NSG 530 Final Exam Actual Exam V1 | NSG 530 Advanced
Pathophysiology (NSG530 Final Exam) [PDF] | Wilkes University
1. A 65-year-old male with a history of chronic smoking presents with a persistent cough and
significant weight loss. A biopsy of the bronchial epithelium reveals that the normal ciliated
columnar cells have been replaced by stratified squamous epithelium. Which cellular
adaptation process is most likely occurring?
A. Atrophy
B. Hyperplasia
C. Metaplasia
D. Dysplasia
Answer: C
Rationale: Metaplasia is a reversible change in which one adult cell type is replaced by
another adult cell type. In this clinical scenario, the chronic irritation from cigarette smoke
induces the bronchial columnar cells to transform into tougher squamous cells. While this
new epithelium is more resistant to smoke, it lacks the protective cilia and mucus secretion
of the original tissue.
2. Following an acute myocardial infarction, which process is responsible for the additional
damage that occurs when blood flow is restored to the ischemic zone?
A. Reperfusion injury
B. Anaerobic glycolysis
C. Apoptosis via extrinsic pathway
D. Autophagy
Answer: A
Rationale: Reperfusion injury occurs when the restoration of blood flow to ischemic
tissues leads to the massive production of reactive oxygen species (ROS). These free
radicals damage cell membranes through lipid peroxidation and trigger the inflammatory
response. This phenomenon often results in greater tissue damage than the initial ischemic
event itself.
3. A 4-year-old child is diagnosed with Cystic Fibrosis. This condition is caused by a mutation
in the CFTR gene, leading to defective chloride transport. Which of the following best
describes the inheritance pattern of this disorder?
A. Autosomal recessive
B. X-linked recessive
,C. Autosomal dominant
D. Mitochondrial inheritance
Answer: A
Rationale: Cystic Fibrosis is an autosomal recessive disorder, meaning an individual must
inherit two copies of the mutated gene to manifest the disease. Carriers who have only one
copy typically do not show symptoms but can pass the gene to their offspring. This specific
genetic defect leads to thick, viscous secretions in the lungs and pancreas, causing
significant morbidity.
4. During an acute inflammatory response, which chemical mediator is primarily responsible
for increasing vascular permeability and inducing pain?
A. C-reactive protein
B. Interferon-gamma
C. Tumor Necrosis Factor
D. Bradykinin
Answer: D
Rationale: Bradykinin is a plasma-derived peptide that causes vasodilation and increased
vascular permeability during inflammation. It also acts directly on nerve endings to
stimulate pain, which is one of the cardinal signs of inflammation. Unlike histamine which
acts early, bradykinin is part of the kinin system that sustains the inflammatory response.
5. A patient presents with a severe allergic reaction to a bee sting, characterized by
bronchospasm and hypotension. Which type of hypersensitivity reaction is occurring?
A. Type I (IgE-mediated)
B. Type II (Cytotoxic)
C. Type III (Immune complex)
D. Type IV (Delayed-type)
Answer: A
Rationale: Type I hypersensitivity involves the binding of an allergen to IgE antibodies
already present on the surface of mast cells and basophils. This cross-linking triggers the
immediate release of preformed mediators like histamine, leading to systemic vasodilation
and smooth muscle contraction. If left untreated, this anaphylactic response can be life-
threatening due to airway obstruction and circulatory collapse.
6. In the development of systemic lupus erythematosus (SLE), what is the fundamental
immunological defect?
A. Deficiency in B-cell maturation
, B. Hyper-activation of T-helper 2 cells
C. Infection by the Human Immunodeficiency Virus
D. Loss of self-tolerance and production of autoantibodies
Answer: D
Rationale: SLE is a complex autoimmune disease characterized by the production of
antibodies against self-antigens, particularly nuclear components. The immune system fails
to maintain self-tolerance, leading to the formation of immune complexes that deposit in
tissues. This deposition causes widespread inflammation and damage to the kidneys, joints,
skin, and heart.
7. Which hormone is inappropriately elevated in a patient with syndrome of inappropriate
antidiuretic hormone (SIADH), leading to hyponatremia?
A. Vasopressin
B. Aldosterone
C. Atrial natriuretic peptide
D. Renin
Answer: A
Rationale: SIADH involves the excessive secretion of antidiuretic hormone (ADH), also
known as vasopressin, despite normal or high plasma volume. This excess ADH causes the
kidneys to reabsorb water excessively, diluting the extracellular fluid and leading to
hyponatremia. The clinical presentation often involves confusion and lethargy due to
cerebral edema caused by the water shift into brain cells.
8. A patient with chronic kidney disease (CKD) develops secondary hyperparathyroidism.
What is the primary stimulus for the increased secretion of parathyroid hormone (PTH)?
A. Hypercalcemia
B. Hypokalemia
C. Elevated Vitamin D levels
D. Hypocalcemia and hyperphosphatemia
Answer: D
Rationale: In CKD, the kidneys fail to excrete phosphate, leading to hyperphosphatemia
which directly lowers serum calcium. Additionally, the kidneys cannot convert Vitamin D to
its active form, further reducing intestinal calcium absorption. These low calcium levels
persistently stimulate the parathyroid glands to release PTH in an attempt to normalize
serum calcium levels.
Pathophysiology (NSG530 Final Exam) [PDF] | Wilkes University
1. A 65-year-old male with a history of chronic smoking presents with a persistent cough and
significant weight loss. A biopsy of the bronchial epithelium reveals that the normal ciliated
columnar cells have been replaced by stratified squamous epithelium. Which cellular
adaptation process is most likely occurring?
A. Atrophy
B. Hyperplasia
C. Metaplasia
D. Dysplasia
Answer: C
Rationale: Metaplasia is a reversible change in which one adult cell type is replaced by
another adult cell type. In this clinical scenario, the chronic irritation from cigarette smoke
induces the bronchial columnar cells to transform into tougher squamous cells. While this
new epithelium is more resistant to smoke, it lacks the protective cilia and mucus secretion
of the original tissue.
2. Following an acute myocardial infarction, which process is responsible for the additional
damage that occurs when blood flow is restored to the ischemic zone?
A. Reperfusion injury
B. Anaerobic glycolysis
C. Apoptosis via extrinsic pathway
D. Autophagy
Answer: A
Rationale: Reperfusion injury occurs when the restoration of blood flow to ischemic
tissues leads to the massive production of reactive oxygen species (ROS). These free
radicals damage cell membranes through lipid peroxidation and trigger the inflammatory
response. This phenomenon often results in greater tissue damage than the initial ischemic
event itself.
3. A 4-year-old child is diagnosed with Cystic Fibrosis. This condition is caused by a mutation
in the CFTR gene, leading to defective chloride transport. Which of the following best
describes the inheritance pattern of this disorder?
A. Autosomal recessive
B. X-linked recessive
,C. Autosomal dominant
D. Mitochondrial inheritance
Answer: A
Rationale: Cystic Fibrosis is an autosomal recessive disorder, meaning an individual must
inherit two copies of the mutated gene to manifest the disease. Carriers who have only one
copy typically do not show symptoms but can pass the gene to their offspring. This specific
genetic defect leads to thick, viscous secretions in the lungs and pancreas, causing
significant morbidity.
4. During an acute inflammatory response, which chemical mediator is primarily responsible
for increasing vascular permeability and inducing pain?
A. C-reactive protein
B. Interferon-gamma
C. Tumor Necrosis Factor
D. Bradykinin
Answer: D
Rationale: Bradykinin is a plasma-derived peptide that causes vasodilation and increased
vascular permeability during inflammation. It also acts directly on nerve endings to
stimulate pain, which is one of the cardinal signs of inflammation. Unlike histamine which
acts early, bradykinin is part of the kinin system that sustains the inflammatory response.
5. A patient presents with a severe allergic reaction to a bee sting, characterized by
bronchospasm and hypotension. Which type of hypersensitivity reaction is occurring?
A. Type I (IgE-mediated)
B. Type II (Cytotoxic)
C. Type III (Immune complex)
D. Type IV (Delayed-type)
Answer: A
Rationale: Type I hypersensitivity involves the binding of an allergen to IgE antibodies
already present on the surface of mast cells and basophils. This cross-linking triggers the
immediate release of preformed mediators like histamine, leading to systemic vasodilation
and smooth muscle contraction. If left untreated, this anaphylactic response can be life-
threatening due to airway obstruction and circulatory collapse.
6. In the development of systemic lupus erythematosus (SLE), what is the fundamental
immunological defect?
A. Deficiency in B-cell maturation
, B. Hyper-activation of T-helper 2 cells
C. Infection by the Human Immunodeficiency Virus
D. Loss of self-tolerance and production of autoantibodies
Answer: D
Rationale: SLE is a complex autoimmune disease characterized by the production of
antibodies against self-antigens, particularly nuclear components. The immune system fails
to maintain self-tolerance, leading to the formation of immune complexes that deposit in
tissues. This deposition causes widespread inflammation and damage to the kidneys, joints,
skin, and heart.
7. Which hormone is inappropriately elevated in a patient with syndrome of inappropriate
antidiuretic hormone (SIADH), leading to hyponatremia?
A. Vasopressin
B. Aldosterone
C. Atrial natriuretic peptide
D. Renin
Answer: A
Rationale: SIADH involves the excessive secretion of antidiuretic hormone (ADH), also
known as vasopressin, despite normal or high plasma volume. This excess ADH causes the
kidneys to reabsorb water excessively, diluting the extracellular fluid and leading to
hyponatremia. The clinical presentation often involves confusion and lethargy due to
cerebral edema caused by the water shift into brain cells.
8. A patient with chronic kidney disease (CKD) develops secondary hyperparathyroidism.
What is the primary stimulus for the increased secretion of parathyroid hormone (PTH)?
A. Hypercalcemia
B. Hypokalemia
C. Elevated Vitamin D levels
D. Hypocalcemia and hyperphosphatemia
Answer: D
Rationale: In CKD, the kidneys fail to excrete phosphate, leading to hyperphosphatemia
which directly lowers serum calcium. Additionally, the kidneys cannot convert Vitamin D to
its active form, further reducing intestinal calcium absorption. These low calcium levels
persistently stimulate the parathyroid glands to release PTH in an attempt to normalize
serum calcium levels.
