,South University NSG 5003 Week 10 Knowledge Check Quiz
| Adv Pathophysiology (2026) Q&A
1. A 55-year-old patient with chronic hypertension develops left ventricular
hypertrophy. Which cellular adaptation primarily drives this change?
A) Increased apoptosis
B) Mechanical stretch and angiotensin II signaling leading to increased protein
synthesis in cardiomyocytes
C) Decreased ATP production
D) Metaplasia of cardiac myocytes into fibroblasts
Correct Answer: Mechanical stretch and angiotensin II signaling leading to
increased protein synthesis in cardiomyocytes
Rationale: Sustained pressure overload causes cardiomyocyte hypertrophy via
mechanotransduction and neurohormonal activation, increasing contractile
protein synthesis. Apoptosis, decreased ATP production, and metaplasia are
distinct processes not responsible for compensatory hypertrophy. Understanding
this mechanism is essential for managing hypertensive heart disease.
2. Which finding is a hallmark of irreversible cell injury?
A) Cellular swelling
B) Detachment of ribosomes
C) Mitochondrial calcium influx and loss of mitochondrial membrane potential
D) Decreased glycogen stores
,Correct Answer: Mitochondrial calcium influx and loss of mitochondrial
membrane potential
Rationale: Irreversible injury is characterized by mitochondrial permeability
transition, calcium overload, and loss of oxidative phosphorylation, leading to cell
death. Cellular swelling, ribosomal detachment, and glycogen depletion are
reversible changes. Recognizing irreversible injury guides prognostication in
ischemic and toxic injuries.
3. A 4-year-old child with recurrent infections and failure to thrive is diagnosed
with severe combined immunodeficiency. Which defect underlies this condition?
A) B-cell deficiency only
B) Defective phagocyte function
C) Deficiency of both T-cell and B-cell immunity due to mutations in adenosine
deaminase or cytokine receptor genes
D) Overproduction of IgE
Correct Answer: Deficiency of both T-cell and B-cell immunity due to mutations
in adenosine deaminase or cytokine receptor genes
Rationale: SCID results from impaired development of both T and B
lymphocytes, often due to adenosine deaminase deficiency or cytokine receptor
mutations. Isolated B-cell deficiency, phagocyte defects, and IgE overproduction
cause different immunodeficiency syndromes. Early recognition is critical for
curative hematopoietic stem cell transplantation.
4. A 62-year-old man with a 40-pack-year smoking history presents with weight
loss, hemoptysis, and a persistent cough. Which pathophysiologic mechanism best
explains his symptoms?
, A) Chronic inflammation and metaplasia progressing to dysplasia
B) Autoimmune destruction of alveolar walls
C) IgE-mediated bronchoconstriction
D) Alpha-1 antitrypsin deficiency
Correct Answer: Chronic inflammation and metaplasia progressing to dysplasia
Rationale: Chronic smoking causes inflammation, metaplasia, and dysplasia that
can progress to bronchogenic carcinoma, presenting with hemoptysis, weight loss,
and persistent cough. Autoimmune alveolar destruction causes emphysema, IgE-
mediated bronchoconstriction causes asthma, and alpha-1 antitrypsin deficiency
causes early-onset emphysema. Recognizing this progression aids timely
diagnosis.
5. Which immunoglobulin is primarily responsible for mediating type I
hypersensitivity reactions?
A) IgA
B) IgG
C) IgM
D) IgE
Correct Answer: IgE
Rationale: IgE binds to mast cells and basophils, and cross-linking by antigen
triggers degranulation and release of histamine and other mediators. IgA protects
mucosal surfaces, IgG is involved in type II and III reactions, and IgM is the first
antibody produced. Identifying IgE is fundamental to allergy pathophysiology.
| Adv Pathophysiology (2026) Q&A
1. A 55-year-old patient with chronic hypertension develops left ventricular
hypertrophy. Which cellular adaptation primarily drives this change?
A) Increased apoptosis
B) Mechanical stretch and angiotensin II signaling leading to increased protein
synthesis in cardiomyocytes
C) Decreased ATP production
D) Metaplasia of cardiac myocytes into fibroblasts
Correct Answer: Mechanical stretch and angiotensin II signaling leading to
increased protein synthesis in cardiomyocytes
Rationale: Sustained pressure overload causes cardiomyocyte hypertrophy via
mechanotransduction and neurohormonal activation, increasing contractile
protein synthesis. Apoptosis, decreased ATP production, and metaplasia are
distinct processes not responsible for compensatory hypertrophy. Understanding
this mechanism is essential for managing hypertensive heart disease.
2. Which finding is a hallmark of irreversible cell injury?
A) Cellular swelling
B) Detachment of ribosomes
C) Mitochondrial calcium influx and loss of mitochondrial membrane potential
D) Decreased glycogen stores
,Correct Answer: Mitochondrial calcium influx and loss of mitochondrial
membrane potential
Rationale: Irreversible injury is characterized by mitochondrial permeability
transition, calcium overload, and loss of oxidative phosphorylation, leading to cell
death. Cellular swelling, ribosomal detachment, and glycogen depletion are
reversible changes. Recognizing irreversible injury guides prognostication in
ischemic and toxic injuries.
3. A 4-year-old child with recurrent infections and failure to thrive is diagnosed
with severe combined immunodeficiency. Which defect underlies this condition?
A) B-cell deficiency only
B) Defective phagocyte function
C) Deficiency of both T-cell and B-cell immunity due to mutations in adenosine
deaminase or cytokine receptor genes
D) Overproduction of IgE
Correct Answer: Deficiency of both T-cell and B-cell immunity due to mutations
in adenosine deaminase or cytokine receptor genes
Rationale: SCID results from impaired development of both T and B
lymphocytes, often due to adenosine deaminase deficiency or cytokine receptor
mutations. Isolated B-cell deficiency, phagocyte defects, and IgE overproduction
cause different immunodeficiency syndromes. Early recognition is critical for
curative hematopoietic stem cell transplantation.
4. A 62-year-old man with a 40-pack-year smoking history presents with weight
loss, hemoptysis, and a persistent cough. Which pathophysiologic mechanism best
explains his symptoms?
, A) Chronic inflammation and metaplasia progressing to dysplasia
B) Autoimmune destruction of alveolar walls
C) IgE-mediated bronchoconstriction
D) Alpha-1 antitrypsin deficiency
Correct Answer: Chronic inflammation and metaplasia progressing to dysplasia
Rationale: Chronic smoking causes inflammation, metaplasia, and dysplasia that
can progress to bronchogenic carcinoma, presenting with hemoptysis, weight loss,
and persistent cough. Autoimmune alveolar destruction causes emphysema, IgE-
mediated bronchoconstriction causes asthma, and alpha-1 antitrypsin deficiency
causes early-onset emphysema. Recognizing this progression aids timely
diagnosis.
5. Which immunoglobulin is primarily responsible for mediating type I
hypersensitivity reactions?
A) IgA
B) IgG
C) IgM
D) IgE
Correct Answer: IgE
Rationale: IgE binds to mast cells and basophils, and cross-linking by antigen
triggers degranulation and release of histamine and other mediators. IgA protects
mucosal surfaces, IgG is involved in type II and III reactions, and IgM is the first
antibody produced. Identifying IgE is fundamental to allergy pathophysiology.
