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COMAT Pathophysiology and Disease Processes Flashcards

6 cards from real COMAT practice questions. Tap to flip, then mark Knew It or Still Learning — missed cards come back until you master them.

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  1. Which pathologic process characterizes the liver histology seen in alcoholic hepatitis?

    Answer: Hepatocyte ballooning, Mallory-Denk bodies, and neutrophilic infiltrate

    Alcoholic hepatitis shows hepatocyte ballooning degeneration, intracytoplasmic Mallory-Denk bodies, and neutrophil infiltration on histology.

  2. In acute pancreatitis, release of pancreatic enzymes into the parenchyma causes tissue destruction primarily through which mechanism?

    Answer: Autodigestion by activated trypsin, lipase, and phospholipase

    Premature intrapancreatic activation of digestive enzymes (especially trypsin) initiates autodigestion of pancreatic parenchyma, fat necrosis, and systemic inflammation.

  3. Rheumatoid arthritis preferentially affects which joint compartment compared to osteoarthritis?

    Answer: Synovial membrane (pannus formation) with secondary cartilage and bone erosion

    RA is primarily a synovitis — inflammatory pannus tissue invades and erodes cartilage and bone — whereas OA is primarily cartilage degeneration.

  4. A patient with community-acquired pneumonia has a PaO2/FiO2 ratio of 180 — which respiratory condition does this indicate?

    Answer: Moderate ARDS (acute respiratory distress syndrome)

    A P/F ratio of 100–200 meets criteria for moderate ARDS (Berlin definition), indicating diffuse alveolar damage impairing gas exchange beyond simple pneumonia.

  5. Which mechanism explains the nephrolithiasis risk in a patient with gout and hyperuricemia?

    Answer: Uric acid stones formed in acidic urine due to reduced urate solubility

    Hyperuricemia combined with low, acidic urine pH reduces uric acid solubility, promoting precipitation and uric acid stone formation.

  6. The pathophysiology of disseminated intravascular coagulation (DIC) involves which primary initiating event?

    Answer: Widespread tissue factor exposure activating simultaneous clotting and fibrinolysis

    DIC is triggered by massive tissue factor release (from sepsis, trauma, or malignancy) causing uncontrolled systemic thrombin generation, consuming clotting factors and platelets while activating fibrinolysis.