NR283 PATHOPHYSIOLOGY EXAM 3
PRACTICE QUESTIONS AND ANSWERS
1. A patient presents with a ‘blown’ pupil, bradycardia, and widening pulse pressure
following a head injury. Which pathophysiology mechanism explains these findings?
A. Diffuse axonal injury causing global ischemia
B. Transient ischemic attack involving the carotid arteries
C. Sympathetic nervous system activation causing a hypertensive crisis
D. Increased intracranial pressure leading to brainstem herniation
Answer: D
Conceptual Explanation: The symptoms describe Cushing’s Triad (bradycardia, widening
pulse pressure, irregular respirations) and a fixed, dilated pupil, which are signs of severe
increased intracranial pressure (ICP) and impending transtentorial herniation.
2. Which of the following describes the primary pathophysiology of Multiple Sclerosis?
A. Autoimmune destruction of the acetylcholine receptors at the neuromuscular junction
B. Degeneration of the substantia nigra resulting in decreased dopamine production
C. Demyelination of the central nervous system neurons mediated by T-cells and B-cells
,D. Ascending demyelination of the peripheral nerves following a viral infection
Answer: C
Conceptual Explanation: Multiple Sclerosis is a chronic autoimmune disease
characterized by the inflammation and demyelination of the CNS (brain and spinal cord).
3. A patient with a history of atrial fibrillation suddenly experiences aphasia and right-sided
hemiplegia. A CT scan shows no hemorrhage. What is the most likely cause?
A. Arteriovenous malformation rupture
B. Lacunar stroke
C. Hemorrhagic stroke
D. Embolic ischemic stroke
Answer: D
Conceptual Explanation: Atrial fibrillation is a major risk factor for embolic strokes,
where a clot travels from the heart to the cerebral arteries, blocking blood flow without
causing immediate bleeding.
4. During the recovery phase of a spinal cord injury at T4, the patient experiences sudden
severe hypertension, a pounding headache, and bradycardia. What is the priority concern?
A. Spinal shock
B. Brown-Sequard syndrome
C. Neurogenic shock
, D. Autonomic dysreflexia
Answer: D
Conceptual Explanation: Autonomic dysreflexia occurs in patients with injuries at T6 or
above; it is triggered by noxious stimuli below the injury level, leading to uninhibited
sympathetic discharge and severe hypertension.
5. What is the hallmark physiological finding in Parkinson’s Disease?
A. Amyloid plaques and neurofibrillary tangles
B. Deficiency of dopamine in the basal ganglia due to loss of nigrostriatal neurons
C. Loss of acetylcholine-producing neurons in the hippocampus
D. Excessive glutamate excitation leading to neuronal death
Answer: B
Conceptual Explanation: Parkinson’s Disease is primarily caused by the degeneration of
dopamine-producing neurons in the substantia nigra, which leads to motor symptoms like
tremors and rigidity.
6. A patient is diagnosed with Myasthenia Gravis. What is the underlying cause of the muscle
weakness?
A. Antibodies block or destroy nicotinic acetylcholine receptors at the motor endplate
B. Failure of the pre-synaptic membrane to release calcium
C. Rapid breakdown of dopamine in the synaptic cleft
PRACTICE QUESTIONS AND ANSWERS
1. A patient presents with a ‘blown’ pupil, bradycardia, and widening pulse pressure
following a head injury. Which pathophysiology mechanism explains these findings?
A. Diffuse axonal injury causing global ischemia
B. Transient ischemic attack involving the carotid arteries
C. Sympathetic nervous system activation causing a hypertensive crisis
D. Increased intracranial pressure leading to brainstem herniation
Answer: D
Conceptual Explanation: The symptoms describe Cushing’s Triad (bradycardia, widening
pulse pressure, irregular respirations) and a fixed, dilated pupil, which are signs of severe
increased intracranial pressure (ICP) and impending transtentorial herniation.
2. Which of the following describes the primary pathophysiology of Multiple Sclerosis?
A. Autoimmune destruction of the acetylcholine receptors at the neuromuscular junction
B. Degeneration of the substantia nigra resulting in decreased dopamine production
C. Demyelination of the central nervous system neurons mediated by T-cells and B-cells
,D. Ascending demyelination of the peripheral nerves following a viral infection
Answer: C
Conceptual Explanation: Multiple Sclerosis is a chronic autoimmune disease
characterized by the inflammation and demyelination of the CNS (brain and spinal cord).
3. A patient with a history of atrial fibrillation suddenly experiences aphasia and right-sided
hemiplegia. A CT scan shows no hemorrhage. What is the most likely cause?
A. Arteriovenous malformation rupture
B. Lacunar stroke
C. Hemorrhagic stroke
D. Embolic ischemic stroke
Answer: D
Conceptual Explanation: Atrial fibrillation is a major risk factor for embolic strokes,
where a clot travels from the heart to the cerebral arteries, blocking blood flow without
causing immediate bleeding.
4. During the recovery phase of a spinal cord injury at T4, the patient experiences sudden
severe hypertension, a pounding headache, and bradycardia. What is the priority concern?
A. Spinal shock
B. Brown-Sequard syndrome
C. Neurogenic shock
, D. Autonomic dysreflexia
Answer: D
Conceptual Explanation: Autonomic dysreflexia occurs in patients with injuries at T6 or
above; it is triggered by noxious stimuli below the injury level, leading to uninhibited
sympathetic discharge and severe hypertension.
5. What is the hallmark physiological finding in Parkinson’s Disease?
A. Amyloid plaques and neurofibrillary tangles
B. Deficiency of dopamine in the basal ganglia due to loss of nigrostriatal neurons
C. Loss of acetylcholine-producing neurons in the hippocampus
D. Excessive glutamate excitation leading to neuronal death
Answer: B
Conceptual Explanation: Parkinson’s Disease is primarily caused by the degeneration of
dopamine-producing neurons in the substantia nigra, which leads to motor symptoms like
tremors and rigidity.
6. A patient is diagnosed with Myasthenia Gravis. What is the underlying cause of the muscle
weakness?
A. Antibodies block or destroy nicotinic acetylcholine receptors at the motor endplate
B. Failure of the pre-synaptic membrane to release calcium
C. Rapid breakdown of dopamine in the synaptic cleft
