NCLEX Pathophysiology Exam Guide: Master Disease Processes ????

NCLEX Pathophysiology Exam Guide: Master Disease Processes
???? Key Learning Objectives
Understanding pathophysiology is crucial for NCLEX success! This comprehensive guide breaks down
how diseases alter normal body functions, helping you recognize clinical manifestations, anticipate
complications, and implement appropriate nursing interventions.
Understand disease mechanisms and progression
Connect pathophysiology to clinical manifestations
Identify early warning signs and complications
Apply pathophysiological knowledge to nursing interventions
Master system-by-system disease processes
❤ Cardiovascular System Pathophysiology
Myocardial Infarction (MI)
Pathophysiology
Mechanism: Coronary artery occlusion → myocardial ischemia → tissue necrosis
Atherosclerotic plaque rupture → platelet aggregation → thrombus formation Ischemia cascade: Decreased oxygen → anaerobic metabolism → cellular death Infarct zones: Necrosis (center) → injury zone → ischemic zone
Clinical Manifestations
Classic Symptoms:
✅ Chest pain: Crushing, substernal, radiating to left arm/jaw ✅ Diaphoresis (profuse sweating)
✅ Nausea and vomiting
✅ Shortness of breath
✅ Anxiety ("sense of impending doom") Atypical Presentations (especially in women, elderly, diabetics):
Fatigue, indigestion, back pain, silent MI
Diagnostic ChangesECG: ST elevation (STEMI) or depression (NSTEMI)
Cardiac enzymes: Troponin elevation (gold standard)
CK-MB: Rises 4-6 hours post-MI
Complications
Cardiogenic shock
Arrhythmias (VF, VT most dangerous)
Papillary muscle rupture
Ventricular septal defect
Pericarditis
Heart Failure
Pathophysiology
Frank-Starling Mechanism Failure: Heart cannot maintain adequate cardiac output
Compensatory mechanisms: SNS activation, RAAS activation, ventricular remodeling Eventually: Compensatory mechanisms become maladaptive
Left-Sided Heart Failure
Pathophysiology: Left ventricle cannot pump effectively → blood backs up into lungs Clinical Manifestations:
✅ Dyspnea (exertional, then at rest)
✅ Orthopnea (difficulty breathing when lying flat)
✅ Paroxysmal nocturnal dyspnea (PND)
✅ Crackles in lungs
✅ S3 gallop
✅ Pulmonary edema (pink, frothy sputum)
Right-Sided Heart Failure
Pathophysiology: Right ventricle cannot pump effectively → systemic congestion Clinical Manifestations:
✅ Peripheral edema (dependent, pitting) ✅ Jugular venous distention (JVD)
✅ Hepatomegaly ✅ Ascites✅ Weight gain
✅ Fatigue
Nursing Considerations
Daily weights (same time, scale, clothes)
I&O monitoring
Sodium restriction (2g/day typically)
Medication compliance (ACE inhibitors, diuretics, beta-blockers)
Hypertension
Pathophysiology
Primary (Essential) HTN: Unknown cause, multifactorial
Genetic predisposition
Environmental factors: Diet, stress, obesity
Vascular changes: Arteriosclerosis, increased peripheral resistance Secondary HTN: Identifiable cause
Renal disease
Endocrine disorders
Medications
Complications
Target organ damage: Heart, brain, kidneys, eyes Hypertensive crisis: BP >180/120 with organ damage Silent killer: Often asymptomatic until complications occur
???? Respiratory System Pathophysiology
Chronic Obstructive Pulmonary Disease (COPD)
Pathophysiology
Two main components:
1. Chronic Bronchitis: Inflammation → mucus hypersecretion → airway obstruction 2. Emphysema: Alveolar destruction → loss of elastic recoil → air trapping
Progressive Disease: Irreversible airflow limitationInflammatory cascade: Neutrophils, macrophages → tissue destruction Alpha-1 antitrypsin deficiency: Genetic cause of early emphysema
Clinical Manifestations
Early Disease:
✅ Chronic cough with sputum production
✅ Shortness of breath with exertion
✅ Frequent respiratory infections
Advanced Disease:
✅ Barrel chest (increased AP diameter)
✅ Use of accessory muscles
✅ Pursed-lip breathing
✅ Tripod positioning
✅ Cyanosis (late sign)
✅ Right heart failure (cor pulmonale)
Nursing Considerations
Oxygen therapy: Low flow (1-2 L/min) - avoid suppressing respiratory drive Bronchodilators: β2-agonists, anticholinergics
Pulmonary rehabilitation
Smoking cessation
Asthma
Pathophysiology
Type I hypersensitivity reaction:
1. Trigger exposure → IgE-mediated mast cell degranulation
2. Inflammatory mediators released (histamine, leukotrienes)
3. Three responses:
Bronchospasm (immediate)
Inflammation (delayed) Airway remodeling (chronic)
TriggersAllergens: Dust mites, pollen, pet dander
Irritants: Smoke, pollution, strong odors
Other: Exercise, cold air, stress, infections
Clinical Manifestations
Classic Triad:
✅ Wheezing (expiratory, then both phases)
✅ Cough (often nonproductive, worse at night)
✅ Dyspnea
Severe Attack:
✅ Use of accessory muscles
✅ Inability to speak in full sentences
✅ Peak flow <50% of personal best
✅ Cyanosis
Status Asthmaticus (Medical Emergency)
Life-threatening bronchospasm
Unresponsive to usual medications
Risk of respiratory failure
Pulmonary Embolism (PE)
Pathophysiology
Virchow's Triad: Conditions promoting thrombosis
1. Venous stasis (immobility, heart failure)
2. Endothelial injury (surgery, trauma)
3. Hypercoagulability (cancer, pregnancy, oral contraceptives)
Mechanism: Thrombus (usually from DVT) → travels to pulmonary circulation → blocks blood flow V/Q mismatch: Ventilation without perfusion
Increased pulmonary vascular resistance
Right heart strain
Clinical Manifestations
Classic Triad (only 20% have all three):✅ Dyspnea (sudden onset) ✅ Chest pain (pleuritic) ✅ Hemoptysis
Other Signs:
✅ Tachycardia
✅ Anxiety
✅ Cough
✅ Syncope (if massive PE)
???? Neurological System Pathophysiology
Stroke (Cerebrovascular Accident)
Types and Pathophysiology
Ischemic Stroke (85%):
Thrombotic: Clot forms in cerebral artery
Embolic: Clot travels from elsewhere (usually heart)
Mechanism: Decreased blood flow → ischemia → infarction Hemorrhagic Stroke (15%):
Intracerebral: Bleeding within brain tissue
Subarachnoid: Bleeding in subarachnoid space
Mechanism: Blood vessel rupture → increased ICP → tissue damage Clinical Manifestations (Location-Dependent)
FAST Assessment:
✅ Face drooping (facial weakness) ✅ Arm drift (arm weakness) ✅ Speech slurred (speech difficulties) ✅ Time (note time of onset)
Additional Signs:
✅ Hemiparesis/hemiplegia ✅ Visual field defects✅ Aphasia (language difficulties)
✅ Dysphagia (swallowing difficulties)
✅ Altered level of consciousness
Nursing Priorities
1. ABCs (airway, breathing, circulation)
2. Time is brain - rapid intervention critical
3. Blood pressure management
4. Swallow assessment before giving anything by mouth
5. Neurological monitoring
Seizures
Pathophysiology
Abnormal electrical brain activity:
Hyperexcitability of neurons
Loss of inhibitory mechanisms
Synchronous neuronal firing
Types
Generalized Seizures:
Tonic-clonic: Stiffening (tonic) then jerking (clonic)
Absence: Brief loss of consciousness (petit mal)
Focal Seizures:
Simple: Consciousness maintained
Complex: Consciousness impaired
Status Epilepticus
Medical emergency: Continuous seizure >5 minutes or recurrent seizures without full recovery Risk: Brain damage from hypoxia and metabolic changes
Nursing Care During Seizure
✅ Protect airway - turn to side
✅ Do NOT restrain or put anything in mouth ✅ Time the seizure✅ Observe and document seizure activity
✅ Post-ictal care: Positioning, monitoring
Parkinson's Disease
Pathophysiology
Dopamine depletion:
Loss of dopaminergic neurons in substantia nigra Imbalance: Decreased dopamine vs. acetylcholine Progressive degeneration
Clinical Manifestations
Cardinal Signs:
✅ Resting tremor (pill-rolling)
✅ Bradykinesia (slow movements) ✅ Muscle rigidity (cogwheel, lead-pipe) ✅ Postural instability
Other Features:
✅ Masklike face (hypomimia)
✅ Shuffling gait
✅ Micrographia (small handwriting) ✅ Soft, monotone voice
???? Endocrine System Pathophysiology
Diabetes Mellitus
Type 1 Diabetes
Pathophysiology:
Autoimmune destruction of pancreatic beta cells Absolute insulin deficiency
Usually childhood/young adult onset Type 2 Diabetes
Pathophysiology:Insulin resistance + relative insulin deficiency
Progressive beta cell dysfunction
Associated with obesity, metabolic syndrome
Acute Complications
Diabetic Ketoacidosis (DKA):
Mechanism: Insulin deficiency → fat breakdown → ketone production
Signs: Fruity breath, Kussmaul respirations, altered mental status Lab values: Glucose >250, pH <7.3, ketones present
Hyperosmolar Hyperglycemic State (HHS):
Mechanism: Severe hyperglycemia without ketosis
Signs: Severe dehydration, altered mental status
Lab values: Glucose >600, high osmolality
Hypoglycemia:
Mechanism: Too much insulin, too little food, or increased activity
Signs: Shakiness, sweating, confusion, rapid pulse
Treatment: 15g fast-acting carbohydrate Chronic Complications
Retinopathy (leading cause of blindness)
Nephropathy (leading cause of kidney failure)
Neuropathy (peripheral and autonomic) Macrovascular disease (CAD, stroke, PVD)
Thyroid Disorders
Hypothyroidism
Pathophysiology:
Primary: Thyroid gland dysfunction
Secondary: Pituitary/hypothalamic dysfunction Decreased T3/T4 → increased TSH (primary)
Clinical Manifestations: ✅ Fatigue, weakness✅ Cold intolerance
✅ Weight gain
✅ Dry skin, hair loss
✅ Bradycardia
✅ Depression
Myxedema Coma (Emergency):
Severe hypothyroidism
Altered mental status, hypothermia
High mortality rate
Hyperthyroidism
Pathophysiology:
Graves' disease: Autoimmune (most common) Toxic nodular goiter
Excessive T3/T4 → decreased TSH
Clinical Manifestations:
✅ Heat intolerance, diaphoresis
✅ Weight loss despite increased appetite ✅ Nervousness, anxiety, tremor
✅ Tachycardia, palpitations ✅ Exophthalmos (Graves' disease)
Thyroid Storm (Emergency): Extreme hyperthyroidism High fever, severe tachycardia Altered mental status
???? Renal System Pathophysiology
Acute Kidney Injury (AKI) Pathophysiology Categories Pre-renal (60-70%):Decreased blood flow to kidneys
Causes: Dehydration, shock, heart failure
Mechanism: Hypoperfusion → ischemia
Intrarenal (25-40%):
Direct kidney damage
Causes: Nephrotoxic drugs, contrast dye, rhabdomyolysis
Mechanism: Tubular necrosis, glomerular damage
Post-renal (5-15%):
Obstruction of urine flow
Causes: Kidney stones, BPH, tumors
Mechanism: Back-pressure → kidney damage
Stages (RIFLE Criteria)
Risk: Creatinine ↑ 1.5x baseline
Injury: Creatinine ↑ 2x baseline
Failure: Creatinine ↑ 3x baseline
Loss: Persistent failure >4 weeks
ESRD: Failure >3 months
Clinical Manifestations
Oliguria: <400 mL/day (most common) Anuria: <100 mL/day Other signs: ✅ Fluid retention (edema, weight gain)
✅ Electrolyte imbalances
✅ Metabolic acidosis
✅ Uremic symptoms (if severe)
Chronic Kidney Disease (CKD)
Pathophysiology
Progressive, irreversible loss of nephrons
Common causes: Diabetes, hypertension, polycystic kidney disease Compensatory mechanisms initially maintain function Eventually: Compensation fails → uremiaStages (Based on GFR)
1. Stage 1: GFR ≥90 (normal with kidney damage)
2. Stage 2: GFR 60-89 (mild decrease)
3. Stage 3: GFR 30-59 (moderate decrease)
4. Stage 4: GFR 15-29 (severe decrease)
5. Stage 5: GFR <15 (kidney failure - dialysis needed)
Complications
Bone disease: Calcium/phosphorus imbalance Anemia: Decreased erythropoietin Cardiovascular disease: Leading cause of death Metabolic acidosis Fluid/electrolyte imbalances
???? Gastrointestinal System Pathophysiology
Peptic Ulcer Disease (PUD)
Pathophysiology
Imbalance: Aggressive factors vs. protective factors
Aggressive: H. pylori, NSAIDs, acid, pepsin
Protective: Mucus, bicarbonate, prostaglandins, blood flow H. pylori (80% of duodenal, 60% of gastric ulcers):
Mechanism: Bacterial infection → inflammation → ulceration Clinical Manifestations
Duodenal ulcers:
✅ Pain 2-3 hours after meals
✅ Pain at night
✅ Relieved by food
Gastric ulcers:
✅ Pain 30-60 minutes after eating ✅ May worsen with food
✅ Weight loss common
ComplicationsBleeding (hematemesis, melena)
Perforation (acute abdomen)
Obstruction (gastric outlet)
Inflammatory Bowel Disease (IBD)
Crohn's Disease
Pathophysiology:
Transmural inflammation (all layers) Skip lesions (patchy distribution)
Can affect entire GI tract
Clinical Manifestations:
✅ Abdominal pain (RLQ common)
✅ Diarrhea (may be bloody)
✅ Weight loss
✅ Fistula formation
Ulcerative Colitis
Pathophysiology:
Mucosal inflammation only Continuous lesions (starts in rectum, moves up) Limited to colon
Clinical Manifestations:
✅ Bloody diarrhea
✅ Tenesmus (feeling of incomplete evacuation) ✅ Lower abdominal cramping
Hepatitis
Viral Hepatitis
Hepatitis A (HAV):
Transmission: Fecal-oral
Course: Acute, self-limiting
Prevention: Vaccine availableHepatitis B (HBV):
Transmission: Blood, sexual, perinatal
Course: Can become chronic
Prevention: Vaccine available
Hepatitis C (HCV):
Transmission: Blood (primary)
Course: Often becomes chronic Leading cause of liver transplant
Clinical Manifestations
Acute phase:
✅ Jaundice (icterus)
✅ Fatigue
✅ Anorexia, nausea
✅ RUQ pain
✅ Dark urine, clay-colored stools
???? Immune System & Inflammatory Pathophysiology
HIV/AIDS
Pathophysiology
HIV (Human Immunodeficiency Virus):
Target: CD4+ T-helper cells
Mechanism: Reverse transcriptase → viral DNA integration
Result: Progressive immune system destruction Disease Progression
1. Acute HIV syndrome (2-4 weeks post-infection)
2. Asymptomatic period (can last years)
3. AIDS (CD4+ count <200 or opportunistic infections) Clinical Manifestations
AIDS-defining conditions:✅ Opportunistic infections (PCP, CMV, MAC) ✅ Opportunistic cancers (Kaposi's sarcoma) ✅ Wasting syndrome
✅ Dementia
Autoimmune Disorders
Systemic Lupus Erythematosus (SLE) Pathophysiology:
Type II and III hypersensitivity Autoantibodies (ANA, anti-DNA)
Immune complex deposition
Multi-system involvement
Clinical Manifestations:
✅ Butterfly rash (malar)
✅ Joint pain (arthralgia)
✅ Photosensitivity
✅ Renal involvement (nephritis)
✅ Fatigue
Rheumatoid Arthritis (RA)
Pathophysiology:
Autoimmune synovial inflammation Pannus formation (inflammatory tissue)
Joint destruction
Symmetric involvement
Clinical Manifestations:
✅ Morning stiffness >1 hour
✅ Symmetric joint swelling
✅ Rheumatoid nodules
✅ Systemic symptoms (fatigue, low-grade fever)
???? NCLEX-Style Practice QuestionsQuestion 1
A patient with heart failure is prescribed furosemide. Which assessment finding indicates the medication is effective?
A. Increased peripheral edema
B. Weight loss of 2 pounds in 24 hours
C. Blood pressure increase
D. Decreased urine output
Answer: B - Weight loss indicates fluid removal, showing diuretic effectiveness.
Question 2
A patient is experiencing a stroke. Which assessment finding requires immediate intervention?
A. Blood pressure 180/100 mmHg
B. Slurred speech
C. Respiratory rate 8/min
D. Arm weakness
Answer: C - Respiratory rate of 8/min indicates potential airway compromise requiring immediate intervention.
Question 3
Which clinical manifestation is most concerning in a patient with COPD?
A. Productive cough
B. Use of accessory muscles
C. Confusion and restlessness
D. Barrel chest appearance
Answer: C - Confusion and restlessness may indicate hypoxemia and CO2 retention.
Question 4
A patient with Type 1 diabetes presents with fruity breath odor and deep, rapid respirations. What condition should the nurse suspect?
A. Hypoglycemia
B. Diabetic ketoacidosis
C. Hyperglycemic hyperosmolar state
D. Diabetic nephropathy
Answer: B - Fruity breath and Kussmaul respirations are classic signs of DKA.Question 5
Which assessment finding in a patient with acute kidney injury indicates improvement?
A. Urine output increases from 20 mL/hr to 50 mL/hr
B. Serum creatinine increases
???? Study Strategies for Pathophysiology Success
C. BUN increases
D. Development of peripheral edema
Answer: A - Increasing urine output indicates improved kidney function.
Understanding Disease Processes
1. Learn normal physiology first - understand what should happen
2. Identify the disruption - what goes wrong in disease
3. Connect pathophysiology to clinical manifestations - why symptoms occur
4. Anticipate complications - what could happen next
5. Apply nursing interventions - how to help restore function
Memory Techniques
Concept Mapping:
Put disease in center
Branch out: causes → pathophysiology → manifestations → complications → interventions Acronyms and Mnemonics:
FAST for stroke assessment
RICE for injury management
ABCs for priorities
Visual Learning:
Draw pathophysiology flowcharts
Use diagrams to show disease progression Create comparison charts for similar conditions
Clinical Application
Think like a nurse: What would you assess? What would you do first? Prioritize systematically: Life-threatening issues firstConsider the whole patient: Multiple systems often involved Prevention focus: How can complications be prevented?
???? Quick Reference Tables
Normal vs. Abnormal Lab Values
Test
Normal Range
Critical Values
Glucose
70-100 mg/dL
<50 or >400 mg/dL
Creatinine
0.6-1.2 mg/dL
>4.0 mg/dL
BUN
10-20 mg/dL
>100 mg/dL
Troponin
<0.04 ng/mL
>0.04 ng/mL
INR
0.8-1.1
>5.0
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Emergency Recognition
System
Red Flag Symptoms
Action
Cardiac
Chest pain, SOB, diaphoresis
ECG, oxygen, IV access
Respiratory
Stridor, severe dyspnea, cyanosis
Airway support, oxygen
Neurologic
Sudden weakness, severe headache
FAST assessment, CT
Endocrine
Altered mental status, fruity breath
Blood glucose, ABG
Renal
Oliguria, confusion, edema
Labs, fluid assessment
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Medication Classes by System
System
Common Medications
Key Actions
Cardiac
ACE inhibitors, beta-blockers
Monitor BP, HR
Respiratory
Bronchodilators, corticosteroids
Assess breathing
Neurologic
Antiepileptics, dopaminergics
Monitor consciousness
Endocrine
Insulin, thyroid hormones
Monitor glucose, vitals
Renal
Diuretics, ACE inhibitors
Monitor I&O, electrolytes
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Remember: Pathophysiology is about understanding WHY things happen in the body during disease. Connect the mechanisms to the manifestations, and you'll excel on the NCLEX and in clinical practice!