NREMT-P Pathology Practice Questions (220 Flashcards)

Stable angina is characterized by a fixed atherosclerotic plaque causing predictable ischemia during periods of increased myocardial oxygen demand. Pathologically, the fibrous cap remains intact. In contrast, unstable angina involves plaque rupture or erosion with overlying non-occlusive thrombus formation, leading to unpredictable pain at rest or with minimal exertion. \n\nExam Strategy: NREMT focuses on the predictability of stable angina vs. the dynamic nature of unstable angina. If the pain pattern changes in frequency or intensity, it is pathologically classified as unstable (part of ACS).

TXA is an antifibrinolytic. It competitively inhibits the activation of plasminogen to plasmin. Plasmin is the enzyme responsible for breaking down fibrin clots (fibrinolysis). By preventing clot breakdown, TXA stabilizes existing clots. Exam Tip: 2026 NREMT standards emphasize that TXA must be given within 3 hours of injury and is most effective when given as soon as possible after hemorrhage is identified.

Pathophysiology: SDH is typically a venous bleed from the bridging veins between the dura and arachnoid mater. \nRisk Factors: Brain atrophy (common in aging and alcoholism) puts these bridging veins under tension and creates more space in the skull. This allows for more movement of the brain during minor trauma, leading to vein shearing.\n\nClinical Appearance: Onset is often slower (subacute/chronic) compared to epidural bleeds. Symptoms may mimic dementia or stroke in the elderly.

This is Hyperosmolar Hyperglycemic State (HHS), typical of T2DM. In T2DM, there is enough circulating insulin to inhibit lipolysis and the subsequent formation of ketones (ketogenesis), but not enough to facilitate glucose uptake. In DKA (T1DM), the absolute lack of insulin triggers the breakdown of fats into fatty acids, which the liver converts into ketoacids. NREMT Tip: HHS typically presents with much higher glucose levels (>600 mg/dL) and more severe dehydration than DKA.

Rapid/Brisk Upper GI Bleeding. If an Upper GI bleed is massive (typically >1,000 mL), the blood acts as a potent cathartic, increasing intestinal motility. This causes the blood to pass through the entire GI tract so quickly that it does not undergo digestion (remaining red). Exam Strategy: If a patient has hematochezia AND signs of hemodynamic instability (shock), suspect a massive Upper GI source (like varices) rather than a lower source, as LGIBs are less frequently associated with immediate shock.