Western Governors University
AO • 5 1 1 D
WGU College of Health Professions — Nursing Program
THE UNIVERSITY OF YOU
EST. 1997
D115 — Objective Assessment (OA)
A D VA N C E D PAT H O P H YS I O LO G Y — H I G H -Y I E L D O A R E V I E W
INSTITUTION Western Governors University — College COURSE CODE D115
of Health Professions
PROGRAM BSN Pre-Licensure / MSN Pathway ACADEMIC YEAR
EXAM TITLE Objective Assessment — High-Yield OA TOTAL QUESTIONS 90 Questions
Review
ACCREDITATION CCNE — Commission on Collegiate FORMAT Multiple Choice — Select the Single Best
Nursing Education Answer
EXAMINATION INSTRUCTIONS
▸ Select the single best answer for each question based on WGU D115 Advanced Pathophysiology content.
▸ Questions cover neuro (myasthenia gravis, Bell's palsy, cerebral palsy, posturing), genetics (Turner, Down, Marfan, Klinefelter),
cardiac (HF, HTN, shock), immunology (hypersensitivity types), hematology (anemia, sickle cell, leukemia), renal (AKI, CKD,
nephritic/nephrotic, pyelonephritis, glomerulonephritis), GI (Crohn's, UC), dermatology (lesion types), endocrine (PCOS),
reproductive, and burns.
▸ Correct answers and pathophysiological rationales appear below each question for OA preparation.
▸ All content aligns with WGU BSN curriculum and CCNE accreditation standards.
SECTION I — D115 OBJECTIVE ASSESSMENT: HIGH-YIELD REVIEW Questions 1 – 90
1. What is the pathophysiology and key feature of myasthenia gravis?
A. Demyelination of CNS white matter; weakness is constant
B. Autoimmune destruction of acetylcholine receptors at the neuromuscular junction causing FATIGABLE weakness —
worsens with activity and improves with rest
C. Degeneration of anterior horn cells; weakness is progressive
D. Acetylcholine excess at the synapse; muscle spasms
CORRECT ANSWER B — Autoimmune destruction of ACh receptors at NMJ; FATIGABLE weakness worsening with activity,
improving with rest
RATIONALE Myasthenia gravis (MG) is a Type II hypersensitivity (autoimmune) disorder where antibodies attack
postsynaptic acetylcholine receptors at the neuromuscular junction. This reduces the number of functional
receptors → muscle weakness that is FATIGABLE — worsens with repeated use and improves with rest.
CRANIAL NERVES commonly affected: CN III (ptosis, diplopia — often the first symptoms), CN V
(mastication/chewing weakness), CN VII (facial weakness), CN IX/X (dysphagia, swallowing difficulty), CN XII
(tongue weakness). DIAGNOSIS: acetylcholine receptor antibody testing (edrophonium/Tensilon test is
historical). MYASTHENIC CRISIS: respiratory muscle weakness → respiratory failure — medical emergency
requiring mechanical ventilation, plasmapheresis, or IVIG. Treatment: anticholinesterase medications
(pyridostigmine), immunosuppressants, thymectomy.
, 2. How do you differentiate Bell's palsy from a stroke?
A. Bell's palsy spares the forehead; stroke affects the forehead
B. Bell's palsy (CN VII) affects the FOREHEAD (cannot wrinkle); stroke SPARES the forehead because of bilateral cortical
innervation of upper face
C. Both present identically
D. Bell's palsy only affects the lower face
CORRECT ANSWER B — Bell's palsy (peripheral CN VII) affects the entire ipsilateral face including FOREHEAD; stroke
(central/UMN) spares the forehead due to bilateral cortical innervation
RATIONALE This is a classic clinical distinction. Bell's palsy is a peripheral CN VII (facial nerve) lesion — the entire
ipsilateral face is affected, including the forehead (patient cannot wrinkle forehead or raise eyebrow on that
side). Stroke is an upper motor neuron (central) lesion — the lower face is affected (contralateral), but the
FOREHEAD IS SPARED because the upper face receives BILATERAL cortical innervation from both
hemispheres. Bell's palsy is often linked to viral infections (HSV, herpes zoster, Lyme disease). It is typically
self-limiting, with most patients recovering within weeks to months. Treatment: corticosteroids (prednisone),
antivirals if viral cause suspected, eye protection (incomplete eyelid closure).
3. What is the difference between decorticate and decerebrate posturing and what does each indicate?
A. Decorticate: extended arms/legs, damage below red nucleus; Decerebrate: flexed arms, extended legs, damage
above red nucleus
B. Decorticate (flexor): arms flexed toward core, legs extended — damage ABOVE red nucleus (cerebral hemispheres,
internal capsule); Decerebrate (extensor): all four extremities extended — damage BELOW red nucleus
(midbrain/pons) — WORSE prognosis
C. Both indicate identical levels of injury
D. Decorticate is always fatal; decerebrate is recoverable
CORRECT ANSWER B — Decorticate (flexor): arms flexed toward core, damage ABOVE red nucleus; Decerebrate (extensor):
all four extended, damage BELOW red nucleus — WORSE prognosis
RATIONALE Posturing indicates the level of brain dysfunction. DECORTICATE (abnormal flexion): arms flexed and
adducted toward chest ("like holding a teddy bear"), legs extended, feet plantar flexed. Indicates damage
ABOVE the red nucleus — cerebral hemispheres, internal capsule, thalamus. DECEREBRATE (abnormal
extension): arms extended and externally rotated, jaw clenched, neck extended, legs extended. Indicates
damage AT or BELOW the red nucleus — midbrain or pons damage. Decerebrate has a WORSE prognosis. The
progression from decorticate → decerebrate represents rostral-to-caudal deterioration (brain herniation). A
rapid change in posturing indicates worsening brain injury, increased ICP, or herniation — a medical
emergency.
AO • 5 1 1 D
WGU College of Health Professions — Nursing Program
THE UNIVERSITY OF YOU
EST. 1997
D115 — Objective Assessment (OA)
A D VA N C E D PAT H O P H YS I O LO G Y — H I G H -Y I E L D O A R E V I E W
INSTITUTION Western Governors University — College COURSE CODE D115
of Health Professions
PROGRAM BSN Pre-Licensure / MSN Pathway ACADEMIC YEAR
EXAM TITLE Objective Assessment — High-Yield OA TOTAL QUESTIONS 90 Questions
Review
ACCREDITATION CCNE — Commission on Collegiate FORMAT Multiple Choice — Select the Single Best
Nursing Education Answer
EXAMINATION INSTRUCTIONS
▸ Select the single best answer for each question based on WGU D115 Advanced Pathophysiology content.
▸ Questions cover neuro (myasthenia gravis, Bell's palsy, cerebral palsy, posturing), genetics (Turner, Down, Marfan, Klinefelter),
cardiac (HF, HTN, shock), immunology (hypersensitivity types), hematology (anemia, sickle cell, leukemia), renal (AKI, CKD,
nephritic/nephrotic, pyelonephritis, glomerulonephritis), GI (Crohn's, UC), dermatology (lesion types), endocrine (PCOS),
reproductive, and burns.
▸ Correct answers and pathophysiological rationales appear below each question for OA preparation.
▸ All content aligns with WGU BSN curriculum and CCNE accreditation standards.
SECTION I — D115 OBJECTIVE ASSESSMENT: HIGH-YIELD REVIEW Questions 1 – 90
1. What is the pathophysiology and key feature of myasthenia gravis?
A. Demyelination of CNS white matter; weakness is constant
B. Autoimmune destruction of acetylcholine receptors at the neuromuscular junction causing FATIGABLE weakness —
worsens with activity and improves with rest
C. Degeneration of anterior horn cells; weakness is progressive
D. Acetylcholine excess at the synapse; muscle spasms
CORRECT ANSWER B — Autoimmune destruction of ACh receptors at NMJ; FATIGABLE weakness worsening with activity,
improving with rest
RATIONALE Myasthenia gravis (MG) is a Type II hypersensitivity (autoimmune) disorder where antibodies attack
postsynaptic acetylcholine receptors at the neuromuscular junction. This reduces the number of functional
receptors → muscle weakness that is FATIGABLE — worsens with repeated use and improves with rest.
CRANIAL NERVES commonly affected: CN III (ptosis, diplopia — often the first symptoms), CN V
(mastication/chewing weakness), CN VII (facial weakness), CN IX/X (dysphagia, swallowing difficulty), CN XII
(tongue weakness). DIAGNOSIS: acetylcholine receptor antibody testing (edrophonium/Tensilon test is
historical). MYASTHENIC CRISIS: respiratory muscle weakness → respiratory failure — medical emergency
requiring mechanical ventilation, plasmapheresis, or IVIG. Treatment: anticholinesterase medications
(pyridostigmine), immunosuppressants, thymectomy.
, 2. How do you differentiate Bell's palsy from a stroke?
A. Bell's palsy spares the forehead; stroke affects the forehead
B. Bell's palsy (CN VII) affects the FOREHEAD (cannot wrinkle); stroke SPARES the forehead because of bilateral cortical
innervation of upper face
C. Both present identically
D. Bell's palsy only affects the lower face
CORRECT ANSWER B — Bell's palsy (peripheral CN VII) affects the entire ipsilateral face including FOREHEAD; stroke
(central/UMN) spares the forehead due to bilateral cortical innervation
RATIONALE This is a classic clinical distinction. Bell's palsy is a peripheral CN VII (facial nerve) lesion — the entire
ipsilateral face is affected, including the forehead (patient cannot wrinkle forehead or raise eyebrow on that
side). Stroke is an upper motor neuron (central) lesion — the lower face is affected (contralateral), but the
FOREHEAD IS SPARED because the upper face receives BILATERAL cortical innervation from both
hemispheres. Bell's palsy is often linked to viral infections (HSV, herpes zoster, Lyme disease). It is typically
self-limiting, with most patients recovering within weeks to months. Treatment: corticosteroids (prednisone),
antivirals if viral cause suspected, eye protection (incomplete eyelid closure).
3. What is the difference between decorticate and decerebrate posturing and what does each indicate?
A. Decorticate: extended arms/legs, damage below red nucleus; Decerebrate: flexed arms, extended legs, damage
above red nucleus
B. Decorticate (flexor): arms flexed toward core, legs extended — damage ABOVE red nucleus (cerebral hemispheres,
internal capsule); Decerebrate (extensor): all four extremities extended — damage BELOW red nucleus
(midbrain/pons) — WORSE prognosis
C. Both indicate identical levels of injury
D. Decorticate is always fatal; decerebrate is recoverable
CORRECT ANSWER B — Decorticate (flexor): arms flexed toward core, damage ABOVE red nucleus; Decerebrate (extensor):
all four extended, damage BELOW red nucleus — WORSE prognosis
RATIONALE Posturing indicates the level of brain dysfunction. DECORTICATE (abnormal flexion): arms flexed and
adducted toward chest ("like holding a teddy bear"), legs extended, feet plantar flexed. Indicates damage
ABOVE the red nucleus — cerebral hemispheres, internal capsule, thalamus. DECEREBRATE (abnormal
extension): arms extended and externally rotated, jaw clenched, neck extended, legs extended. Indicates
damage AT or BELOW the red nucleus — midbrain or pons damage. Decerebrate has a WORSE prognosis. The
progression from decorticate → decerebrate represents rostral-to-caudal deterioration (brain herniation). A
rapid change in posturing indicates worsening brain injury, increased ICP, or herniation — a medical
emergency.
