NUR 546/NUR546 Exam 4 V1 | Advanced
Pathophysiology Q&A with Rationale |
William Paterson University
1. Which physiological change is a hallmark of Multiple Sclerosis (MS)?
A. Autoimmune-mediated demyelination of the central nervous system
B. Degeneration of dopaminergic neurons in the substantia nigra
C. Development of neurofibrillary tangles and amyloid plaques
D. Destruction of acetylcholine receptors at the neuromuscular junction
Answer: A
Rationale: Multiple Sclerosis is characterized by an autoimmune response where T-cells
attack the myelin sheath of axons in the brain and spinal cord. This demyelination slows or
blocks nerve impulses, leading to the various neurological symptoms observed in patients.
Inflammation and subsequent scarring, or gliosis, are also core components of the disease
process.
2. A patient presents with a ‘pill-rolling’ tremor and bradykinesia. Which neurotransmitter
deficiency is most likely responsible?
A. Serotonin
B. Acetylcholine
C. Dopamine
,D. GABA
Answer: C
Rationale: Parkinson’s disease is caused by the progressive loss of dopamine-producing
neurons in the substantia nigra. The resulting lack of dopamine disrupts the balance of the
basal ganglia, leading to motor symptoms like tremors and rigidity. Therapeutic
interventions often focus on restoring dopamine levels or mimicking its effects.
3. Which clinical sign is included in Cushing’s Triad, indicating increased intracranial pressure?
A. Tachycardia
B. Hypotension
C. Hyperventilation
D. Bradycardia
Answer: D
Rationale: Cushing’s triad consists of systolic hypertension with a widened pulse pressure,
bradycardia, and irregular respiratory patterns. It is a late sign of increased intracranial
pressure and suggests that the brainstem is being compressed. Prompt recognition and
intervention are necessary to prevent brain herniation.
4. Which pathophysiological mechanism underlies Myasthenia Gravis?
A. Loss of lower motor neurons in the spinal cord
B. Overproduction of cholinesterase in the synaptic cleft
, C. Autoimmune destruction of acetylcholine receptors at the NMJ
D. Demyelination of peripheral nerves following a viral infection
Answer: C
Rationale: Myasthenia Gravis involves the production of IgG antibodies that block or
destroy acetylcholine receptors at the postsynaptic membrane of the neuromuscular
junction. This leads to reduced muscle activation and progressive weakness, particularly in
muscles used for eye movement and swallowing. The thymus gland is often abnormal and
thought to play a role in this autoimmune response.
5. Which type of stroke is most commonly associated with atrial fibrillation?
A. Hemorrhagic stroke
B. Lacunar stroke
C. Embolic stroke
D. Thrombotic stroke
Answer: C
Rationale: Atrial fibrillation causes blood to pool in the left atrium, which can lead to the
formation of a thrombus. If this clot dislodges, it travels through the circulation and can
lodge in a cerebral artery, causing an embolic stroke. Anticoagulation therapy is often
prescribed to patients with atrial fibrillation to reduce this specific risk.
Pathophysiology Q&A with Rationale |
William Paterson University
1. Which physiological change is a hallmark of Multiple Sclerosis (MS)?
A. Autoimmune-mediated demyelination of the central nervous system
B. Degeneration of dopaminergic neurons in the substantia nigra
C. Development of neurofibrillary tangles and amyloid plaques
D. Destruction of acetylcholine receptors at the neuromuscular junction
Answer: A
Rationale: Multiple Sclerosis is characterized by an autoimmune response where T-cells
attack the myelin sheath of axons in the brain and spinal cord. This demyelination slows or
blocks nerve impulses, leading to the various neurological symptoms observed in patients.
Inflammation and subsequent scarring, or gliosis, are also core components of the disease
process.
2. A patient presents with a ‘pill-rolling’ tremor and bradykinesia. Which neurotransmitter
deficiency is most likely responsible?
A. Serotonin
B. Acetylcholine
C. Dopamine
,D. GABA
Answer: C
Rationale: Parkinson’s disease is caused by the progressive loss of dopamine-producing
neurons in the substantia nigra. The resulting lack of dopamine disrupts the balance of the
basal ganglia, leading to motor symptoms like tremors and rigidity. Therapeutic
interventions often focus on restoring dopamine levels or mimicking its effects.
3. Which clinical sign is included in Cushing’s Triad, indicating increased intracranial pressure?
A. Tachycardia
B. Hypotension
C. Hyperventilation
D. Bradycardia
Answer: D
Rationale: Cushing’s triad consists of systolic hypertension with a widened pulse pressure,
bradycardia, and irregular respiratory patterns. It is a late sign of increased intracranial
pressure and suggests that the brainstem is being compressed. Prompt recognition and
intervention are necessary to prevent brain herniation.
4. Which pathophysiological mechanism underlies Myasthenia Gravis?
A. Loss of lower motor neurons in the spinal cord
B. Overproduction of cholinesterase in the synaptic cleft
, C. Autoimmune destruction of acetylcholine receptors at the NMJ
D. Demyelination of peripheral nerves following a viral infection
Answer: C
Rationale: Myasthenia Gravis involves the production of IgG antibodies that block or
destroy acetylcholine receptors at the postsynaptic membrane of the neuromuscular
junction. This leads to reduced muscle activation and progressive weakness, particularly in
muscles used for eye movement and swallowing. The thymus gland is often abnormal and
thought to play a role in this autoimmune response.
5. Which type of stroke is most commonly associated with atrial fibrillation?
A. Hemorrhagic stroke
B. Lacunar stroke
C. Embolic stroke
D. Thrombotic stroke
Answer: C
Rationale: Atrial fibrillation causes blood to pool in the left atrium, which can lead to the
formation of a thrombus. If this clot dislodges, it travels through the circulation and can
lodge in a cerebral artery, causing an embolic stroke. Anticoagulation therapy is often
prescribed to patients with atrial fibrillation to reduce this specific risk.
