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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 mechanism best explains the pain of angina pectoris in coronary artery disease?

    Answer: Ischemia-induced accumulation of metabolites stimulating cardiac nociceptors

    Myocardial ischemia causes metabolite accumulation (adenosine, lactate, H+) that stimulates cardiac sympathetic afferents, producing the characteristic chest pain of angina.

  2. Type 2 diabetes mellitus is primarily characterized by which underlying pathophysiologic mechanism?

    Answer: Peripheral insulin resistance with relative insulin deficiency

    Type 2 DM involves peripheral tissue insulin resistance (especially muscle and liver) combined with progressive beta cell dysfunction leading to relative insulin deficiency.

  3. A patient with COPD has a PaCO2 of 55 mmHg chronically — which acid-base disorder is present?

    Answer: Chronic respiratory acidosis with metabolic compensation

    Chronic CO2 retention in COPD leads to respiratory acidosis with compensatory renal bicarbonate retention, resulting in a near-normal pH (chronic respiratory acidosis).

  4. The pathophysiology of nephrotic syndrome involves loss of which glomerular barrier property?

    Answer: Charge selectivity allowing albumin to cross the GBM

    Nephrotic syndrome results from loss of the glomerular basement membrane's negative charge barrier, permitting albumin (normally repelled) to pass into the filtrate.

  5. Which cytokine is primarily responsible for the fever response during acute systemic infection?

    Answer: IL-1β

    IL-1β (along with IL-6 and TNF-α) is an endogenous pyrogen that acts on the hypothalamus to raise the thermoregulatory set point, producing fever.

  6. In left heart failure, pulmonary edema occurs primarily due to which hemodynamic change?

    Answer: Elevated pulmonary capillary wedge pressure exceeding oncotic pressure

    Left ventricular failure raises left atrial and pulmonary venous pressure (PCWP), which when it exceeds plasma oncotic pressure (~25 mmHg), forces fluid into alveoli.