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1. A 68-year-old patient with peripheral artery disease develops a non-healing
wound on the lower leg. Microscopic examination shows coagulative necrosis with
preservation of cellular outlines. Which pathophysiological process best explains
this tissue death?
• A) Autolysis from enzymatic digestion by the cell's own enzymes
• B) Ischemia causing denaturation of structural proteins without enzymatic
degradation
• C) Liquefactive necrosis from bacterial infection and neutrophil activity
• D) Caseous necrosis from granulomatous inflammation
Answer: B
Rationale: Coagulative necrosis is characteristic of ischemic injury in most tissues except
the brain. Ischemia inhibits lysosomal enzymes that would otherwise digest the tissue,
causing denaturation of structural proteins while preserving cellular architecture
temporarily—creating "ghost outlines" of cells .
2. A patient presents with redness, heat, swelling, and pain at a surgical incision
site 48 hours postoperatively. Which vascular event initiates this acute
inflammatory response?
• A) Vasoconstriction of arterioles to reduce blood flow
• B) Vasodilation of arterioles and increased vascular permeability
• C) Lymphatic vessel constriction to trap fluid in tissues
• D) Platelet aggregation and thrombosis in microcirculation
,Answer: B
Rationale: The classic signs of acute inflammation (rubor, calor, tumor, dolor) are
initiated by vasoactive mediators (histamine, prostaglandins, leukotrienes) causing
transient vasoconstriction followed by prolonged vasodilation of arterioles (increased
blood flow = redness and heat) and increased vascular permeability of venules (allows
protein-rich fluid exudation = swelling/edema) .
3. During the proliferative phase of wound healing, which cell type is primarily
responsible for collagen synthesis and wound contraction?
• A) Neutrophils
• B) Macrophages
• C) Fibroblasts
• D) Epithelial cells
Answer: C
Rationale: The proliferative phase (days 3–21) is characterized by fibroblast migration
and activation. Fibroblasts synthesize type III collagen (later replaced by type I), secrete
fibronectin, and differentiate into myofibroblasts containing actin filaments that contract
the wound .
4. A patient with diabetes mellitus has impaired wound healing. Which
pathophysiological mechanism contributes most to this delayed healing?
• A) Excessive collagen cross-linking causing tissue stiffness
• B) Decreased angiogenesis and impaired macrophage function
• C) Hyperproliferation of fibroblasts causing excessive scar formation
• D) Increased neutrophil apoptosis leading to premature inflammation resolution
Answer: B
Rationale: Diabetes impairs wound healing through microvascular disease (reduced
angiogenesis limiting oxygen/nutrient delivery) and impaired immune function
(macrophages show defective phagocytosis, chemotaxis, and cytokine production).
, Advanced glycation end-products (AGEs) cross-link collagen abnormally and impair cell
signaling .
5. A patient with chronic hypertension develops left ventricular hypertrophy. This
cellular adaptation is best described as:
• A) Hyperplasia
• B) Hypertrophy
-- C) Metaplasia
• D) Dysplasia
Answer: B
Rationale: Hypertrophy is an increase in cell size without an increase in cell number. In
hypertension, the heart works harder against high pressure, causing cardiac muscle cells
to enlarge .
6. A patient with long-standing GERD undergoes an esophageal biopsy. The
pathology report indicates columnar epithelium in the distal esophagus, replacing
the normal squamous epithelium. This change is termed:
• A) Hyperplasia
• B) Metaplasia
• C) Dysplasia
• D) Atrophy
Answer: B
Rationale: Metaplasia is the reversible replacement of one mature cell type by another.
In Barrett's esophagus (caused by chronic acid reflux), the more acid-resistant columnar
epithelium replaces squamous epithelium as a protective adaptation .
7. Which characteristic distinguishes necrosis from apoptosis?
• A) Cell shrinkage