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WGU D115 Advanced Pathophysiology Rapid Review | 100-Question Practice Exam | Units 2-7 Mixed Graduate MCQs with Rationales | OA Ready 2025/2026

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ACCELERATE YOUR WGU D115 ADVANCED PATHOPHYSIOLOGY PREP! This 100-question rapid-review set covers Units 2-7 with mixed graduate-level MCQs, each featuring concise rationales. Perfect for final review before your Objective Assessment (OA) in the 2025/2026 academic year. Designed specifically for time-efficient study, this resource presents challenging graduate-level pathophysiology questions in a mixed-format to simulate the actual OA experience. Each four-option multiple-choice question includes a single best answer followed by a targeted rationale that reinforces key concepts without unnecessary detail—ideal for last-minute mastery and confidence building. WHAT MAKES THIS RAPID-REVIEW SET ESSENTIAL: 100 MIXED-FORMAT QUESTIONS covering Units 2-7 of WGU D115 curriculum GRADUATE-LEVEL PATHOPHYSIOLOGY - Advanced complexity for MSN/NP students CONCISE, TARGETED RATIONALES - Quick reinforcement of key concepts OA-STYLE QUESTIONS - Four-option MCQs with single best answer format 2025/2026 CURRICULUM ALIGNED - Updated for current academic year requirements TIME-EFFICIENT DESIGN - Perfect for final review sessions and knowledge gaps identification Don't waste time on inefficient studying. Get the focused rapid-review that targets exactly what you need for the D115 OA. Purchase now and master advanced pathophysiology concepts quickly and effectively!

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WGU D115 Advanced Pathophysiology
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Institution
WGU D115 Advanced Pathophysiology
Course
WGU D115 Advanced Pathophysiology

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Uploaded on
December 1, 2025
Number of pages
22
Written in
2025/2026
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1



WGU D115 Advanced Pathophysiology
Rapid Review | 100-Question Practice
Exam | Units 2-7 Mixed Graduate MCQs
with Rationales | OA Ready 2025/2026
1. Which best explains why the β-globin Glu→Val mutation produces sickling under
deoxygenated conditions?
A. Val adds a negative charge → electrostatic repulsion
B. Val is hydrophobic → accepts a complementary pocket on an adjacent deoxy-HbS →
polymer
C. Val forms a new hydrogen bond with α-chain
D. Val increases 2,3-BPG affinity → left-shifted curve
Key: B | Rationale: Hydrophobic valine allows longitudinal polymerization of deoxy-
HbS, rigidifying the RBC.

2. A renal graft biopsy shows “muddy-brown” granular casts. The patient received NSAIDs
for gout yesterday. Which mechanism caused the cast?
A. Afferent arteriole dilatation → hyper-filtration injury
B. Efferent vasoconstriction → prerenal azotemia → ischemic ATN → sloughed tubule
cells in TAL
C. Direct tubular toxicity by NSAID metabolites
D. Crystal obstruction by uric acid
Key: B | Rationale: NSAIDs block renal prostaglandins → lose afferent vasodilatory
brake → cortical ischemia → ATN.

3. Microscopic polyangiitis is strongly associated with which auto-antibody?
A. Anti-PR3
B. Anti-MPO
C. Anti-GBM
D. Anti-CCP
Key: B | Rationale: p-ANCA (anti-myeloperoxidase) is characteristic of microscopic
polyangiitis.

, 2



4. A 30-year-old woman with RRMS has new T2 lesions on MRI. Which cytokine
predominates in her acute plaques?
A. IL-4
B. IL-10
C. IL-17
D. TGF-β
Key: C | Rationale: Th17/IL-17 drives neutrophil recruitment and blood-brain-barrier
breakdown in MS.

5. The “pink puffer” COPD phenotype is linked to which underlying pathophysiology?
A. Centrilobular emphysema with α-1-antitrypsin deficiency
B. Pan-acinar emphysema with preserved airway elastic recoil
C. Chronic bronchitis with mucous gland hyperplasia
D. Small-airway fibrosis without parenchymal destruction
Key: B | Rationale: Pan-acinar loss increases lung compliance → patient breathes at high
lung volumes to maintain flow.

6. In cardiogenic shock, which Starling curve shift best describes the ventricle?
A. Up and to the left (increased contractility)
B. Down and to the right (decreased contractility)
C. Up and to the right (increased afterload)
D. Down and to the left (volume depletion)
Key: B | Rationale: Primary pump failure flattens the curve → lower stroke volume at
any filling pressure.

7. A patient with Addisonian crisis has Na 124 mmol/L and K 6.2 mmol/L. The
hyperkalemia is primarily due to:
A. Reduced distal Na delivery →↓K secretion
B. Aldosterone deficiency →↓ENaC expression →↓K excretion
C. Metabolic acidosis → K shift out of cells
D. Increased urine flow → K loss → total-body depletion
Key: B | Rationale: Aldosterone normally up-regulates ENaC and ROMK; lack thereof
blocks K secretion.

, 3



8. Which mutation produces the “gain-of-function” in the ACTH receptor seen in primary
bilateral macronodular adrenal hyperplasia?
A. GNAS
B. MC2R (activating)
C. PRKAR1A
D. TP53
Key: B | Rationale: Activating MC2R mutations cause ACTH-independent cortisol over-
production.

9. A 2-day-old newborn has bilious vomiting and a “double-bubble” X-ray. Which
embryologic mechanism failed?
A. Recanalization of the duodenum
B. Rotation of the midgut around SMA
C. Fusion of the pancreatic buds
D. Septation of cloaca
Key: A | Rationale: Failure of duodenal recanalization → congenital duodenal atresia.

10. Which clotting factor is NOT in the intrinsic pathway yet its deficiency prolongs the
aPTT?
A. VIII
B. IX
C. XII
D. VII
Key: D | Rationale: High-dose factor VIIa can shorten aPTT in vitro; physiologic levels
do not, but severe VII deficiency (<1 %) can mildly prolong aPTT because tissue-factor
pathway feeds IX.

11. A patient with CLL develops warm-antibody autoimmune hemolysis. The antibody
isotype is:
A. IgM
B. IgG
C. IgA
D. IgE
Key: B | Rationale: Warm autoantibodies are typically IgG, detected by DAT.

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