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Examen

NSG 5140 Advanced Pathophysiology – NSG 5140 – Midterm 1 Exam with Questions, Correct Answers, and Rationales (Latest A+ Graded)

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Subido en
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Escrito en
2025/2026

This document features the latest NSG 5140 Advanced Pathophysiology Midterm 1 exam, including exam-style questions with 100% correct answers and clear, detailed rationales. It covers foundational and system-based pathophysiology concepts commonly assessed in the first midterm. The material is graded A+ and is ideal for structured midterm review and exam preparation.

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NSG 5140 ADVANCED PATHOPHYSIOLOGY
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NSG 5140 ADVANCED PATHOPHYSIOLOGY











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Institución
NSG 5140 ADVANCED PATHOPHYSIOLOGY
Grado
NSG 5140 ADVANCED PATHOPHYSIOLOGY

Información del documento

Subido en
20 de enero de 2026
Número de páginas
37
Escrito en
2025/2026
Tipo
Examen
Contiene
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NSG 5140 ADVANCED PATHOPHYSIOLOGY –
MIDTERM 1 EXAM QUESTIONS AND CORRECT
ANSWERS WITH RATIONALES GRADED A+
LATEST

1. Which of the following is the primary mechanism of cellular injury in
hypoxic conditions?
A. DNA mutation
B. ATP depletion leading to loss of ion homeostasis
C. Free radical formation
D. Protein misfolding
Answer: B
Rationale: Hypoxia limits oxidative phosphorylation → decreased ATP → Na⁺/K⁺
pump failure → cell swelling and injury.


2. A patient presents with edema due to heart failure. Which mechanism is
primarily responsible?
A. Increased plasma oncotic pressure
B. Increased hydrostatic pressure in capillaries
C. Decreased capillary permeability
D. Lymphatic obstruction
Answer: B
Rationale: Elevated hydrostatic pressure pushes fluid into interstitial spaces,
causing edema in CHF.


3. Which electrolyte imbalance is most likely in a patient with Addison’s
disease?
A. Hypernatremia, hypokalemia
B. Hypercalcemia, hypermagnesemia

,C. Hyponatremia, hyperkalemia
D. Hypokalemia, hypernatremia
Answer: C
Rationale: Addison’s disease causes aldosterone deficiency → Na⁺ loss
(hyponatremia) and K⁺ retention (hyperkalemia).


4. The hallmark of acute inflammation is:
A. Fibrosis
B. Vasodilation and increased vascular permeability
C. Neoplasia
D. Autoantibody formation
Answer: B
Rationale: Acute inflammation triggers redness, heat, swelling, and pain through
vascular changes.


5. Which intracellular signaling pathway is most directly involved in
apoptosis?
A. MAPK
B. Caspase cascade
C. JAK/STAT
D. PI3K/Akt
Answer: B
Rationale: Caspases mediate programmed cell death by cleaving cellular
substrates.


6. In a patient with chronic liver disease, which lab value best reflects
impaired synthetic function?
A. AST
B. ALT
C. Albumin
D. Bilirubin

,Answer: C
Rationale: Albumin production is reduced in liver dysfunction; low albumin
indicates impaired synthetic capacity.


7. Which type of shock is caused by severe allergic reactions?
A. Cardiogenic
B. Hypovolemic
C. Distributive (anaphylactic)
D. Obstructive
Answer: C
Rationale: Anaphylaxis causes vasodilation and capillary leak → distributive
shock.


8. A patient with type 1 diabetes presents with hyperglycemia, ketonuria, and
acidosis. This is indicative of:
A. HHNS
B. DKA (Diabetic Ketoacidosis)
C. Hypoglycemia
D. Metabolic alkalosis
Answer: B
Rationale: DKA occurs in insulin deficiency → hyperglycemia, lipolysis, ketone
production, and metabolic acidosis.


9. Which type of hypersensitivity reaction is mediated by IgE?
A. Type I
B. Type II
C. Type I
D. Type IV
Answer: C
Rationale: Type I hypersensitivity involves IgE binding to mast cells → histamine
release → allergic reactions.

, 10. The most common cause of primary hyperthyroidism is:
A. Pituitary adenoma
B. Thyroid carcinoma
C. Graves’ disease
D. Iodine deficiency
Answer: C
Rationale: Graves’ disease is an autoimmune disorder causing thyroid hormone
overproduction.


11. Which of the following best describes metabolic acidosis?
A. Increased HCO₃⁻, decreased H⁺
B. Decreased HCO₃⁻, decreased pH
C. Increased HCO₃⁻, increased pH
D. Decreased H⁺, increased pH
Answer: B
Rationale: Metabolic acidosis is caused by a primary loss of bicarbonate or
accumulation of acids → low pH.


12. A patient with cirrhosis has ascites. Which mechanism primarily
contributes?
A. High plasma oncotic pressure
B. Portal hypertension and hypoalbuminemia
C. Renal sodium loss
D. Hyperkalemia
Answer: B
Rationale: Increased hydrostatic pressure in portal circulation and low albumin
reduce plasma oncotic pressure → fluid accumulation.
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