Page 1 of 126
NR 507 EDAPT WEEK 7: CENTRAL NERVOUS
SYSTEM SENSORY AND MOTOR DISORDERS |
COMPREHENSIVE PRACTICE QUESTION BANK |
WITH DETAILED RATIONALES | GRADUATE
NURSING STUDENTS | ADVANCED
PATHOPHYSIOLOGY | CHAMBERLAIN UNIVERSITY |
NR 507 WEEK 7 EDAPT MODULE ASSESSMENT |
TABLE OF CONTENTS
| Section | Topic | Questions |
|---------|-------|-----------|
| I | Neurodegenerative Disorders: Alzheimer's Disease & Dementia | 1–35 |
| II | Neurodegenerative Disorders: Parkinson's Disease | 36–65 |
| III | Demyelinating Disorders: Multiple Sclerosis & Related Conditions | 66–95 |
| IV | Motor Neuron Disorders: ALS & Related Conditions | 96–115 |
| V | Neuromuscular Junction Disorders: Myasthenia Gravis | 116–135 |
| VI | Cerebrovascular Disorders: Stroke & TIA | 136–165 |
| VII | Seizure Disorders & Epilepsy | 166–185 |
| VIII | Increased Intracranial Pressure & Headache Disorders | 186–200 |
| IX | Integrative & Cross-Topic Questions | 201–215 |
,Page 2 of 126
SECTION I: NEURODEGENERATIVE DISORDERS — ALZHEIMER'S DISEASE & DEMENTIA
**Question 1**
Which pathophysiological mechanism is primarily responsible for the formation of extracellular
senile plaques associated with Alzheimer's disease?
A) Hyperphosphorylation of intracellular tau proteins leading to microtubule destabilization
B) Deposition and aggregation of misfolded beta-amyloid proteins in the neural parenchyma
C) Autoimmune-mediated destruction of central cholinergic neurons in the nucleus basalis of
Meynert
D) Massive expansion of the cerebral ventricles secondary to normal-pressure hydrocephalus
**Correct Answer: B**
**Rationale:** Alzheimer's disease is characterized pathologically by two hallmark protein
abnormalities: extracellular senile plaques (formed by the accumulation of insoluble beta-
amyloid peptides) and intracellular neurofibrillary tangles (composed of hyperphosphorylated
tau proteins). The cleavage of amyloid precursor protein (APP) by aberrant secretase activity
yields sticky beta-amyloid fragments that clump together, disrupting synaptic communication
and inciting a localized inflammatory response. Option A describes neurofibrillary tangles, not
plaques. Option C describes a consequence of cholinergic loss, not plaque formation. Option D
describes hydrocephalus ex vacuo, a secondary finding.
**Question 2**
A 72-year-old patient presents with progressive memory loss, disorientation to time and place,
and difficulty finding words. Family reports the patient has become increasingly dependent for
activities of daily living. Which brain region is most characteristically affected early in the
disease process?
A) Cerebellum
,Page 3 of 126
B) Hippocampus
C) Medulla oblongata
D) Primary motor cortex
**Correct Answer: B**
**Rationale:** The hippocampus is critical for converting short-term memory into long-term
memory, and it is one of the earliest and most severely affected regions in Alzheimer's disease.
Its shrinkage on imaging correlates with the profound short-term memory loss that is an early
and prominent symptom. The cerebellum (A) is involved in motor coordination, the medulla (C)
regulates autonomic functions, and the primary motor cortex (D) controls voluntary movement—
none of which are the earliest sites of Alzheimer's pathology.
**Question 3**
The cholinergic hypothesis of Alzheimer's disease serves as the foundational rationale for
administering which class of medications to manage cognitive decline?
A) N-methyl-D-aspartate (NMDA) receptor antagonists
B) Dopamine receptor agonists
C) Acetylcholinesterase inhibitors
D) Monoamine oxidase B (MAO-B) inhibitors
**Correct Answer: C**
**Rationale:** The brains of individuals with Alzheimer's disease exhibit a marked deficit in
acetylcholine (ACh), a key neurotransmitter vital for memory, learning, and synaptic plasticity.
Because acetylcholinesterase is the enzyme responsible for degrading synaptic ACh,
administering an acetylcholinesterase inhibitor (e.g., donepezil) blocks this breakdown, thereby
, Page 4 of 126
increasing the availability of acetylcholine within the synaptic cleft to temporarily sustain
cognitive function. Memantine (an NMDA receptor antagonist) is used for moderate to severe
disease but does not directly target the cholinergic deficit.
**Question 4**
Which medication is used for moderate to severe Alzheimer's disease and acts as an NMDA
receptor antagonist?
A) Donepezil
B) Rivastigmine
C) Memantine
D) Galantamine
**Correct Answer: C**
**Rationale:** Memantine is an NMDA receptor antagonist that blocks glutamate-mediated
excitotoxicity. It is approved for moderate to severe Alzheimer's disease, often in combination
with an acetylcholinesterase inhibitor. Donepezil, rivastigmine, and galantamine are all
acetylcholinesterase inhibitors, not NMDA receptor antagonists.
**Question 5**
The strongest genetic risk factor for late-onset Alzheimer's disease is:
A) APOE2 allele
B) APOE3 allele
C) APOE4 allele
D) Presenilin-1 gene mutation
NR 507 EDAPT WEEK 7: CENTRAL NERVOUS
SYSTEM SENSORY AND MOTOR DISORDERS |
COMPREHENSIVE PRACTICE QUESTION BANK |
WITH DETAILED RATIONALES | GRADUATE
NURSING STUDENTS | ADVANCED
PATHOPHYSIOLOGY | CHAMBERLAIN UNIVERSITY |
NR 507 WEEK 7 EDAPT MODULE ASSESSMENT |
TABLE OF CONTENTS
| Section | Topic | Questions |
|---------|-------|-----------|
| I | Neurodegenerative Disorders: Alzheimer's Disease & Dementia | 1–35 |
| II | Neurodegenerative Disorders: Parkinson's Disease | 36–65 |
| III | Demyelinating Disorders: Multiple Sclerosis & Related Conditions | 66–95 |
| IV | Motor Neuron Disorders: ALS & Related Conditions | 96–115 |
| V | Neuromuscular Junction Disorders: Myasthenia Gravis | 116–135 |
| VI | Cerebrovascular Disorders: Stroke & TIA | 136–165 |
| VII | Seizure Disorders & Epilepsy | 166–185 |
| VIII | Increased Intracranial Pressure & Headache Disorders | 186–200 |
| IX | Integrative & Cross-Topic Questions | 201–215 |
,Page 2 of 126
SECTION I: NEURODEGENERATIVE DISORDERS — ALZHEIMER'S DISEASE & DEMENTIA
**Question 1**
Which pathophysiological mechanism is primarily responsible for the formation of extracellular
senile plaques associated with Alzheimer's disease?
A) Hyperphosphorylation of intracellular tau proteins leading to microtubule destabilization
B) Deposition and aggregation of misfolded beta-amyloid proteins in the neural parenchyma
C) Autoimmune-mediated destruction of central cholinergic neurons in the nucleus basalis of
Meynert
D) Massive expansion of the cerebral ventricles secondary to normal-pressure hydrocephalus
**Correct Answer: B**
**Rationale:** Alzheimer's disease is characterized pathologically by two hallmark protein
abnormalities: extracellular senile plaques (formed by the accumulation of insoluble beta-
amyloid peptides) and intracellular neurofibrillary tangles (composed of hyperphosphorylated
tau proteins). The cleavage of amyloid precursor protein (APP) by aberrant secretase activity
yields sticky beta-amyloid fragments that clump together, disrupting synaptic communication
and inciting a localized inflammatory response. Option A describes neurofibrillary tangles, not
plaques. Option C describes a consequence of cholinergic loss, not plaque formation. Option D
describes hydrocephalus ex vacuo, a secondary finding.
**Question 2**
A 72-year-old patient presents with progressive memory loss, disorientation to time and place,
and difficulty finding words. Family reports the patient has become increasingly dependent for
activities of daily living. Which brain region is most characteristically affected early in the
disease process?
A) Cerebellum
,Page 3 of 126
B) Hippocampus
C) Medulla oblongata
D) Primary motor cortex
**Correct Answer: B**
**Rationale:** The hippocampus is critical for converting short-term memory into long-term
memory, and it is one of the earliest and most severely affected regions in Alzheimer's disease.
Its shrinkage on imaging correlates with the profound short-term memory loss that is an early
and prominent symptom. The cerebellum (A) is involved in motor coordination, the medulla (C)
regulates autonomic functions, and the primary motor cortex (D) controls voluntary movement—
none of which are the earliest sites of Alzheimer's pathology.
**Question 3**
The cholinergic hypothesis of Alzheimer's disease serves as the foundational rationale for
administering which class of medications to manage cognitive decline?
A) N-methyl-D-aspartate (NMDA) receptor antagonists
B) Dopamine receptor agonists
C) Acetylcholinesterase inhibitors
D) Monoamine oxidase B (MAO-B) inhibitors
**Correct Answer: C**
**Rationale:** The brains of individuals with Alzheimer's disease exhibit a marked deficit in
acetylcholine (ACh), a key neurotransmitter vital for memory, learning, and synaptic plasticity.
Because acetylcholinesterase is the enzyme responsible for degrading synaptic ACh,
administering an acetylcholinesterase inhibitor (e.g., donepezil) blocks this breakdown, thereby
, Page 4 of 126
increasing the availability of acetylcholine within the synaptic cleft to temporarily sustain
cognitive function. Memantine (an NMDA receptor antagonist) is used for moderate to severe
disease but does not directly target the cholinergic deficit.
**Question 4**
Which medication is used for moderate to severe Alzheimer's disease and acts as an NMDA
receptor antagonist?
A) Donepezil
B) Rivastigmine
C) Memantine
D) Galantamine
**Correct Answer: C**
**Rationale:** Memantine is an NMDA receptor antagonist that blocks glutamate-mediated
excitotoxicity. It is approved for moderate to severe Alzheimer's disease, often in combination
with an acetylcholinesterase inhibitor. Donepezil, rivastigmine, and galantamine are all
acetylcholinesterase inhibitors, not NMDA receptor antagonists.
**Question 5**
The strongest genetic risk factor for late-onset Alzheimer's disease is:
A) APOE2 allele
B) APOE3 allele
C) APOE4 allele
D) Presenilin-1 gene mutation
