Pathophysiology & Disease Management Flashcards

A patient presents with acute decompensated heart failure (ADHF). Echocardiogram shows EF of 25%, BNP 2,400 pg/mL, BP 85/55 mmHg, and warm/wet profile on the Forrester-Stevenson hemodynamic classification. What does the warm/wet profile indicate and what is the treatment priority?

Answer: Warm/wet indicates adequate perfusion with congestion — IV diuresis is first-line therapy

Warm/wet profile (quadrant B) means adequate perfusion (warm extremities) with congestion (wet — elevated filling pressures) — IV diuresis is the treatment priority.

A patient develops acute liver failure (ALF) with encephalopathy. The pathophysiology of hepatic encephalopathy (HE) involves which primary mechanism?

Answer: Accumulation of neurotoxins (primarily ammonia) due to impaired hepatic detoxification, causing cerebral edema and astrocyte dysfunction

HE is primarily caused by ammonia accumulation — impaired liver fails to convert ammonia to urea; ammonia crosses the BBB, causes astrocyte swelling, cerebral edema, and neurotoxicity.

A 45-year-old patient with longstanding poorly controlled type 2 diabetes presents with painless vision loss in one eye. Funduscopy shows neovascularization and preretinal hemorrhage. What is the pathophysiological mechanism driving proliferative diabetic retinopathy?

Answer: Chronic retinal ischemia leading to upregulation of VEGF and pathological retinal neovascularization

Proliferative diabetic retinopathy results from chronic retinal ischemia triggering VEGF upregulation, driving pathological neovascularization that is fragile and prone to hemorrhage.

A patient with chronic kidney disease stage 4 develops normocytic anemia with low reticulocyte count. Which pathophysiological mechanism is primarily responsible?

Answer: Reduced erythropoietin production by diseased kidneys causing inadequate red blood cell production

The kidney produces 90% of circulating erythropoietin; CKD progressively reduces EPO production, causing normocytic, normochromic anemia of CKD with low reticulocyte response.

A 60-year-old patient develops sudden onset severe headache described as 'the worst headache of my life,' nausea, and nuchal rigidity. CT head is negative. What is the most critical next step and underlying pathophysiology if subarachnoid hemorrhage (SAH) is confirmed?

Answer: Lumbar puncture for xanthochromia; SAH results from arterial blood in the subarachnoid space causing meningeal irritation and cerebral vasospasm

LP for xanthochromia is essential when CT is negative but SAH is suspected — blood in CSF (or xanthochromia after 6+ hours) confirms SAH; early angiography identifies the aneurysm source.

A patient on mechanical ventilation develops worsening hypoxemia despite FiO2 0.80 and PEEP 12 cmH2O. ABG: PaO2 55 mmHg, PaCO2 38 mmHg, pH 7.38. Chest X-ray shows bilateral infiltrates. P/F ratio is 69. Which pathophysiological mechanism best explains this presentation?

Answer: Refractory hypoxemia from intrapulmonary shunting due to ARDS — alveolar flooding and collapse prevent oxygen exchange

P/F ratio 69 (PaO2/FiO2 = 55/0.8 = 69) meets severe ARDS criteria (<100); refractory hypoxemia despite high FiO2 and PEEP indicates intrapulmonary shunt (alveolar flooding/collapse).