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NR 283 PATHOPHYSIOLOGY EXAM 150 QUESTIONS AND ANSWERS

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NR 283 PATHOPHYSIOLOGY EXAM 150 QUESTIONS AND ANSWERS

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NR 283 PATHOPHYSIOLOGY
Course
NR 283 PATHOPHYSIOLOGY

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NR 283 PATHOPHYSIOLOGY EXAM 150
QUESTIONS AND ANSWERS




Page 1 of 225

,Question 1
Healing of large areas of skin loss (including dermis and epidermis) would be most
successful through:

a. rapid mitosis and regeneration of skin layers.
b. resolution of damaged cells in the area.
c. covering the area with biosynthetic skin substitute.
d. graft of fibrous tissue to the area.

Correct Answer
c. covering the area with biosynthetic skin substitute.

Question 1: A patient with chronic hypertension develops left ventricular
hypertrophy. Which cellular adaptation BEST explains this finding?

A. Hyperplasia

B. Atrophy

C. Hypertrophy

D. Metaplasia

CORRECT ANSWER: C. Hypertrophy

Rationale: Hypertrophy is an increase in cell size in response to increased workload,
such as pressure overload from hypertension. Cardiac myocytes are terminally
differentiated and cannot undergo hyperplasia (A). Atrophy (B) is decreased cell size
from disuse or decreased stimulation. Metaplasia (D) is reversible replacement of
one differentiated cell type with another, typically in response to chronic irritation.

#Tags: #CellularAdaptation #Hypertrophy #CardiovascularPathophysiology

Question 2: A patient with severe ischemic stroke develops brain tissue necrosis.
Which type of necrosis is MOST characteristic of cerebral infarction?

A. Coagulative necrosis

B. Liquefactive necrosis

C. Caseous necrosis

D. Fat necrosis

CORRECT ANSWER: B. Liquefactive necrosis




Page 2 of 225

,Rationale: Liquefactive necrosis occurs in the brain due to high lysosomal enzyme
content and low structural protein, causing tissue digestion into a liquid viscous
mass. Coagulative necrosis (A) occurs in heart, kidney, and liver ischemia where
architecture is preserved. Caseous necrosis (C) is characteristic of tuberculosis. Fat
necrosis (D) occurs in pancreatitis or breast trauma.

#Tags: #CellularInjury #Necrosis #NeurologicPathophysiology

Question 3: A patient with chronic gastroesophageal reflux disease (GERD)
develops Barrett esophagus. Which cellular adaptation is present?

A. Dysplasia

B. Hyperplasia

C. Metaplasia

D. Anaplasia

CORRECT ANSWER: C. Metaplasia

Rationale: Barrett esophagus involves metaplasia—replacement of normal stratified
squamous epithelium with intestinal-type columnar epithelium in response to
chronic acid exposure. Dysplasia (A) is abnormal cellular growth and organization
(premalignant). Hyperplasia (B) is increased cell number. Anaplasia (D) is loss of
differentiation in malignant cells.

#Tags: #CellularAdaptation #Metaplasia #GastrointestinalPathophysiology

Question 4: A patient with a deep venous thrombosis develops pulmonary
embolism. Which type of cellular injury is PRIMARILY responsible for the lung tissue
damage?



A. Hypoxic injury

B. Chemical injury

C. Infectious injury

D. Immunologic injury



CORRECT ANSWER: A. Hypoxic injury




Page 3 of 225

, Rationale: Pulmonary embolism obstructs pulmonary arterial blood flow, causing
ischemia and hypoxic injury to lung tissue distal to the occlusion. Chemical (B),
infectious (C), and immunologic (D) injuries have different mechanisms not primarily
involved in acute PE.



#Tags: #CellularInjury #Hypoxia #RespiratoryPathophysiology




Question 5: A patient with end-stage renal disease develops anemia. Which
mechanism BEST explains this finding?



A. Decreased erythropoietin production

B. Increased red blood cell destruction

C. Iron deficiency from gastrointestinal bleeding

D. Bone marrow suppression from uremic toxins



CORRECT ANSWER: A. Decreased erythropoietin production



Rationale: The kidneys produce erythropoietin, which stimulates red blood cell
production in bone marrow. Renal failure reduces erythropoietin synthesis, causing
normocytic, normochromic anemia. While uremic toxins (D) and GI bleeding (C) can
contribute, erythropoietin deficiency is the primary mechanism.



#Tags: #HematologicPathophysiology #Anemia #RenalPathophysiology




Page 4 of 225

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Course
NR 283 PATHOPHYSIOLOGY

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