Mixed Hospital Problems-FAST

20 Mixed Hospital Problems-FAST, High-Yield (Option 1)

1. Congestive Heart Failure (CHF):  acute decompensated

Pathophysiology: Ventricular systolic or diastolic dysfunction reduces forward cardiac output → neurohormonal activation (SNS, RAAS) → fluid retention and increased preload/afterload. Fluid backs into lungs (pulmonary edema) and/or periphery. Chronic remodeling worsens symptoms over time.

 Diagnosis: BNP/NT-proBNP ↑, CXR pulmonary congestion/edema, bedside echo shows reduced EF or diastolic dysfunction, JVD/leg edema, orthopnea.

 Management: Rapid IV diuresis (loop diuretics), oxygen/CPAP/BiPAP if hypoxic, vasodilators (nitro) if hypertensive, treat triggers (ischemia, arrhythmia, infection), start/optimize GDMT once stable.

2. COPD Exacerbation

Pathophysiology: Acute increase in airway inflammation, bronchoconstriction, mucus production and/or infection → worsened airflow limitation and V/Q mismatch causing hypoxemia/hypercapnia. Baseline emphysema/bronchitis predisposes to frequent exacerbations.

 Diagnosis: Increased dyspnea/wheeze/sputum; CXR to rule out pneumonia; ABG for hypercapnia/respiratory acidosis; spirometry not acute.

 Management: Short-acting bronchodilators (albuterol ± ipratropium), systemic steroids (oral/IV), antibiotics if bacterial features, oxygen titrated to target (88–92%), consider NIPPV for CO₂ retention.

3. Community-Acquired Pneumonia (CAP)

Pathophysiology: Pathogen (bacterial/viral) invades alveoli → local inflammation, consolidation, impaired gas exchange and systemic inflammatory response. Severity depends on host factors and organism virulence.

 Diagnosis: Fever, cough, consolidation on CXR, leukocytosis; blood/ sputum cultures in admitted pts; consider procalcitonin.

 Management: Empiric antibiotics per severity (cover typical/atypical), oxygen, IV fluids as needed, source control (drain empyema if present), escalate to ICU for respiratory failure or septic shock.

4. Sepsis / Septic Shock

Pathophysiology: Dysregulated host response to infection → systemic inflammation, endothelial dysfunction, vasodilation, capillary leak → tissue hypoperfusion and organ dysfunction. Progresses to refractory hypotension in septic shock.

 Diagnosis: Suspected/known infection + new organ dysfunction (SOFA qSOFA screening), lactate ↑, blood cultures prior to antibiotics.

 Management: Early broad-spectrum antibiotics (within 1 hour if septic shock), aggressive IV crystalloids (30 mL/kg initial), vasopressors (norepinephrine) for persistent hypotension, source control (drain/remove devices).

5. Acute Kidney Injury (AKI)

Pathophysiology: Sudden decline in GFR due to prerenal (hypoperfusion), intrinsic (ATN, glomerulonephritis), or postrenal (obstruction) causes → accumulation of nitrogenous wastes, electrolytes, and fluid. Ischemia/toxins damage tubules in intrinsic AKI.

 Diagnosis: Rise in creatinine and/or reduced urine output; urine studies (Na, FeNa, osm) to differentiate prerenal vs intrinsic; renal ultrasound for obstruction.

 Management: Treat underlying cause (restore perfusion, stop nephrotoxins), optimize volume status, correct electrolytes, renal replacement therapy for severe acidosis, hyperkalemia, volume overload, or uremia.

6. Diabetic Ketoacidosis (DKA)

Pathophysiology: Absolute/relative insulin deficiency → lipolysis and ketogenesis → metabolic acidosis, osmotic diuresis → dehydration and electrolyte disturbances (notably total body K⁺ depletion).

 Diagnosis: Hyperglycemia, high anion gap metabolic acidosis, serum/urine ketones, low bicarbonate, elevated anion gap.

 Management: IV fluids (restore volume), IV insulin infusion (after K⁺ checked), aggressive potassium repletion as needed, correct acidosis and precipitating cause (infection, MI).

7. Acute Ischemic Stroke

Pathophysiology: Sudden cerebral artery occlusion → focal ischemia → energy failure, cytotoxic edema, potential infarction if not reperfused. Time-dependent neuronal loss.

 Diagnosis: Focal neuro deficits; non-contrast CT to exclude hemorrhage; CT angiography/perfusion or MRI for vessel status and penumbra assessment.

 Management: Rapid stroke stroke-team evaluation, IV tPA if eligible (within window and no hemorrhage), thrombectomy for large vessel occlusion when indicated, blood pressure management, neurological ICU care.

8. Atrial Fibrillation with RVR (rapid ventricular response)

Pathophysiology: Chaotic atrial electrical activity → loss of organized atrial contraction and irregular rapid ventricular response → reduced cardiac output and risk of thromboembolism. Can be triggered by infection, ischemia, electrolyte imbalance.

 Diagnosis: Irregularly irregular rhythm on ECG, absent P waves, rapid ventricular rate; check electrolytes, TSH, and troponin if indicated.

 Management: Rate control (beta-blocker, diltiazem), rhythm control if indicated (cardioversion, antiarrhythmics), anticoagulation based on stroke risk (CHA₂DS₂-VASc) once stabilized/assessed.

9. Upper Gastrointestinal (UGI) Bleed

Pathophysiology: Bleeding from esophagus/stomach/duodenum (peptic ulcer, varices, erosive gastritis) → hematemesis/melena; severe bleeds cause hypovolemia and shock. Variceal bleeds due to portal hypertension.

 Diagnosis: Hematemesis/melena, Hb/hematocrit drop, hemodynamic instability; NG lavage sometimes; urgent endoscopy for localization.

 Management: ABCs, IV fluids/blood transfusion as needed, PPI infusion for suspected peptic bleed, octreotide and antibiotics for variceal bleed, urgent endoscopic therapy (banding/clip), ICU monitoring.

10. NSTEMI / Acute Coronary Syndrome (ACS)

Pathophysiology: Atherosclerotic plaque rupture or erosion → partial coronary occlusion → myocardial ischemia and necrosis without classic ST elevation. Inflammatory/thrombotic cascade enlarges injury.

 Diagnosis: Chest pain, troponin rise, ECG changes (ST-depression/T-wave inversions), coronary angiography for definitive anatomy.

 Management: MONA-B (oxygen if hypoxic, antiplatelet, anticoagulation), high-intensity statin, beta-blocker, risk-stratify for early cath/revascularization; manage complications (HF, arrhythmia).

11. Acute Respiratory Distress Syndrome (ARDS)

Pathophysiology: Severe inflammatory lung injury → increased alveolar-capillary permeability → noncardiogenic pulmonary edema, diffuse alveolar damage and severe hypoxemia. Often secondary to sepsis, aspiration, or trauma.

 Diagnosis: Acute hypoxemia with bilateral infiltrates on CXR/CT not explained by cardiac failure; PaO₂/FiO₂ ratio defines severity.

 Management: Lung-protective ventilation (low tidal volumes 6 mL/kg PBW), adequate PEEP, conservative fluids, prone positioning for severe ARDS, treat underlying cause.

12. Pulmonary Embolism (PE)

Pathophysiology: Thrombus (often from DVT) embolizes to pulmonary arteries → obstruction of flow, increased RV afterload → RV strain/failure and hypoxemia; massive PE causes hemodynamic collapse.

 Diagnosis: Sudden dyspnea, pleuritic chest pain, tachycardia; D-dimer for low-risk; CT pulmonary angiography is diagnostic; bedside echo may show RV strain.

 Management: Anticoagulation (heparin) unless contraindicated, thrombolysis for massive PE with hemodynamic instability, catheter/surgical embolectomy if needed, supportive care and oxygen.

13. Cirrhosis Complications (Ascites / Variceal Bleed / Encephalopathy)

Pathophysiology: Chronic liver fibrosis → portal hypertension and decreased synthetic function → ascites, varices, reduced detoxification (NH₃ accumulation → encephalopathy).

 Diagnosis: Clinical ascites, abdominal ultrasound, endoscopy for varices; elevated INR/low albumin; encephalopathy diagnosed clinically with precipitant search.

 Management: Sodium restriction, diuretics/paracentesis for ascites; variceal bleed: resuscitate, vasoactive agents (octreotide), antibiotics, urgent endoscopy with banding; hepatic encephalopathy: lactulose, rifaximin, treat precipitating causes.

14. Hyperkalemia

Pathophysiology: Reduced renal excretion, cellular shift, or excessive intake → increased serum K⁺ → membrane depolarization → cardiac conduction abnormalities and risk of fatal arrhythmias.

 Diagnosis: ECG changes (peaked T waves, widened QRS), serum K⁺ elevation, correlate with clinical context and renal function.

 Management: Stabilize myocardium (IV calcium), shift K⁺ intracellularly (insulin + glucose, beta-agonists, bicarbonate if acidotic), remove K⁺ (diuretics, cation exchangers, dialysis).

15. Hyponatremia

Pathophysiology: Excess free water relative to sodium from volume status changes, SIADH, or diuretics → hypo-osmolar state that can cause cerebral edema when acute or severe.

 Diagnosis: Low serum Na, assess volume status, urine osmolality and urine sodium to determine cause.

 Management: Treat underlying cause; acute/symptomatic hyponatremia → cautious hypertonic saline; chronic → fluid restriction, salt tablets, demeclocycline or vasopressin antagonists in select cases (specialist input).

16. Hypovolemic Shock / Volume Depletion

Pathophysiology: Loss of intravascular volume (hemorrhage, GI loss, diuresis) → decreased preload, reduced cardiac output, tissue hypoperfusion and organ dysfunction.

 Diagnosis: Hypotension, tachycardia, low JVP, low urine output, elevated lactate; bedside fluid responsiveness tests.

 Management: Rapid IV crystalloid resuscitation, stop ongoing losses (control bleeding), blood transfusion for hemorrhage, vasopressors only after adequate volume if needed.

17. Cellulitis / Severe Soft-Tissue Infection

Pathophysiology: Bacterial invasion of dermal/subcutaneous tissues (often streptococci/staph) causing localized inflammation; can progress to necrotizing infection if virulent organisms present.

 Diagnosis: Erythema, warmth, swelling, pain; systemic signs if severe; ultrasound/CT if abscess suspected.

 Management: Empiric IV antibiotics for moderate/severe cases, incision and drainage for abscess, MRSA coverage when risk factors present, escalate to surgical debridement if necrotizing infection suspected.

18. Deep Vein Thrombosis (DVT)

Pathophysiology: Virchow’s triad (stasis, endothelial injury, hypercoagulability) → thrombus formation in deep veins that can embolize to lungs.

 Diagnosis: Unilateral leg swelling/pain; duplex ultrasound is diagnostic; D-dimer for low-probability cases.

 Management: Anticoagulation (heparin → DOAC/warfarin), IVC filter if anticoagulation contraindicated, compression stockings and mobilization.

19. Acute Pancreatitis

Pathophysiology: Premature activation of pancreatic enzymes → autodigestion of pancreas → local inflammation, systemic inflammatory response, possible necrosis or organ failure. Common causes: gallstones, alcohol.

 Diagnosis: Epigastric pain radiating to back, elevated amylase/lipase, CT abdomen for complications.

 Management: NPO, aggressive IV fluids, pain control, treat underlying cause (ERCP for choledocholithiasis), ICU care for severe disease and complications.

20. Hypokalemia

Pathophysiology: Loss of potassium (GI losses, diuretics) or intracellular shift → hyperpolarization of cell membranes causing muscle weakness, ileus, and cardiac arrhythmias.

 Diagnosis: Low serum K⁺, ECG may show U waves/flattened T waves, assess magnesium (often low).

 Management: Oral or IV potassium repletion depending on severity, correct associated hypomagnesemia, identify and treat underlying cause (stop offending diuretics).