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WGU C777 Objective Assessment 2 – Pathophysiology 2025 Actual Exam Versions A & B with Verified Answers (Graded A+)

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This document provides the full WGU C777 Objective Assessment 2 for Pathophysiology, featuring the latest 2025 Actual Exam Versions A and B. It includes verified questions with correct answers that have been graded A+, ensuring reliability and accuracy for exam preparation. The exam covers essential pathophysiology topics such as cellular injury and adaptation, inflammation, immune response, cardiovascular and respiratory disorders, endocrine and renal dysfunctions, neurological conditions, and disease processes across multiple body systems. With detailed explanations for each answer, this resource is designed to enhance understanding and help students prepare confidently for success in the WGU C777 exam.

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2025/2026
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WGU C777 Objective Assessment 2 –
Pathophysiology 2025 Actual Exam Versions
A & B with Verified Answers (Graded A+)
Complete 200 Questions with Correct Detailed Answers and
Rationales
Verified Answers | Already Graded A+

This exam for WGU C777 Objective Assessment 2 (Pathophysiology) includes Versions A and
B, totaling 200 questions. It covers cellular injury, inflammation, immune responses, genetic
disorders, neoplasia, and system-specific pathophysiology (cardiovascular, respiratory, renal,
etc.). Each question is followed by the correct answer in dark red and a detailed rationale based
on 2025 guidelines.

Version A (Questions 1-100)



1. What is Starling's Law of Capillary Forces, and how does it explain edema in
malnutrition?
Fluid movement across capillaries depends on hydrostatic and oncotic pressures; low
albumin reduces oncotic pressure, causing fluid leakage and edema.
Rationale: Starling's forces balance fluid movement; malnutrition (e.g., kwashiorkor) lowers
plasma albumin, reducing oncotic pull, leading to ascites and peripheral edema.



2. How does the body respond to bacterial infection?
Innate immunity (neutrophils, macrophages) phagocytoses pathogens; adaptive immunity
(T/B cells) produces antibodies.
Rationale: PAMPs trigger TLRs, releasing cytokines (TNF-alpha, IL-1) for inflammation and
fever; B cells produce specific IgG for opsonization.



3. What role do DNA mutations play in congenital abnormalities?
Mutations during gametogenesis or embryogenesis disrupt development, causing structural
defects.
Rationale: Trisomy 21 or teratogens (e.g., thalidomide) alter gene expression, leading to
anomalies like heart defects or spina bifida.

,4. How do developmental disruptions cause congenital anomalies?
Disruptions during organogenesis (weeks 3-8) cause malformations; later disruptions affect
function.
Rationale: Critical periods are vulnerable; e.g., folate deficiency in week 4 causes neural tube
defects.



5. A patient has +3 pitting edema and ascites. Which lab value is critical to monitor?
Albumin level
Rationale: Low albumin (<3 g/dL) reduces oncotic pressure, causing fluid extravasation per
Starling’s Law, common in liver failure or nephrotic syndrome.



6. What is the primary mechanism of aspiration pneumonia?
Inhalation of oropharyngeal contents causes chemical pneumonitis and bacterial infection.
Rationale: Gastric acid damages alveoli; right lower lobe involvement is common in dysphagia
(e.g., post-stroke).



7. In anorexia nervosa, what causes bradycardia?
Hypothermia and hypokalemia slow cardiac conduction.
Rationale: Starvation reduces metabolic rate; low potassium prolongs QT, risking arrhythmias.



8. What triggers migraine headaches?
Cortical spreading depression activates trigeminovascular system, releasing CGRP.
Rationale: Vasodilation causes pain; triptans block CGRP; triggers include stress, hormones.



9. What causes beta-cell destruction in type 1 diabetes?
Autoimmune T-cell attack triggered by environmental factors.
Rationale: HLA-DR3/4 and viral triggers cause insulitis, leading to insulin deficiency and DKA.



10. What molecular change causes sickle cell anemia?
HbS point mutation (valine for glutamic acid) polymerizes under hypoxia.
Rationale: Causes vaso-occlusion and hemolysis; hydroxyurea reduces crises.

, 11. What initiates disseminated intravascular coagulation (DIC)?
Endothelial damage triggers tissue factor release, activating coagulation.
Rationale: Sepsis or trauma causes microthrombi and bleeding from factor depletion; treat
underlying cause.



12. In ischemic cardiomyopathy, what causes ventricular dilation?
Myocyte necrosis and fibrosis impair contractility, causing volume overload.
Rationale: EF <40% leads to dilation; ACE inhibitors and beta-blockers improve outcomes.



13. What causes a holosystolic murmur in mitral regurgitation?
Incompetent mitral valve allows LV-to-LA backflow during systole.
Rationale: Turbulence heard at apex; chordae rupture or dilation is common cause.



14. What is the mechanism of pain in urolithiasis?
Ureteral obstruction and distension from stones.
Rationale: Calcium oxalate stones cause renal colic; hydration and alpha-blockers aid passage.



15. In diabetic nephropathy, what causes proteinuria?
Hyperglycemia-induced glomerular basement membrane damage.
Rationale: Podocyte injury increases permeability; ACE inhibitors slow progression.



16. What causes condyloma acuminata?
HPV 6/11 induces epithelial hyperplasia via E6/E7 oncoproteins.
Rationale: Benign warts; treated with imiquimod or cryotherapy; HPV vaccine prevents.



17. What underlies peptic ulcer disease?
H. pylori or NSAIDs disrupt mucosal barrier via urease or prostaglandin inhibition.
Rationale: Acid erodes mucosa; PPI and antibiotics eradicate H. pylori.

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