AANPCB Pathophysiology Flashcards
6 cards from real AANPCB practice questions. Tap to flip, then mark Knew It or Still Learning — missed cards come back until you master them.
Read the first 6 AANPCB Pathophysiology flashcards as text
Which mechanism explains the development of compensatory polycythemia in patients with chronic obstructive pulmonary disease (COPD)?
Answer: Hypoxia-stimulated erythropoietin release from the kidneys
Chronic hypoxia in COPD stimulates the kidneys to release erythropoietin, which drives increased red blood cell production to improve oxygen-carrying capacity.
In rheumatoid arthritis, what is the primary driver of joint destruction?
Answer: Pannus formation from activated synovial fibroblasts and immune cells
RA joint destruction is driven by pannus, an invasive tissue formed by activated synoviocytes and infiltrating immune cells that erodes cartilage and bone.
What pathophysiological mechanism explains why hypothyroidism causes hyperlipidemia?
Answer: Decreased LDL receptor expression leading to impaired LDL clearance
Thyroid hormone normally upregulates LDL receptors on hepatocytes; its deficiency reduces receptor expression and slows clearance of LDL from the bloodstream.
Which pathophysiological process is central to the development of Alzheimer's disease?
Answer: Amyloid-beta plaque accumulation and tau neurofibrillary tangles
Alzheimer's disease is characterized by extracellular amyloid-beta plaques and intracellular neurofibrillary tau tangles that disrupt neuronal function and lead to cell death.
What is the underlying pathophysiology of peripheral edema in right-sided heart failure?
Answer: Elevated venous hydrostatic pressure due to impaired right ventricular output
Right ventricular failure raises systemic venous pressure, increasing hydrostatic force in capillaries and forcing fluid into the interstitial space of dependent tissues.
In peptic ulcer disease, how does H. pylori infection contribute to mucosal injury?
Answer: Producing urease, disrupting the mucus layer, and triggering inflammation
H. pylori produces urease that neutralizes gastric acid locally, disrupts the protective mucus layer, and induces an inflammatory response that damages the gastric epithelium.