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WGU D115 ADVANCED PATHOPHYSIOLOGY NEWEST EXAM 2026 | QUESTIONS AND VERIFIED ANSWERS | ALREADY A GRADED | NEW AND REVISED!!

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Escrito en
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WGU D115 ADVANCED PATHOPHYSIOLOGY NEWEST EXAM 2026 | QUESTIONS AND VERIFIED ANSWERS | ALREADY A GRADED | NEW AND REVISED!!

Institución
WGU D115 ADVANCED PATHOPHYSIOLOGY
Grado
WGU D115 ADVANCED PATHOPHYSIOLOGY











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Institución
WGU D115 ADVANCED PATHOPHYSIOLOGY
Grado
WGU D115 ADVANCED PATHOPHYSIOLOGY

Información del documento

Subido en
23 de enero de 2026
Número de páginas
44
Escrito en
2025/2026
Tipo
Examen
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Preguntas y respuestas

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WGU D115 ADVANCED
PATHOPHYSIOLOGY NEWEST EXAM
2026 | QUESTIONS AND VERIFIED
ANSWERS | ALREADY A GRADED | NEW
AND REVISED!!




Question 1
A patient with chronic inflammation exhibits increased levels of
tumor necrosis factor-alpha (TNF-α). Which pathophysiologic
effect is most directly associated with TNF-α overexpression?
A. Enhanced insulin sensitivity
B. Decreased endothelial permeability
C. Promotion of apoptosis and cachexia
D. Suppression of acute-phase reactants
TNF-α is a pro-inflammatory cytokine that promotes
apoptosis, muscle wasting, and systemic inflammatory
responses, contributing to cachexia.
Question 2
During hypoxic injury, which cellular adaptation occurs first to
preserve ATP production?
A. Lysosomal rupture
B. Shift to anaerobic glycolysis
C. Mitochondrial swelling
D. DNA fragmentation

,2|Page


Cells initially compensate for hypoxia by increasing anaerobic
glycolysis to maintain ATP production.
Question 3
A patient with metabolic acidosis presents with Kussmaul
respirations. This compensatory mechanism primarily aims to:
A. Increase bicarbonate retention
B. Decrease PaCO₂
C. Increase renal hydrogen excretion
D. Reduce serum lactate
Deep, rapid respirations lower carbon dioxide levels, helping to
correct metabolic acidosis.
Question 4
Which mechanism best explains edema formation in nephrotic
syndrome?
A. Increased hydrostatic pressure
B. Decreased plasma oncotic pressure
C. Lymphatic obstruction
D. Increased capillary permeability alone
Loss of albumin reduces oncotic pressure, allowing fluid to
shift into interstitial spaces.
Question 5
A patient with uncontrolled diabetes mellitus develops non-
enzymatic glycosylation of proteins. This process most directly
contributes to:
A. Improved capillary integrity
B. Reduced oxidative stress
C. Microvascular complications
D. Enhanced immune function

,3|Page


Advanced glycation end products damage small blood vessels,
leading to neuropathy, nephropathy, and retinopathy.
Question 6
Which electrolyte imbalance is most likely to cause ventricular
arrhythmias?
A. Hypernatremia
B. Hyperkalemia
C. Hypocalcemia
D. Hypomagnesemia
Elevated potassium alters cardiac membrane potentials,
increasing arrhythmia risk.
Question 7
In left-sided heart failure, pulmonary edema develops primarily
due to:
A. Decreased pulmonary capillary permeability
B. Increased pulmonary venous pressure
C. Right ventricular hypertrophy
D. Reduced alveolar surfactant
Left ventricular dysfunction increases pressure in pulmonary
veins, forcing fluid into alveoli.
Question 8
A patient with septic shock has persistent hypotension despite
fluid resuscitation. Which pathophysiologic process is most
responsible?
A. Decreased cytokine release
B. Increased systemic vascular resistance
C. Widespread vasodilation from nitric oxide
D. Enhanced myocardial contractility

, 4|Page


Sepsis causes nitric-oxide–mediated vasodilation, leading to
distributive shock.
Question 9
Which immune cell is primarily responsible for antibody
production?
A. T lymphocyte
B. B lymphocyte
C. Natural killer cell
D. Macrophage
B lymphocytes differentiate into plasma cells that secrete
antibodies.
Question 10
A patient with asthma experiences bronchoconstriction mediated
by which immunologic mechanism?
A. Type II hypersensitivity
B. IgE-mediated mast cell degranulation
C. Immune complex deposition
D. Delayed T-cell response
Asthma is a type I hypersensitivity reaction involving IgE and
mast cells.


Question 11
Chronic hypoxemia in COPD patients often leads to secondary
polycythemia due to:
A. Bone marrow suppression
B. Increased erythropoietin production
C. Reduced plasma volume
D. Impaired iron metabolism
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