Western Governors University
MAXE • 511D
WGU College of Health Professions — Leavitt School of Health
A NEW KIND OF U.
D115 PATHO
D115 — Advanced Pathophysiology
CO M P R E H E N S I V E O A R E A D I N E SS E X A M I N AT I O N • G E N E T I CS T H R O U G H M U LT I SYST E M
INSTITUTION Western Governors University (WGU) COURSE CODE D115
PROGRAM M.S.N. — Family Nurse Practitioner (FNP) ACADEMIC YEAR
EXAM TITLE D115 Advanced Pathophysiology — TOTAL QUESTIONS 40 Questions
Comprehensive Exam
FORMAT Multiple Choice — Select the Single Best
Answer
EXAMINATION INSTRUCTIONS
▸ Select the single best answer for each question based on D115 Advanced Pathophysiology content.
▸ Questions cover genetic disorders, chromosomal abnormalities, hematologic conditions, cardiovascular pathology,
neurological disorders, GI diseases, endocrine dysfunction, and infectious diseases.
▸ Pay close attention to inheritance patterns, pathognomonic findings, and distinguishing features between similar conditions.
▸ Correct answers and detailed rationales appear below each question for OA preparation.
SECTION I — GENETICS, HEMATOLOGY, CARDIOVASCULAR, NEUROLOGY, Questions 1
GI & ENDOCRINE – 40
1. Turner syndrome is a chromosomal disorder characterized by which karyotype and clinical findings?
A. XXY — tall stature, gynecomastia, small testes
B. XO (monosomy X) — short stature, webbed neck, underdeveloped ovaries (sterile), wide-spaced nipples, edema
C. Trisomy 21 — intellectual disability, flat facial profile, simian crease
D. Trisomy 18 — clenched fists, rocker-bottom feet, severe intellectual disability
CORRECT ANSWER B — XO (monosomy X) — short stature, webbed neck, underdeveloped ovaries, wide-spaced nipples,
edema
RATIONALE Turner syndrome (45,XO) is a chromosomal disorder in females caused by complete or partial absence of one
X chromosome. The classic clinical features: SHORT STATURE (average adult height ~4'7"), WEB OF SKIN on
the neck (webbed neck/pterygium colli), UNDERDEVELOPED OVARIES (streak gonads → infertility), widely
spaced nipples (shield chest), lymphedema of hands and feet at birth, and low hairline. Many Turner
conceptuses are spontaneously aborted. Diagnostic testing includes karyotype (genetic testing),
echocardiogram (cardiac anomalies, especially coarctation of aorta and bicuspid aortic valve), bone density,
and bone age testing. Treatment involves growth hormone administration and estrogen replacement therapy.
XXY (A) is Klinefelter syndrome. Trisomy 21 (C) is Down syndrome. Trisomy 18 (D) is Edwards syndrome.
,2. Marfan syndrome is caused by a mutation in which gene, and what is its inheritance pattern?
A. CFTR gene; autosomal recessive
B. FBN1 (fibrillin-1) gene; autosomal dominant
C. HTT gene; autosomal dominant
D. HBB gene; autosomal recessive
CORRECT ANSWER B — FBN1 (fibrillin-1) gene; autosomal dominant
RATIONALE Marfan syndrome is an autosomal dominant connective tissue disorder caused by mutations in the FBN1
gene on chromosome 15, which encodes fibrillin-1 — a glycoprotein essential for the formation of elastic
fibers in connective tissue. Defective fibrillin leads to weakened connective tissue throughout the body.
Clinical features: tall stature with disproportionately long limbs (dolichostenomelia), arachnodactyly (long,
spider-like fingers), joint hypermobility, lens dislocation (ectopia lentis — upward and outward), aortic root
dilation with risk of aortic dissection (most life-threatening complication), and mitral valve prolapse. At least
25% of cases result from a NEW (de novo) mutation — meaning there is no family history. CFTR (A) causes
cystic fibrosis. HTT (C) causes Huntington disease. HBB (D) causes sickle cell disease and beta-thalassemia.
3. What is the pathophysiologic mechanism of pernicious anemia?
A. Iron deficiency due to chronic blood loss
B. Autoimmune destruction of gastric parietal cells or intrinsic factor, leading to inability to absorb vitamin B12
C. Inherited defect in hemoglobin synthesis
D. Bone marrow failure with pancytopenia
CORRECT ANSWER B — Autoimmune destruction of gastric parietal cells or intrinsic factor → B12 malabsorption
RATIONALE Pernicious anemia is a type of macrocytic (megaloblastic) anemia caused by VITAMIN B12 DEFICIENCY due to
impaired absorption — specifically, autoimmune destruction of either the gastric parietal cells (which
produce intrinsic factor/IF) or intrinsic factor itself. Without IF, vitamin B12 cannot be absorbed in the terminal
ileum, regardless of dietary intake. This results in: macrocytic anemia (high MCV), neurological deficits
(paresthesia, gait disturbances, cognitive changes — because B12 is needed for myelin synthesis), glossitis
(beefy red tongue), and fatigue. Causes of B12 deficiency beyond pernicious anemia include: atrophic
gastritis, conditions affecting the small intestine (Crohn's, celiac, bacterial overgrowth), heavy alcohol use,
and medications that interfere with B12 absorption (PPIs, H2 blockers, metformin). Iron deficiency (A) causes
microcytic anemia. Bone marrow failure (D) is aplastic anemia.
, 4. What is the difference between mitral regurgitation and mitral stenosis?
A. Regurgitation: valve fails to close completely → backflow during systole. Stenosis: valve opening narrowed →
restricts forward flow from LA to LV
B. Regurgitation: narrowed valve opening. Stenosis: leaky valve
C. Both describe the same valvular abnormality
D. Regurgitation affects the aortic valve only; stenosis affects the mitral valve only
CORRECT ANSWER A — Regurgitation: fails to close → backflow during systole. Stenosis: narrowed → restricts forward
flow
RATIONALE Valvular heart disease includes two primary dysfunctions. MITRAL REGURGITATION (insufficiency): the mitral
valve fails to CLOSE completely → during ventricular systole, blood flows BACKWARD from the left ventricle
into the left atrium → volume overload, left atrial enlargement, and eventually heart failure. It produces a
pansystolic murmur at the apex radiating to the axilla. Causes include papillary muscle rupture, mitral valve
prolapse, and infective endocarditis. MITRAL STENOSIS: the mitral valve opening is NARROWED → restricts
forward blood flow from the left atrium to the left ventricle → left atrial pressure increases → left atrial
enlargement → pulmonary congestion. It produces a diastolic rumbling murmur at the apex. Aortic stenosis:
narrowed aortic valve → left ventricular hypertrophy. Aortic regurgitation: leaky aortic valve → backflow into
LV during diastole. Heart vegetations (infective endocarditis) are abnormal bacterial growths on valves that
damage them.
5. What is the difference between ischemic and hemorrhagic stroke?
A. Ischemic: vessel rupture. Hemorrhagic: vessel occlusion
B. Ischemic: thrombus/embolus occludes cerebral artery (85% of strokes). Hemorrhagic: cerebral artery ruptures and
bleeds (15% of strokes)
C. Both have identical mechanisms and presentation
D. Ischemic is always fatal; hemorrhagic is always survivable
CORRECT ANSWER B — Ischemic: occlusion (85%). Hemorrhagic: rupture (15%)
RATIONALE Stroke is classified by mechanism. ISCHEMIC STROKE (85%): caused by thrombus or embolus occluding a
cerebral artery → ischemia → cerebral infarction (death of brain tissue). Risk factors: hypertension,
atherosclerosis (carotid stenosis), atrial fibrillation (embolic source), diabetes, smoking, hyperlipidemia, oral
contraceptives, and sickle cell anemia. HEMORRHAGIC STROKE (15%): caused by rupture of a cerebral artery
→ bleeding into brain tissue (intracerebral) or subarachnoid space → compression and toxicity to brain cells.
MAJOR risk factor: HYPERTENSION. Other risks: weakened vessel walls (aneurysm, AVM), age,
anticoagulant/antiplatelet use. Cerebral contusion (brain bruising from trauma) symptoms: severe headache,
dizziness, N/V, ipsilateral pupil dilation, and possible LOC. Bell's Palsy: CN VII paralysis (unilateral facial droop,
cannot wrinkle forehead — peripheral LMN lesion). Most common cause: herpes simplex virus.
MAXE • 511D
WGU College of Health Professions — Leavitt School of Health
A NEW KIND OF U.
D115 PATHO
D115 — Advanced Pathophysiology
CO M P R E H E N S I V E O A R E A D I N E SS E X A M I N AT I O N • G E N E T I CS T H R O U G H M U LT I SYST E M
INSTITUTION Western Governors University (WGU) COURSE CODE D115
PROGRAM M.S.N. — Family Nurse Practitioner (FNP) ACADEMIC YEAR
EXAM TITLE D115 Advanced Pathophysiology — TOTAL QUESTIONS 40 Questions
Comprehensive Exam
FORMAT Multiple Choice — Select the Single Best
Answer
EXAMINATION INSTRUCTIONS
▸ Select the single best answer for each question based on D115 Advanced Pathophysiology content.
▸ Questions cover genetic disorders, chromosomal abnormalities, hematologic conditions, cardiovascular pathology,
neurological disorders, GI diseases, endocrine dysfunction, and infectious diseases.
▸ Pay close attention to inheritance patterns, pathognomonic findings, and distinguishing features between similar conditions.
▸ Correct answers and detailed rationales appear below each question for OA preparation.
SECTION I — GENETICS, HEMATOLOGY, CARDIOVASCULAR, NEUROLOGY, Questions 1
GI & ENDOCRINE – 40
1. Turner syndrome is a chromosomal disorder characterized by which karyotype and clinical findings?
A. XXY — tall stature, gynecomastia, small testes
B. XO (monosomy X) — short stature, webbed neck, underdeveloped ovaries (sterile), wide-spaced nipples, edema
C. Trisomy 21 — intellectual disability, flat facial profile, simian crease
D. Trisomy 18 — clenched fists, rocker-bottom feet, severe intellectual disability
CORRECT ANSWER B — XO (monosomy X) — short stature, webbed neck, underdeveloped ovaries, wide-spaced nipples,
edema
RATIONALE Turner syndrome (45,XO) is a chromosomal disorder in females caused by complete or partial absence of one
X chromosome. The classic clinical features: SHORT STATURE (average adult height ~4'7"), WEB OF SKIN on
the neck (webbed neck/pterygium colli), UNDERDEVELOPED OVARIES (streak gonads → infertility), widely
spaced nipples (shield chest), lymphedema of hands and feet at birth, and low hairline. Many Turner
conceptuses are spontaneously aborted. Diagnostic testing includes karyotype (genetic testing),
echocardiogram (cardiac anomalies, especially coarctation of aorta and bicuspid aortic valve), bone density,
and bone age testing. Treatment involves growth hormone administration and estrogen replacement therapy.
XXY (A) is Klinefelter syndrome. Trisomy 21 (C) is Down syndrome. Trisomy 18 (D) is Edwards syndrome.
,2. Marfan syndrome is caused by a mutation in which gene, and what is its inheritance pattern?
A. CFTR gene; autosomal recessive
B. FBN1 (fibrillin-1) gene; autosomal dominant
C. HTT gene; autosomal dominant
D. HBB gene; autosomal recessive
CORRECT ANSWER B — FBN1 (fibrillin-1) gene; autosomal dominant
RATIONALE Marfan syndrome is an autosomal dominant connective tissue disorder caused by mutations in the FBN1
gene on chromosome 15, which encodes fibrillin-1 — a glycoprotein essential for the formation of elastic
fibers in connective tissue. Defective fibrillin leads to weakened connective tissue throughout the body.
Clinical features: tall stature with disproportionately long limbs (dolichostenomelia), arachnodactyly (long,
spider-like fingers), joint hypermobility, lens dislocation (ectopia lentis — upward and outward), aortic root
dilation with risk of aortic dissection (most life-threatening complication), and mitral valve prolapse. At least
25% of cases result from a NEW (de novo) mutation — meaning there is no family history. CFTR (A) causes
cystic fibrosis. HTT (C) causes Huntington disease. HBB (D) causes sickle cell disease and beta-thalassemia.
3. What is the pathophysiologic mechanism of pernicious anemia?
A. Iron deficiency due to chronic blood loss
B. Autoimmune destruction of gastric parietal cells or intrinsic factor, leading to inability to absorb vitamin B12
C. Inherited defect in hemoglobin synthesis
D. Bone marrow failure with pancytopenia
CORRECT ANSWER B — Autoimmune destruction of gastric parietal cells or intrinsic factor → B12 malabsorption
RATIONALE Pernicious anemia is a type of macrocytic (megaloblastic) anemia caused by VITAMIN B12 DEFICIENCY due to
impaired absorption — specifically, autoimmune destruction of either the gastric parietal cells (which
produce intrinsic factor/IF) or intrinsic factor itself. Without IF, vitamin B12 cannot be absorbed in the terminal
ileum, regardless of dietary intake. This results in: macrocytic anemia (high MCV), neurological deficits
(paresthesia, gait disturbances, cognitive changes — because B12 is needed for myelin synthesis), glossitis
(beefy red tongue), and fatigue. Causes of B12 deficiency beyond pernicious anemia include: atrophic
gastritis, conditions affecting the small intestine (Crohn's, celiac, bacterial overgrowth), heavy alcohol use,
and medications that interfere with B12 absorption (PPIs, H2 blockers, metformin). Iron deficiency (A) causes
microcytic anemia. Bone marrow failure (D) is aplastic anemia.
, 4. What is the difference between mitral regurgitation and mitral stenosis?
A. Regurgitation: valve fails to close completely → backflow during systole. Stenosis: valve opening narrowed →
restricts forward flow from LA to LV
B. Regurgitation: narrowed valve opening. Stenosis: leaky valve
C. Both describe the same valvular abnormality
D. Regurgitation affects the aortic valve only; stenosis affects the mitral valve only
CORRECT ANSWER A — Regurgitation: fails to close → backflow during systole. Stenosis: narrowed → restricts forward
flow
RATIONALE Valvular heart disease includes two primary dysfunctions. MITRAL REGURGITATION (insufficiency): the mitral
valve fails to CLOSE completely → during ventricular systole, blood flows BACKWARD from the left ventricle
into the left atrium → volume overload, left atrial enlargement, and eventually heart failure. It produces a
pansystolic murmur at the apex radiating to the axilla. Causes include papillary muscle rupture, mitral valve
prolapse, and infective endocarditis. MITRAL STENOSIS: the mitral valve opening is NARROWED → restricts
forward blood flow from the left atrium to the left ventricle → left atrial pressure increases → left atrial
enlargement → pulmonary congestion. It produces a diastolic rumbling murmur at the apex. Aortic stenosis:
narrowed aortic valve → left ventricular hypertrophy. Aortic regurgitation: leaky aortic valve → backflow into
LV during diastole. Heart vegetations (infective endocarditis) are abnormal bacterial growths on valves that
damage them.
5. What is the difference between ischemic and hemorrhagic stroke?
A. Ischemic: vessel rupture. Hemorrhagic: vessel occlusion
B. Ischemic: thrombus/embolus occludes cerebral artery (85% of strokes). Hemorrhagic: cerebral artery ruptures and
bleeds (15% of strokes)
C. Both have identical mechanisms and presentation
D. Ischemic is always fatal; hemorrhagic is always survivable
CORRECT ANSWER B — Ischemic: occlusion (85%). Hemorrhagic: rupture (15%)
RATIONALE Stroke is classified by mechanism. ISCHEMIC STROKE (85%): caused by thrombus or embolus occluding a
cerebral artery → ischemia → cerebral infarction (death of brain tissue). Risk factors: hypertension,
atherosclerosis (carotid stenosis), atrial fibrillation (embolic source), diabetes, smoking, hyperlipidemia, oral
contraceptives, and sickle cell anemia. HEMORRHAGIC STROKE (15%): caused by rupture of a cerebral artery
→ bleeding into brain tissue (intracerebral) or subarachnoid space → compression and toxicity to brain cells.
MAJOR risk factor: HYPERTENSION. Other risks: weakened vessel walls (aneurysm, AVM), age,
anticoagulant/antiplatelet use. Cerebral contusion (brain bruising from trauma) symptoms: severe headache,
dizziness, N/V, ipsilateral pupil dilation, and possible LOC. Bell's Palsy: CN VII paralysis (unilateral facial droop,
cannot wrinkle forehead — peripheral LMN lesion). Most common cause: herpes simplex virus.
