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Advanced Pathophysiology Midterm Practice Exam: Comprehensive 150 Question Review

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ADVANCED PATHOPHYSIOLOGY MIDTERM PRACTICE EXAM: COMPREHENSIVE 150 QUESTION REVIEW

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ADVANCED PATHOPHYSIOLOGY MIDTERM PRACTICE EXAM: COMPREHENSIVE 150-
QUESTION REVIEW




SECTION A: CELLULAR ADAPTATION AND INJURY

1. A patient's cardiac muscle cells enlarge in response to chronic hypertension. This
cellular adaptation is best described as:

A. Hyperplasia
B. Metaplasia
C. Hypertrophy
D. Dysplasia

Rationale: Hypertrophy is an increase in cell size without an increase in cell number,
typical of permanent tissues like cardiac muscle.



2. Which cellular adaptation involves the replacement of one mature cell type with
another mature cell type?

A. Dysplasia
B. Metaplasia
C. Anaplasia
D. Atrophy

Rationale: Metaplasia is a reversible substitution of one differentiated cell type for another.



3. A biopsy shows disordered cell growth with variation in size and shape but no
invasion of the basement membrane. This is most consistent with:

,A. Dysplasia
B. Metaplasia
C. Hypertrophy
D. Neoplasia

Rationale: Dysplasia features disordered growth and pleomorphism but remains confined.



4. Which of the following is the most common cause of reversible cellular injury?

A. Ischemia
B. Apoptosis
C. Necrosis
D. Calcification

Rationale: Ischemia is the most common cause of reversible injury due to ATP depletion.



5. Coagulative necrosis is most likely to occur in which tissue following ischemia?

A. Brain
B. Heart
C. Pancreas
D. Lung

Rationale: Coagulative necrosis preserves tissue architecture and is classically seen in
ischemic injury to the heart.



6. Liquefactive necrosis is characteristically seen in:

A. Myocardial infarction
B. Bacterial abscess and brain infarction
C. Tuberculosis
D. Pancreatitis

Rationale: Liquefactive necrosis involves enzymatic digestion, seen in brain infarcts and
abscesses.



7. Caseous necrosis is most strongly associated with which condition?

,A. Acute pancreatitis
B. Tuberculosis
C. Myocardial infarction
D. Gangrenous appendicitis

Rationale: Caseous necrosis is a hallmark of tuberculosis infection.



8. Apoptosis differs from necrosis in that apoptosis:

A. Triggers a strong inflammatory response
B. Is an energy-dependent, programmed process
C. Causes cell swelling and lysis
D. Is always pathologic

Rationale: Apoptosis is ATP-dependent and genetically programmed.



9. Which intracellular accumulation is most commonly associated with alcoholic liver
disease?

A. Fat (steatosis)
B. Glycogen
C. Hemosiderin
D. Lipofuscin

Rationale: Alcohol metabolism promotes hepatic fat accumulation.



10. Dystrophic calcification is best characterized as:

A. Calcification in injured or dead tissue with normal serum calcium
B. Calcification in normal tissue with hypercalcemia
C. Calcification in metastatic bone lesions
D. Calcification in the thyroid gland only

Rationale: Dystrophic calcification occurs in damaged tissues despite normal serum
calcium.



SECTION B: INFLAMMATION AND REPAIR

, 11. Which vascular change is the earliest manifestation of acute inflammation?

A. Increased capillary permeability
B. Vasodilation
C. Neutrophil margination
D. Fibroblast proliferation

Rationale: Vasodilation is the earliest hemodynamic change.



12. The cardinal sign "dolor" in inflammation is primarily caused by:

A. Vasodilation
B. Prostaglandins and bradykinin
C. Neutrophil degranulation
D. Fibrin deposition

Rationale: Prostaglandins and bradykinin sensitize pain receptors.



13. Which cell is the predominant phagocyte in acute inflammation within the first 6 to
24 hours?

A. Macrophage
B. Neutrophil
C. Lymphocyte
D. Eosinophil

Rationale: Neutrophils are the first responders in early acute inflammation.



14. Which cell type predominates in chronic inflammation?

A. Neutrophil
B. Eosinophil
C. Macrophage and lymphocyte
D. Basophil

Rationale: Chronic inflammation is characterized by macrophages and lymphocytes.



15. Which mediator is responsible for the wheal-and-flare reaction?

Información del documento

Subido en
27 de septiembre de 2026
Número de páginas
37
Escrito en
2026/2027
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