive protein
Granulomatous (Crohn's CT or MRI of abdomen
Colitis): Only LI Colonoscopy
 lOMoARcPSD|22650627

Crohn's Disease
Signs and Symptoms - Pt has flare-ups and remission cycles
Adults: Children:
Crampy ab pain in RLQ Wt loss May not show digestive symptoms
Abdominal bloating Ulcers (mouth & GI tract) Slow growth
Chronic diarrhea Anal fissures (w/bleeding) Joint inflammation
Fever Malnourished Fever
Loss of appetite Weakness
Fatigue

Complications
Obstruction - due to scarring
Other parts of body:
Perforation - from ulcers
Gallstones
Abscesses - pockets of infection
Urinary tract infections
Fistulas - due to ulcer or abscess formation
Kidney stones
Anal fissures
Colon cancer

Intervention
**No cure**
Meds as prescribed
Educate pt on disease - no cure Meds
Encourage no smoking Anti-inflammatory - Sulfasalazine;
May require TPN in severe cases Prednisone
Monitor I/O and GI symptoms Immuno-suppressors - Azathioprine;
Surgery Imuran
May be necessary w/complications Biologic agents - Adalimumab;
May end up with ileostomy Infliximab
Ostomy care Antibiotics - Ciprofloxacin
Diet: Probiotics
Goal is to avoid flare-ups (individual to Anti-diarrheal - take PO before meals
each person) No NSAIDS! Cause flare-ups
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
 lOMoARcPSD|22650627

Ulcerative Colitis
An IBD characterized by inflammation and ulcers in the large intestine and rectum.
Affects the inner lining in a continuous pattern, starting in the rectum.

Cause Diagnosis
**Exact cause unknown** Blood & stool tests to check:
Possibly: Overactive immune response to something in Anemia
the environment, diet or an infectious agent. May be WBC count
Albumin
hereditary.
C-Reactive protein
Barium enema w/x-ray
→ →
Intense inflammation in LI cells die ulcers form, Colonoscopy
→
bleed and create pus LI can no longer absorb water
→ →
stool remains watery diarrhea (bloody) flare-→ Signs and Symptoms
→
up cycles cause polyps and scar tissue to form bowel Symptoms will depend on severity
→
narrows due to scar tissue LI loses shape and of flare-up and how much of LI is
becomes smooth affected
Frequent BM
Wt loss
Continuous Anemia
inflammation in Painful abdominal cramps
Rectal bleeding
the LI from
Severe diarrhea
Ulcerative Fever
Colitis Blood/mucus in stool

4 Types of UC
Ulcerative Proctitis: Rectum -
Mildest
Complications Proctosigmoiditis: Rectum and
Bleeding - most common (leads to anemia) Sigmoid colon
Toxic colitis - (rare, severe) Pancolitis: entire colon -
May lead to toxic megacolon - LI SEVERE
becomes paralyzed and may rupture Left-sided colitis: Descending
Colon cancer colon, sigmoid colon, rectum
Peritonitis - leaking intestinal contents into
abdominal cavity
 lOMoARcPSD|22650627

Ulcerative Colitis
Intervention
**Only cure is surgery**
Meds as prescribed
May be NPO w/IV hydration Meds
Monitor:
Anti-inflammatory - Sulfasalazine;
Bowel movements
Prednisone
Wts
Immuno-suppressors - Azathioprine;
GI system- sounds, distention
Imuran
Educate pt on disease - no cure
Biologic agents - Adalimumab;
Surgery
Infliximab
Proctocolectomy - complete removal of
Antibiotics - Ciprofloxacin
colon and rectum - will end in ileostomy
Probiotics
Ileoanal anastomosis (J-pouch) - colon
Anti-diarrheal - take PO before meals
and rectum removed - pouch attached to
No NSAIDS! Cause flare-ups
ileum - no ileostomy needed
Diet:
Goal is to avoid flare-ups (individual to
each person)
May cause flare-ups:
High fiber foods
Hard to digest foods (nuts, seeds)
Typical allergen foods (i.e. dairy,
wheat)
Preferred diet: Low fiber and high protein

Differences between Crohn's and UC

Crohn's Ulcerative Colitis
Can affect any part of GI tract mouth → anus Only colon and rectum affected
Can affect entire thickness of bowel wall Affects inner-most lining of LI only
Scattered patches Continuous (starts in rectum)
No cure Colectomy is cure

Similarities between Crohn's and UC

Pt has flare-ups and remission Prescribed diets similar
Cause unknown Prescribed meds similar
↑ risk of colon cancer
 lOMoARcPSD|22650627

Diverticul -osis and -itis

Two types of diverticular disease: a condition where small sacs called diverticula form in
the intestine (usually the wall of the large intestine).

Diverticula are created when the thin inner layer Large Intestine
of the bowel bulges out through a defect in the
middle layer. May be caused by spasms of the
muscular layer of the intestine. Found most
often in the sigmoid colon.

Diverticulosis: Presence of 1 or more diverticula

Diverticulitis: When diverticula become inflamed
(with or without infection)

Diverticulosis
Cause Diagnosis
**Exact cause unknown**
Possibly: Low-fiber diet, sedentary lifestyle, obesity, smoking, Colonoscopy
certain drugs (NSAIDs), constipation/straining during bowel CT scan

movements; risk increases with age

Signs and Symptoms

Usually asymptomatic
Intervention
Sometimes: None if symptom-free
Painful cramps Diet changes if symptoms present:
Sudden High-fiber diet (Fruits/vegetables/whole grains)
constipation/diarrhea Adequate fluids for fiber
Abdominal bloating May need daily fiber supplement (psyllium)
Treat bleeding that does not stop on own
Complications Colonoscopy to coagulate
Angiography
Diverticulitis Surgery to remove part of LI (rare)
GI Bleed
Bowel obstruction
Fistula
 lOMoARcPSD|22650627

Diverticulitis
Cause
Diagnosis
**Exact cause unknown**
Colonoscopy
Possibly:
→
Stool stuck in diverticulum infection
CT scan
MRI (pregnant or
Pressure from straining during bowel movement tears the young)
diverticulum leading to inflammation

Signs and Symptoms

Complications
Pain/tender (LLQ)
Fistula - When inflamed diverticulum touches another
Fever
organ
Nausea/vomiting
Abscess - Pocket of pus around diverticulum
Abdominal bloating
Peritonitis - Infection of the abdominal cavity, which
Cramps
develops if wall of diverticulum ruptures
Constipation
Obstruction - due to inflammation and scarring of tissue
Bloody stool

Intervention
Risk Factors
Mild case:
Over age 40 Liquid diet, rest
Corticosteroid After a few days, ↓ fiber diet, then once
use recovered, ↑ fiber diet (same as diverticulosis)
HIV + Severe case:
Chemotherapy IV fluids/ABx/TPN
Bed rest
NPO
Then clear liquids, then ↓ fiber diet until recovered
and then ↑ fiber diet (same as diverticulosis)
Drain abscess if necessary
Surgery rarely: partial colectomy
 lOMoARcPSD|22650627

Celiac Disease
A hereditary autoimmune disorder involving intolerance to gluten. The intolerance causes
damage to the lining of the small intestine, resulting in malabsorption.

Gluten is a protein found in wheat, barley and rye. It is comprised of

gliadin and glutenin. In celiac disease, gliadin is seen as a foreign -AKA -
invader (like a bacteria or virus) because it cannot be broken down Gluten Enteropathy
properly.

Cause Villi are finger-like

Gluten stimulates the immune system to produce certain projections along the
antibodies which damage the lining of the small intestine (mostly lining of the SI that aid
the jejunum). This flattens the villi that line the SI. These villi are in the absorption of
necessary for absorption so malabsorption results. nutrients

Normal Flattened
VIlli VIlli

Signs and Symptoms Develops in children OR adults

Adults: Children:
May or may not have digestive Upset stomach
symptoms Abdominal bloating
Weak Steatorrhea
No appetite Failure to thrive
Diarrhea/oily or greasy stool Weak, pale, listless
Mild wt loss Short stature
Anemia Anemia
Mouth sores/inflamed tongue Edema (due to ↓ protein)
Osteoporosis/osteopenia Nerve damage ( due to
Dermatitis herpetiformis (rash malabsorption of B12)
with blisters) Broken bones, tooth discoloration
Lactose intolerance (due to ↓ calcium absorption)
 lOMoARcPSD|22650627

Celiac Disease
Intervention
Diagnosis
May need test for vit deficiencies If gluten-free diet does not
Blood test to Vit/Min supps such as folate & Fe cure symptoms, pt may have
measure If severe in children, may need refractory celiac disease
antibodies IV feeding at first which is then treated with
Biopsy of SI to Strict gluten-free diet for life corticosteroids (such as
check villi Encourage to join Celiac Support prednisone)
Group

Celiac Diet
Avoid: Encourage:
Wheat
Choose WHOLE FOODS over
Barley
PROCESSED FOODS
Rye
Meats
Malt
Rice, corn, soy, millet, quinoa,
Triticale
tapioca, chia, buckwheat
Beer
Vegetables and fruits
Pasta (made from wheat)
Nuts, beans, legumes
Most seasonings
Dairy (if pt is not lactose
All breads not gluten-free
intolerant)
Many processed foods
Eggs
Breadings, coatings
Fish/seafood
Soups, dressings

Look for 'Gluten-free'

on the label!
If it does not have it,
avoid it!

Always check the label

for hidden ingredients
that may contain
gluten.
 lOMoARcPSD|22650627

Hepatitis
Inflammation of the liver
Can be either ACUTE: lasting < 6 months or CHRONIC: lasting > 6 months

The Liver
Functions
Makes about 1/2 the body's cholesterol
Cholesterol is used to make bile (aids in digestion)
LARGEST ORGAN IN
Cholesterol also used to make many hormones BODY NEXT TO
Makes clotting factors and albumin (to maintain fluid pressure in SKIN
the bloodstream)
Stores sugar as glycogen and releases it into bloodstream as
VERY COMPLEX
needed
Breaks down harmful substances and secretes them
AND IMPORTANT!!
Metabolizes drugs
Produces immune factor proteins and eliminates bacteria from MANY
blood
FUNCTIONS
Turns ammonia (from breakdown of proteins) into urea via urine
Breaks down RBCs into bilirubin which is excreted via stool
(gives it brown color)

Hepatic
Liver
vein Receives blood via the portal vein (oxygen-
poor, rich in nutrients, filtered in liver)
Portal and the hepatic artery (oxygenated blood
vein from heart). Blood leaves liver via the
Gallbladder
Hepatic hepatic vein.
artery

Causes
of Hepatitis Most cases of acute
AKA: Viral Hepatitis
hepatitis are caused
Virus - A, B, C, D, or E When a virus attacks the by a virus and
**Main cause** cells of the liver causing resolve on their own,
Excessive alcohol intake them to malfunction but some progress to
Nonalcoholic fatty liver chronic
disease
Certain drugs
 lOMoARcPSD|22650627

Hepatitis A
Transmitted
Most common cause of acute viral
Via contaminated food or water by the hepatitis.
stool of an infected person
→
(fecal oral route)
Acute infection only!

Signs and Symptoms- for ALL types of Hepatitis

May be asymptomatic at first
Jaundice, itchy skin When liver does not filter bilirubin out of
Whites of eyes turn yellow blood, it builds up in blood and deposits in
Nausea/vomiting skin (jaundice) and whites of eyes.
Stomach pain (URQ) Bilirubin is normally secreted in intestine
No appetite
and excreted in stool. Instead, with
Fever
General ill feeling Hepatitis, it is eliminated in the urine.
Dark urine Hence, pale stool and dark urine.
Clay-colored stool

Diagnosis Treatment
Pt may be
Blood test to check for: contagious 2 weeks Rest
anti-HAV before s/s appear Supportive care
IgM (active) Avoid alcohol until
and 1-3 weeks after
IgG (recovered, has healed
they appear Cholestyramine for
immunity)
itching
Recovery usually
Prevention complete

Handwashing - especially after

using bathroom, after changing
diaper, and before handling food
Vaccine Vaccines available
Immune globin (IG) if came in for Hepatitis A and
contact with virus (contains Hepatitis B only!
antibodies)
Avoid water supply in developing
countries
 lOMoARcPSD|22650627

Hepatitis B
Transmitted
Via blood and body fluids Second most common cause of
IV drug use (sharing needles) acute viral hepatitis.
Reusing needles to apply tattoos
Sexual contact
Acute and chronic infections!
Birth if mom is Hep B+

Signs and Symptoms Diagnosis

See s/s for Hepatitis A, plus: Blood test to check for:
HBsAg (shows infectious)
Joint pain
Anti-HBs (pt recovered and immune)
Itchy red hives on skin (wheals)

Chance of developing
~ 5-10% of people with If Hep B becomes
chronic after acute:
acute Hep B develop chronic, severe
chronic. The younger Infants 90% scarring of liver
the person the higher Children 1-5 yrs (cirrhosis), liver
the chance of old 25-50% failure or cancer can
developing chronic. Adults 5% develop.

Treatment Prevention
Acute: Avoid sharing needles
Rest Avoid multiple sex partners
Supportive care Pregnant mothers tested
Avoid alcohol until Vaccine
healed Those exposed but not vaccinated
Cholestyramine for should receive Hep B immune
itching globulin
Chronic:
Antiviral meds
Liver transplant if
severe
 lOMoARcPSD|22650627

Hepatitis C
Transmitted
Acute and chronic infections!
Via blood and body fluids
IV drug use (sharing needles)
**Most common
Reusing needles to apply tattoos Signs and Symptoms
Sexual contact Often asymptomatic. If symptoms
Long-term dialysis present, see s/s for Hepatitis A

Diagnosis Having the antibody to Hep C

Blood test to check for: does NOT protect from
Antibodies to Hep C getting it again (unlike A & B)

Chronic Hep C is
75% of people
usually MILD but There is no
with acute Hep C
may develop vaccine for
develop chronic
cirrhosis or liver Hep C!
Hep C.
cancer over time.

Treatment Prevention
Antiviral meds
Avoid sharing needles
Avoid alcohol until
Avoid multiple sex partners
healed
Blood and organ donor screening
 lOMoARcPSD|22650627

Hepatitis D
Transmitted Acute and chronic infections!
Via blood and body fluids Very rare in the U. S.
IV drug use (sharing needles)
Reusing needles to apply tattoos
Only affects a person who already has
Sexual contact
Hepatitis B! Hepatitis D is an
Signs and Symptoms incomplete virus and needs Hepatitis
B to reproduce.
See s/s for Hepatitis A.
Makes current symptoms of
Hepatitis B more severe! Prevention
Diagnosis Treatment Avoid sharing needles
Avoid multiple sex partners
Blood test to check for: Antiviral meds Vaccine for Hep B (no vaccine for
HDAg Interferon alfa Hep D or post-exposure IG)
anti-HDV Avoid alcohol until
healed

Hepatitis E
Transmitted Almost all acute infections.
Via contaminated food or water by the Chronic infections rarely with
stool of an infected person immunosuppressed people.
→
(fecal oral route)

Can cause severe symptoms,

Signs and Symptoms especially in pregnant women.
See s/s for Hepatitis A.

Prevention
Diagnosis Treatment
Handwashing - especially after
Rest
Blood test to check for: using bathroom, after changing
Supportive care
anti-HEV diaper, and before handling food
No alcohol until healed
No vaccine in the U. S.
Ribavirin for chronic
 lOMoARcPSD|22650627

Cirrhosis
Disease of the liver where healthy liver tissue is replaced with scar tissue due to repeated
or continuous damage. The damage and scar tissue are permanent.

The liver performs many important

The liver consists of 2 main lobes.
functions in the body. In cirrhosis, the
Within these lobes are thousands of
liver is not able to perform these
lobules. Within the lobules are
functions and the whole body suffers.
hepatocytes and Kupffer cells.
Hepatocytes- make up 80% of
Healthy Liver
liver's mass and do most of the
metabolic, endocrine and secretory
functions
Kupffer cells- macrophages that
remove bacteria, debris, parasites Cirrhosis Liver
and old RBCs

The liver receives blood via the

portal vein (oxygen-poor, rich in
nutrients, filtered in liver) and the
hepatic artery (oxygenated blood
from heart). Blood leaves liver via
the hepatic vein.
Causes of Cirrhosis
Chronic alcohol use (one of most
common)
Hepatic Chronic Hep C or B (one of most
Liver
vein common)
Fatty liver (nonalcoholic): obesity,
Portal diabetes, hyperlipidemia
vein Any disorder, drug or toxin that
Gallbladder causes fibrosis (e.g. autoimmune)
Hepatic
artery Bile duct problems: bile remains in
liver and damages cells
 lOMoARcPSD|22650627

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, ↓ platelets, ↓ WBCs
musty smell to breath (buildup of Edema - legs
toxins) Varices

Impaired Liver Function Complication

Detoxification (break down and Toxins accumulate in bloodstream, side
secretion of harmful substances): ↑
effects of meds , alcohol not excreted as
well, estrogen not metabolized
RBC breakdown into bilirubin to
Leaks into blood then skin/eyes- Jaundice
excrete in stool:

Makes cholesterol (used to make ↓ fat absorption and digestion is affected

bile to aid digestion):

Turns ammonia (from

Neuro changes, asterixis, hepatic
breakdown of protein) into urea
encephalopathy
excreted via urine:
Blood glucose levels may be high as excess
Stores excess sugar as glycogen is not turned to glycogen OR blood glucose
and releases as BG level :↓ levels may be low as liver not able to
release stored glycogen as needed.

Produces blood clotting Fluid pressure interrupted, clotting

factors and albumin: problems
 lOMoARcPSD|22650627

Cirrhosis
Complications

Portal Hypertension - Portal vein narrows due to scar tissue → ↓

blood flow to liver → ↑ pressure in portal vein
Most serious complication
Leads to enlarged spleen (splenomegaly)
Spleen cannot release platelets and WBCs → ↓ platelet and
WBC count
Leads to esophageal/gastric/rectal varices
Increase pressure in veins may rupture and may be 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
 lOMoARcPSD|22650627

Cirrhosis
Treatment
No cure
Treat cause
Stopping alcohol use, drugs, etc
Hepatitis - give antivirals
Transplant
Treat complications:
↓ fluids/diuretics
Vit supps
Beta blockers (to ↓ BP in liver's blood vessels)
Shunting surgery - blood rerouted to bypass liver
Alleviates ascites
Vit K (help with clotting)
Lactulose (↓ ammonia level)
Paracentesis (remove fluid from abdomen)

Intervention
Monitor:
Bleeding (PT/INR)
Vomiting/coughing blood (for esophageal varices)
Mental status - irritable, confused, asterixis
BG levels
I/Os, daily wt, swelling, ascites
Diet:
If neuro problems → ↓ protein
If not, ↑ lean protein (no raw seafood - bacteria)
No ETOH
Restrict fluids
Vits/lactulose per MD orders
 lOMoARcPSD|22650627

Pancreatitis
Inflammation of the pancreas that occurs when the pancreatic digestive enzymes start
digesting the pancreas itself. Can be either ACUTE: lasts up to a few weeks or CHRONIC:
persists and destroys pancreatic function

Pancreas
Leaf-shaped organ located behind the lower part of the stomach and duodenum. Has 2 types
of tissue: Pancreatic acini and Islets of Langerhans

Pancreatic acini cells- Produce the digestive enzymes and secrete them into the duodenum
where they are activated. Also secrete large amounts of sodium bicarbonate which
neutralizes acid from the stomach.
The Islets of Langerhans- Produce hormones which are secreted into the blood. The
hormones are:
Insulin - Decreases the level of sugar (glucose) in the blood
Glucagon - Raises the level of sugar in the blood (stimulates liver to
release its stores)
Somatostatin - Stops the release of insulin and glucagon

Stomach
3 Digestive Enzymes:
Liver
Amylase-digests
carbohydrates
Lipase - digests fats
Trypsin - digests protein Gallbladder
**Enzymes not activated until
they reach the duodenum**
Sphincter
of Oddi Pancreatic
Bile sent to pancreas from duct
gallbladder to increase absorption
of fats Duodenum Pancreas
 lOMoARcPSD|22650627

Acute Pancreatitis
The digestive enzymes inside the pancreas are activated and the pancreas begins to
digest itself. Can be reversed with prompt proper treatment.

Causes
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
Slow onset- alcohol
Alcohol use (damaged cells produce
Sitting up and moving forward
thick fluid that clog ducts)- 30% of makes the pain recede
cases N/V, dry heaving
Hereditary Hyperglycemia
Some medications ↓ BP
Viruses Fever
Swelling upper abdomen
Tumor
Sweaty
↑ HR
Diagnosis Shallow, rapid breathing
↑ amylase/lipase
Blood tests - amylase, lipase, WBC, Severe case: (due to
BUN (all ↑) retroperitoneal bleeding)
Imaging - x-ray, CT, ultrasound Cullen's Sign - bluish skin
Urine test - trypsinogen (↑) around belly button
Endoscopic Retrograde Cholangio- Greg-Turner's Sign - bluish
Pancreatography (ERCP)- uses skin around flanks
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 → ↓ BP and damage
to organs such as lungs and kidneys
 lOMoARcPSD|22650627

Intervention - Tx depends on severity

IV fluids Pain meds - NO morphine - will cause
NPO, then liquids, then ↓ fat, soft diet spasm of Sphincter of Oddi
May need tube feed or TPN No supine position
Monitor: PPIs, H2 blockers, antacids (to ↓ acid
BG for hyperglycemia secretion)
WBC, BUN Pancreatic enzymes - give b4 meals
Stools with acidic foods
Daily wts, I/Os Abx (for any infection)
Pseudocyst - drained via endoscope
NG tube - remove fluid and air

Chronic Pancreatitis
Chronic inflammation that has led to Signs and Symptoms
irreversible damage.
Severe upper ab pain (until late, then stops)
Worse after greasy, fatty meals & ETOH
Causes Lessens sitting upright or leaning forward
Heavy alcohol use Pancreatic insufficiency - ↓ amt of dig enz in
(50% cases in U.S.) pancreatic fluid → malabsorption →
Smoking steatorrhea, light colored, oily stool
Wt loss
Cystic fibrosis
Possible mass in abdomen due to pseudocyst
Hereditary Jaundice - due to damaged bile duct
Autoimmune Dark urine
Tumor Signs of diabetes b/c Islet of Langerhans not
working (regulating BG)

Diagnosis Intervention
Imaging - CT, x-ray, ERCP No ETOH
Blood tests - amylase, lipase, BG No smoking
(all ↑) Pain control:
4 or 5 small meals; ↓ fat
Opioids w/antidepressants, SSRIs
Complications Corticosteroids for autoimmune
Pancreatic pseudocyst ERCP - drain duct
Diabetes Pancreatic enzymes w/meals
Pancreatic cancer H2 blockers, PPIs
Fat supps - A, D, E, K
Manage DB
 lOMoARcPSD|22650627

Cholecystitis
Inflammation of the gallbladder usually caused by a gallstone blocking the cystic duct. can
be ACUTE: high intensity, rapid onset or CHRONIC: lower intensity, lasting long time

Gallbladder
Small, pear-shaped storage sac located under the liver that holds bile and is connected to the
liver by ducts. Secretes bile post-meal into duodenum.

Bile: greenish, yellow/brown thick sticky fluid (created by liver). Composed of bile salts,
electrolytes, bile pigments (specifically bilirubin), cholesterol and other fats. Two main
functions:
Aid in digestion of fats - If gallbladder not working we can't digest fats and they exit the
body via stool (steatorrhea/light color)
Eliminate certain waste products - excess cholesterol and Hg (breaks down into bilirubin)
- If gallbladder not working the bilirubin builds up in blood and leaks into skin and eyes
(yellow) and urine (dark)

Liver
Bile flows out of liver via Right Hepatic
hepatic ducts which connect Duct
with cystic duct to form Left Hepatic
common bile duct. From there Gallbladder Duct
it enters SI at the Sphincter of
Oddi.
Stomach
Cystic
Duct
Gallbladder not necessary for
body to function. If removed, the Common Bile
bile will move directly from liver Duodenum Duct
Sphincter of
to SI.
Oddi

Gallstones: Hard masses made of cholesterol. May form in gallbladder or bile ducts.
Usually no symptoms unless they block bile flow out of gallbladder.
Cause not completely known.
 lOMoARcPSD|22650627

Acute and Chronic Cholecystitis

Cause Risk Factors Complications

ACUTE: Almost always gallstones Women Abscess
blocking the cystic duct. Bile then Obese Perforation
becomes trapped in the gallbladder > 60 yrs Pancreatitis
Pregnant
causing irritation and pressure that
Estrogen replacement
leads to inflammation. therapy Diagnosis
CHRONIC: Gallstones and Birth control
Ultrasound
prior attacks of acute. Gallbladder Large wt loss
CT
may become thick-walled, scarred ↑ fat diet
HIDA scan
and small.

Signs and Symptoms

Acute Acalculous
Severe upper ab pain radiating to right
Rare form of acute cholecystitis shoulder blade (Chronic less severe)
without gallstones. VERY serious. Peaks after 15-60 minutes and remains
Bile becomes very thick, gallbladder constant
not contracting. Occurs in very ill Breathing deeply worsens pain
patients (usually already in (+ Murphy's sign)
N/V
hospital): Mech. vent, sepsis, severe
Fever (Chronic no fever)
burns or trauma, prolonged TPN. Chills
May be overlooked: Look for fever Elderly - no appetite, tired, weak, vomiting
and swollen, tender abdomen. Jaundice
Steatorrhea, dark urine, light stools

Intervention - Hospitalization for both acute and chronic

NPO, recover → clear liquids, adv as tol per Most will need surgery (Cholecystectomy)-
MD order Bile will then drain from liver via bile duct
IV fluids/electrolytes/ABx into duodenum
GI suction Laparoscopic procedure
Analgesics / antremics Monitor for infection
ERCP to remove gallstones Ambulate post-procedure
If not candidate for surgery - Encourage deep breathing
Cholecystostomy - C-tube to remove bile T-tube (drains excessive bile)
Maintain at waist level Keep upright in Semi-Fowler's
Record drainage; monitor color position; monitor drainage
Flush per MD order only MD order to flush and clamp (to allow
bile into SI)
 lOMoARcPSD|22650627

Appendicitis
Inflammation of the appendix

Appendix
Finger-shaped tube connected to the large intestine at the end of the ascending colon
Not an essential organ. May play a role in immune function or maintaining healthy flora in
the GI tract
Over 5% of population in U.S. develops appendicitis at some point in their lives (usually in
adolescence or 20s)
In women, appendicitis may cause ovaries and fallopian tubes to become infected which
could cause scarring and infertility

Cause Transverse
Not 100% known. Most likely:
Blockage/obstruction Ascending
Descending
From hard, small piece of Cecum (rt)
(lt)
stool (fecalith)
Foreign body Sigmoid
Worms (rare) Appendix Rectum
Swollen lymph nodes Anus
Trauma
Pathophysiology
Diagnosis Blockage causes:
Build up of mucous, fluids,
Imaging test:
CT bacteria →
Ultrasound Increased pressure →
Laparoscopy Venous obstruction →
Blood test Occlusion of blood flow →
↑ WBCs
Stagnant blood coagulation →
Clot formation →
Treatment is surgery!
Ischemia →
Break down of walls →
Open or laparoscopic. Leak contents into ab. cavity →
Abscess and peritonitis
 lOMoARcPSD|22650627

Signs and Symptoms

Pain upper abdomen around navel
N/V Watch for:
Pain moves after ~1-2 hours to rt lower
part of abdomen **Pain lessening for several hours**
Worst pain at McBurney's point
Rebound tenderness: press and release → Appendix may have burst!
pain WORSE
Peritonitis will occur and then pain
Fever
Fetal position feels best and fever severe: may lead to shock
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 Bowel sounds
Pain lessens for several hrs, then Maintain drain if have one
intense pain and fever Keep pt on right side
Signs of peritonitis Ambulate
↑ HR, resp, temp, pain Encourage coughing/deep breathing
Pain relief IV abx/pain relief per MD order
Avoid: heat, enemas, laxatives (↑ risk of NG tube (NPO until removed)
rupture) Diet: clears → full liquid → solids as tol
 lOMoARcPSD|22650627

Hematologic Disorders
Components of Blood

Plasma White Blood Cells

Liquid component of blood AKA leukocytes
Where RBCs, WBCs and platelets are Fewer than RBCs
suspended Defend against infection
When low called leukopenia
Red Blood Cells Infections more likely
When high called leukocytosis
AKA erythrocytes
May indicate underlying
40% of blood volume
disorder
Contain hemoglobin
Gives blood red color
Helps to carry oxygen to tissues Platelets
Carry C02 from tissues to lungs AKA thrombocytes
When low called anemia Help in clotting process
Low oxygen → fatigue When low called thrombocytopenia
When high called erythrocytosis Bruising and abnormal bleeding
Blood thickens When high called thrombocythemia
Clot risk increases Blood clotting may cause
↑ risk of stroke and MI transient ischemic attack

Normal Lab Values Thrombocytopenia PLT <150,000

WBC: 4,500-11,000 Pathology: ↓ platelets → ↓ clotting → bruising and
RBCs: 4.5-5.5 abnormal bleeding
PLT: 150,000-450,000
Hgb: Causes: Anemia Toxins
Leukemia Cirrhosis
Female: 12-16 g/dL
Platelet disorders Infections
Male: 13-18 g/dL
Enlarged spleen RBC transfusions
Hct:
Female: 36-48% Signs: Treatment:
Male: 39-54% Prolonged bleeding time Treat cause
PT: 10-13 seconds Petechiae on lower legs No aspirin
PTT: 25-35 seconds Purpura (bruising) Avoid injury
aPTT: 30-40 seconds Bleeding gums Use electric razors
INR: Blood in stool/urine Possible:
NOT on warfarin: Heavy menstrual cycles Platelet transfusion
<1 sec ↑ INR, ↑ PT/PTT BMT
ON warfarin: 2-3 sec
MCV: 80-100 fL
 lOMoARcPSD|22650627

Anemia Condition is which the number of RBCs is Vitamin B12 Deficiency Anemia
low. Blood cannot get enough oxygen!
Pathology: Signs:
Most ↓ levels of B12 Weak, pale
Iron-Deficiency Anemia Common
Anemia Causes: SOB
Gastric Bypass Nerve malfunction
Pathology: Diagnosis: PPI use Tingling
Low or depleted Blood test: ↓ Fe, Alcohol Loss of sensation
iron stores ↓ Hct, ↓ Hgb Low dietary intake Muscle weakness
(needed to Treatment: (esp. vegans)
produce RBCs)
Stop bleeding Treatment:
Diagnosis: B12 injection/nose spray/tablet
Iron supplements Blood test:
Causes: Usually PO, large High-B12 foods (eggs, chicken,
↓ B12,
Excessive bleeding amounts by IV red meat, milk)
MCV>100
(GI tract, menstrual) Side effects: stool
Inadequate dietary dark, constipation Folate Deficiency Anemia
intake Take 30 min b4
Decreased Fe absorption breakfast with Vit C Pathology: Signs:
Iron-rich foods: ↓ levels of folate Pale
Signs: Egg yolks Causes: SOB
Weak Spinach Dizzy
Alcoholism
Shortness of breath Red meat Irritable
Malabsorption
Pale Beans Weight loss
Chrohn's/Celiac
Fatigue Seafood Pregnancy
Pica Raisins/apricots Treatment:
Diagnosis: Folate tablet PO
Blood test: High-folate foods
Aplastic Anemia ↓ folate, (oranges, peanuts, lentils,
MCV>100 leafy greens)
Pathology: Signs:
Damage to bone
marrow cells
Fatigue Sickle Cell Disease
Weakness Pathology:
causes bone
Paleness Inherited genetic abnormality of
marrow failure
Hgb → sickle-shaped RBCs
Causes: Treatment:
Signs:
Autoimmune Stem cell transplant
Chronic anemia
Infection Transfusion
Jaundice
Toxins Meds to help
Fatigue/weakness
Chemo tx regenerate bone Diagnosis:
Pain on exertion
Pregnancy marrow Blood test-
Hepatitis electrophoresis
Treatment:
Blood test (↓RBCs,
Stem cell transplant
Diagnosis: ↓WBCs, ↓PLT)
Oxygen therapy
Bone marrow exam
 lOMoARcPSD|22650627

Musculoskeletal System
Purpose: To protect body organs, provide support and stability for the
body and allow coordinated movement

Key Definitions
Bone Bone
Function: support, protect internal organs,
voluntary movement, blood cell production and
mineral storage
Ligament
Muscle
Classified as cortical (compact and dense) or
cancellous (spongy)
Cartilage
Bone Cells Bursa
Osteoblasts - synthesize collagen; the basic bone-
forming cells
Tendon
Osteocytes - mature bone cells
Bone
Osteoclasts - assist in the breakdown of bone
tissue

Joints Cartilage
Place where the ends of 2 bones are in proximity Flexible tissue that is the main connective tissue
and move in relation to each other in body
3 types:
Muscle Hyaline - most common; contains mostly
3 types:
collagen fibers
Cardiac - involuntary; in heart only
Elastic - more flexible; contains collagen and
Smooth - involuntary; found in airways,
elastic fibers
arteries, GI tract, urinary bladder, uterus
Fibrous - tough, shock absorber; contains
Skeletal - voluntary; half of body's weight,
mostly collagen fibers
requires neuronal stimulation to contract
Contractions: Ligaments
Isometric - Increased tension within muscle Dense connective tissue connecting bones to
but no movement bones
Isotonic - Shortens muscle and produces
movement Tendons
Flexion: bending a joint Dense connective tissue connecting muscles to
Extension - straightening a joint bones

Fascia Bursae
Layers of connective tissue that surround muscles, Small sacs of connective tissue filled with synovial
nerves, blood vessels, organs and holds them in fluid; located in joints to decrease pressure &
place friction
 lOMoARcPSD|22650627

Musculoskeletal Assessment
Muscle Strength Scale Assess
Range of motion
0 = No muscle contraction
Goniometer - measures ROM of joint
1 = A barely detectable contraction
Muscle strength
2 = Active movement of body part without gravity
Look for normal spinal curvatures
3 = Active movement of body part against gravity
Asymmetry
4 = Active movement of body part against gravity
Joint swelling / tenderness
and some resistance
Look for abnormalities
5 = Active movement of body part against full
resistance without evident fatigue
↓
Atrophy - size/strength of muscle
Ankylosis - Stiffness and fixation of joint
Kyphosis - exaggerated thoracic curvature
Swayback - exaggerated lumbar curvature
Older Adults
Inquire about exercise practices; type and Scoliosis - asymmetric elevation of shoulders
frequency
Determine age-related changes of
musculoskeletal system on functional status (ADL,
Older Adults - instruct
etc) Use ramps in buildings and at street corners
↑ ↓
risk of falls due to muscle mass and instead of steps
strength and changes in patient's balance Eliminate scatter rugs at home
Bone resorption increases and bone formation Use a walker or cane
decreases with age which leads to osteopenia and Avoid excessive weight gain
osteoporosis Get regular and frequent exercise
30% of muscle mass lost by age 70 Use shoes with good support
Tendons and ligaments less flexible with leads to Avoid walking on uneven ground and wet floors
rigid movement Avoid sudden change in position to prevent
Joints often have osteoarthritis dizziness, falls, etc

R est → To prevent further injury

I ce → To reduce inflammation and pain

C ompression → To prevent edema and encourage

fluid return

E levation → To mobilize excess fluid and prevent

further edema
 lOMoARcPSD|22650627

Musculoskeletal Trauma
Soft tissue injury - damage to any skin, muscle, tendon or ligament
Sprains and Strains Dislocation
Sprain - an injury to ligaments surrounding a Complete displacement of the joint
joint usually caused by wrenching or twisting Results from severe injury of the ligaments
motion in ankle, wrist or knee joint surrounding the joint
Strain - excessive stretching of a muscle, its Usually in thumb, elbow, shoulder, hip, kneecap
facial sheath or a tendon Subluxation - partial displacement of the joint
↓
S/S of strain or sprain: pain, edema, fnx in S/S - deformity, local pain, tenderness, loss of
injured area, contusion; usually occur during fnx of injured area, swelling near joint
vigorous activities Tx: requires prompt attention; orthopedic
↓
Tx: RICE to local inflammation & pain; ice & emergency b/c may include vascular injury;
elevate 24-48 hrs post injury; full function realignment 1st action, then immobilize to allow
returns in 3-6 weeks to heal

Repetitive Strain Injury Carpal Tunnel Syndrome

Injuries resulting from prolonged force or Caused by compression of the median nerve in
repetitive movements and awkward postures the wrist
Tendons, ligaments and muscles are strained May be caused by hormones - often occurs
causing tiny tears that become inflamed during PMS, pregnancy, menopause
At risk: musicians, dancers, those who use At risk: those with DB, PVD, rheum arthritis
mouse/keyboard often, competitive athletes S/S: weakness, pain, numbness, impaired
S/S: pain, weakness, numbness sensation in thumb, index and middle fingers
Tx: stop activity causing RSI, heat/cold, NSAIDs, Tx: stop repetitive motions, fix ergonomics,
rest, PT splint, PT, corticosteroids, surgery

Rotator Cuff Injury Meniscus Injury

Rotator cuff = 4 muscles in the shoulder Menisci - cartilage in the knee, AC and other
May be gradual, degenerative process or from joints
injury while falling Usually caused by rotational stress when knee is
Often due to repetitive motions in flexion and foot is planted or fixed
↓
S/S: shoulder weakness, pain and ROM; At risk: athletes (basketball, football, soccer)
positive drop arm test S/S: pain upon flexion, unstable, 'pops' in knee
Tx: rest, ice and heat, NSAIDS, corticosteroids, Tx: ice, immobility, crutches, PT, surgery;
PT, surgery instruct importance of warming up b4 exercise

Anterior Cruciate Ligament (ACL) Injury Bursitis

Most commonly injured knee ligament Inflammation of the bursa from repeated or
Usually occurs in athletes while pivoting or excessive trauma/ friction, or from gout,
landing from jump rheumatoid arthritis or infection
S/S: hear 'pop,' then pain, swelling, knee Affects hands, elbows, shoulders, knees, hip
unstable S/S: warmth, pain, swelling, limited ROM in
Tx: rest, ice, NSAIDs, elevate, crutches, knee affected part
brace, PT, surgery; full recovery 6-8 months Tx: rest, splint, ice, NSAIDs, corticosteroids
 lOMoARcPSD|22650627

Fracture
A break or crack in a bone caused by traumatic injury or disease such as cancer
or osteoporosis
Classifications
Open (Compound) or Closed (Simple)
Open - Skin broken, bone exposed, soft tissue injury
Closed - Skin remains intact Oblique
Complete or Incomplete
Complete - Break goes completely through the bone
Incomplete - fracture goes partly across bone shaft
Comminuted
Displaced or Nondisplaced
Transverse
Displaced - 2 ends of broken bone separated and out
of alignment
Comminuted - 3 or more fragments
Oblique - fractured at a slant
Nondisplaced - bone fragments aligned Spiral
Transverse - fracture straight across bone
Spiral - fracture in spiral direction down bone
Greenstick - one side of bone bent, other side Greenstick
splintered; incomplete; common in pediatrics

Types of Fractures
Colles' fracture - in distal radius (forearm); most common; > 50 years old; risk w/osteoporosis
Humeral shaft - shaft of humerus (long bone in arm); common among young and middle-aged
Pelvic fracture - small percentage; associated with mortality rate ↑
Hip - common in older adults; > 95% resulting from fall
Stable vertebral fracture - car crashes, falls; fragments unlikely to cause spinal cord damage

Signs and Symptoms

Immediate, localized pain, tenderness Deformity (abnormal position)
↓ function in affected part Contusion/bruising
Unable to bear weight on affected part Crepitation - grating or crunching of bone
Edema and swelling fragments; audible sounds
 lOMoARcPSD|22650627

Treatment
Goal: Traction
Realign bone fragments (via closed or Aligns the bone with a constant steady
open reduction) pulling action
Immobilize to maintain realignment Electrical Bone Growth Stimulation
Restoration of normal function To facilitate the healing process
Closed reduction Increases Ca uptake of bone, activates
Nonsurgical, manual realignment intracellular Ca stores, increases
Under local or general anesthesia production of bone growth factors
Traction, cast, splint, or brace used after Electrodes in band applied to skin 10-12
Open reduction hrs/day (sleeping)
Correction of alignment through surgery Meds
Wires, screws, pins, plates internal or Muscle relaxants - Soma, Robaxin
external Tetanus shot if open fracture
Traction, cast, splint, or brace used after Bone-penetrating Abx (Kefzol)
Facilitates early ambulation Nutrition
Protein 1g/kg BW
Vits B, C, D; Ca, Ph, Mg

Intervention
Immediately after injury - immobilize Traction -
w/splint Wts need to hang freely (not on floor)
Apply pressure w/sterile dressing if open Monitor pin sites for infection
Elevate extremity Encourage pt to participate in ROM
↓
Apply ice to swelling activities (as allowed)
NPO until evaluated by surgeon Casts
X-ray Keep elevated above heart level
Pain meds - monitor to see if pain relieved 1st 2 days ice packs
Monitor for: Monitor for hot spots, pain, foul odor,
Compartment syndrome (see next page) swelling, 6 Ps
Fat embolism (see next page) Monitor skin integrity - use moleskin
Asses 6 Ps (see next page) around top edge of cast
Prep for surgery if needed Keep dry!
Post op:
Monitor vitals and Assess 6 Ps
Watch dressing for bleeding or excessive
drainage
 lOMoARcPSD|22650627

Complications of Fractures
Infection -
↑
Open fractures and soft tissue injuries have incidence of infection
May require aggressive surgical debridement
May have IV Abx 3-7 days post op phase
Compartment syndrome -
↑
Swelling causes pressure within muscle compartment
Fascia surrounding muscle has limited ability to stretch
Continued swelling decreases function of blood vessels and nerves and decreases blood
flow to muscle
2 causes:
Decreased compartment size from restrictive dressings, splints, casts, traction
Increased compartment contents from bleeding, inflammation, edema
Usually associated with:
Trauma, large bone fractures, extensive tissue damage and crush injury
MUST be treated within 6 hours or nerve damage will result!
S/S: Look for the 6 Ps:
Pain - out of proportion to injury and not managed with meds -- early sign!
Paresthesia - numbness/tingling -- early sign!
Poikilothermia - affected limb cooler than non-affected limb
Pallor - coolness, loss of normal color in distal extremity
Paralysis - loss of function in extremity; late sign
Pulselessness - decreased or absent peripheral pulse; late sign
Intervention:
Regular neuro assessments on all patients with fractures
Notify HCP of pain and paresthesia as these are the 1st signs!
Keep extremity at heart level and NOT below
Monitor UO: look for dark reddish-brown color, may be from damaged muscles
Fat Embolism Syndrome -
Systemic fat globules from fractures travel to tissues, lungs and other organs after a
traumatic skeletal injury
Usually seen with long bone, rib, tibia, pelvis fractures
Need to recognize early on!
Usually occurs 24-48 hours post injury
↓
S/S: chest pain, tachypnea, cyanosis, dyspnea, tachycardia, PaO2, changes in mental
status, restlessness, confusion, petechiae
Tx: fluid resuscitation, correct acidosis, blood transfusion
Intervention: Encourage coughs/deep breathing, O2 for hypoxia
 lOMoARcPSD|22650627

Osteoarthritis
Progressive joint disorder that develops due to the deterioration of
articular cartilage.
AKA Degenerative Arthritis and Degenerative Joint Disease

*Most common type of arthritis*

3 Types of
Pathophysiology Cartilage:
Articular cartilage (hyaline cartilage found in synovial Hyaline - most
joints) begins to deteriorate due to tissue damage common - end of
Normally soft, smooth, white cartilage becomes less bones (joints),
elastic, dull, yellow and granular ribs, nose
→
Joint space decreases bones begin to grate against Fibrous -
→
each other bone erosion follows along with intervertebral
osteophyte (bone spur) formation discs, knee
Pieces of cartilage and bone break off and float Elastic - external
around in the joint space ear, epiglottis

Joint
Capsule Causes / Risk Factors
Synovial A condition damages cartilage
Membrane (gout, rheumatoid arthritis)
Bone
Synovial An event damages cartilage
Fluid or causes joint instability (e.g.
ACL knee injury)
Bone ends
Bone Low estrogen at menopause
Cartilage rub together
Bone
Obesity (increases stress on
joints)
Bone
spur Repetitive motions (e.g.
Healthy Joint
Bone occupations that require
Thinned Broken
frequent kneeling and
cartilage pieces of
cartilage and stooping have high risk of
bone knee OA)
Genetics
Osteoarthritis
 lOMoARcPSD|22650627

NOT a normal part of aging process

Begins between 20 - 30 yrs and the majority of adults affected by age 40. Symptoms
appear after age 50 - 60 yrs
Men affected more than women before age 40
Women affected more than men between 40 -70 yrs, then both the same after 70 yrs

Signs and Symptoms

*Joint pain * - Main sign - gets worse with use
Early stages gets better w/rest
Later stages pain still at rest Diagnosis
Pain leads to disability and loss of function No single test
Early morning stiffness - disappears after 30 Analyze symptoms and rule
minutes out other disorders such as
Crepitation - grating caused by bones rubbing or rheumatoid arthritis and gout
loose cartilage X-ray to see:
Deformity, bone spur formation and tenderness at Dense bone
specific joints Osteophytes
Heberden's Node (joint closest to fingernail) Decreased joint space
Bouchard's Node (joint in middle of finger)
Affects hands, knees, hips and spine
Asymmetrical
Treatment / Intervention
No cure - Focus on managing pain and joint inflammation and maintain/improve joint function
Rest when joints acutely inflamed Exercise - necessary to preserve articular
Use splints/brace if needed during acute cartilage health
inflammation but not longer than 1 week Low-impact (walking, water aerobics),
Knee OA: avoid standing/kneeling/squatting weight training, ROM exercises
for long periods Avoid high-impact
Assistive devices to decrease joint stress Meds
Heat/cold to decrease pain and stiffness Tylenol for mild pain
Ice for acute inflammation Capsaicin cream
Heat best for stiffness Bengay, Arthricare (contain camphor,
Nutrition - educate on weight loss if eucalyptus oil, menthol)
overweight Topical Salicylates (Aspercreme)
Alternative therapies: NSAIDs
Acupuncture, Massage, Tai Chi Intraarticular injections:
Surgery - arthroscopy for knee OA corticosteroids (temp relief 1-2 mos)
 lOMoARcPSD|22650627

Rheumatoid Arthritis
Chronic autoimmune disease that causes inflammation in the joints.

Pathophysiology
Starts with initial immune response to antigen
The antigen triggers formation of an abnormal immunoglobulin G (IgG)
The body reacts with autoantibodies known as rheumatoid factor (RF) which land on
the synovial membranes and cartilage in joints
Inflammation results which triggers release of neutrophils (Stage 1 Synovitis)
→
Proteolytic enzymes released damage to cartilage and thickening of synovial lining
Pannus (layer of vascular fibrous tissue) forms (Stage 2)
Pannus grows and damages bone & cartilage (Stage 3)
Ankylosis develops (fusion of bone) (Stage 4) Cause
Exact cause unknown- most
likely a combination of genetics
Healthy Joint and environmental trigger
Joint (smoking, infection, etc)
Capsule

Synovial Stage 1: Synovitis

Bone Membrane Synovial membrane
Synovial inflamed & fluid
Fluid thickened
Bone & cartilage
Bone Cartilage gradually eroded

Stage 2: Stage 3: Fibrous Stage 4: Bony

Pannus Ankylosis Ankylosis
Pannus forms, Fibrous Bones fused
cartilage connective
eroded, bones tissue
exposed invades joint
 lOMoARcPSD|22650627

Signs and Symptoms

Late stages - Deformity and disability
Occurs at any age, peaking between 30-50 yrs
May spread to other parts of body:
Occurs in women 3x more than men
Cataracts, vision loss
Onset slow, insidious
Pleurisy
Fatigue, anorexia, wt loss, generalized
Pleural effusion
stiffness
Pericarditis
Stiffness becomes localized
Pericardial effusion
Joints become painful, stiff with limited ROM
Cardiomyopathy
Joints soft and inflamed (hot, swollen, tender)
Sjogren's syndrome:
Symmetrical (Bilateral)
dry mouth/eyes
Typically in small bones of hands, wrists, feet
photosensitivity
But may also be in elbows, shoulders, knees,
Felty syndrome:
hips, ankles and jaw
enlarged spleen
Morning stiffness lasting 60+ minutes
Rheumatoid nodules - develop in 50% of pt
↓ WBC count
Depression
Firm masses subcutaneous (usually on
fingers and elbows)
↓ self-care capabilities

Treatment
No cure BRMs (Biologic Response Modifiers) -
Meds (main tx): for moderate to severe cases who do
DMARDs (Disease-modifying antirheumatic not respond to DMARDs
drugs), helps slow disease progression; may Enbrel, Remicade, Humira, Cimzia,
be prescribed more than 1 at a time: Simponi
Methotrexate (Trexall) - Immunosuppressants -
Side effect: bone marrow Azathioprine/cyclosporine (side
suppression; hepatotoxicity (rare); effects: liver dz, infections)
Needs frequent lab monitoring Corticosteroids - Prednisone (oral for
Sulfasalazine (Azulfidine) - May cause a limited time, injection into joint for
neutropenia acute relief)
Hydroxychloroquine (Plaquenil)- may Celebrex, NSAIDs/salicylates
cause vision problems; needs vision Surgery - may be needed to relieve
check-ups regularly severe pain and increase fnx of
Leflunomide (Avava)- teratogenic - severely damaged joints
cannot be pregnant and need adequate Synovectomy - remove joint lining
contraception Arthroplasty - total joint
replacement
 lOMoARcPSD|22650627

Diagnosis
Blood tests to check: Check synovial fluid for:
+RF (Rheumatoid factor) ↑ WBC
ESR (Erythrocyte Sedimentation Rate) MMP-3 (enzyme)
CRP (C-Reactive Protein) X-ray to show joint deterioration (will see
ANA (Antinuclear antibody) titers later in disease process)
Anti-CCP (Antibodies to citrullinated
peptide)

Intervention
Flare-ups Educate:
Inflamed joints - rest and ice On disease; no cure, how to manage
Splints Importance of balanced diet and
Heat for stiffness maintaining healthy weight
Monitor for anemia (pale, fatigued, SOB on Exercise - importance of; as tolerated;
exertion, palpations) low-impact; ROM exercises
May need supplements: Fe, folic acid, Vit Schedule rest and activity so no over-
B12 exertion
Monitor for GI bleed (look for dark, tarry Meds to take and side effects
stool) Importance of follow-up visits

Difference between Osteoarthritis and Rheumatoid Arthritis

Osteoarthritis Rheumatoid Arthritis
Deterioration of articular hyaline cartilage Autoimmune disease that causes
of bones inflammation of the synovium in joints
Non-symmetrical Symmetrical
Hands/knees/hips/spine Fingers/wrists/feet
Not systemic (joints only) Systemic
Cause: Wear and tear/overuse/injury Cause: Unknown
Older adults Any age
No systemic inflammation Systemic inflammation
Osteophytes No osteophytes
AM stiffness < 30 minutes AM Stiffness > 60 minutes
 lOMoARcPSD|22650627

Osteoporosis
Chronic, progressive bone disease characterized by decreased bone mass
and deterioration of bone tissue, leading to increased bone fragility
Pathophysiology Stages of Osteoporosis
There are 2 types of bone:
Compact: rigid, outer bone
Spongy (cancellous): porous, inner bone
Bones are in a constant state of remodeling
Bone is deposited by osteoblasts (built up) Normal Bone Osteopenia
Bone is resorbed by osteoclasts (broken down)
Usually this remodeling is in a state of equality
In osteoporosis, bone resorption > bone deposition
This inequality causes bone (specifically spongy bone)
to become very porous and thus bone density
Severe
decreases, making the bone weak Osteoporosis
Osteoporosis

Hormones involved in bone health

Parathyroid Hormone - When blood Ca levels are low, the PTH gland secretes PTH.
This causes osteoclasts to break down stores of Ca in the bone and enter the blood.
PTH also increases SI reabsorption of Ca and decreases kidney excretion of Ca.
Calcitonin - When Ca levels are too high, the thyroid creates calcitonin to decrease
the activity of osteoclasts
Growth hormone - Stimulates osteoblasts to build bone
Estrogen - keeps bones strong by preventing bone resorption by the osteoclasts
Testosterone - converts to estrogen and thus helps keep bones strong

Osteoporosis is more common in women

than in men because:
Women consume less calcium
Known as the
Women have less bone mass due to smaller frames 'Silent Thief'
Bone resorption begins earlier in women and because it slowly
becomes more rapid at menopause
steals a person's
Pregnancy and breast feeding deplete a woman's
skeletal reserves (unless Ca intake is adequate) bone health
Women live longer (higher chance of developing it)
 lOMoARcPSD|22650627

Risk Factors
> 65 years old Low intake of Ca and/or Vit D Deficiency
Female (8x more common than men) > 2 alcohol drinks/day
↓ BW (BMI < 19) ↓ testosterone in men
White/Asian ethnicity Long-term use: Corticosteroids (major
Cigarette smoking contributor), thyroid replacement, heparin,
Sedentary lifestyle long-acting sedatives, aluminum-containing
Family history antacids, anticonvulsants (phenobarbital,
Estrogen-deficient (surgical or age- Dilantin, Depakote, Tegretol),
related menopause) glucocorticoids (for > 3 months)

Signs and Symptoms

During menopause
Early sign - pain in back, neck, hip
there is rapid bone or spontaneous fracture
loss when Osteoporosis most common in
estrogen decline is spine, hips, wrists
Loss of height and humped
greatest, then
thoracic spine (kyphosis -
bone loss slows to dowager's hump) - happens over
equal men's loss time from vertebral fracture
and wedging

Diagnosis
Bone mineral density (BMD) test
All women over 65+ yrs should get tested
Diseases associated with
Measured by:
Quantitative ultrasound (QUS) - for Osteoporosis
heel, kneecap, shin Inflammatory Bowel Disease
Dual-energy x-ray absorptiometry Intestinal malabsorption
(DXA) - *Gold standard - for spine, Kidney disease
hips, forearm - (No Ca supplements Rheumatoid arthritis
24 hr before test) Hyperthyroidism
Results listed as T-score and Alcoholism
compared to healthy 30-yr old Cirrhosis of the liver
0 = normal for healthy young adult Hypogonadism
+1 to -1 is normal Diabetes
-1 to -2.5 = osteopenia
-2.5 or lower = osteoporosis
 lOMoARcPSD|22650627

Treatment/Intervention
Treatment focuses on: proper nutrition, calcium supplements, meds, exercise, fall prevention
Loss of bone cannot be significantly reversed but further loss can be prevented
Treatment begins when:
T-score less than -2.5 OR
Fall Prevention
-1 to -2.5 with add'l risk factors OR
History of hip or vertebral fracture Educate patient:
Goal for Ca intake: Rooms clutter-free
1000 mg/day for women 19-50 yrs and men 19-70 yrs Non-slip socks, shoes
1200 mg/day for women 51+ yrs and men 71+ yrs Avoid throw rugs
Assistive devices
Calcium Supplementation
Meds
Ca supps hard to absorb in single doses > 500 mg
↑
Take in divided doses to absorption Biphosphonates -
Ca Carbonate - has 40% elemental Ca Fosamax - Daily or weekly oral tablet
Take w/meals because stomach acid needed to Boniva - once-per-month oral tablet
dissolve and absorb Actonel - daily, weekly, monthly dep on dose
Ca Citrate - has 20% elemental Ca Reclast - once yearly IV infusion to treat
Not dependent on stomach acid to absorb osteoporosis or every 2 yrs for prevention
Better for pt on PPIs or H2 Blockers Main side effect is GI upset:
Ca Lactate and Ca Gluconate NOT recommended Take with full glass of water in morning
Vit D important for Ca absorption and function and on empty stomach with no other meds;
bone formation sit upright for 30-60 min and nothing to
Get it from sun 20+ min/day eat for 1 hr
Supplemental D recommended for post- Rare side effect is osteonecrosis (bone
menopausal women or those homebound, in LTC death) of jaw so pt should be evaluated by
or northern climates dentist before starting meds
Calcitonin - interacts with osteoclasts
IM, subcutaneous, intranasal (alternate
Nutrition
nostrils)
High calcium foods Side effects - nausea, facial flushing, nasal
Milk, cheese Ice cream
dryness
Yogurt Sardines, salmon
Monitor for hypocalcemia
Turnip Greens Spinach
Evista - selective estrogen receptor modulator
Cottage cheese Tofu, almonds
(SERM) - mimics estrogen -
↓ alcohol intake and quit smoking Side effects - leg cramps, hot flashes, blood
clots (monitor for DVT)
Exercise Forteo - form of PTH, increases action of
osteoblasts; for severe osteoporosis
Important for building and maintaining bone
Side effects - leg cramps/dizziness
mass
Prolia - used for postmenopausal women with
Best exercises are weight bearing
osteoporosis who are at a high risk for fractures
Walking, hiking, weight training, tennis, etc
Subcutaneous injection every 6 months
Rec 30 min 3 x/week
 lOMoARcPSD|22650627

Gout
Type of acute arthritis characterized by hyperuricemia and deposits of
uric acid crystals in one or more joints. AKA Gouty Arthritis
Uric acid (UA) is the major end product of purine catabolism; excreted by kidneys via urine
Hyperuricemia - 2 types
Primary - hereditary error of purine metabolism leading to overproduction or retention
of UA
Secondary -
Related to another disorder such as: acidosis/ketosis, diabetes, renal insufficiency,
atherosclerosis
Caused by certain drugs: Thiazide diuretics, B-blockers, ACE inhibitors, niacin,
aspirin, cyclosporine
Gout can be acute or chronic

Risk Factors
Causes Obesity **
Excessive alcohol consumption
Decreased excretion of UA by
kidneys (most common)
↑
Prolonged fasting ( ketoacids
inhibit UA excretion)
Increased in UA production
CKD
High intake of
Metabolic syndrome
foods/beverages containing
Dehydration
purines (small factor)
Physical stress on body
More common in men
Pt on cyclosporine

Diagnosis High Purine Foods/Beverages

Synovial fluid aspiration to look for Red meat
monosodium urate crystals; also helps Organ meats (liver, kidney, sweetbread)
decompress a swollen joint capsule; Beer
* main diagnostic test Shellfish (sardines, herring, mussels)
24-hr urine test to see if disease is from Fructose drinks (fruit juice, soda)
decreased renal excretion or Venison, goose
overproduction of UA Anchovies
 lOMoARcPSD|22650627

Signs and Symptoms

Marked by painful flares lasting days to weeks with long periods of no symptoms
Sharp urate crystals form around the joints causing intense inflammation/pain/redness
Most commonly occurs in BIG toe (podagra), but also affects fingers, elbows, knees, wrists
Cool areas: crystals form more readily in cool areas on the body than warm areas

Acute Chronic
Usually starts in big toe in middle of night Multiple joint involvement
Inflammation Visible deposits of sodium urate crystals
Joints dusky or cyanotic (tophi)
Sudden swelling Tophi - white/yellow nodules under skin;
Severe pain - peaks within several hours appear years after onset
Area sensitive to touch Joints become damaged; cartilage
Random flare-ups, may have 1-2 episodes destruction may lead to secondary OA
and no more Excessive UA excretion may lead to
Attacks end in 2-10 days with or w/o tx kidney or urinary tract stone formation

Treatment
Main treatment: Colchicine (anti- Maintenance meds (to prevent future attacks):
inflammatory agent) within 12-24 hrs Drugs to lower urate level: Allopurinol
of attack (Zyloprim, Aloprim); helps prevent attacks
Usually combined w/NSAIDs Drugs to increase excretion of UA in urine:
NO Aspirin Probenecid
Weight loss if needed Uloric for chronic gout
Avoid alcohol and foods high in purine Krystexxa for those who can't take allopurinol
Corticosteroids or ACTH for acute (given via IV)
attack Serum UA monitored regularly if on meds
Intervention
Acute attack: Hydrate 2-3 L/day
Cold and warm compresses (alternating) Bed rest with cradle or foot board
If on Colchicine: Educate:
Monitor for GI upset, neutropenia (slow Weight loss if needed
wound healing), toxicity (muscle pain, Discuss flare-ups and possible
easy bleeding) contributor
Do not give with grapefruit juice Low-purine diet
If on Allopurinol: Regular assessment of UA levels if on
No vit C Supplements meds
Encourage regular eye exams Avoid fasting
 lOMoARcPSD|22650627

Brain Anatomy & Physiology

The brain is composed of the cerebrum, cerebellum and brainstem
Cerebrum - largest part; split into right and left hemispheres and 4 main lobes;
for higher functions like speech, reasoning, emotions, learning
Cerebellum - coordinates muscle movement, maintains posture and balance
Brainstem - relay center; connects cerebrum and cerebellum to spinal cord;
performs many automatic functions
The central nervous system is composed of the brain and spinal cord
The peripheral nervous system is composed of the spinal nerves and cranial nerves

t rip rip
o r s ry st
Frontal Lobe ot nso
M Se Parietal Lobe
Broca's
Cerebrum
Area Wernicke's
Area
Occipital
Temporal Lobe
Lobe

Cerebellum
Brainstem

The Brain Lobes and Functions

Frontal Lobe Parietal Lobe Temporal Lobe
Behavior/emotions Senses - Hearing
Planning/problem solving touch/pain/temp Memory
Thinking/concentration (Sensory strip) Understanding language
Expressive speech (Broca's Interprets signals - (Wernicke's area) - if damaged,
area) - if damaged, can vision/hearing/motor cannot understand speech and
understand speech but not Interprets languages speaks in sentences with no
speak clearly and words meaning
Body movement (Motor
Occipital Lobe
strip)
Interprets vision - color/light/movement
 lOMoARcPSD|22650627

Left Side vs Right Side Functions

**Nerves in the brain cross over to the other side of the
body. The left side of the brain controls the right side of
the body and vice versa.**

Left Side Functions Right Side Functions

Logical Side Creative Side
"Dominant side" Creativity
Speaking/Language Imagination
Reading Music Awareness
Writing Showing emotions
Math Art awareness
Analysis
Planning

Function of Cranial Nerves I-XII

I - Olfactory - Smell
II - Optic - Sight
III - Oculomotor - eye movement, pupil dilation
IV - Trochlear - vertical eye movement
V - Trigeminal - moves face muscles, face sensations
VI - Abducens - lateral eye movement
VII - Facial - moves face, salivate
VIII - Vestibulocochlear (Auditory) - hearing, balance
IX - Glossopharyngeal - taste, swallowing
X - Vagus - heart rate, digestion, gag reflex
XI - Accessory - head and shoulder movement
XII - Hypoglossal - tongue movement
 lOMoARcPSD|22650627

Blood Supply to the Brain

Cerebral arteries
Blood is supplied to the brain
from the heart via the
internal carotid arteries and
External External the vertebral arteries
carotid carotid These arteries join the Circle
artery artery of Willis where they branch
off into cerebral arteries
Circle of that supply blood to the two
Willis hemispheres
The carotid arteries and
Vertebral Internal carotid vertebral arteries
arteries arteries communicate in the Circle of
Willis. If a vessel becomes
Common carotid artery Common carotid artery blocked, blood from the
other side can be supplied to
prevent brain damage

Neurons
Dendrites
The neuron is the basic
working unit of the brain
that transmits information Cell
to other nerve cells body Nucleus
Comprised of the cell body
(with nucleus), dendrites and
axon (covered by a myelin Direction
of impulse
sheath) Axon
Myelin Sheath
The impulse starts in the
nucleus and travels through
the axon to the axon
terminals
The dendrites receive nerve Axon
impulses from the axon terminals
terminals of other neurons
Neuron
 lOMoARcPSD|22650627

Stroke
Blockage or rupture of an artery in the brain that results in death of
brain cells. AKA Cerebrovascular Accident (CVA)
Cerebral arteries
Blood supply to the brain comes from the
heart through the internal carotid
arteries and the vertebral arteries
External External These arteries branch into the cerebral
carotid carotid arteries that feed the brain
artery artery
Collateral arteries (not shown) are small
Circle of arteries that run between other arteries,
Willis making connections
These collateral arteries can form
Vertebral Internal carotid different pathways for blood when an
arteries arteries
artery becomes blocked.
People with small collateral arteries are
Common carotid artery Common carotid artery more likely to experience a stroke than
those with large collateral arteries.
Blood Supply to the Brain

Types of Stroke
Ischemic Stroke Hemorrhagic Stroke
Ischemic Stroke Hemorrhagic Stroke
80% of all strokes 20% of all strokes
Usually due to a blocked artery Due to bleeding blood vessel in and
(often blocked by a blood clot) around the brain
Brain cells do not receive enough Blood vessel ruptures, blood leaks
oxygen/glucose and can soon die into brain tissue or around the
Causes: brain →↓ blood to brain cells and
Embolism - clot forms in ↑swelling in brain
another part of the body and Causes:
travels to the brain Rupture of brain aneurysm
Thrombosis - clot forms in the Uncontrolled HTN
artery in neck or brain Age of blood vessels

Transient Ischemic Attack (TIA) - AKA Ministroke

Early warning sign of impending stroke
Caused by a brief interruption of the blood supply to part of the brain
Blood supply restored quickly, no tissue dies, brain function returns quickly
 lOMoARcPSD|22650627

Strokes usually damage one side of the brain

Signs, symptoms and effects of strokes will depend on the location of the
stroke
The nerves in the brain cross over to the other side of the body. The left side
of the brain controls the right side of the body and vice versa.

Left Side Effects when stroke Right Side Effects when stroke
Functions on LEFT side of brain Functions on RIGHT side of brain
Logical Side Right side hemiplegia Creative Side Left side hemiplegia
"Dominant side" (paralysis) Creativity (paralysis)
Speaking/Language Trouble forming words Imagination Impulsive
Reading and comprehending Music Awareness Unable to recognize
Writing them Showing emotions people
Math Cautious Art awareness Short attention span
Analysis Aware of deficits Denies problems / ignores
Planning Depressed damaged side (neglect
syndrome)

The Brain Lobes and Functions

Frontal Lobe Parietal Lobe
Behavior/emotions Senses - touch/pain/temp (Sensory strip)
Planning/problem solving Interprets signals - vision/hearing/motor
Thinking/concentration Interprets languages and words
Expressive speech (Broca's
Occipital Lobe
area) - if damaged, can
Interprets vision - color/light/movement
understand speech but not
speak clearly
rip p
Body movement (Motor strip) r st stri
o r y
Frontal Lobe ot nso
M Se Parietal Lobe
Temporal Lobe
Broca's
Hearing Cerebrum
Area Wernicke's
Memory Area
Occipital
Temporal Lobe
Understanding language Lobe
(Wernicke's area) - if damaged,
cannot understand speech and
speaks in sentences with no Cerebellum
Brainstem
meaning
 lOMoARcPSD|22650627

Risk Factors
Conditions that lead to strokes develop over time
95% of strokes are the result of modifiable risk factors
More common among older people and women vs men
Black people 2x more likely to have a stroke than white people
Also higher incidence in Hispanics, Native Americans and Asian Americans
than in white people
Risk factors:
↑BP (single most important factor) Cocaine, amphetamine use

↑ cholesterol Previous stroke

Heredity
Diabetes
Oral contraceptives (when combined
Insulin Resistance
Smoking
↑
with smoking and BP)
Atherosclerosis (ischemic)
Obesity
Blood thinners (hemorrhagic)
Older age
↑ alcohol use
Clotting disorders (ischemic)

↓ physical activity
Afib (ischemic)

↑
Diet - salt, sat fat, trans fat and calories
Cerebral aneurysm (hemorrhagic)

Signs and Symptoms - SUDDEN!!

Will depend on location of blockage or
bleeding: National Stroke Association Signs of
Weakness or paralysis, loss of sensation on a Stroke:
one side of body
Difficulty speaking; slurred speech; -- Face Drooping
confusion
Loss of vision in one eye -- Arm Weakness
Dizziness; problems with coordination
TIA s/s same as above but disappear
-- Speech Difficulty
within minutes to 1 hr.
Hemorrhagic s/s also include:
Severe headache, N/V -- Time to Call 911
Loss of consciousness
↑
Very BP

Call rapid response (or 911 if not in hospital). Record signs/symptoms

and the exact time they occurred.
 lOMoARcPSD|22650627

Effects
Effects of an ischemic stroke are usually greatest immediately after the stroke
With a hemorrhagic stroke effects progress between minutes to hours after
the stroke
Some function may be regained- due to plasticity (healthy areas of brain take
over for damaged areas)
However, many effects remain and a stroke is a lifelong change for the patient
and family
Effects may include:
Motor - most obvious effects
Mobility
Respiratory
Dysphagia - problems swallowing (weak muscles)
Gag reflex
Self-care
Hemiparesis - weakness on one side of the body
Hemiplegia - paralysis on one side of body
Communication
Aphasia - Inability to speak
Receptive - unable to comprehend speech (damage to Wernicke's area)
Expressive - comprehends speech but can't respond (damage to Broca's area)
Global - inability to understand speech and speak
Dysarthria - slurred speech due to weak muscles
Affect - trouble controlling emotions
Intellectual
Memory
Judgment (left-side damage = cautious; right-side damage = impulsive)
Agraphia- loss of ability to write
Alexia - loss of ability to read
Agnosia - does not understand sensations or recognize familiar objects
Spatial-Perceptual alterations
Denies illness, ignores damaged side
Hemianopia - sees only half of visual field in each eye
Agnosia - inability to recognize objects
Apraxia - inability to carry out normal movements (despite muscles working fine)
Elimination - typically temporary; may be due to inability to communicate
 lOMoARcPSD|22650627

Complications
Aspiration may lead to aspiration
pneumonia Diagnosis
Malnutrition from undereating CT scan or MRI
Difficulty breathing To distinguish what type
Muscle loss, pressure sores, blood clots, of stroke and identify
contractures from not moving location and size
Clots may lead to pulmonary embolism CTA or MRA (angiography)
Urinary tract infections Cardiac imagery to check
Hemorrhagic - herniation where brain heart
pushes through structures that separate Blood tests- platelets,
brain; may lead to loss of consciousness, glucose, PT
coma, death

Prognosis
The sooner the patient is treated, the less severe brain damage will result
Strokes that impair consciousness or effect a large part of the left side (language)
fair worse
→
Faster improvement in the few days post stroke better chances of good recovery
Ischemic - at 12 months post, problems that remain will most likely be permanent
Hemorrhagic - If not massive, outcome better than ischemic with similar symptoms
Depression common

Prevention
Decrease risk factors: Antiplatelet drugs - reduce risk if
Normal BP already had ischemic stroke or TIA
Normal BW Aspirin
↑ physical activity Clopidogrel (Plavix)
No smoking Aggrenox
Limit alcohol Anticoagulants (for pt w/Afib)
Diet: Warfarin
↓ salt/sat fat/trans fat/chol Dabigatran
↑ fruits/veges Apixaban
Rivaroxaban
 lOMoARcPSD|22650627

Treatment
Measures to support vitals (if needed): Hemorrhagic may need:
O2, mechanical vent Help to get blood to clot (Vit K and
IV hypertensives plasma/platelet transfusion)
↓ ↑
swelling in brain, HOB, head in midline Meds to control BP
Adequate hydration Shunt in skull to pressure ↓
Ischemic may need: Stent to treat ruptured brain aneurysm
Antiplatelet drugs, anticoagulants, BP meds
Mechanical thrombectomy, angioplasty, stent insertion Intervention for tPA
tPA - Tissue plasminogen activator
To reestablish blood flow through a blocked artery Monitor vitals during and 24 hrs
MUST be given within 3-4 1/2 hrs post stroke post
MUST be screened closely before administering Monitor labs
Make certain not hemorrhagic stroke Watch for bleeding
No recent: GI bleeding, head trauma, Watch for neuro changes
major surgery, active internal bleeding Will go to ICU for monitoring
No heparin or anticoagulants
Labs normal: Glucose, INR, platelets
BP: SBP < 185 and DBP <110

Intervention
Record time of onset of symptoms Turn every 2 hrs - to optimize musculoskeletal fnx
Assess using NIH Stroke Scale (NIHSS) and maintain skin integrity
0 - 42 scale Side - back - side (weak side only 30 min)
0 = No symptoms GI - May need stool softener or laxative
21 - 42 = severe symptoms take to bathroom on regular schedule
Monitor vitals and neuro - BP VERY important Nutrition -
Airway - at risk for aspiration pneumonia Speech therapist for evaluation before oral
Kept at NPO until screened for ability to intake initiated
swallow Check gag reflex (tongue blade - back of
Elevate HOB, encourage deep breathing throat)
Monitor: Food - should be easy to swallow; will need
Cardiac rhythms assistance eating; monitor for food left in
Murmurs mouth
I/Os Communication - Assess ability
Lung sounds for crackles and wheezes Use gestures, visual cues, picture board
Keep pt moving Short phrases
ROM exercises (active and passive) Be patient
↑
Monitor for ICP Use questions with simple answers
↑ ↓
Headache/ BP/ HR Family -
N/V Provide info and emotional support
Pupils not responding Family and pt will have varying feelings
Monitor for neglect syndrome and hemianopsia Social service referral will be needed
 lOMoARcPSD|22650627

Seizure
A brief, uncontrolled electrical discharge of neurons in the brain that
interrupts normal function.

Provoked seizure - a seizure that has a direct cause (head injury, hypoglycemia,
infection, reaction to drug, alcohol or drug withdrawal)
Unprovoked seizure - a seizure that does NOT have an immediate cause
Epilepsy - a chronic disorder, characterized by recurring, unprovoked seizures
Seizures are the primary sign of epilepsy, but not all seizures are a sign of epilepsy

Neurotransmitters

Neuron
Neuron
Receptor

Pathophysiology
Neurons release different types of neurotransmitters
Some are Excitatory neurotransmitters that tell the neuron receptors to relay
an electrical message
Others are Inhibitory neurotransmitters that tell the neuron to stop the
electrical message
During a seizure, a cluster of neurons become impaired and start sending out a
ton of excitatory signals
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Type of Seizures
Two main types - Generalized Onset and Focal Onset

Generalized Onset
Affects both sides of brain Atypical absence -
Most cases lose consciousness Staring with eye blinking or movement of lips
Tonic-Clonic - formerly known as Grand Mal Usually continues into adulthood
Most common Generalized Onset Lasts 10-30 seconds
Pt loses consciousness and falls to ground if Clonic -
upright Loss of muscle tone then jerking
Stiffens body (tonic phase) for 10-20 seconds Not very common
Jerkiness follows (clonic phase) for 30-40 sec Myoclonic -
Cyanosis, salivating, tongue or cheek biting, Sudden jerkiness of body
incontinence Lasts a few seconds
In postictal phase - muscle soreness, tired, sleep Remains conscious and aware
No memory of seizure Atonic - AKA drop seizure or drop attack
Absence - formerly known as Petit Mal Loss of muscle tone; usually falls to ground
Usually in children; rarely continues to Lasts <15 seconds
adolescence Usually not aware; risk of injury
Brief staring spell (looks like daydreaming) <10 Tonic -
seconds Sudden stiff muscles, usually occurs in sleep
No memory of seizure <20 seconds
May take months to years to recognize Remains conscious and aware

Focal Onset (formerly known as Partial Onset)

Affects specific part of brain Focal to Bilateral Tonic-Clonic - AKA Secondary

Symptoms based on area of brain affected Generalized Tonic-Clonic
Focal Onset Aware - formerly Simple Partial When focal seizure spreads to other side of
Experiences unusual feelings and sensations brain
May hear/taste/see things not real Any Tonic-Clonic seizure preceded by an aura is
Remains conscious and aware a focal seizure that generalized secondarily
Called an aura if happens before another seizure May result in a brief residual neurologic deficit
Focal Impaired Awareness - formerly Complex Partial in postictal phase called Todd's Paralysis
Loses awareness (resolves itself)
Eyes open - cannot interact
Displays automatisms - repetitive actions (e.g. lip
smacking)
Lasts 30 seconds - 2 minutes
Tired and confused after
Generalized
Aura may happen before it Focal Onset
Onset
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Phases of a Seizure
**Not everyone will go through each phase**
Causes
Cause often dependent on age of seizure
Prodrome - feelings, sensations, changes in behavior
1st 6 months of life - severe birth injury,
hours or days before seizure
congenital defects of CNS, infection
Aura - doesn't happen with all types of seizures; first 2-20 years - birth injury, infection, trauma,
symptom, happens within seconds to minutes before genetic factors, fever
seizure; sudden weird feelings (fear, panic, racing 20-50 years - structural lesions (trauma,
thoughts), dizzy, headache, nausea brain tumors, vascular disease)
50 + years - stroke, metastatic brain
Ictal - actual seizure, electrical activity in brain tumors
occurs; symptoms vary widely 1/3 of all cases no cause known
Genetic link- epilepsy often runs in
Postictal - after the seizure; recovery period; may families
recover immediately or take minutes to hours; may be
extremely tired, confused, have difficulty talking

Complications
Status epilepticus - continuous seizure activity in which seizures recur in rapid succession without return to
consciousness between seizures
OR any seizure lasting longer than 5 minutes
Neurologic emergency! Can lead to brain damage if not treated
Any injury that may have occurred during a seizure
Mortality rate of people with epilepsy = 2-3x the rate of the general population
Psychosocial - difficult to cope with seizures; depression; social stigma; transportation and employment are
difficult

Diagnosis
Thorough review of history of seizures and health history needed
EEG - may show abnormal findings which will help determine type of seizure
Should be done within 24 hours of seizure
Usually need repeated EEGs or continuous EEG monitoring
NOT definitive test (false + and false -)
Magnetoencephalography (with EEG)
CBC, check on liver/kidney function, urinalysis - to rule out metabolic disorders and recreational drugs
as cause of seizures
CT/MRI - to rule out structural lesions
 lOMoARcPSD|22650627

Treatment
No cure, goal is to prevent seizures with minimal Side effects:
side effects from drugs Diplopia, drowsiness, ataxia
Medications - Mental slowness
Antiseizure drugs (primary treatment) Phenobarbital - watch for respiratory
Tonic-Clonic and focal seizures - depression and hypotension
Phenytoin (Dilantin) Phenytoin - watch for gingival hyperplasia
Tegretol (instruct on good oral hygiene); hirsutism,
Phenobarbital rash (report immediately); avoid taking
Divalproex with milk or antacids
Mysoline Older adults: respond better to meds but side
Absence and Myoclonic - effects are worse
Zarontin Surgery -
Divalproex If unresponsive to drug therapy
Klonopin Remove part of brain causing the seizure
For status epilepticus - Vagal nerve stimulation -
Rapid-acting IV antiseizure drug Used when a specific area of brain cannot be
Lorazepam (Ativan) identified
Diazepam (Valium) Interrupts the brain wave activity to stop the
Most drugs have a long 1/2 life, so given in once neurons
or twice daily doses Sends electrical impulse to vagus nerve
↑ ↓
Ketogenic diet - fat, carb diet

Intervention
Seizure precautions - Note how pt acted immediately prior to
Suction and O2 ready seizure and during
IV access Which body part affected 1st
Padded side rails After seizure -
Pillow under head Assess pt status - responsive/tired/any
Bed lowest position injury?
Remove restrictive clothing/glasses Maintain airway
During seizure - Monitor vitals, LOC, O2 sat, pupil
Lie pt down; turn on side size/reactivity
Ensure pt airway cleared Clean pt if incontinence occurred
Protect from injury - side rails, pillow under Educate patient -
head, remove anything that may break Importance of taking meds regularly
Remove/loosen tight clothing All side effects - plus need to report them
Do NOT restrain Assist in finding resources (Epilepsy
Stay with pt until seizure passes Foundation), social worker
IV access for meds if needed Suggest med alert bracelet/necklace/ID card
Suction as needed Factors that may cause seizure:
Note time start/stop Stress, trauma to head, pregnancy, lack of
If > 5 minutes or no return to baseline = sleep, hypoglycemia, dehydration, fever,
→
Status Epilepticus activate ESR team strobe lights, recreational drugs, alcohol
 lOMoARcPSD|22650627

Increased Intracranial Pressure

Potentially life-threatening condition where the pressure builds within
the skull.

The skull is an enclosed space with 3 essential CSF Blood

volume components:
Brain tissue, blood and cerebrospinal fluid
(CSF)
Intracranial Pressure (ICP) - the pressure in
the skull created by the 3 components
Normal ICP = 5-15 mm Hg
Under normal circumstances, ICP is influenced
by:
Brain tissue
Arterial pressure Posture
Venous pressure Temperature
Intraabdominal pressure Blood gases Components of the Brain
Intrathoracic pressure (esp. CO2)

The Monro-Kellie doctrine states that the 3 components must remain at a

relatively constant volume within the skull. If the volume of 1 component
increases and the volume of another component decreases, the total
intracranial volume will not change (provided the skull is closed).
The body adapts to volume changes within the skull in 3 different ways:
CSF volume: by altering CSF absorption and production or displacing CSF
Intracranial blood volume: by collapsing cerebral veins & dural sinuses;
cerebral vasoconstriction or dilation; changes in venous outflow
Brain tissue volume: by distention of the dura or compression of brain tissue

The ability to compensate for changes in volume is limited!

As the volume continues to increase, the ICP rises and decompensation ultimately
occurs, resulting in compression and ischemia.
 lOMoARcPSD|22650627

Cerebral blood flow (CBF) - amount of blood in ml passing through 100 g of brain
tissue in 1 minute
Maintenance of blood flow to brain is critical because the brain requires a
constant supply of O2 and glucose
The brain regulates its own blood flow via autoregulation
Autoregulation - the automatic adjustment in the diameter of the cerebral blood
vessels by the brain to maintain constant blood flow during changes in arterial
blood pressure; also helps maintain cerebral perfusion pressure

Cerebral perfusion pressure (CPP) - the pressure needed to ensure blood flow to
the brain.
→
If CPP falls too low autoregulation fails CBF decreases →
Normal CPP = 60-100 mm Hg CPP = MAP - ICP
CPP < 50 mmHg = ischemia and neuronal death MAP = SBP + 2 (DBP)
CPP < 30mmHg = ischemia and incompatible with life 3
CPP = MAP (mean arterial pressure) - ICP SBP = systolic BP
Critical to maintain MAP when ICP is elevated! DBP = diastolic BP

Mechanisms of Increased Intracranial Pressure

ICP begins to increase due to tissue edema from head injury, hemorrhage or
another cause (see list next page)
↑ ↓ ↓
ICP leads to CPP which leads to cerebral blood flow
↓ CBF leads to ischemia, swelling and more edema
Brain will try to maintain cerebral perfusion by increasing systolic BP
This will lead to systolic HTN, widening pulse pressure, bradycardia with a full,
bounding pulse and altered respirations = CUSHING'S TRIAD = neurologic
emergency!
Leads to herniation (shifting inside the skull) and displacement
→
Herniation forces the brainstem downward respiratory arrest due to
compression of the respiratory control center in the medulla
 lOMoARcPSD|22650627

Causes of ↑ ICP Diagnosis

Head Injury
Hemorrhage CT
Hematoma MRI
Brain tumor EEG
Brain abscess Cerebral angiography
Encephalitis ICP mmnt
Meningitis Transcranial Doppler studies
Cerebral Infarction Evoked potential studies
Hydrocephalus PET
Hepatic encephalopathy

Signs and Symptoms

Change in LOC - Earliest sign
BEST indicator of pt neurologic status
↓
Appears restless or confused; level of attention
Headache - nocturnal or early morning
Vomiting - without nausea (unexpected vomiting), may be projectile
Seizures
Change in body temperature
Irregular breathing
Ocular:
Double vision
Swelling of optic nerve (papilledema)
Pupils - increase or decrease in size or unequal in size
No response to light
Check oculocephalic reflex - if eyes stay midline = brain stem damage
Muscular -
Weakness on one side
Decorticate - stiff with arms bent in toward body, clenched fists, legs held out
straight/rotated internally
Decerebrate - arms and legs straight, feet flexed - worst of the two- more serious
damage
Change in vitals - Cushing's triad - appears late- emergency!
 lOMoARcPSD|22650627

Treatment
Identify/treat underlying cause of ICP↑
Support brain function
Maintain adequate oxygenation, may need:
Endotracheal tube
Tracheostomy
Mechanical vent
Removal of brain lesion if necessary
Meds -
Mannitol (Osmitrol) - osmotic diuretic given via IV
Decreases ICP by plasma expansion and osmotic effect
Draws the water pooling in the brain back to the blood
Hypertonic saline solution
Moves water out of swollen brain cells
Corticosteroids - not for TBI, used for tumors and abscesses
Monitor glucose, GI bleeds - H2 Blockers and PPIs to prevent GI ulcers/bleeding
↓
Barbiturates (help ICP and cerebral edema), opioids

Intervention
↑
Focus on preventing further ICP and Monitor -
monitor current ICP Glasgow Coma Scale (see next page)
Respiratory - Maintaining airway critical! Neuro checks
Need to prevent hypoxia and Monitor ICP - usually via
↓ ↑
hypercapnia ( O2 or CO2 can ventriculostomy:
↑
cause ICP) Catheter in lateral ventricle
Suction only as little as possible as may coupled to external transducer
↑ ICP Levels >20 mm Hg report to MD
Elevate HOB 30 degrees, head midline, I/Os
no flexion of neck or hips Electrolytes - glucose, Na, K, Mg,
NG tube to aspirate stomach contents osmolality
(prevents abdominal distention) Turn at least every 2 hours
Temp - Restraints only if absolutely necessary
↑
Prevent elevated temp (will ICP) Nutrition - enteral/parenteral as
↓
Antipyretics, room temp, cool bath prescribed
(but prevent shivering) Watch for FVO from diuretics
Quiet, calm environment Renal function
Attempt to avoid: coughing/ sneezing/ s/s of heart failure, pulmonary edema
valsalva maneuver/ rapid movements
 lOMoARcPSD|22650627

Glasgow Coma Scale

Behavior Response plus points

+1 No response
+2 Abnormal extension (decerebrate)
+3 Abnormal flexion (decorticate)

+4 Flexion withdrawal from pain

Motor Response
+5 Moves to localized pain
+6 Obeys commands

+1 No response
+2 Incomprehensible sounds
+3 Inappropriate words
Verbal Response +4 Confused conversation
+5 Oriented to time, person, place

+1 No response
+2 Responds to pain
+3 Responds to speech
Eye Opening Response
+4 Spontaneously opens eyes

Severe head injury: Score of 8 or less

Moderate head injury: Score of 9-12
Mild head injury: Score of 13-15
ICP should be monitored in patient with GCS score of 8 or less and abnormal
CT scan or MRI
 lOMoARcPSD|22650627

Multiple Sclerosis
Disorder where patches of myelin and underlying nerve fibers in the
brain and spinal cord are damaged or destroyed.
Neurons
Dendrites
The neuron is the basic
working unit of the brain
that transmits information Cell
to other nerve cells body Nucleus
Comprised of the cell body
(with nucleus), dendrites and
axon (covered by a myelin Direction
of impulse
sheath) Axon
Myelin Sheath
The impulse starts in the
nucleus and travels through
the axon to the axon
terminals
The dendrites receive nerve Axon
impulses from the axon terminals
terminals of other neurons
Neuron

Pathophysiology
Unknown trigger in genetically susceptible person activates T cells which then
migrate to brain and spinal cord
This causes an inflammatory response which leads to demyelination of the
axons
At first, nerve fibers are not affected and transmission of nerve impulses
occurs but is slowed
Myelin regenerates, symptoms disappear, patient goes into remission
Inflammation later occurs again but this time myelin loses its ability to
→
regenerate axon then becomes damaged
Nerve impulse transmission halted and permanent loss of nerve function
occurs
 lOMoARcPSD|22650627

Risk Factors
Causes
Unknown Genetic
Possibly autoimmune where immune Climate during first 15 years of
system attacks myelin sheath life:
Develops in genetically susceptible people Temperate climates worst
as a result of exposure to (possibly): Tropical and near equator
Infection best
Smoking May be related to Vitamin D
Emotional stress level from sun
Excessive fatigue Smoking
Pregnancy 2-3x more likely in women than
The autoimmune reaction results in men
inflammation which damages the myelin Shows up between 20 - 40 years
sheath and nerve fiber old

Diagnosis
No single test to diagnose
Assess symptoms, history and tests
MRI - detects areas of demyelination of CNS
MRI with contrast agent - used to determine recent vs old areas of damage
Spinal tap (lumbar puncture) - to detect oligoclonal bands (immunoglobulins);
shows inflammation
Evoked responses - electric signals sent to CNS to activate certain areas;
brain's responses recorded
Other test to rule out MS:
AIDS
Guillain-Barre
Lupus
Lyme

Most people with MS have periods of good health (remissions) alternating with
periods of worsening symptoms (flare-ups/relapses). Recovery during remission
is good but often incomplete leading to MS worsening slowly over time.
 lOMoARcPSD|22650627

Signs and Symptoms

Will vary depending on which nerve fibers are Lhermitte's sign - feels like an electric shock
damaged radiating down the spine into the limbs upon
Symptoms begin long before diagnosed flexion of neck
Fatigue Bowel/bladder -
Dizziness/vertigo Constipation
Tingling, numbness (face, extremities) Spastic bladder - urinary
Pain in arms, legs, trunk urgency/frequency/incontinence
Involuntary tremors Flaccid bladder - No sensation to void
Muscle spasms Sexual dysfunction; no libido
Muscle weakness Cognitive - problems with short-term
Speech impediment memory, attention, information processing
Loss of dexterity/coordination Emotion - anger, depression, euphoria
Vision problems- blurred, double, red-green Romberg's sign - sway when eyes closed and
color distortion, pain moving eyes standing with feet together
Nystagmus - problems controlling eye Uhthoff's sign - symptoms get worse with
movement heat

Treatment
No cure so need to treat disease process and provide symptom relief
→
Ideally start early in course of MS better prognosis
Medications: For spasticity - muscle relaxants (Baclofen,
↓
Immunomodulator drugs - to inflammation Diazepam)
and immune system response For fatigue - Amantadine, Modafinil
Beta interferon (Rebif, Plegridy, For bladder - Overactive -anticholinergics
Avonex, Betaseron, Extavia, Copaxone) (Oxybutynin) or underactive - cholinergics
Corticosteroids - to treat exacerbations (Bethanechol)
Methylprednisolone, Prednisone For walking - Dalfampridine (Ampyra)
IV immunoglobulin G - may be needed when For tremors - Propranolol (beta blocker),
steroids not sufficient Isoniazid (antibiotic)

Intervention
Assist patient in identifying triggers that Encourage - light exercise and rest, well
cause exacerbations (heat, overexertion, etc) ↑
balanced diet ( fiber), stool softeners,
May need to be taught self-catherization ↓ caffeine, adequate fluids (1-2 L/day)
Speech and PT consult Administer meds as prescribed and educate
Safety considerations (vision, coordination) pt on meds
 lOMoARcPSD|22650627

Parkinson's Disease
Chronic, progressive neurodegenerative disorder.

Basal Ganglia in the Brain

Cerebrum
Basal Ganglia
1 Caudate nucleus
1
2 Globus pallidus 2 3
3 Putamen 4
5 Thalamus
4 Subthalamic nucleus

5 Substantia nigra
Amygdala

Brain stem Cerebellum

The basal ganglia are collections of nerve cells deep in the brain
They help initiate and smooth out voluntary muscle movements, suppress
involuntary movements and coordinate changes in posture

Pathophysiology
In Parkinson's Disease, the nerve cells in the substantia nigra (in the basal
ganglia) degenerate
These cells produce dopamine which helps increase nerve impulses to muscles
When they degenerate, dopamine level decreases and the number of
connections between nerve cells in the basal ganglia decrease
This leads to the inability of the basal ganglia to control muscle movement
properly
Plus, the levels of acetylcholine and dopamine are altered (normally equal)
with an excess of acetylcholine floating around (contributes to tremors)
PD symptoms do not show up until at least 80% of neurons in the substantia
nigra are lost
 lOMoARcPSD|22650627

Cause Risk Factors

Exact cause unknown 60+ years old
May be presence of Lewy bodies in Slight genetic link
the substantia nigra Possibly:
Lewy bodies are clumps of synuclein Well water
(a protein in the brain) Pesticides/herbicides
Rural residence
Signs and Symptoms
Will begin subtly and progress gradually
May start on one side/extremity and progress to the other side
Tremors Depression
Often 1st sign and starts in hand Anxiety
Affects handwriting Apathy
Appears to be rolling a pill or coin between Fatigue
thumb and forefinger (pill-rolling) Pain
Coarse and rhythmic Constipation
Occurs at rest (resting tremor) Urinary retention
May move to tongue, jaw, voice Erectile dysfunction
Rigidity Memory changes
Muscles become stiff, making movement Sleep problems
difficult REM sleep behavior disorder (limbs
Muscles resist passive movement move suddenly and violently)
Cogwheel rigidity - jerky movement Urinate frequently
Akinesia Scales on scalp and face
No control over voluntary movement Loss of smell
Bradykinesia - slowness of movements, ADL all become difficult due to stiff
especially automatic movements (blinking muscles and tremors
eyelids, swallowing, postural adjustments) Turning in bed
Seen as stooped posture, masked face, Getting out of car
drooling, shuffling Standing up
Postural instability Dressing, combing hair
Unable to stop moving forward (propulsion) Eating
or backward (retropulsion) Writing
 lOMoARcPSD|22650627

Complications Diagnosis
Falls/injury Difficult to diagnose due to same s/s as
Aspiration (esophagus moves contents slowly) aging
↓
Sudden BP (orthostatic hypotension) No specific test
Malnutrition Based on evaluation
Dementia - 1/3 develop late in disease Positive response to antiparkinsonian drugs
Hallucinations, delusions, paranoia - may be caused by provides confirmation of PD
disease OR meds

Treatment
No cure, so focus is on symptom management
Medications -
Antiparkinsonian drugs
Main one is Levodopa combined with Carbidopa (Sinemet) - has many side effects
May stop working after several years (called 'on-off effect')
Levodopa
Converted into dopamine in the basal ganglia
Reduces muscle stiffness; improves movement; reduces tremors
May take up to 3 weeks to take effect
MANY side effects (N/V, orthostatic hypotension, flushing, nightmares, hallucinations,
confusion, obsessive compulsive behavior)
MD must find best dose by balancing control of disease with side effects
Don't take with foods high in B6 or high protein foods
Carbidopa
Prevents levodopa from being converted to dopamine in intestine and CV system (helps
decrease GI side effects)
Anticholinergic drugs - Cogentin - used to treat tremors; may be taken alone or with Levodopa; NO
alcohol
Dopamine agonists - may be used instead of Sinemet
Mirapax or Requip (taken PO- drowsiness major side effect)
Neupro (skin patch)
Apomorphine (injected under skin) - can be used as rescue therapy for 'off' effects of Sinemet
MAO Inhibitors - Eldepryl, Azilect - used w/Levodopa or alone; beware taking with foods containing
tyramine- risk of hypertensive crisis
Amantadine - may help with on-off effect; used alone or w/Levodopa; only provides MILD relief
COMT Inhibitors - Comtan, Tasmar (Help Levodopa last longer)
Domperidone- treats side effects (N/V, orthostatic hypotension)
Antipsychotics if needed - Quetrapine, Clozapine
Exelon or Aricept for dementia
Amitryptyline for depression
Surgery- For those unresponsive to drug therapy; 3 types
Deep Brain Stimulation - electrodes in basal ganglia; electricity sent to areas responsible for tremors
Ablation - ultrasound waves applied to areas of the brain affected by Parkinson's
Stem cell transplantation - ongoing research in this area
 lOMoARcPSD|22650627

Intervention
Goal for patient:
Maintain good health (eating/movement)
Maintain independence
Avoid complications
Stay safe
Optimize psychosocial well-being
Major concerns - exercise and well-balanced diet
Exercise to limit:
Muscle atrophy
Contractures
Constipation
Nutrition
At risk for wt loss due to difficulty chewing/swallowing
Foods need to be soft and easy to swallow
2 L of fluids - goal during day
↑ fiber diet; may need stool softener
↑
Don't take meds with protein meals (will absorption) ↓
Educate on dosages and side effects of meds (see Treatment)
Discuss environmental changes to assure safety
Removing area rugs
Removing excess furniture
Elevated toilet seat
Handrails
Use of cane
Clothing
Slip on shoes (rather than shoelaces)
Hooks and velcro rather than zippers and buttons
Educate on how to deal with freezing episodes - patient feels like feet stuck to ground and
unable to move
Change direction
Think about stepping over imaginary line on floor
Rock from side to side
Take a step back then try to go forward again
↓
Discuss support groups and need for stress as stress may increase symptoms
 lOMoARcPSD|22650627

Myasthenia Gravis
Autoimmune disorder of the neuromuscular junction that results in
muscle weakness.
Pathophysiology
The neuromuscular junction is where the Neuromuscular Junction
motor neuron and muscle fiber meet and
send signals
Motor
Acetylcholine (ACh) is released from the
Neuron
motor neuron
(Nerve)
Receptors on the muscle fiber are
stimulated by the ACh Acetylcholine
The receptors contract the muscle fibers (ACh)
causing movement Antibody
AChE then breaks down the ACh to avoid
constant muscle stimulation
ACh
However, in Myasthenia Gravis the
Receptors
receptors are attacked by antibodies from Muscle
the immune system
Acetylcholinesterase
This leaves fewer receptors on the fiber to
(AChE)
contract the muscles
Leads to muscle weakness

Signs and Symptoms

Cause Main sign: Weakness of skeletal muscles that

becomes worse with activity and BETTER with
Exact cause unknown rest
May be malfunction of Usually noticed first in eyes:
thymus gland where it Weak, drooping eyelids (ptosis)
does not decrease in size Weak eye muscles - double vision
after puberty and (strabismus)
develops tumors Difficulty speaking/swallowing
These tumors may Energy fades as day progresses
produce autoantibodies No expression on face
Shortness of breath
 lOMoARcPSD|22650627

Diagnosis
Symptom assessment - muscles tested with repetition, patient rests and
→
then tested again improvement shows possible MG
↓
EMG to show response to muscle stimulation
Blood tests - to show antibodies
Tensilon test - Injection with Edrophonium Chloride (Tensilon). If shows
improved muscle contractility = myasthenia gravis
MRI or CT - to evaluate thymus for tumors

Treatment
No cure
Medications -
Anticholinesterase (Pyridostigmine)
Stops acetylcholinesterase from breaking down acetylcholine
This leaves more acetylcholine floating around and prolongs its action
Therefore more chance for muscle contraction
May cause Myasthenic Crisis (see next page)
Corticosteroids (Prednisone) - given on alternate days
Immunosuppressants - Azothioprine (Imuran), Mycophinolate (CellCept), Cyclosporine
(Sandimmune)
Thymectomy - remove thymus gland (not a cure but decreases symptoms)
Plasmapheresis (plasma exchange) or IV immunoglobulin G - Both used to provide short-
term results in myasthenic crisis or before surgery when avoiding corticosteroids

Contraindications
The following meds are contraindicated in patients with MG

Anesthetics Diuretics
Antidysrhythmics Opioids
Antibiotics Cathartics
Quinine Muscle relaxants
Antipsychotics Thyroid preparations
Barbiturates Tranquilizers
 lOMoARcPSD|22650627

Intervention
Assess severity: Fatigue level, muscles affected, muscle strength, swallowing, speech, cough
and gag reflexes
Acute phase -
Monitor: respiratory (RR, O2 Sat), vision, voice, swallowing, strength, cranial nerves,
aspiration
Nutrition -
May have feeding tube
If not, instruct:
Balanced diet, foods easily chewed and swallowed
Schedule meds 30 - 60 minutes before eating to take advantage of strong muscles
Instruct -
Plan day with activities early when strength is best
Necessity of medication adherence
Adverse reactions to meds to look for
↑
Avoid activities that risk of crisis

Myasthenic Crisis vs Cholinergic Crisis

Severe episode of MG due to infection, Reaction to too much anticholinesterase
surgery, stress, starting Leads to too much ACh at receptor site
corticosteroids or not taking enough Signs and Symptoms:
anticholinesterase Respiratory failure (may need vent)
Leads to not enough ACh at receptor Muscle weakness
site Muscle fasciculation (twitching)
Signs and Symptoms: Blurry vision
Respiratory failure (may need ↓ BP
vent) Pupils constricted
Muscle weakness Lacrimation
Difficulty speaking ↑ salivation
No cough/gag reflexes Diarrhea
↑ BP N/V
Bowel/bladder incontinence Ab cramps
Pupils normal Sweating

To determine if pt is experiencing MC or CC, Tensilon test will be administered.

If pt weakness improves = positive test for MC = Give anticholinesterase per MD order
If pt weakness worsens = negative test for MC = Administer Atropine per MD order
Downloaded by REGINA CARLA ARQUINES ([Link]@[Link])
 lOMoARcPSD|22650627

Guillain-Barré Syndrome
Disorder in which the immune system attacks the peripheral
nervous system.
Peripheral Nervous System (PNS)- System of nerves that provides connection
between brain/spinal cord and rest of body. Consists of Somatic Nervous System
and Autonomic Nervous System. SNS = Voluntary functions (muscles, etc) ANS =
Involuntary functions (BP, HR, RR, Temp, Vision, Renal, Digestion)

Neurons
Dendrites
The neuron is the basic
working unit of the brain
that transmits information Cell
to other nerve cells body Nucleus
Comprised of the cell body
(with nucleus), dendrites and
axon (covered by a myelin Direction
of impulse
sheath) Axon
Myelin Sheath
The impulse starts in the
nucleus and travels through
the axon to the axon
terminals
The dendrites receive nerve Axon
impulses from the axon terminals
terminals of other neurons
Neuron

Pathophysiology
Patient experiences illness, then 1-2 weeks later the immune system begins to
attack the PNS and cranial nerves
The myelin sheath (necessary for nerve conduction) begins to deteriorate
Demyelination occurs, transmission of nerve impulses stops
Muscles innervated by these nerves undergo denervation and atrophy
Most common type of GBS: Acute Inflammatory Demyelinating
Polyneuropathy (AIDP) - discussed in this study guide
 lOMoARcPSD|22650627

Causes/Risk Factors
Most likely autoimmune reaction 1-2 weeks
after one of the following: Miller-Fisher Syndrome
Viral or bacterial infection
Variant of GBS
Viral - Cytomegalovirus
Only few symptoms develop:
Bacterial - Campylobacter Jejuni
Eye paralysis
(thought to be the most common)
Walking unsteady
Surgery
Normal reflexes disappear
Vaccination
Flu
Typically upper respiratory illness or GI
infection is the starting incident

Signs and Symptoms

Main feature is ascending, progressive, symmetrical weakness in limbs
Begins in both legs
Pain
Paresthesia (numbness & tingling)
↓
Hypotonia ( muscle tone) Max symptoms reached in 2-4 weeks
Leads to paralysis after start, then recovery begins.
Leads to Areflexia (lack of reflexes) Damage stops at 8 weeks.
Then moves to ANS in severe cases: No treatment = improve slowly over
BP fluctuates several months
Cardiac dysrhythmias Early treatment = improve quickly in
Urine retention days or weeks
Severe constipation Recovery takes 1-2 years to return to
Body temp fluctuations baseline
Facial flushing
Cranial nerve involvement soon after:
Facial weakness/paresthesia
Eye movement problems
Dysphagia
Respiratory failure if progresses (most serious complication)
 lOMoARcPSD|22650627

Treatment Diagnosis
Can worsen rapidly so treat as a medical emergency Assess symptoms plus test results
Ventilation may become necessary CSF analysis via spinal tap (lumbar
Feeding- enteral or parenteral puncture)
IV fluids Looking for elevated protein
If within 1st 2 weeks of symptom onset, one of the without elevated WBCs
following: Electromyography and nerve
IV immunoglobulin conduction studies
From donor, stops antibodies Looking for demyelination of
Plasmapheresis nerves
Filters antibodies from blood

Intervention
During acute phase:
Monitor:
Motor function for ascending paralysis Pain- provide meds as needed
Reflexes Turn patient every 2 hours
Cranial nerve function Encourage movement if possible
Gag May need to provide passive ROM
Cornea stretching
Swallow Provide enteral/parenteral nutrition
LOC as prescribed
ABGs Support/communicate with pt often
Vital capacity as this is a scary time for him/her and
BP family - Let them know this is a
Cardiac rate/rhythm for dysrhythmias temporary condition
I/Os
Respiratory status ***
Bowel sounds

Around 28 days after first symptom, patient will start to recover spontaneously.
~80% completely recover within a few years
~65% have minor residual symptoms
 lOMoARcPSD|22650627

The Kidneys
Major function: To remove waste products and excess fluid from the body

Bean-shaped organs about the size of a fist

All Functions
located on either side of the spine at lowest
level of rib cage Remove waste products from blood
Kidneys filter 150-200 qts of blood and Remove drugs from the blood
produce 1-2 qts of H2O every 24 hrs Help balance the body's fluids
Each kidney contains over a million nephrons Release hormones that regulate
(the functional unit where blood is filtered blood pressure
and urine is produced) Produce active form of Vitamin D
Each kidney connects to a ureter which leads for bones
to the bladder Control production of RBCs
Glomerulus Filtration Rate (GFR) measures
the total amount of filtrate formed/min by
the kidneys. Normal = 90-120ml/min
Kidney
Anatomy of Kidney
1. Renal Capsule - outermost layer; gives kidney
shape an protects from infections Ureter
2. Renal Cortex - outer layer within the kidney;
where the majority of the blood filtration and
urine production occurs; contains most of the Bladder
nephron structure minus the loop of Henle
3. Renal Medulla - inside layer; hypertonic; helps
3. Medulla
maintain water and salt balance; contains part
of the nephrons (loop of Henle)
4. Artery
4. Renal Artery - Brings fresh oxygenated blood
2.
from heart to be filtered; branches off into 5. Vein Cortex
afferent and efferent arterioles
Ureter 1.
5. Renal Vein - takes filtered blood back to heart Capsule
to be re-oxygenated and pumped to body
Kidney Cross Section
 lOMoARcPSD|22650627

Nephrons
Functions Each nephron consists of two parts:
Renal Corpuscle (Glomerulus and Bowman's
Filters blood (in the renal
Capsule)
corpuscle)
Renal Tubule
Reabsorbs minerals/H2O
Blood enters glomerulus, is filtered, then passes out to
and secretes waste (in
the body, the filtrate drips into the Bowman's capsule
renal tubule)
and then passes into the tubule
Produces urine (drains
In the tubule chemicals and H2O are added to or
into ureters)
removed from the fluid and then excreted down
ureters, stored in bladder, voided out via the urethera

In the glomerulus (in Renal Cortex); very

high pressure causes ultrafiltration;
Glomerulus filters out: H2O,
filtrate collects in bowman's capsule
ions, AA, glucose,
creatinine, urea from blood
Unfiltered blood enters
Glomerulus Efferent
nephron from renal artery
Filtered blood exits via Arteriole Afferent
efferent arteriole to Proximal Arteriole
Convoluted
renal vein Leaves as urine
Tubule
to ureter
Distal
Filtrate flows through Bowman's Convoluted
Proximal Convoluted Capsule Tubule
Tubule; where it Collecting In Collecting
reabsorbs: H2O, ions, Tubule tubule reabsorbs
Renal Cortex
urea, glucose, AA Na, H2O, urea
Renal Medulla

Filtrate enters loop of Henle In distal convoluted

Loop of tubule - Reabsorbs Na,
(in the Renal Medulla). Goal To Ureter
Henle H2O, Cl, Ca, HCO3;
here is to concentrate urine.
Secretes K, H
In descending limb -
In ascending limb -
permeable to H2O
permeable to ions
only- H2O leaves
only- Na, Cl, K
filtrate
Nephron pumped out of
filtrate
 lOMoARcPSD|22650627

RAAS: Renin-Angiotensin-Aldosterone System

A series of reactions designed to help regulate blood pressure.

1. Blood pressure falls → Kidneys release RENIN

2. Renin activates ANGIOTENSINOGEN (from

liver)
ACE Inhibitors
work by blocking
3. Angiotensinogen turns into ANGIOTENSIN I this step

Angiotensin-Converting Enzyme (ACE) from lungs

converts Angiotensin I into ANGIOTENSIN II (the
4.
main product of RAAS). Then:

ANGIOTENSIN II:

Causes vasoconstriction of venous and arterial

vessels→↑ BP

Triggers release of Aldosterone from adrenal glands:

Causes kidneys to retain Na and H2O
Causes kidneys to secrete K

Triggers release of ADH from pituitary gland:

Causes kidneys to retain H2O

Increased Na and H2O retention causes increased blood pressure

 lOMoARcPSD|22650627

Chronic Kidney Disease

Slow and progressive decline in the kidneys' ability to filter blood properly.

Causes Stages of Kidney Disease

Normal GFR = 90-120 ml/min
Diabetes - glucose sticks to artery
Stage 1: Damage with normal renal fnx:
walls → ↓ blood supply to kidneys -
GFR: > 90 ml/min
** Most common
Stage 2: Mild loss of renal fnx:
↑ BP - constant pressure damages
GFR: 60-89 ml/min
artery walls → ↓ blood supply to
Stage 3: Mild-severe loss of fnx:
kidneys - ** Most common
GFR: 30-59 ml/min
Urinary tract obstruction
Stage 4: Severe loss of fnx:
Polycystic kidney disease
GFR: 15-29 ml/min
Autoimmune disorder (ex. lupus)
Stage 5: End stage renal disease
Infections
GFR: < 15 ml/min
Certain meds (NSAIDS,
aminoglycosides, chemotherapy
drugs) Signs/Symptoms
-Usually asymptomatic at first-
Diagnosis Early stages:
Blood and urine tests to look for: Nocturia (early on)
↑ urea and creatinine Fatigue/weak (due to metabolic waste in
↑ K, PO4 and PTH blood and anemia)
↓ Ca and calcitrol ↓ appetite, N/V
↓ Hg SOB
Blood more acidic Unpleasant taste in mouth
Ultrasonography to rule out Easily bruise and bleed
obstruction Gout/joint pain/swelling
Advanced stages:
Muscle: twitches/weakness/cramps/pain
Risk Factors Restless legs syndrome
Diabetes Encephalopathy
↑ BP Heart failure; pericarditis
Heart Disease GI ulcers
Family history Uremic frost (deposits of urea crystals
on skin)
 lOMoARcPSD|22650627

The progressive decline in kidney function will cause many problems:

Inability to remove waste from blood: Inability to regulate electrolytes:
Uremia ↑ K (can cause heart problems)
Metabolic Acidosis ↑ PO4 (will bind to Ca and
Proteinuria decrease it)
Hematuria ↓ Ca levels (will increase PTH -
↑
Gout (from uric acid levels) cause Ca to leak from bones -
→
Filtering less H2O kidney renal osteodystrophy)
thinks BP is low →↑ renin ↑ Mg
release →↑ BP
Inability to help Inability to
Inability to balance body fluids: produce RBCs: create urine:
Hypervolemia Anemia Oliguria/
Edema Anuria
↑ BP
Treatment
Inability to Activate Vit D:
Vit D not available to help Treat condition that worsens fnx:
reabsorb Ca →↓ Ca Meds for ↑ BP
Diet and meds for DB
Remove UTI obstruction
Intervention
Clear infection
Monitor for Kussmaul breathing Reduce meds that cause damage
(due to metabolic acidosis) Dietary changes
Iron supps: IV, subq, or blood Meds
transfusions Dialysis/Transplant (for advanced)
Monitor EKG (cardiac events)
Monitor lab values (esp. K) Diet
May provide Keyexalate
PO4 binders (with food) ↓ Protein; consume sufficient carbs
Avoid antacids/laxatives with Mg to offset calories
IV Ca if ordered ↓ K (avoid: potatoes, avocadoes,
Monitor I/Os; daily wts strawberries, tomatoes, oranges,
Monitor BP/swelling bananas)
Educate on diet ↓ PO4 (avoid: poultry, fish, dairy,
nuts, sodas)
↓ Mg (avoid: pumpkin seeds,
almonds, spinach, cashews)
↓ Na
 lOMoARcPSD|22650627

Acute Kidney Injury

Rapid decline in the kidneys' ability to filter blood properly.

Causes
Prerenal Injury - Due to decreased blood flow to the kidneys from:
Sepsis *most common Loss of large amounts of Na and fluid
Hemorrhage Shock
↓ CO Meds (aminoglycosides & contrast agents)
Heart failure Injury that blocks blood vessels
MI Liver failure
Dehydration

Intrarenal Injury - Due to damage to the nephrons in the kidney from:

Meds (NSAIDS, contrast agents Glomerulonephritis
used in imagery tests, poisons, (inflammation of glomeruli)
chemotherapy drugs) Sepsis
Trauma Tumors within kidneys
Rhabdomyolysis

Postrenal Injury - Due to blockage in the urinary tract (between

kidneys and urethra) from:
Enlarged prostate Tumor in urinary tract
Narrowing of urethra Stones in ureters or bladder
Bladder cancer Renal calculi

Signs/Symptoms
Early stages: Middle stages: Left untreated:
H2O retention → Oliguria/anuria Chest pain
swelling of Fatigue Seizures
feet/ankles/face/hands ↓ concentration SOB
↓ UO No appetite
Nausea
Itchiness (pruritus)
 lOMoARcPSD|22650627

Diagnosis Treatment
Blood tests to look for: Urine tests to look for:
Treat cause
↑ BUN and Cr Na, K, Ca, PO4
Dialysis may be nec.
↑ K and PO4 Ultrasonography or CT to
↓ fluids, Na, PO4, K
↓ Na check for hydronephrosis
PO4 binders
Blood acidosis or enlarged bladder

Stages of AKI

Onset Stage: Lasts a few

Kidney injury occurs hours to
S/S start to appear several days
Oliguric Phase: Intervention
Glomerulus not filtering ↓ K & ↓ pro diet
blood properly (↓ GFR) Safety (due to neuro changes)
UO < 400 ml/day Monitor EKG and lab values
Spec. grav > 1.020 May give kayexalate
↑ BUN, Cr, K, PO4 ↓ fluids Lasts 8-14
↓ Ca Strict I/Os / Daily wts days
Hypervolemia Monitor RR & O2 Sat
Metabolic acidosis Watch for Kussmaul breathing
** Pt may go on dialysis Give PO4 binders

Diuresis Stage: Intervention

Cause of AKI has been Strict I/Os
corrected Daily wts Lasts 7-14
UO 3-6 L/day due to Monitor: days
osmotic diuresis Dehydration
Pt now more alert Hypovolemia
Urine now diluted (spec. ↓ BP
grav. < 1.020)

Recovery Stage:
Lasts a few
↓ edema / UO normal BUN/Cr/K/PO4/Ca all
months- 1 year
GFR returns to normal return to normal
 lOMoARcPSD|22650627

Renal Calculi (Kidney Stones)

Hard deposits of minerals and salts that form out of the filtrate produced
by the nephron.
The nephron filters waste from the blood into
Staghorn
a filtrate that is excreted in urine
Sometimes the minerals and salts in the
filtrate become concentrated, form crystals Stones in
and turn into stone kidneys
These stones either stay in kidney or travel
through the urinary tract
Vary in size
From microscopic to 1 in or more
Stone in
Largest is the 'staghorn' which can fill
ureter
entire renal pelvis
Vary in material/type
Calcium Oxalate (most common) Stone in
Uric Acid bladder
Cystine
Struvite
Vary in location Signs and Symptoms
Kidneys (most common)
Depends on type and location
Ureters
Small stones often no symptoms
Bladder
Pain in lower abs (stone in bladder)
Risk Factors Renal colic: Pain in between ribs
and hips to abs and back (stone in
Hyperparathyroidism renal pelvis)
Dehydration Ureteral colic: Pain in waves in
Renal tubular acidosis genital area (stone in ureter)
Diets low in Ca or high in: N/V
Animal protein Restlessness
Vit C (increases oxalate in urine) Sweating/chills/fever
Family history Blood may be in urine
Bariatric surgery Frequent urge to urinate (↓ UO)
Decreased mobility Cloudy, foul-smelling urine
Hypocitraturia - citrate helps stop stone
formation & keeps urine alkaline
 lOMoARcPSD|22650627

Types of Renal Calculi

Calcium Oxalate stones: Causes of ↑Ca in filtrate:

Hypercalcemia:
Most common
Excessive Ca supps
Forms in acidic urine
↑
Forms when concentration
Eating too much salt
Renal tubule problems
of Ca or oxalate in filtrate Too much animal protein in diet
Hyperparathyroidism:
Too much PTH released which ↑
Uric Acid stones: Ca release from bones
Forms when too much uric acid in Causes of ↑oxalate in filtrate:
urine ↑ intake of high-oxalate foods
Causes of too much uric acid in urine: GI disorders (UC, Crohn's)
Diet ↑ in purine Fats aren't digested so they
Diet ↑ in animal protein bind with Ca and leave oxalate
Dehydration behind (oxalate normally
Gout binds with Ca)
Diabetes

Cystine stones: Struvite stones:

Forms when too much amino acid Due to urinary tract infections
cysteine in urine Mg, NH3 and PO4 crystallize
Cysteine not properly reabsorbed Very large stone
in nephron AKA Staghorn
Rare, genetic Rare

Diagnosis
Renal colic- good IVP (Intravenous Pyelogram) 24-hr urine test:
indication of stones Check for allergies to Measures ions, uric
Hard to dx otherwise; shellfish or iodine, if on acid, Cr, Citrate, Ph
need to eliminate other metformin, pregnant or Keep on ice
causes of pain breast feeding Strain for stones!
CT; Ultrasound Urinalysis to show: (need to test to
KUB xrays blood/pus/infection/crystals determine what type)
 lOMoARcPSD|22650627

Treatment/Intervention
Small stone: Wait for it to Stone removal:
pass: Extracoporeal Shock Wave Therapy
Keep pt pain ↓ with (ESWL): For stones 1/2 in (1 cm) or less
round-the-clock pain Noninvasive
meds (NSAIDS/opioids) Maintain fluid intake
3-4 L/day fluids Pain medication/Keep mobile
Helps move stone Strain urine
Keeps urine diluted to Percutaneous Nephrolithotomy: For
prevent infection and large stones or where ESWL not option
add'l stone formation Invasive
Monitor I/Os Incision in back: nephroscope &
Check for s/s of UTI probe used to remove/break stone
Strain for stones! Maintain fluid needs 3-4 L/d
Keep mobile Maintain nephrostomy (empty bag,
Small stones that block UT or monitor for infection)
w/infection will need to be Strain urine (if stone not removed)
removed Uteroscopy: to remove stones in lower
Large stone > 3/16 in (5 mm) part of ureter
or close to kidneys probably Scope inserted from urethra to
won't pass on own kidneys to remove or break stone
Maintain fluids
Pain medication/Keep mobile
Strain urine (if stone not removed)

Prevention
Maintain hydration 2L/d Diet:
Alluprinol - to ↓ uric acid ↓ animal protein
levels ↓ food high in purine
HCTZ (hydrocholorthiazide) - Bacon, liver, sardines, anchovies, dried
to ↓ Ca in urine peas, beans, beer
ABx to prevent UTIs ↓ foods high in oxalate
Do not ↓ intake of Ca other Rhubarb, spinach, cocoa, nuts, pepper,
than in med form tea
Instruct on how to strain urine and keep stone
 lOMoARcPSD|22650627

Urinary Tract Infections

Infection in the urinary tract caused by bacteria, virus or fungus.

Upper Tract
Infection of kidneys Kidneys
(Pyelonephritis)

Ureters

Lower Tract
Infection of bladder
(Cystitis) Bladder
Infection of urethra
Urethra
(Urethritis)

Urinary Tract Infection Overview

Infections usually start in urethra and spread to bladder
If unchecked, can spread to ureters and kidneys
Cystitis most common
Pyelonephritis can spread to bloodstream and lead to sepsis
Women at greater risk of infection due to anatomy: Shorter urethra and closeness
to rectum (spread of bacteria)
Urinary tract has several defense mechanisms against infection:
Valves - at ureters and bladder (one-way)
Muscles of bladder - squeeze urine out
Pressure in bladder - pushes urine out
Urine is sterile with antiseptic qualities
Lining of urinary system has immune cells
Male prostate glands secrete fluid with antimicrobial properties
Bacteria in vagina - lactobacilli - keeps area acidic
 lOMoARcPSD|22650627

Urethritis - infection of the urethra

Causes: Signs/symptoms:
Bacteria, fungus, virus Pain during urination Left
E. Coli (common) Frequent need to urinate unchecked
STD (common) Occ discharge in men
can lead to
Diagnosis: Treatment: narrowing
Urinalysis Abx
of urethra
Urethral swab Antiviral for herpes
Urine culture STD infections > treat partners

Cystitis- infection of the bladder

Causes:
Bacteria (E. Coli) Common among women during
Diaphragm use reproductive years, especially
Condom w/spermicide use
during pregnancy.
Catheter infected w/bacteria
Wiping back to front
Signs/symptoms:
Bubble baths/scented tampons
Hormonal changes Burning/painful during urination
Abx (change flora of body) Frequent need to urinate
Immobility Pain lower back
VUR in children (genetic, valves don't Nocturia
close properly, urine backflows to Cloudy urine (severe infection)
kidneys) Elderly: fever, confusion, no
Obstruction (stone in bladder or symptoms related to urination
urethra) Diagnosis:
Enlarged prostate Urinalysis
Narrowing of urethra Treatment: Urine culture
Abx
Treat cause if not bacteria (e.g. obstruction)
 lOMoARcPSD|22650627

Pyelonephritis- infection of the kidney

Causes: More common among

women than men.
Bacteria (E. Coli) (~90% cases)
Physical blockage of urine: ↑ risk during pregnancy
Structural abnormality (enlarged uterus puts
Kidney stone pressure on the ureters)
Enlarged prostate ↑ risk with diabetes or
Backflow of urine
Infection through bloodstream (~5%)
↓ immune system
Diagnosis:
Signs/symptoms:
Urinalysis - RBCs, WBCs,
Sudden: bacteria
Chills Urine culture - bacteria
Fever Blood test: WBCs, bacteria,
Pain in lower back on either kidney damage
side
N/V
Treatment:
Frequent, painful urination Abx (PO or IV with
Elderly: confusion, fever or sepsis hospitalization)

Prevention
Intervention
Drink 2-3 L fluids/day
Maintain I/Os Void every 2-3 hours
Make sure UO >30 cc/hr Avoid spermicides and diaphragms
Tylenol/NSAIDS Wipe front to back
Meds per MD order: Avoid tight, non-porous underwear
Pyridium (will cause Urinate immediately after intercourse
orange-colored urine) Take all abx as prescribed
Sulfonamide (bactrim) Specimen collection:
Instruct on proper specimen Wipe w/antiseptic wipe
collection Void small amount
Instruct on prevention Collect urine midstream
Keep cup few inches from urethra
 lOMoARcPSD|22650627

Glomerulonephritis
Condition in which inflammation of the glomerulus causes the release of
RBCs and protein into the urine
Glomerulus
Efferent
Arteriole Afferent
The nephron is the part of the kidney that Proximal Arteriole
filters blood and produces urine Convoluted
The glomerulus filters out water, ions, urea, Tubule

glucose and amino acids from the blood Distal

Bowman's Convoluted
It does NOT filter out protein and blood Capsule Tubule
cells Collecting
Tubule
However, when the glomerulus is damaged it
will filter protein and blood cells allowing
them to be excreted via the filtrate into the Renal Cortex

urine Renal Medulla

Loop of
Glomerulonephritis leads to hematuria and Henle To Ureter
small amounts of proteinuria
Nephron

Glomerulonephritis can be Acute or Chronic

Causes of Acute Causes of Chronic

Infections (bacterial, fungal, parasitic, viral) Cause often unclear
Most common infection is from Strep throat: Develops very slowly over years
Called Acute Glomerulonephritis If pt had acute glomerulonephritis
Poststreptococcal it may develop into chronic
Appears 2 weeks after strep throat infection
Usually in pediatric population 2-10 yrs
Immune system actually causes the
inflammation of the glomerulus
Lupus and Goodpasture syndrome (autoimmune)
Granulomatosis w/polyangiitis (blood vessel
inflammation)
 lOMoARcPSD|22650627

Signs and Symptoms

S/S of Acute
50% have no symptoms Hematuria leads to dark urine
Edema - first face/eyelids later legs Proteinuria leads to edema b/c
↓ UO low albumin in blood causes
Dark urine
water to move out of capillaries
↓ kidney function →↑ BP/Cr/BUN, ↓GFR into tissues
Drowsy, confused
Elderly - Nausea, malaise

S/S of Chronic
No symptoms for a long time
↑
Later: BP & Edema

Diagnosis Treatment
Acute: Chronic:
Blood and urine tests: Treat the ACE
Protein disorder/infection Inhibitors
Blood cells Diet: ↓ protein & Na or ARBs
GFR Diuretics ↓ Na diet
BUN/Cr HTN meds
Biopsy to confirm Possibly Abx or
glomerulonephritis corticosteroids

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 Monitor:
I/Os K, BUN, Cr, BP
Daily wts Provide meds per MD order:
Void 30 cc/hr or 1 m/kg/hr (kids) Diuretics
Monitor for swelling and lung sounds Antihypertensives
↓ fluids; diet: ↓ protein & Na Abx
 lOMoARcPSD|22650627

Nephrotic Syndrome
Condition in which damage to the glomerulus causes excessive amounts of
protein to be excreted into the urine.

↑ protein in urine (>3 gm/day) → ↓ protein in blood

↓ protein (albumin) in blood → edema (water leaves capillaries into tissues)
Liver senses hypoalbuminemia and makes more albumin and at the same time
makes cholesterol and TG → hyperlipidemia
Also lose
Immunoglobulins from blood → increase risk for infections
Proteins that prevent clot formation → increase risk of clot formation

Causes Signs and Symptoms

Primary - (originates in kidneys): No appetite; malaise
Minimal Change Disease - most common cause Proteinuria (>3 gm/day)
in children **Frothy urine (from protein)
Focal Segmental Glomerulosclerosis - most Puffy face/hands/legs, ascites
common cause in adults - scar tissue forms in Ab pain
part of glomeruli
Secondary (>50% of adult NS cases are secondary): Diagnosis
Usually a systemic disease like lupus or DB
May be mistaken for heart
NSAIDS
failure in older adults
Glomerulonephritis
Urine/blood tests: Cr,
Certain allergies
albumin, lipids

Intervention
Treatment Monitor fluid status:
Treat cause if known I/Os
Meds: ACE Inhibitors, ARBs, Daily wts
statins, possibly: Void 30 cc/hr adults or 1 ml/kg/hr
corticosteroids, Watch for infection (↓ immune system)
immunosuppressants, anti- Watch for blood clots: swelling, pain in
coags legs, arms (DVT)
Diuretics Monitor pulmonary status
Diet: ↓ sat fat/chol/Na Diet: ↓ sat fat/chol/Na
 lOMoARcPSD|22650627

Dialysis
Artificial process for removing waste products and excess fluids from the
body when kidneys are not functioning properly.
Two types of dialysis: Hemodialysis and Peritoneal Dialysis

Goal of Dialysis
Patient with kidney failure may need to go
on dialysis when: ↓ waste in blood
Correct acidosis
Very high levels of K or Ca
Uremic encephalopathy
Reverse electrolyte
Pericarditis imbalances
Acidosis Remove excess fluid
Heart failure
Excessive fluid in body
Pulmonary edema Two other options to filter blood:
Symptoms of renal failure
Hemofiltration - done in ICU as a
GFR < 10-15 ml/min
continuous procedure; can filter large
amounts of blood
Hemoperfusion - used to treat
poisoning; charcoal filter absorbs poison

Blood removed from body and

Hemodialysis
pumped into a dialyzer (artificial Complications
kidney) which filters metabolic
waste, electrolytes and fluids. Blood
↓ BP (most common) Dysrhythmias
Infection of graft or Air embolus
returned purified. fistula Bleeding in the
Total amount of fluid returned can be Fever intestine, brain,
adjusted Anaphylaxis (allergy to eyes or abdomen
Total time is about 3-5 hours 3 times substance in dialyzer or from too much
per week tubing) heparin in dialyzer
Can be done at home or dialysis
center
Most common dialysis
 lOMoARcPSD|22650627

Peritoneal Dialysis
Uses the peritoneum (membrane that lines the
abdominal cavity) to act as a natural filter Complications
Fluid (dialysate) infused through catheter into
peritoneal space
↓ BP (most common)
Bleeding (irritation of peritoneum)
Dialysate sits for a period of time, absorbs waste Infection (at insertion site)
products, electrolytes and then is drained and Hypoalbuminemia
discarded. Repeated 4-5 times/day. Scarring of peritoneum
↑
Uses osmosis: dialysate has concentration of Hernias (ab or groin)
glucose attracting fluid (more fluid is drained Constipation - interferes with
than was instilled) dialysate flow
Less efficient than hemo, but can be run for
longer times
Done at home; can use machine or manually

Venous Access
External shunt/catheter - Arteriovenous fistulas - Arteriovenous graft - Uses a
Cannula placed in large vein Large artery and vein sewn synthetic connector to
and large artery near each together below surface of connect artery and vein
other; for immediate use; skin (creates one blood (also creates one blood
usually short-term. Prone vessel for both withdraw vessel for both withdraw
to infection, clotting, skin and return) and return)
erosion Requires surgery and Requires surgery and
healing time (up to 6 wks) healing time (up to 2 mos)

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) Peritoneal: Color of fluid removed
Diet peritoneal: adequate pro & cal; low to (bloody effluent may be bleeding inside)
no salt (table or K-containing) Peritoneal: Cloudy discharge may mean
Diet hemo: Na and K restricted, phosphorus infection
limited
 lOMoARcPSD|22650627

Diuretics
Medications used to remove extra fluid volume from blood through
increased urination. They work by altering the processes in the nephrons.

Glomerulus
Efferent
4 main types of diuretics Arteriole Afferent Thiazide
Proximal Arteriole
Convoluted
Tubule
Loop - work in the loop of Henle - K-sparing
mainly the thick ascending limb Distal
Bowman's Convoluted
Thiazide - work in the first part Osmotic Capsule Tubule
Collecting
of the distal convoluted tubule Duct
Potassium-sparing - work in last
part of distal convoluted tubule
Loop
and collecting duct
Loop of
Osmotic - work in the proximal Henle To Ureter

convoluted tubule and descending

limb of loop of Henle Nephron

Location of action in the nephron

Diuretics Overview
Loop are the most powerful diuretics
Thiazide best for HTN
Both Loop and Thiazide cause K LOSS
K-Sparing are rather weak, so used w/Loop and Thiazide to help spare K
Remember water loves Na and will follow it!
All diuretics increase urination, so dehydration main concern for use
along with maintaining electrolyte balance
 lOMoARcPSD|22650627

Loop Diuretics **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) →↑ Na in
Torsemide (Demadex) filtrate→↑ H2O excreted as urine
Ethacrynic acid (H2O loves Na and will follow it)

Used for Nursing Considerations

Pulmonary edema Monitor:
HTN (Thiazides work better) Dehydration
↑ Ca levels Hypotension
Edema Vitals
Heart failure I/Os and Daily wts
Liver impairment w/ascites Look for signs of gout
Slow IV route for furosemide to avoid
Side Effects damaging inner ear (ototoxicity)
Monitor labs:
↓Ca, K, Na and Mg levels Hypokalemia (will need to
↓ BP supplement if <3.5 mEq/L) (if on
↑ uric acid levels → gout digoxin, monitor level)
Ototoxicity Hypocalcemia
Hyponatremia (if on lithium,
monitor level)
Interactions
Hypomagnesemia
NSAIDS: ↓ blood flow to Educate:
kidneys → ↓diuretic effects S/S of dehydration
Lithium:↓Na →↑lithium BP and HR mmnt
Digoxin:↓K → ↑digoxin Wt daily & notify MD if +3 lbs in 1
day
↑
Encourage K foods
 lOMoARcPSD|22650627

Thiazide Diuretics Not as powerful as Loop

Names Action
Hydrochlorothiazide (HCTZ) Blocks reabsorption of Na and Cl in
Indapamide the first part of the distal convoluted
Chlorothiazide tubule (where 5-7% of Na is absorbed
Metolazone from filtrate) →↑ →
Na in filtrate
Chlorthalidone ↑ H2O excreted as urine (H2O loves
Na and will follow it)
Used for
Nursing Considerations
HTN (best)
Heart failure Monitor:
Renal calculi from Ca Dehydration
Hypotension
Vitals
Side Effects
I/Os
↓Na levels Daily wts
↑ Ca (helps with Look for signs of gout
preventing renal stones and Monitor glucose in DB pt
↑ bone density) ↓
Give with meals to GI upset
↓K and loss of H+ ions Monitor labs:
↓BP Hypokalemia (will need to
Hyperglycemia supplement if <3.5 mEq/L) (if on
↑uric acid levels (gout) digoxin, monitor level)
Hypercalcemia
Contraindications Hyponatremia (if on lithium,
Renal impairment monitor level)
Pregnancy Educate:
S/S of dehydration
↑
Diet in K
Wt daily & notify MD if +3 lbs in 1
day
Monitor BG if DB
 lOMoARcPSD|22650627

Potassium-sparing Diuretics Keeps K in blood

Names Action
Spironolactone (Aldactone) Works in 2 ways:
*Most common Directly inhibit Na channels (in DCT
Eplerenone and CD) so Na can't go thru and is
Triamterene therefore excreted
Amiloride By working against aldosterone
(most common); Aldosterone's role
Side Effects
is to cause nephron to reabsorb
Hyperkalemia more Na & H20 into blood
Spironolactone may cause Does NOT decrease K levels like the
antiandrogen effects: other diuretics do
Gynecomastia Often prescribed with loop or thiazide
Menstrual irregularity to spare K
Sexual dysfunction
Used for
Nursing Considerations
HTN
Monitor: Edema due to
Dehydration Heart failure
Vitals Liver impairment
I/Os Nephrotic syndrome
Daily wts Hypokalemia (due to other diuretics)
↓
Give with meals to GI upset Hyperaldosteronism
Monitor labs:
Hyperkalemia (EKG changes - Interactions
Tall peaked T waves) May increase K:
Educate: ACE inhibitors
S/S of dehydration ARBs
↓
Diet in K and no salt NSAIDS
substitutes If on lithium, monitor level
Wt daily & notify MD if +3 lbs
in 1 day
 lOMoARcPSD|22650627

Osmotic Diuretics Least common

Names Action
Mannitol (Osmitrol) - Exhibits osmotic pressure in renal
*Most common tubules that inhibits fluid reabsorption
(specifically in the proximal tubule and
first part of loop of Henle)
Nursing Considerations
Administer via IV
Used for
Monitor:
Vitals Treat cerebral edema
I/Os ↓
To intraocular pressure
Daily wts Treat or avoid Dialysis Disequilibrium
Instruct pt to report changed in Syndrome - neurological condition
LOC from dialysis (rare)

Side Effects
Heart failure
Pulmonary congestion
Pulmonary edema
Hyponatremia
 lOMoARcPSD|22650627

Respiratory Disorders
Lung Anatomy and Physiology

Trachea
Right Lung Carina
*Has three lobes Left Lung
Primary *Has two lobes
Bronchi
Secondary
Bronchi

Tertiary
Bronchioles Bronchi

Alveolar Sacs
Notch for heart

Physiology of Gas Exchange

Inhaled air moves down the trachea to the carina where it splits into the right and
left primary bronchi. The primary bronchi break down into the secondary and
tertiary bronchi then into the bronchioles. From there into the alveolar sacs for gas
exchange.

RBCs from RBCs to body

heart (oxygenated)
(deoxygenated)
Air

Alveolus wall CO2 O2

Capillary wall

Alveolus
 lOMoARcPSD|22650627

Pneumonia
Respiratory tract infection that causes inflammation of the alveoli sacs.

Causes- Microorganism The inflamed alveoli sacs lose their ability to inflate
and deflate and perform gas exchange. The pt then
**May involve more than one** starts to experience hypoxemia (low oxygen in the
Bacteria - **Very common blood) which leads to respiratory acidosis.
Virus - **Very common
Mycobacteria Risk Factors
Fungi
65+ years of age Heart failure
Parasites
Diabetes COPD, asthma
Lung cancer Impaired immune
Smoking system
Usually the body can fight off these Immobile (e.g. stroke) AIDS
microorganisms, but sometimes it Post abdominal Infants
can't and pneumonia results. surgery Elderly
Prior infection

Signs and Symptoms Two main types of pneumonia:

Cough (produces sputum) Community-acquired (contracted outside the
Chest pain (pleuritic) healthcare community)
Chills
Hospital-acquired (contracted in hospital- developed
Fever, aching
SOB
48-72 hrs after admission)
Rhonchi/Wheezes
Oxygen sat <90% Diagnosis
Nausea/vomiting
Chest x-ray
Abnormal lung sounds
Medications Sputum culture

Antibiotics
Antivirals Intervention
Bronchodilator
Monitor: Encourage:
Mucolytic (thins mucus)
Respiratory system Coughing
for lung sounds Deep breathing
Oxygen sat. should Fluids
be >95% Educate:
Suction as needed Stop smoking
Oxygen therapy Vaccinations
 lOMoARcPSD|22650627

COPD
Chronic obstructive pulmonary disease is the persistent narrowing (blocking or obstruction) of
the airways. This occurs with emphysema, chronic obstructive bronchitis, or both.

Emphysema Chronic Bronchitis

**Pink Puffers** **Blue Bloaters**
Alveoli sacs are inflamed and cannot inflate Bronchioles become damaged → increased
and deflate. Inhaled air is stuck in sac, causing sputum production → hard to exhale →
hyperinflation → diaphragm flattens → unable increased air volume → hyperinflation along
to fully exhale → hyperventilation with ↓ O2 levels and ↑ CO2 levels in blood

'Pink Puffers' nickname comes from pink skin 'Blue Bloaters' nickname comes from
color (vs blue) and hyperventilating cyanosis from hypoxia and bloating from
right-sided heart failure

Signs and Symptoms- Takes years to develop and show symptoms

Decreased energy Cough (dry or productive) Pursed lip breathing
SOB Coarse crackles or Breathing with tripod
Weight loss wheezing stance
Respiratory acidosis Barrel chest (emphysema) Cyanosis (bronchitis)
PCO2>45, PO2<90 May cough up blood

Risk Factors Diagnosis

Smoking!! Spirometry (pulmonary function test)
Environmental pollution Chest Xrays
Occupational (chemicals, dust) ABGs

Intervention
Medications Educate:
Smoking cessation!!
Inhaled bronchodilators Supplemental oxygen Vaccines
Inhaled corticosteroids (keep oxygen at 88- Pursed-lip
Take bronchdilators 1st!! 93%) breathing
Rinse mouth after use to Educate: Diaphragm
avoid thrush Avoid sick people breathing
Avoid extreme High-cal diet in
temperatures small meals
 lOMoARcPSD|22650627

ASTHMA
Chronic lung disease that causes narrowing and inflammation of the airways

Causes: Unknown (May be genetic or environmental)

Pathology Asthma Attack

Bronchi and bronchioles are Smooth muscles surround the airway and
chronically inflamed help with dilating and constricting. These
muscles constrict during asthma attack.
May lead to Asthma attack
Chest tightness and difficulty breathing
result. Then goblet cells produce excess
Asthma attack triggers amounts of mucous. Air becomes trapped in
Allergens (pollens, dust mites, animal alveoli inhibiting proper gas exchange →
dander) respiratory acidosis.
Infections (colds, bronchitis)
Irritants (tobacco, fumes, air pollution)
Exercise
Asthma categories
Stress/anxiety Intermittent
NSAIDS, aspirin, sulfites Symptoms 2 days/week or less
No interference w/daily life
Mild persistent
Signs and Symptoms Symptoms >2 days/week
Slightly interfere w/daily life
Early Active Moderate persistent
SOB Tight chest Symptoms occur daily
Fatigue Wheezing Interfere w/daily life
Wheezing Difficulty Severe persistent
Coughing at night breathing Occur often throughout day
Incresed resp rate Increased RR Greatly interfere w/daily life
↓ Peak flow best

Needs Medical Intervention! Intervention

Inhaler won't work Cyanosis
Can't talk Sweaty Keep pt calm
Monitor skin color
Monitor vitals
Monitor lungs
Position in high Fowler's
Diagnosis Educate:
Medications Bronchodilators/
Avoiding triggers
oxygen/corticosteroids
Dr eval s/s
Bronchodilators
Spirometry
Corticosteroids
X-Ray
 lOMoARcPSD|22650627

ACUTE RESPIRATORY DISTRESS SYNDROME

(ARDS)
Respiratory failure when the capillary membrane surrounding the alveoli sac is damaged.

Pathology Fast onset!

→
Capillary membrane is damaged fluid
→
leaks into the alveoli sac collapse of sac Occurs often in people already hospitalized
→ →
lungs become stiff decreased gas who develop a complication.
→ →
exchange hypoxemia organs suffer High mortality rate

Cause- Indirect or Direct

Indirect Direct Diagnosis
Sepsis **Most common Pneumonia
Pulse oximetry
Burns Aspiration
(measures O2 levels)
Blood transfusion Inhalation of toxic
Chest x-ray
Pancreatitis substance
Drug overdose Embolism
Drowning
Chest injury

Signs and Symptoms

Usually develop within 24-48 hrs post-injury or disease
SOB Cyanosis
Rapid, shallow breaths Increased heart rate
Crackles Confusion
Wheezing Sleepiness

Medications Intervention
Usually mechanical intervention w/PEEP
Corticosteroids Pressure kept at 10-20 cm H2O
Antibiotics Prone position (so heart does not compress
lungs)
Monitor:
Urine output
BP
CO
Mental status
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PLEURAL EFFUSION
Abnormal collection of fluid in pleural space

Cause Pleural space is the area between the two

Heart failure layers of the membrane that covers the
Tumors lungs
Pneumonia
Pulmonary embolus
Coronary artery bypass
Diagnosis Fluid is either:
surgery Chest x-ray ** Rich in protein (exudate)
Chest injury Ultrasonography OR
Cirrhosis Lab tests on fluid
** Watery (transudate)
Kidney failure (will determine cause)

Signs and Symptoms Medications

**Usually no symptoms**
SOB IV Antibiotics if caused by
Chest pain (pleuritic) pneumonia
Decreased chest sounds

Intervention
Will need to treat the disorder causing PE
Small effusions may not need treatment
Large effusions may require drainage via
thoracentesis

Lung Terminology
Spirometry- test to evaluate
Tidal volume: Amount of air moved
respiratory function and assess
in and out of lungs with each
pulmonary disorders
respiratory cycle
Forced expiratory volume
Residual volume: Amount of air in
(FEV)- measures how much
lungs after forced expiration
air a person can exhale
Peak Flow Meter: Measures how well air during a forced breath
moves out of lungs Forced vital capacity (FVC)-
Personal Best is the highest number total amount of air exhaled
over a 2-week period (when asthma is during the FEV test. Normal
controlled) is 80-120%
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Shock
Condition characterized by decreased tissue perfusion and impaired
cellular metabolism.

Shock in a nutshell
Shock occurs when the blood pressure
becomes so low that the body's cells do not
Types of Shock
receive enough blood and therefore not Cardiogenic
enough oxygen Hypovolemic
Organ cells stop functioning normally due to Distributive
the low oxygen supply Septic
The cells become irreversibly damaged and Neurogenic
die and the organ begins to fail Anaphylactic
When 2 or more organs fail = Multiple Organ
Dysfunction Syndrome (MODS)
MODS = high likelihood of death

Causes
Cardiogenic - Due to inadequate pumping of the heart
Complications of MI, pulmonary embolism, malfunction of a heart valve,
arrhythmia, myocarditis, endocarditis, cardiac tamponade
Hypovolemic - Due to low blood volume
Severe bleeding - External (injury) or Internal (ulcer, GI bleed, ruptured
blood vessel)
Excessive loss of body fluids - major burn, severe diarrhea/vomiting,
pancreatitis, untreated diabetes
Distributive - Due to excessive dilation of blood vessels (vasodilation)
Septic - severe bacterial infection
Neurogenic - injury to spinal cord (or occasionally to brain)
Anaphylactic - serious allergic reaction
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Stages of Shock
Initial Stage- Not clinically apparent
Cardiac Output (CO) very low and cell hypoxia occurs
Cells change from aerobic to anaerobic (without oxygen) metabolism
Anaerobic metabolism creates lactic acid
Liver not receiving enough oxygen so can't metabolize the lactic acid
→
Buildup of lactic acid in blood pH drops
Serum lactate > 4 mmol/L = lactic acidosis

Compensatory Stage - Body tries to recover

Goal is to increase CO or Blood Volume (BV) to help tissue perfusion:
Baroreceptors stimulate the SNS to release epinephrine and norepinephrine
This will cause vasoconstriction →↑ BP and HR ↑ →↑
perfusion to vital
↓
organs and to non-vital organs (puts at risk for paralytic ileus)
Body shifts fluid from interstitial compartment to intravascular →↑
CO & BP
→
Kidneys activate the RAS produces Angiotensin II (a vasoconstrictor) →
↑ →↑
more blood to heart and BP tissue perfusion and cells more oxygen
Aldosterone released due to Angiotensin II kidneys keep Na & H2O→ →↑ BV
Kidneys retaining Na →↑ serum osmolality →
this tells pituitary gland to
→
release ADH keeps H2O in kidneys BV →↑
At this stage if cause of shock is corrected patient can recover

Progressive Stage- All major organs begin to die

If patient hits this stage, the compensatory stage has failed and patient
moving to MODS
Cells swelling now and capillary permeability is ↑
Fluids and protein drawn into interstitial space edema and BV → ↓
↓ →↓
BV ↓
CO and tissue perfusion
Mental status changes /ARDS / GI bleeding / Ulcers / Toxic waste buildup
Cardiac dysrhythmias leading to complete deterioration of CV system
DIC - (disseminated intravascular coagulation) - leads to massive bleeding
Refractory Stage - Cannot be reversed. All organs begin to shut down.
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Signs and Symptoms Treatment/Intervention

↓Capillary refill EKG

↓BP, ↓CO, ↑HR, ↓UO Monitor - HR, rhythm, BP, CO

Cardiogenic
Watch for fluid overload
Crackles, tachypnea
Asses heart sounds, lung sounds
Cyanosis & cool, pale, clammy skin
Supplemental O2
Weak peripheral pulse
Intubate/mech vent if necessary
Anxious, confused
Meds:
N/V
Nitrates, inotropes, diuretics

UO beginning to ↓ Stop loss of fluids, restore volume

↓ ↓ ↓ ↑
SV, CO, BP, HR Supplemental O2
Hypovolemic

↓ Capillary refill Monitor fluid overload & UO

Tachypnea No specific meds
Weak peripheral pulse
Cool, clammy skin
Anxious, confused

May not have signs at 1st Fluid replacement 1st

Vasodilation Then vasopressors (norepinephrine)
Warm/flushed skin early, then Inotropes (dobutamine)
cool/clammy later Abx - Start within 1st hour! (obtain culture
Septic

Pulse strong (bounding) at 1st right before start)

↓ ↑ ↓
BP, HR, UO Monitor glucose closely
GI bleeding/paralytic ileus Supplemental O2
Hyperventilation, confused Intubate/mech vent if necessary
Crackles, respiratory failure

Vasodilation Maintain pt airway

↓ ↓
BP, HR Supplemental O2
Neurogenic

Unable to regulate body temp Intubate/mech vent if necessary

Warm, dry skin at 1st Vasopressors
Cool, dry skin later on Atropine (for bradycardia)
Bowel dysfunction Stabilize spine
Loss of reflex activity Monitor temp and UO

Vasodilation Maintain pt airway

↑ ↓HR, BP Supplemental O2
Anaphylactic

Sudden dizziness, chest pain Fluid resuscitation w/colloids

Incontinence Meds: epinephrine 1st tx (IM or IV),
Swelling of lips and tongue antihistamines, zantac, albuterol,
Wheezing, SOB, stridor, flushing corticosteroids if hypotension persists > 2 hr
↓
Anxious and confused, LOC * Prevention
Cramping/ab pain/N/V/D * Carry epipen