NSG 530 Exam 4 Actual Exam V3 | NSG 530 Advanced
Pathophysiology (NSG530 Exam 4) [PDF] | Wilkes University
1. A 52-year-old female presents with fatigue, pallor, and a smooth, beefy red tongue.
Laboratory findings reveal a high mean corpuscular volume (MCV) and a low hemoglobin
level. Which pathophysiological mechanism is most likely responsible for these findings?
A. Impaired DNA synthesis due to Vitamin B12 deficiency
B. Defective heme synthesis due to iron deficiency
C. Chronic blood loss leading to microcytic anemia
D. Premature destruction of erythrocytes in the spleen
Answer: A
Rationale: The clinical presentation of macrocytic anemia and atrophic glossitis suggests
Vitamin B12 or folate deficiency. Vitamin B12 is essential for DNA synthesis and nuclear
maturation in erythroid precursors; its absence leads to megaloblastic changes. The lack of
intrinsic factor or dietary intake results in ineffective erythropoiesis and large, fragile red
blood cells.
2. Which of the following describes the primary mechanism by which proto-oncogenes
contribute to malignant transformation?
A. They act as ‘brakes’ to stop the cell cycle during DNA damage
B. They are silenced by methylation, leading to increased cell proliferation
C. They induce apoptosis in cells with genetic instability
D. They undergo gain-of-function mutations to become oncogenes that promote
unregulated growth
Answer: D
Rationale: Proto-oncogenes are normal genes that regulate cell growth and differentiation.
When these genes undergo point mutations, amplifications, or translocations, they become
oncogenes that drive constitutive cellular proliferation. This represents a gain-of-function
mechanism, unlike tumor suppressor genes, which typically require a loss-of-function to
contribute to cancer.
3. A patient with a history of systemic lupus erythematosus (SLE) presents with new-onset
edema and hypertension. A renal biopsy shows immune complex deposition in the glomeruli.
This is an example of which type of hypersensitivity reaction?
A. Type I (IgE-mediated)
B. Type II (Cytotoxic)
,C. Type IV (Delayed-type)
D. Type III (Immune-complex mediated)
Answer: D
Rationale: Type III hypersensitivity involves the formation of antigen-antibody complexes
that circulate and deposit in tissues like the kidneys or joints. These complexes activate the
complement system, leading to neutrophil recruitment and subsequent tissue damage. In
SLE, the deposition of these complexes in the glomerular basement membrane results in
lupus nephritis.
4. In the pathophysiology of Multiple Sclerosis (MS), what is the primary target of the
immune-mediated attack?
A. Myelin sheaths within the central nervous system
B. Dopaminergic neurons in the substantia nigra
C. Acetylcholine receptors at the neuromuscular junction
D. Peripheral nerve axons in the lower extremities
Answer: A
Rationale: Multiple Sclerosis is a chronic autoimmune disease characterized by
inflammation and demyelination of the central nervous system (CNS). T-cells and B-cells
cross the blood-brain barrier and attack the myelin sheath, which is produced by
oligodendrocytes. This disruption leads to slowed nerve conduction and a variety of
neurological symptoms depending on the location of the plaques.
5. A 68-year-old male presents with resting tremor, bradykinesia, and postural instability. The
underlying pathology involves the loss of neurons in which brain region?
A. Cerebral cortex
B. Substantia nigra
C. Hippocampus
D. Hypothalamus
Answer: B
Rationale: Parkinson’s disease is characterized by the progressive loss of dopaminergic
neurons in the substantia nigra pars compacta of the basal ganglia. This depletion of
dopamine leads to an imbalance between excitatory and inhibitory pathways, resulting in
the classic motor symptoms. The presence of Lewy bodies, which are intracellular
inclusions of alpha-synuclein, is a hallmark histological finding.
, 6. Which mediator is primarily responsible for the systemic vasodilation and increased
capillary permeability observed during septic shock?
A. Epinephrine
B. Vasopressin
C. Angiotensin II
D. Nitric oxide
Answer: D
Rationale: In septic shock, the host response to infection triggers the release of pro-
inflammatory cytokines like TNF-alpha and IL-1. These cytokines induce the expression of
inducible nitric oxide synthase (iNOS), leading to excessive production of nitric oxide.
Nitric oxide is a potent vasodilator that causes significant drops in systemic vascular
resistance and blood pressure.
7. During an acute exacerbation of Rheumatoid Arthritis (RA), which biological process is
driving the joint destruction?
A. Formation of a pannus that invades the joint space
B. Wear-and-tear degradation of articular cartilage
C. Deposition of urate crystals in the synovial fluid
D. Decrease in synovial fluid production
Answer: A
Rationale: Rheumatoid Arthritis is a chronic inflammatory disorder where the immune
system attacks the synovium. This leads to the formation of a ‘pannus,’ a layer of
inflammatory granulation tissue that releases enzymes like collagenase. The pannus
eventually invades and destroys the underlying cartilage and bone, distinguishing it from
the non-inflammatory degradation seen in osteoarthritis.
8. A 25-year-old male is admitted with a severe head injury. His intracranial pressure (ICP) is
rising. Which compensatory mechanism occurs first according to the Monro-Kellie doctrine?
A. Increase in cerebral blood flow
B. Herniation of brain tissue through the foramen magnum
C. Displacement of cerebrospinal fluid (CSF) into the spinal subarachnoid space
D. Expansion of the cranial vault
Answer: C
Rationale: The Monro-Kellie doctrine states that the cranial vault is a fixed volume
containing brain tissue, blood, and CSF. When one component increases (like brain edema),
Pathophysiology (NSG530 Exam 4) [PDF] | Wilkes University
1. A 52-year-old female presents with fatigue, pallor, and a smooth, beefy red tongue.
Laboratory findings reveal a high mean corpuscular volume (MCV) and a low hemoglobin
level. Which pathophysiological mechanism is most likely responsible for these findings?
A. Impaired DNA synthesis due to Vitamin B12 deficiency
B. Defective heme synthesis due to iron deficiency
C. Chronic blood loss leading to microcytic anemia
D. Premature destruction of erythrocytes in the spleen
Answer: A
Rationale: The clinical presentation of macrocytic anemia and atrophic glossitis suggests
Vitamin B12 or folate deficiency. Vitamin B12 is essential for DNA synthesis and nuclear
maturation in erythroid precursors; its absence leads to megaloblastic changes. The lack of
intrinsic factor or dietary intake results in ineffective erythropoiesis and large, fragile red
blood cells.
2. Which of the following describes the primary mechanism by which proto-oncogenes
contribute to malignant transformation?
A. They act as ‘brakes’ to stop the cell cycle during DNA damage
B. They are silenced by methylation, leading to increased cell proliferation
C. They induce apoptosis in cells with genetic instability
D. They undergo gain-of-function mutations to become oncogenes that promote
unregulated growth
Answer: D
Rationale: Proto-oncogenes are normal genes that regulate cell growth and differentiation.
When these genes undergo point mutations, amplifications, or translocations, they become
oncogenes that drive constitutive cellular proliferation. This represents a gain-of-function
mechanism, unlike tumor suppressor genes, which typically require a loss-of-function to
contribute to cancer.
3. A patient with a history of systemic lupus erythematosus (SLE) presents with new-onset
edema and hypertension. A renal biopsy shows immune complex deposition in the glomeruli.
This is an example of which type of hypersensitivity reaction?
A. Type I (IgE-mediated)
B. Type II (Cytotoxic)
,C. Type IV (Delayed-type)
D. Type III (Immune-complex mediated)
Answer: D
Rationale: Type III hypersensitivity involves the formation of antigen-antibody complexes
that circulate and deposit in tissues like the kidneys or joints. These complexes activate the
complement system, leading to neutrophil recruitment and subsequent tissue damage. In
SLE, the deposition of these complexes in the glomerular basement membrane results in
lupus nephritis.
4. In the pathophysiology of Multiple Sclerosis (MS), what is the primary target of the
immune-mediated attack?
A. Myelin sheaths within the central nervous system
B. Dopaminergic neurons in the substantia nigra
C. Acetylcholine receptors at the neuromuscular junction
D. Peripheral nerve axons in the lower extremities
Answer: A
Rationale: Multiple Sclerosis is a chronic autoimmune disease characterized by
inflammation and demyelination of the central nervous system (CNS). T-cells and B-cells
cross the blood-brain barrier and attack the myelin sheath, which is produced by
oligodendrocytes. This disruption leads to slowed nerve conduction and a variety of
neurological symptoms depending on the location of the plaques.
5. A 68-year-old male presents with resting tremor, bradykinesia, and postural instability. The
underlying pathology involves the loss of neurons in which brain region?
A. Cerebral cortex
B. Substantia nigra
C. Hippocampus
D. Hypothalamus
Answer: B
Rationale: Parkinson’s disease is characterized by the progressive loss of dopaminergic
neurons in the substantia nigra pars compacta of the basal ganglia. This depletion of
dopamine leads to an imbalance between excitatory and inhibitory pathways, resulting in
the classic motor symptoms. The presence of Lewy bodies, which are intracellular
inclusions of alpha-synuclein, is a hallmark histological finding.
, 6. Which mediator is primarily responsible for the systemic vasodilation and increased
capillary permeability observed during septic shock?
A. Epinephrine
B. Vasopressin
C. Angiotensin II
D. Nitric oxide
Answer: D
Rationale: In septic shock, the host response to infection triggers the release of pro-
inflammatory cytokines like TNF-alpha and IL-1. These cytokines induce the expression of
inducible nitric oxide synthase (iNOS), leading to excessive production of nitric oxide.
Nitric oxide is a potent vasodilator that causes significant drops in systemic vascular
resistance and blood pressure.
7. During an acute exacerbation of Rheumatoid Arthritis (RA), which biological process is
driving the joint destruction?
A. Formation of a pannus that invades the joint space
B. Wear-and-tear degradation of articular cartilage
C. Deposition of urate crystals in the synovial fluid
D. Decrease in synovial fluid production
Answer: A
Rationale: Rheumatoid Arthritis is a chronic inflammatory disorder where the immune
system attacks the synovium. This leads to the formation of a ‘pannus,’ a layer of
inflammatory granulation tissue that releases enzymes like collagenase. The pannus
eventually invades and destroys the underlying cartilage and bone, distinguishing it from
the non-inflammatory degradation seen in osteoarthritis.
8. A 25-year-old male is admitted with a severe head injury. His intracranial pressure (ICP) is
rising. Which compensatory mechanism occurs first according to the Monro-Kellie doctrine?
A. Increase in cerebral blood flow
B. Herniation of brain tissue through the foramen magnum
C. Displacement of cerebrospinal fluid (CSF) into the spinal subarachnoid space
D. Expansion of the cranial vault
Answer: C
Rationale: The Monro-Kellie doctrine states that the cranial vault is a fixed volume
containing brain tissue, blood, and CSF. When one component increases (like brain edema),
