NUR 555 — Quiz 4 Exam
Question and answers| SNHU
Q1. Which mechanism best explains why a rise in intracranial pressure
(ICP) can progress rapidly once the brain's compensatory limits are
exceeded?
A. The skull is a closed, rigid compartment (Monro-Kellie doctrine), so once
compensatory volume shifts in CSF and venous blood are exhausted, small
volume increases cause large pressure increases
B. Neurons regenerate faster than the pressure can build
C. Increased ICP always resolves spontaneously through increased CSF
production
D. The dura mater expands to accommodate excess volume
Answer: A
Rationale: Per the Monro-Kellie doctrine, the skull holds a fixed total volume of
brain tissue, blood, and CSF. Initially, small increases in one component (e.g., a
hematoma) are compensated by displacing CSF and venous blood. Once that
buffering capacity is exhausted, the pressure-volume curve steepens sharply,
and small further increases in volume cause disproportionately large rises in
ICP.
Q2. Cushing's triad (hypertension with widening pulse pressure,
bradycardia, and irregular respirations) is a late clinical sign of which
process?
A. Early compensated increased ICP
B. Severe increased ICP causing brainstem compression/herniation
C. Normal autoregulation of cerebral blood flow
D. Peripheral nerve demyelination
Answer: B
, Rationale: Cushing's triad reflects the brainstem's response to severe,
sustained increased ICP: systemic hypertension develops as the body attempts
to maintain cerebral perfusion pressure against rising ICP, triggering
baroreceptor-mediated reflex bradycardia, while irregular respirations signal
brainstem (medullary) compression — a late and ominous sign of impending
herniation.
Q3. Uncal (transtentorial) herniation classically produces which early
finding due to compression of the third cranial nerve on the affected side?
A. Bilateral pinpoint pupils
B. A unilateral fixed, dilated ('blown') pupil
C. Loss of the gag reflex only
D. Sudden bilateral hearing loss
Answer: B
Rationale: As the uncus of the temporal lobe herniates medially through the
tentorial notch, it compresses cranial nerve III (oculomotor), whose
parasympathetic fibers control pupillary constriction. Compression classically
causes ipsilateral pupillary dilation and sluggish or absent light response before
other signs progress.
Q4. Cellular death from prolonged cerebral ischemia is primarily driven by
which pathophysiologic cascade?
A. Excess GABA release causing sustained neuronal inhibition
B. Excitotoxicity from excess glutamate release, calcium influx, and free
radical-mediated membrane damage
C. Overproduction of myelin by oligodendrocytes
D. Decreased intracellular sodium causing cell shrinkage
Answer: B
Rationale: When cerebral blood flow drops, ATP-dependent ion pumps fail,
neurons depolarize, and excess glutamate is released. This over-activates
NMDA/AMPA receptors, driving massive calcium influx that activates
proteases, lipases, and free-radical generation — the excitotoxic cascade
responsible for infarction and irreversible neuronal death.
Question and answers| SNHU
Q1. Which mechanism best explains why a rise in intracranial pressure
(ICP) can progress rapidly once the brain's compensatory limits are
exceeded?
A. The skull is a closed, rigid compartment (Monro-Kellie doctrine), so once
compensatory volume shifts in CSF and venous blood are exhausted, small
volume increases cause large pressure increases
B. Neurons regenerate faster than the pressure can build
C. Increased ICP always resolves spontaneously through increased CSF
production
D. The dura mater expands to accommodate excess volume
Answer: A
Rationale: Per the Monro-Kellie doctrine, the skull holds a fixed total volume of
brain tissue, blood, and CSF. Initially, small increases in one component (e.g., a
hematoma) are compensated by displacing CSF and venous blood. Once that
buffering capacity is exhausted, the pressure-volume curve steepens sharply,
and small further increases in volume cause disproportionately large rises in
ICP.
Q2. Cushing's triad (hypertension with widening pulse pressure,
bradycardia, and irregular respirations) is a late clinical sign of which
process?
A. Early compensated increased ICP
B. Severe increased ICP causing brainstem compression/herniation
C. Normal autoregulation of cerebral blood flow
D. Peripheral nerve demyelination
Answer: B
, Rationale: Cushing's triad reflects the brainstem's response to severe,
sustained increased ICP: systemic hypertension develops as the body attempts
to maintain cerebral perfusion pressure against rising ICP, triggering
baroreceptor-mediated reflex bradycardia, while irregular respirations signal
brainstem (medullary) compression — a late and ominous sign of impending
herniation.
Q3. Uncal (transtentorial) herniation classically produces which early
finding due to compression of the third cranial nerve on the affected side?
A. Bilateral pinpoint pupils
B. A unilateral fixed, dilated ('blown') pupil
C. Loss of the gag reflex only
D. Sudden bilateral hearing loss
Answer: B
Rationale: As the uncus of the temporal lobe herniates medially through the
tentorial notch, it compresses cranial nerve III (oculomotor), whose
parasympathetic fibers control pupillary constriction. Compression classically
causes ipsilateral pupillary dilation and sluggish or absent light response before
other signs progress.
Q4. Cellular death from prolonged cerebral ischemia is primarily driven by
which pathophysiologic cascade?
A. Excess GABA release causing sustained neuronal inhibition
B. Excitotoxicity from excess glutamate release, calcium influx, and free
radical-mediated membrane damage
C. Overproduction of myelin by oligodendrocytes
D. Decreased intracellular sodium causing cell shrinkage
Answer: B
Rationale: When cerebral blood flow drops, ATP-dependent ion pumps fail,
neurons depolarize, and excess glutamate is released. This over-activates
NMDA/AMPA receptors, driving massive calcium influx that activates
proteases, lipases, and free-radical generation — the excitotoxic cascade
responsible for infarction and irreversible neuronal death.
