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Disease Pathology

Pathophysiology, signs & symptoms, diagnostics, and treatments

High-Yield Conditions

Expand each card to review pathophysiology, signs & symptoms, diagnostics, treatment, and key nursing considerations.

Pathophysiology: Heart can't pump enough blood to meet body's demands. Reduced cardiac output → congestion (left = pulmonary, right = systemic). Types: systolic (HFrEF, EF ≤40%) vs diastolic (HFpEF).
Signs & Symptoms: Dyspnea, orthopnea, JVD, peripheral edema, crackles, S3 gallop.
Key Diagnostics: BNP, echocardiogram, chest X-ray.
Treatment Approach: ACEi/ARBs, beta blockers, diuretics, ARNI (sacubitril/valsartan).
Nursing Considerations: Daily weights — report 2–3 lb gain in 24 hours. Strict I&O monitoring. Administer O₂ as ordered. Assess for fluid overload (crackles, edema, weight gain). Position patient in high Fowler's to ease breathing.
Pathophysiology: Coronary artery occlusion → myocardial ischemia → necrosis. STEMI (full thickness) vs NSTEMI (partial thickness). Irreversible damage begins within 20–40 minutes of occlusion.
Signs & Symptoms: Crushing substernal chest pain radiating to left arm/jaw, diaphoresis, N/V, SOB, sense of impending doom. Women may present atypically: fatigue, indigestion, back pain.
Key Diagnostics: 12-lead ECG (ST elevation in STEMI), elevated troponin I/T, CK-MB.
Treatment Approach: MONA (Morphine, O₂, Nitroglycerin, Aspirin). PCI within 90 minutes of first medical contact. Fibrinolytics if PCI unavailable within 120 min.
Nursing Considerations: Continuous ECG monitoring. Vital signs q15min during acute phase. Assess pain level and location frequently. Maintain IV access. Keep patient on bedrest with head elevated. Prepare for rapid transport to cath lab.
Pathophysiology: Insulin resistance + progressive beta-cell dysfunction → chronic hyperglycemia. Peripheral tissues (muscle, fat, liver) fail to respond to insulin, and the pancreas cannot compensate with enough insulin production.
Signs & Symptoms: The 3 P's: polyuria, polydipsia, polyphagia. Also fatigue, slow wound healing, recurrent infections (yeast, UTI), blurred vision, acanthosis nigricans.
Key Diagnostics: Fasting plasma glucose ≥126 mg/dL (×2), A1c ≥6.5%, 2-h OGTT ≥200 mg/dL, or random glucose ≥200 with symptoms.
Treatment Approach: Metformin first-line. Add sulfonylureas, GLP-1 agonists (semaglutide), SGLT2 inhibitors, DPP-4 inhibitors, or insulin as disease progresses. A1c target <7% (individualize).
Nursing Considerations: Teach foot care: inspect daily, wear well-fitting shoes, never go barefoot. Monitor blood glucose pre-meal and at bedtime. Teach sick day rules (continue meds, check glucose more often). Rotate injection sites if on insulin. Refer for annual eye and foot exams.
Pathophysiology: Chronic inflammation → airway narrowing + alveolar destruction (emphysema) + mucus hypersecretion (chronic bronchitis). Loss of elastic recoil → air trapping and hyperinflation. Primarily caused by smoking.
Signs & Symptoms: Dyspnea on exertion → at rest, chronic cough with sputum (especially mornings), barrel chest, pursed-lip breathing, prolonged expiratory phase, use of accessory muscles, wheezing.
Key Diagnostics: PFTs: FEV₁/FVC <0.70 post-bronchodilator confirms obstruction. Chest X-ray (hyperinflation, flattened diaphragm). ABG in exacerbation.
Treatment Approach: Bronchodilators: SABA (albuterol) for rescue, LAMA/LABA for maintenance. Inhaled corticosteroids for frequent exacerbators. O₂ therapy if resting SpO₂ ≤88%. Pulmonary rehabilitation. Smoking cessation.
Nursing Considerations: Teach pursed-lip breathing and diaphragmatic breathing. Encourage energy conservation — cluster ADLs, sit for tasks when possible. O₂ safety: no smoking, no open flames. Position in tripod position to ease breathing. Encourage adequate nutrition (small, frequent meals). Monitor for signs of CO₂ retention with high-flow O₂.
Pathophysiology: Progressive, irreversible nephron loss → decreased GFR → waste accumulation, fluid/electrolyte imbalance, decreased erythropoietin and vitamin D activation. Staged 1–5 based on GFR. Leading causes: diabetes and hypertension.
Signs & Symptoms: Often silent until late stages. Fatigue, edema, hypertension, anemia (pallor, weakness), pruritus (uremic), nausea, metallic taste, uremic frost in end-stage.
Key Diagnostics: Serum creatinine and eGFR (staging), BUN, urinalysis (proteinuria, microalbuminuria), renal ultrasound. Kidney biopsy if cause unclear.
Treatment Approach: Manage underlying cause (HTN, DM). ACEi/ARBs to reduce proteinuria and slow progression. Erythropoietin-stimulating agents for anemia. Phosphate binders. Dialysis at Stage 5 (GFR <15). Renal transplant.
Nursing Considerations: Monitor strict I&O and daily weights. Low sodium, potassium, and phosphate diet. Renal dosing — many drugs require dose adjustment. Assess AV fistula/graft (thrill and bruit) if on hemodialysis. Monitor for hyperkalemia (ECG changes, muscle weakness).
Pathophysiology: Chronic, progressive liver damage → diffuse fibrosis and nodular regeneration → portal hypertension and decreased hepatic synthetic function. Common causes: alcohol, viral hepatitis B/C, NAFLD/NASH.
Signs & Symptoms: Jaundice, ascites, spider angiomas, palmar erythema, gynecomastia, caput medusae, hepatic encephalopathy (confusion, asterixis/flapping tremor), bleeding tendency, fetor hepaticus.
Key Diagnostics: LFTs (AST/ALT ratio >2:1 in alcoholic cirrhosis), elevated PT/INR (decreased synthetic function), low albumin, thrombocytopenia. Imaging: ultrasound, CT, FibroScan. Liver biopsy gold standard.
Treatment Approach: Treat underlying cause (abstinence, antivirals). Lactulose for hepatic encephalopathy. Diuretics (spironolactone ± furosemide) for ascites. Non-selective beta blockers for variceal prophylaxis. Paracentesis for tense ascites. Liver transplant in end-stage.
Nursing Considerations: Monitor for bleeding: check gums, IV sites, stool for melena. Daily weights and abdominal girth measurements. Neuro checks q4h for encephalopathy (asterixis, orientation). Low sodium diet (2g/day). Strict I&O. Avoid hepatotoxic drugs (acetaminophen max 2g/day).
Pathophysiology: Ischemic (87%): thrombotic or embolic occlusion of cerebral artery. Hemorrhagic (13%): vessel rupture → bleeding into brain tissue. 'Time is brain' — 1.9 million neurons lost per minute of untreated large-vessel ischemic stroke.
Signs & Symptoms: FAST: Face drooping, Arm weakness, Speech difficulty, Time to call 911. Also: sudden confusion, vision changes (hemianopsia), severe headache (especially hemorrhagic), gait disturbance, unilateral neglect.
Key Diagnostics: Non-contrast CT head first (rule out hemorrhage). MRI with DWI for ischemic stroke. CTA/MRA to identify large vessel occlusion. Carotid ultrasound, echo to find source.
Treatment Approach: Ischemic: IV tPA (alteplase) within 4.5 hours of symptom onset — must rule out hemorrhage first. Mechanical thrombectomy for large vessel occlusion (up to 24h in selected patients). Hemorrhagic: aggressive BP control, reverse any anticoagulation, possible surgical evacuation.
Nursing Considerations: NIHSS assessment on arrival and at regular intervals. Frequent neuro checks (LOC, pupils, motor strength). Swallow screen before any PO intake — NPO until cleared. Aspiration precautions: upright position, chin tuck, thickened liquids. Fall precautions. Monitor for increased ICP (Cushing's triad: HTN, bradycardia, irregular respirations).
Pathophysiology: Dysregulated host response to infection → systemic inflammatory response → massive vasodilation + increased capillary permeability → distributive shock → tissue hypoperfusion → multi-organ failure. Septic shock: sepsis with persistent hypotension requiring vasopressors + lactate >2 mmol/L despite adequate fluid resuscitation.
Signs & Symptoms: Fever (>38°C) or hypothermia (<36°C), tachycardia, tachypnea, altered mental status (early sign!), hypotension unresponsive to fluids (septic shock), decreased urine output, mottled/cool skin, elevated lactate.
Key Diagnostics: Serum lactate >2 mmol/L (tissue hypoperfusion). Blood cultures (×2 sets) before antibiotics. Elevated WBC (or leukopenia). Procalcitonin. Source identification: CXR, UA, wound cultures.
Treatment Approach: Sepsis bundle (within 1 hour): blood cultures, lactate measurement, broad-spectrum antibiotics, IV crystalloid 30 mL/kg for hypotension or lactate ≥4, vasopressors (norepinephrine first-line) if refractory hypotension. Source control: remove lines, drain abscesses.
Nursing Considerations: qSOFA screening: altered mental status, RR ≥22, SBP ≤100. Early recognition saves lives — know your facility's sepsis protocol. Monitor VS q15min during acute phase. Strict I&O (Foley for accurate output). Titrate vasopressors to MAP ≥65. Prepare for possible ICU transfer.
Pathophysiology: Community-acquired pneumonia (CAP): infection of lung parenchyma → alveolar inflammation and consolidation → impaired gas exchange. Most common pathogens: S. pneumoniae, H. influenzae, atypical bacteria (Mycoplasma, Chlamydia). Risk factors: age >65, COPD, smoking, immunocompromised, aspiration.
Signs & Symptoms: Productive cough (purulent sputum), fever with chills/rigors, pleuritic chest pain, dyspnea, tachypnea, crackles/rhonchi on auscultation, dullness to percussion over consolidated areas, tactile fremitus increased.
Key Diagnostics: Chest X-ray (infiltrates, consolidation). Sputum culture and Gram stain. Blood cultures (×2). CBC (leukocytosis). CURB-65 score to determine severity and admission need: Confusion, Urea >7 mmol/L, RR ≥30, low BP (SBP <90 or DBP ≤60), age ≥65.
Treatment Approach: Empiric antibiotics based on setting: outpatient — macrolide or doxycycline; inpatient — beta-lactam + macrolide or respiratory fluoroquinolone. O₂ therapy for hypoxemia. Hydration, antipyretics, chest physiotherapy. Severe: ICU admission, possible mechanical ventilation.
Nursing Considerations: Monitor respiratory status: rate, depth, SpO₂, breath sounds. Encourage deep breathing and coughing (incentive spirometer). Position in semi-Fowler's to high-Fowler's to optimize lung expansion. Encourage fluids (2–3 L/day unless contraindicated). Administer antibiotics on time — timing affects outcomes. Sputum culture before first antibiotic dose.
Pathophysiology: Virchow's triad: venous stasis + endothelial injury + hypercoagulability → thrombus formation in deep veins, most commonly in lower extremities (calf, popliteal, femoral, iliac). Risk factors: immobility, surgery, trauma, pregnancy, OCPs, smoking, obesity, cancer, inherited clotting disorders.
Signs & Symptoms: Unilateral leg swelling and edema, calf pain/tenderness (especially with dorsiflexion — Homan's sign, though unreliable), warmth and erythema over affected area, palpable cord. May be asymptomatic — high index of suspicion needed.
Key Diagnostics: D-dimer (high sensitivity, low specificity — if negative, rules out DVT in low-risk patients). Duplex venous ultrasound (gold standard). Wells criteria for pre-test probability. Venography rarely needed.
Treatment Approach: Anticoagulation: LMWH (enoxaparin) or fondaparinux as bridge to warfarin, or direct oral anticoagulant (rivaroxaban, apixaban). Duration: 3–6 months typically. IVC filter if anticoagulation is contraindicated. Compression stockings post-acute phase. Elevate affected extremity.
Nursing Considerations: Measure bilateral calf and thigh circumference daily at marked locations. Bed rest during acute phase with affected leg elevated above heart level. NEVER massage the affected leg — risk of dislodging clot. Monitor for signs of PE (sudden dyspnea, chest pain, tachycardia). Administer anticoagulants on schedule — do not miss doses. Monitor aPTT/anti-Xa levels as ordered.
Pathophysiology: Most commonly a complication of DVT: thrombus dislodges from deep veins → travels through right heart → lodges in pulmonary artery → obstructs pulmonary blood flow → ventilation-perfusion (V/Q) mismatch → impaired gas exchange and increased pulmonary vascular resistance → right ventricular strain. Massive PE can cause obstructive shock and death.
Signs & Symptoms: Sudden onset dyspnea, pleuritic chest pain, tachypnea, tachycardia, hemoptysis (late sign), apprehension/anxiety, low-grade fever, syncope (massive PE). Signs of DVT may be present. Classic triad (hemoptysis, dyspnea, chest pain) present in <30%.
Key Diagnostics: CTA chest (CT pulmonary angiography) — gold standard, detects filling defects. D-dimer: highly sensitive; if negative in low-risk patient, PE ruled out. ABG (respiratory alkalosis with hypocapnia). ECG: sinus tachycardia, possibly S1Q3T3 pattern. V/Q scan if CTA contraindicated. Troponin and BNP for risk stratification.
Treatment Approach: Anticoagulation: LMWH or fondaparinux bridge to warfarin, or DOAC (rivaroxaban, apixaban). Thrombolytics (tPA/alteplase) for massive PE with hemodynamic instability. Catheter-directed thrombolysis or embolectomy for selected patients. O₂ therapy. Hemodynamic support with IV fluids and vasopressors if needed.
Nursing Considerations: Immediate O₂ to maintain SpO₂ >92%. Continuous cardiac and SpO₂ monitoring. Keep patient in semi-Fowler's. Monitor for bleeding with anticoagulation (gums, IV sites, bruising, melena, hematuria). Assess for right ventricular failure: JVD, peripheral edema, hepatomegaly. Strict bed rest during acute phase. Prepare for possible thrombolytic administration.
Pathophysiology: Most commonly caused by Hashimoto's thyroiditis (autoimmune destruction of thyroid gland). Decreased thyroid hormone production → slowed metabolism → affects virtually every organ system. Secondary causes: thyroidectomy, radioactive iodine, iodine deficiency, pituitary dysfunction, medications (amiodarone, lithium).
Signs & Symptoms: Fatigue, lethargy, cold intolerance, unexplained weight gain, constipation, bradycardia, dry/coarse skin and hair, hair loss, periorbital edema, myxedema (non-pitting edema), slowed speech and cognition, menorrhagia, hoarseness, depression.
Key Diagnostics: Elevated TSH (most sensitive), low free T4. Anti-TPO antibodies positive in Hashimoto's. Lipid panel (elevated cholesterol). Anemia (macrocytic or normocytic). TSH screening in at-risk populations.
Treatment Approach: Levothyroxine (T4) replacement — synthetic T4. Dose based on weight and age; start low and titrate slowly in elderly and cardiac patients. Take on an empty stomach, 30–60 min before breakfast, separated from calcium/iron supplements by 4 hours. Life-long treatment. Monitor TSH every 6–8 weeks until stable, then annually.
Nursing Considerations: Teach patient to take levothyroxine on an empty stomach with full glass of water, at least 30–60 min before breakfast. Do not take with calcium, iron, or antacids (separate by 4 hours). Stress that therapy is life-long — never stop abruptly. Report signs of over-replacement (hyperthyroid symptoms: palpitations, heat intolerance, insomnia, weight loss). Myxedema coma is a medical emergency — severe hypothyroidism with altered mental status, hypothermia, and bradycardia.
Pathophysiology: Graves' disease: autoimmune disorder — TSH receptor antibodies (TRAb) stimulate thyroid → excessive T3/T4 production → hypermetabolic state. Most common cause of hyperthyroidism. Other causes: toxic multinodular goiter, thyroiditis, excessive iodine intake.
Signs & Symptoms: Heat intolerance, diaphoresis, weight loss despite increased appetite, tachycardia/palpitations, tremor, nervousness/anxiety, insomnia, hyperreflexia, warm/moist skin, fine hair, exophthalmos (proptosis) — hallmark of Graves', pretibial myxedema, goiter, lid lag.
Key Diagnostics: Low/suppressed TSH, elevated free T4 and T3. TSH receptor antibodies (TRAb) confirm Graves'. Radioactive iodine uptake (RAIU): increased in Graves', low in thyroiditis. Thyroid ultrasound.
Treatment Approach: Antithyroid drugs: methimazole (first-line, not in 1st trimester pregnancy) or PTU (propylthiouracil — preferred in 1st trimester). Radioactive iodine (¹³¹I) — destroys thyroid tissue. Thyroidectomy if large goiter, suspected malignancy, or refractory to other treatments. Beta blockers (propranolol) for symptomatic tachycardia/tremor until euthyroid.
Nursing Considerations: Monitor for agranulocytosis with methimazole/PTU — teach patient to report sore throat and fever immediately (stop drug, check WBC). Radioactive iodine precautions: isolate patient 24–72 hours, use private bathroom, no contact with pregnant women/children. Post-thyroidectomy: monitor for hypocalcemia (Chvostek's and Trousseau's signs), airway obstruction, and thyroid storm. Maintain cool environment. Reduce stimulation.
Pathophysiology: Most common anemia worldwide. Microcytic hypochromic anemia: inadequate iron → decreased heme synthesis → small (microcytic) and pale (hypochromic) RBCs. Causes: chronic blood loss (GI bleed, heavy menstruation), poor dietary intake, malabsorption (celiac, gastric bypass), increased demand (pregnancy).
Signs & Symptoms: Fatigue, pallor (skin, conjunctiva, nail beds), tachycardia, dyspnea on exertion, brittle/spoon-shaped nails (koilonychia), glossitis (smooth, sore tongue), angular cheilitis, pica (craving ice, dirt, starch — pagophagia is classic for iron deficiency), restless leg syndrome.
Key Diagnostics: CBC: low Hb/Hct, low MCV (<80 fL — microcytic), low MCHC (hypochromic). Low serum ferritin (best indicator of iron stores, <30 ng/mL diagnostic). Low serum iron, elevated TIBC, low transferrin saturation (<16%). Stool guaiac to rule out GI bleed.
Treatment Approach: Ferrous sulfate 325 mg PO — 65 mg elemental iron per tablet. Typically 2–3 tablets daily. Take on an empty stomach with vitamin C (orange juice) to enhance absorption. Expect dark/green/black stools (non-toxic). Duration: 3–6 months to replenish stores (not just until Hb normalizes). IV iron if intolerant to oral or severe deficiency.
Nursing Considerations: Teach patient that ferrous sulfate causes dark stools — this is normal, not GI bleed. Take with vitamin C source for better absorption (orange juice). Avoid taking with calcium, antacids, or tea (tannins inhibit absorption) — separate by 2 hours. GI side effects: constipation, nausea, epigastric pain — can take with food if needed (reduces absorption but improves tolerance). Monitor reticulocyte count (rises in 5–10 days with effective therapy).
Pathophysiology: Premature activation of pancreatic enzymes (trypsinogen → trypsin) within the pancreas → autodigestion of pancreatic tissue → intense inflammation and necrosis. Most common causes: gallstones (obstruct pancreatic duct) and chronic alcohol use (accounts for ~80% of cases). Other causes: hypertriglyceridemia, hypercalcemia, medications, ERCP, trauma, infections.
Signs & Symptoms: Severe epigastric pain radiating to back (band-like), worsened when lying supine, relieved by leaning forward (classic). Nausea and vomiting, low-grade fever, abdominal distension, tachycardia, hypotension (third-spacing and hypovolemia). Severe: Cullen's sign (periumbilical bruising), Grey Turner's sign (flank bruising) — indicate hemorrhagic pancreatitis.
Key Diagnostics: Elevated serum amylase (rises 2–12h, returns to normal in 3–5 days). Elevated serum lipase (more specific, rises 4–8h, peaks at 24h, stays elevated 7–14 days). Imaging: CT abdomen with contrast (severity assessment, necrosis). Ranson's criteria for severity. Abdominal ultrasound to identify gallstones.
Treatment Approach: NPO initially (rest the pancreas). Aggressive IV fluid resuscitation (LR preferred over NS). Pain control (IV opioids — morphine traditionally avoided due to sphincter of Oddi spasm, but evidence is mixed; hydromorphone often used). NG tube if persistent vomiting or ileus. Nutritional support: advance to oral diet as tolerated, or enteral nutrition (NG or NJ) if severe. ERCP for gallstone pancreatitis within 24–48h.
Nursing Considerations: Maintain NPO status — no food, no sips of water until pain resolved and bowel sounds return. Strict I&O and vital signs monitoring — these patients can third-space liters of fluid. Assess pain level, location, and quality regularly. Position patient sitting upright with knees flexed to reduce pain. Monitor for complications: ARDS, AKI, DIC, hypocalcemia (check Chvostek's/Trousseau's). Watch for signs of infection (necrotizing pancreatitis).
Pathophysiology: Bleeding from the upper GI tract (proximal to the ligament of Treitz). Most common causes: peptic ulcer disease (PUD — H. pylori, NSAIDs), esophageal varices (portal hypertension from cirrhosis), Mallory-Weiss tears (forceful vomiting), erosive esophagitis, and gastric/esophageal malignancy. Severity ranges from occult bleeding to life-threatening hemorrhage.
Signs & Symptoms: Hematemesis: frank red blood (active bleeding) or coffee-ground emesis (blood exposed to gastric acid). Melena: black, tarry, foul-smelling stools (oxidized blood). Occult bleeding: positive guaiac, iron deficiency anemia. Signs of hypovolemia: tachycardia, hypotension, orthostasis, pallor, cool/clammy skin.
Key Diagnostics: CBC (Hgb/Hct may be normal acutely — takes 24h to equilibrate), BUN elevated (BUN:Cr ratio >20:1 suggests upper GI source due to digestion and absorption of blood proteins). EGD (esophagogastroduodenoscopy) — diagnostic and therapeutic (gold standard), ideally within 24 hours. Stool guaiac. Type and crossmatch for possible transfusion.
Treatment Approach: ABCDE: airway protection (risk of aspiration), 2 large-bore IVs for fluid resuscitation. IV PPI (pantoprazole 80 mg bolus + 8 mg/hr infusion) for PUD. Octreotide/terlipressin + prophylactic antibiotics for variceal bleed. Endoscopic therapy: epinephrine injection, thermal coagulation, clips, banding (varices). Blood transfusion if Hgb <7 (restrictive strategy). NPO until EGD complete.
Nursing Considerations: Maintain NPO status — nothing by mouth until EGD completed. Monitor vital signs q15min during active bleeding — watch for signs of hemorrhagic shock (tachycardia first, then hypotension). Two large-bore IVs (18G minimum). Assess emesis and stool: color, volume, frequency. Monitor Hgb/Hct trends. Blakemore/Sengstaken-Blakemore tube for refractory variceal bleeding — keep scissors at bedside (cut tube if it migrates and obstructs airway).
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