NRMS 5190 — Pathophysiology Exam 3 SUNY Downstate
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Updated
1. According to the Monro-Kellie doctrine, the cranial vault is a rigid compartment
containing which three components whose volumes must remain in balance?
A. Brain tissue, blood, and cerebrospinal fluid
B. Brain tissue, bone, and dura mater
C. Blood, bone, and scalp tissue
D. Cerebrospinal fluid, dura mater, and skull
Answer: A
Rationale: The Monro-Kellie doctrine states that the skull is a rigid, fixed-volume
compartment containing brain tissue (~80%), blood (~10%), and cerebrospinal fluid
(~10%); an increase in the volume of any one component requires a compensatory
decrease in another to keep intracranial pressure normal.
2. Which of the following is typically the earliest and most sensitive indicator of
increasing intracranial pressure (ICP)?
A. Cushing's triad
B. A decreasing level of consciousness
C. Fixed and dilated pupils
D. Decerebrate posturing
Answer: B
Rationale: A change in level of consciousness (restlessness, confusion, lethargy) is the
earliest and most sensitive sign of rising ICP because the cerebral cortex and reticular
activating system are highly sensitive to changes in oxygenation and perfusion. Cushing's
triad, fixed pupils, and abnormal posturing are late, ominous findings.
3. Cushing's triad (widening pulse pressure, bradycardia, and irregular respirations)
occurs in late-stage increased ICP due to which mechanism?
A. Increased cerebral perfusion pressure with normal brainstem function
, B. The brain's attempt to maintain cerebral perfusion by increasing systemic blood
pressure, which triggers a baroreceptor-mediated reflex bradycardia, while
brainstem compression disrupts the respiratory center
C. Hypovolemic shock
D. A normal physiologic response with no clinical significance
Answer: B
Rationale: As ICP rises and approaches mean arterial pressure, cerebral perfusion
pressure falls; the body compensates by markedly increasing systemic blood pressure to
preserve cerebral blood flow. This severe hypertension triggers a baroreceptor-mediated
reflex bradycardia, while pressure on the brainstem respiratory centers causes irregular
respiratory patterns — together forming Cushing's triad, a sign of impending herniation.
4. Cerebral perfusion pressure (CPP) is calculated using which formula?
A. CPP = ICP - MAP
B. CPP = MAP - ICP
C. CPP = MAP + ICP
D. CPP = ICP / MAP
Answer: B
Rationale: Cerebral perfusion pressure equals mean arterial pressure (MAP) minus
intracranial pressure (ICP). A normal CPP is approximately 60-100 mmHg; as ICP rises,
CPP falls, reducing cerebral blood flow and risking ischemia if not corrected.
5. Which compensatory mechanism is the body's first response to a small increase in
intracranial volume, according to the Monro-Kellie doctrine?
A. Herniation of brain tissue
B. Displacement of cerebrospinal fluid into the spinal subarachnoid space and
increased CSF absorption
C. Cardiac arrest
D. Immediate brain cell death
Answer: B
Rationale: Initially, the brain compensates for a small increase in intracranial volume by
displacing CSF out of the cranial vault into the spinal subarachnoid space and increasing
CSF absorption; venous blood volume may also be reduced. Once these compensatory
mechanisms are exhausted, small further increases in volume cause dramatic rises in ICP.
6. Uncal (transtentorial) herniation classically presents with which early finding due to
compression of the third cranial nerve?
, A. Bilateral pinpoint pupils
B. A unilateral, fixed, and dilated ("blown") pupil on the side of the herniation
C. Bilateral fixed and dilated pupils as the first sign
D. Normal pupillary response
Answer: B
Rationale: As the uncus of the temporal lobe herniates through the tentorial notch, it
compresses the oculomotor nerve (CN III) on the same side, causing ipsilateral pupillary
dilation and sluggish or absent response to light — an early, critical warning sign of
herniation requiring immediate intervention.
7. Which nursing/medical intervention is contraindicated in a client with increased
intracranial pressure because it can raise ICP further?
A. Elevating the head of the bed to 30 degrees
B. Maintaining the head in a neutral, midline position
C. Extreme flexion or rotation of the neck
D. Minimizing environmental stimuli
Answer: C
Rationale: Extreme neck flexion or rotation can compress the jugular veins, impairing
venous outflow from the brain and further increasing ICP; the head and neck should be
maintained in a neutral, midline position, with the head of bed elevated to promote
venous drainage.
8. A client with increased ICP has a PaCO2 of 55 mmHg. Which pathophysiologic effect
does this hypercapnia have on cerebral blood flow?
A. Cerebral vasoconstriction, decreasing ICP
B. Cerebral vasodilation, further increasing cerebral blood volume and ICP
C. No effect on cerebral vessels
D. Decreased cerebral metabolic rate
Answer: B
Rationale: Carbon dioxide is a potent cerebral vasodilator; elevated PaCO2 (hypercapnia)
causes cerebral vessels to dilate, increasing cerebral blood volume and worsening
intracranial pressure. This is why controlled ventilation to maintain a low-normal PaCO2
is used therapeutically to reduce ICP in select situations.
9. Communicating (non-obstructive) hydrocephalus results from which
pathophysiologic mechanism?
, A. A physical blockage within the ventricular system preventing CSF flow
B. Impaired reabsorption of CSF by the arachnoid villi despite normal CSF flow
through the ventricles
C. Complete cessation of CSF production
D. Overproduction of blood within the ventricles only
Answer: B
Rationale: In communicating hydrocephalus, CSF flows freely between the ventricles and
into the subarachnoid space, but reabsorption by the arachnoid villi is impaired (e.g.,
from prior meningitis or hemorrhage), causing CSF to accumulate and the ventricles to
enlarge.
10. Noncommunicating (obstructive) hydrocephalus is caused by which mechanism?
A. A structural blockage (e.g., tumor, congenital malformation) within the ventricular
system that prevents CSF from flowing between ventricles or exiting into the
subarachnoid space
B. Excess absorption of CSF
C. A defect solely in CSF absorption at the arachnoid villi
D. Decreased choroid plexus function
Answer: A
Rationale: Noncommunicating hydrocephalus results from a physical obstruction within
the ventricular system itself (such as a tumor, congenital aqueductal stenosis, or blood
clot) that blocks the normal flow of CSF, causing it to accumulate proximal to the
obstruction and the ventricles to dilate.
11. Which classic triad of symptoms is associated with normal pressure hydrocephalus
(NPH) in older adults?
A. Fever, nuchal rigidity, and photophobia
B. Gait disturbance, urinary incontinence, and cognitive decline (dementia)
C. Tremor, rigidity, and bradykinesia
D. Ptosis, diplopia, and dysphagia
Answer: B
Rationale: Normal pressure hydrocephalus classically presents with the triad of gait
disturbance (often described as "magnetic" or shuffling), urinary incontinence, and
progressive cognitive decline, resulting from ventricular enlargement despite normal-to-
only-intermittently-elevated CSF pressure.
Medical Center Questions with Answers| Pass Guaranteed|
Updated
1. According to the Monro-Kellie doctrine, the cranial vault is a rigid compartment
containing which three components whose volumes must remain in balance?
A. Brain tissue, blood, and cerebrospinal fluid
B. Brain tissue, bone, and dura mater
C. Blood, bone, and scalp tissue
D. Cerebrospinal fluid, dura mater, and skull
Answer: A
Rationale: The Monro-Kellie doctrine states that the skull is a rigid, fixed-volume
compartment containing brain tissue (~80%), blood (~10%), and cerebrospinal fluid
(~10%); an increase in the volume of any one component requires a compensatory
decrease in another to keep intracranial pressure normal.
2. Which of the following is typically the earliest and most sensitive indicator of
increasing intracranial pressure (ICP)?
A. Cushing's triad
B. A decreasing level of consciousness
C. Fixed and dilated pupils
D. Decerebrate posturing
Answer: B
Rationale: A change in level of consciousness (restlessness, confusion, lethargy) is the
earliest and most sensitive sign of rising ICP because the cerebral cortex and reticular
activating system are highly sensitive to changes in oxygenation and perfusion. Cushing's
triad, fixed pupils, and abnormal posturing are late, ominous findings.
3. Cushing's triad (widening pulse pressure, bradycardia, and irregular respirations)
occurs in late-stage increased ICP due to which mechanism?
A. Increased cerebral perfusion pressure with normal brainstem function
, B. The brain's attempt to maintain cerebral perfusion by increasing systemic blood
pressure, which triggers a baroreceptor-mediated reflex bradycardia, while
brainstem compression disrupts the respiratory center
C. Hypovolemic shock
D. A normal physiologic response with no clinical significance
Answer: B
Rationale: As ICP rises and approaches mean arterial pressure, cerebral perfusion
pressure falls; the body compensates by markedly increasing systemic blood pressure to
preserve cerebral blood flow. This severe hypertension triggers a baroreceptor-mediated
reflex bradycardia, while pressure on the brainstem respiratory centers causes irregular
respiratory patterns — together forming Cushing's triad, a sign of impending herniation.
4. Cerebral perfusion pressure (CPP) is calculated using which formula?
A. CPP = ICP - MAP
B. CPP = MAP - ICP
C. CPP = MAP + ICP
D. CPP = ICP / MAP
Answer: B
Rationale: Cerebral perfusion pressure equals mean arterial pressure (MAP) minus
intracranial pressure (ICP). A normal CPP is approximately 60-100 mmHg; as ICP rises,
CPP falls, reducing cerebral blood flow and risking ischemia if not corrected.
5. Which compensatory mechanism is the body's first response to a small increase in
intracranial volume, according to the Monro-Kellie doctrine?
A. Herniation of brain tissue
B. Displacement of cerebrospinal fluid into the spinal subarachnoid space and
increased CSF absorption
C. Cardiac arrest
D. Immediate brain cell death
Answer: B
Rationale: Initially, the brain compensates for a small increase in intracranial volume by
displacing CSF out of the cranial vault into the spinal subarachnoid space and increasing
CSF absorption; venous blood volume may also be reduced. Once these compensatory
mechanisms are exhausted, small further increases in volume cause dramatic rises in ICP.
6. Uncal (transtentorial) herniation classically presents with which early finding due to
compression of the third cranial nerve?
, A. Bilateral pinpoint pupils
B. A unilateral, fixed, and dilated ("blown") pupil on the side of the herniation
C. Bilateral fixed and dilated pupils as the first sign
D. Normal pupillary response
Answer: B
Rationale: As the uncus of the temporal lobe herniates through the tentorial notch, it
compresses the oculomotor nerve (CN III) on the same side, causing ipsilateral pupillary
dilation and sluggish or absent response to light — an early, critical warning sign of
herniation requiring immediate intervention.
7. Which nursing/medical intervention is contraindicated in a client with increased
intracranial pressure because it can raise ICP further?
A. Elevating the head of the bed to 30 degrees
B. Maintaining the head in a neutral, midline position
C. Extreme flexion or rotation of the neck
D. Minimizing environmental stimuli
Answer: C
Rationale: Extreme neck flexion or rotation can compress the jugular veins, impairing
venous outflow from the brain and further increasing ICP; the head and neck should be
maintained in a neutral, midline position, with the head of bed elevated to promote
venous drainage.
8. A client with increased ICP has a PaCO2 of 55 mmHg. Which pathophysiologic effect
does this hypercapnia have on cerebral blood flow?
A. Cerebral vasoconstriction, decreasing ICP
B. Cerebral vasodilation, further increasing cerebral blood volume and ICP
C. No effect on cerebral vessels
D. Decreased cerebral metabolic rate
Answer: B
Rationale: Carbon dioxide is a potent cerebral vasodilator; elevated PaCO2 (hypercapnia)
causes cerebral vessels to dilate, increasing cerebral blood volume and worsening
intracranial pressure. This is why controlled ventilation to maintain a low-normal PaCO2
is used therapeutically to reduce ICP in select situations.
9. Communicating (non-obstructive) hydrocephalus results from which
pathophysiologic mechanism?
, A. A physical blockage within the ventricular system preventing CSF flow
B. Impaired reabsorption of CSF by the arachnoid villi despite normal CSF flow
through the ventricles
C. Complete cessation of CSF production
D. Overproduction of blood within the ventricles only
Answer: B
Rationale: In communicating hydrocephalus, CSF flows freely between the ventricles and
into the subarachnoid space, but reabsorption by the arachnoid villi is impaired (e.g.,
from prior meningitis or hemorrhage), causing CSF to accumulate and the ventricles to
enlarge.
10. Noncommunicating (obstructive) hydrocephalus is caused by which mechanism?
A. A structural blockage (e.g., tumor, congenital malformation) within the ventricular
system that prevents CSF from flowing between ventricles or exiting into the
subarachnoid space
B. Excess absorption of CSF
C. A defect solely in CSF absorption at the arachnoid villi
D. Decreased choroid plexus function
Answer: A
Rationale: Noncommunicating hydrocephalus results from a physical obstruction within
the ventricular system itself (such as a tumor, congenital aqueductal stenosis, or blood
clot) that blocks the normal flow of CSF, causing it to accumulate proximal to the
obstruction and the ventricles to dilate.
11. Which classic triad of symptoms is associated with normal pressure hydrocephalus
(NPH) in older adults?
A. Fever, nuchal rigidity, and photophobia
B. Gait disturbance, urinary incontinence, and cognitive decline (dementia)
C. Tremor, rigidity, and bradykinesia
D. Ptosis, diplopia, and dysphagia
Answer: B
Rationale: Normal pressure hydrocephalus classically presents with the triad of gait
disturbance (often described as "magnetic" or shuffling), urinary incontinence, and
progressive cognitive decline, resulting from ventricular enlargement despite normal-to-
only-intermittently-elevated CSF pressure.
