South College NSG 5140 Advanced Pathophysiology
Final Exam Review | Best Q&A with Explanations
(Latest 2026) instant pdf download
1. Which cellular adaptation represents a reversible replacement of one mature cell
type by another mature cell type, often due to chronic irritation?
A. Hyperplasia
B. Dysplasia
C. Metaplasia
D. Anaplasia
Answer: C. Metaplasia
Metaplasia is a reversible change where one adult cell type is replaced by another
to better withstand chronic stress, such as ciliated columnar epithelium changing to
squamous epithelium in smokers.
2. During myocardial ischemia, what is the primary systemic effect of the failure of the
cellular Na+/K+ ATPase pump?
A. Cellular dehydration
B. Intracellular calcium influx
C. Intracellular potassium accumulation
D. Extracellular sodium influx
Answer: B. Intracellular calcium influx
When ATP is depleted, the Na+/K+ pump fails, leading to sodium accumulation
inside the cell. This reverses the sodium-calcium exchanger, causing a massive
influx of intracellular calcium, which activates destructive enzymes.
3. Which type of necrosis is characteristically seen in hypoxic injury of the central
nervous system (brain)?
A. Coagulative necrosis
B. Liquefactive necrosis
C. Caseous necrosis
D. Fat necrosis
Answer: B. Liquefactive necrosis
Brain tissue contains high amounts of lipids and lysosomal enzymes. When
, ischemic injury occurs, autolytic digestion liquefies the dead tissue, forming a fluid-
filled cavity.
4. A patient is diagnosed with an automated immune disease where antibodies block
acetylcholine receptors at the neuromuscular junction. Which disease is this?
A. Multiple Sclerosis
B. Myasthenia Gravis
C. Amyotrophic Lateral Sclerosis
D. Guillain-Barré Syndrome
Answer: B. Myasthenia Gravis
Myasthenia Gravis is a Type II hypersensitivity disorder characterized by
autoantibodies against nicotinic acetylcholine receptors, leading to progressive
muscle weakness.
5. What is the fundamental pathogenic mechanism behind Type I Hypersensitivity
reactions?
A. Deposition of immune complexes in tissues
B. IgE-mediated mast cell degranulation
C. T-cell mediated cytotoxicity
D. IgG or IgM antibody-mediated cell lysis
Answer: B. IgE-mediated mast cell degranulation
Type I hypersensitivity involves allergen binding to IgE antibodies already attached
to mast cells, triggering the release of histamine and other inflammatory mediators.
6. Which substance is the primary mediator of immediate vascular permeability and
vasodilation during acute inflammation?
A. Leukotrienes
B. Histamine
C. Prostaglandins
D. Interleukin-1
Answer: B. Histamine
Histamine is preformed and stored in mast cells. It is released immediately during
injury, causing rapid endothelial contraction, vasodilation, and increased capillary
permeability.
7. A patient presents with severe edema after suffering from deep vein thrombosis
(DVT). What is the primary Starling force responsible for this edema?
A. Decreased plasma oncotic pressure
B. Increased capillary hydrostatic pressure
, C. Increased interstitial oncotic pressure
D. Decreased interstitial hydrostatic pressure
Answer: B. Increased capillary hydrostatic pressure
A DVT causes venous obstruction, which increases upstream venous pressure. This
elevates capillary hydrostatic pressure, forcing fluid out of the vasculature into the
interstitial space.
8. Which molecular marker is highly specific for evaluating acute myocardial infarction
within the first 4 to 6 hours of chest pain?
A. Myoglobin
B. Creatine Kinase (CK-MB)
C. Cardiac Troponin I (cTnI)
D. Lactate Dehydrogenase (LDH)
Answer: C. Cardiac Troponin I (cTnI)
Cardiac Troponins are highly sensitive and specific structural components of cardiac
muscle. They rise within 3-4 hours of injury and remain elevated for days.
9. What is the primary compensatory neurohormonal mechanism activated in response
to decreased renal perfusion in chronic heart failure?
A. Antidiuretic hormone suppression
B. Natriuretic peptide release
C. Renin-angiotensin-aldosterone system (RAAS) activation
D. Parasympathetic nervous system stimulation
Answer: C. Renin-angiotensin-aldosterone system (RAAS) activation
Decreased renal perfusion causes the juxtaglomerular apparatus to secrete renin.
This leads to angiotensin II formation (vasoconstriction) and aldosterone release
(sodium/water retention) to support blood pressure.
10. In the pathogenesis of atherosclerosis, what occurs immediately after endothelial
injury and LDL oxidation?
A. Smooth muscle cell proliferation
B. Macrophage engulfment of LDL to form foam cells
C. Collagen deposition and fibrous plaque formation
D. Platelet aggregation and thrombus formation
Answer: B. Macrophage engulfment of LDL to form foam cells
Oxidized LDL acts as a chemoattractant for monocytes. Monocytes enter the tunica
intima, mature into macrophages, and engulf the modified lipids, transforming into
lipid-laden foam cells.
Final Exam Review | Best Q&A with Explanations
(Latest 2026) instant pdf download
1. Which cellular adaptation represents a reversible replacement of one mature cell
type by another mature cell type, often due to chronic irritation?
A. Hyperplasia
B. Dysplasia
C. Metaplasia
D. Anaplasia
Answer: C. Metaplasia
Metaplasia is a reversible change where one adult cell type is replaced by another
to better withstand chronic stress, such as ciliated columnar epithelium changing to
squamous epithelium in smokers.
2. During myocardial ischemia, what is the primary systemic effect of the failure of the
cellular Na+/K+ ATPase pump?
A. Cellular dehydration
B. Intracellular calcium influx
C. Intracellular potassium accumulation
D. Extracellular sodium influx
Answer: B. Intracellular calcium influx
When ATP is depleted, the Na+/K+ pump fails, leading to sodium accumulation
inside the cell. This reverses the sodium-calcium exchanger, causing a massive
influx of intracellular calcium, which activates destructive enzymes.
3. Which type of necrosis is characteristically seen in hypoxic injury of the central
nervous system (brain)?
A. Coagulative necrosis
B. Liquefactive necrosis
C. Caseous necrosis
D. Fat necrosis
Answer: B. Liquefactive necrosis
Brain tissue contains high amounts of lipids and lysosomal enzymes. When
, ischemic injury occurs, autolytic digestion liquefies the dead tissue, forming a fluid-
filled cavity.
4. A patient is diagnosed with an automated immune disease where antibodies block
acetylcholine receptors at the neuromuscular junction. Which disease is this?
A. Multiple Sclerosis
B. Myasthenia Gravis
C. Amyotrophic Lateral Sclerosis
D. Guillain-Barré Syndrome
Answer: B. Myasthenia Gravis
Myasthenia Gravis is a Type II hypersensitivity disorder characterized by
autoantibodies against nicotinic acetylcholine receptors, leading to progressive
muscle weakness.
5. What is the fundamental pathogenic mechanism behind Type I Hypersensitivity
reactions?
A. Deposition of immune complexes in tissues
B. IgE-mediated mast cell degranulation
C. T-cell mediated cytotoxicity
D. IgG or IgM antibody-mediated cell lysis
Answer: B. IgE-mediated mast cell degranulation
Type I hypersensitivity involves allergen binding to IgE antibodies already attached
to mast cells, triggering the release of histamine and other inflammatory mediators.
6. Which substance is the primary mediator of immediate vascular permeability and
vasodilation during acute inflammation?
A. Leukotrienes
B. Histamine
C. Prostaglandins
D. Interleukin-1
Answer: B. Histamine
Histamine is preformed and stored in mast cells. It is released immediately during
injury, causing rapid endothelial contraction, vasodilation, and increased capillary
permeability.
7. A patient presents with severe edema after suffering from deep vein thrombosis
(DVT). What is the primary Starling force responsible for this edema?
A. Decreased plasma oncotic pressure
B. Increased capillary hydrostatic pressure
, C. Increased interstitial oncotic pressure
D. Decreased interstitial hydrostatic pressure
Answer: B. Increased capillary hydrostatic pressure
A DVT causes venous obstruction, which increases upstream venous pressure. This
elevates capillary hydrostatic pressure, forcing fluid out of the vasculature into the
interstitial space.
8. Which molecular marker is highly specific for evaluating acute myocardial infarction
within the first 4 to 6 hours of chest pain?
A. Myoglobin
B. Creatine Kinase (CK-MB)
C. Cardiac Troponin I (cTnI)
D. Lactate Dehydrogenase (LDH)
Answer: C. Cardiac Troponin I (cTnI)
Cardiac Troponins are highly sensitive and specific structural components of cardiac
muscle. They rise within 3-4 hours of injury and remain elevated for days.
9. What is the primary compensatory neurohormonal mechanism activated in response
to decreased renal perfusion in chronic heart failure?
A. Antidiuretic hormone suppression
B. Natriuretic peptide release
C. Renin-angiotensin-aldosterone system (RAAS) activation
D. Parasympathetic nervous system stimulation
Answer: C. Renin-angiotensin-aldosterone system (RAAS) activation
Decreased renal perfusion causes the juxtaglomerular apparatus to secrete renin.
This leads to angiotensin II formation (vasoconstriction) and aldosterone release
(sodium/water retention) to support blood pressure.
10. In the pathogenesis of atherosclerosis, what occurs immediately after endothelial
injury and LDL oxidation?
A. Smooth muscle cell proliferation
B. Macrophage engulfment of LDL to form foam cells
C. Collagen deposition and fibrous plaque formation
D. Platelet aggregation and thrombus formation
Answer: B. Macrophage engulfment of LDL to form foam cells
Oxidized LDL acts as a chemoattractant for monocytes. Monocytes enter the tunica
intima, mature into macrophages, and engulf the modified lipids, transforming into
lipid-laden foam cells.
