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NUR 546/NUR546 Final Exam V1 | Advanced Pathophysiology Q&A with Rationale | William Paterson University

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NUR 546/NUR546 Final Exam V1 | Advanced Pathophysiology Q&A with Rationale | William Paterson University

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NUR 546/NUR546 Final Exam V1 |
Advanced Pathophysiology Q&A with
Rationale | William Paterson University
1. A patient with chronic hypertension develops left ventricular hypertrophy. Which of the

following best describes this cellular adaptation?

A. Increase in cell number due to increased workload.


B. Reversible reduction in the size of the heart muscle.


C. Change from one adult cell type to another.


D. Increase in cell size in response to increased afterload.


Correct Answer: D


Expert Explanation: Chronic hypertension increases the resistance the heart must pump

against, known as afterload. The cardiac myocytes respond to this stress by increasing in

size to generate more force. This adaptation is a classic example of hypertrophy rather than

hyperplasia, as heart cells do not readily divide.


2. Which mechanism is primarily responsible for the development of edema in a patient with

nephrotic syndrome?

A. Increased capillary hydrostatic pressure.


B. Decreased plasma oncotic pressure.


C. Increased capillary permeability to water.

,D. Obstruction of the lymphatic flow.


Correct Answer: B


Expert Explanation: Nephrotic syndrome is characterized by massive proteinuria, leading

to a significant loss of albumin in the urine. This loss reduces the plasma oncotic pressure,

which is necessary to pull fluid back into the vasculature. Consequently, fluid moves into

the interstitial space, resulting in widespread edema.


3. A patient is diagnosed with Graves’ disease. What is the underlying pathophysiology of this

condition?

A. Destruction of thyroid follicles by T-cells.


B. Production of antibodies that mimic TSH.


C. TSH-secreting tumor in the pituitary gland.


D. Iodine deficiency leading to goiter formation.


Correct Answer: B


Expert Explanation: Graves’ disease is an autoimmune disorder where the body produces

thyroid-stimulating immunoglobulins (TSI). These antibodies bind to and activate the TSH

receptors on the thyroid gland, leading to overproduction of thyroid hormones. This results

in the clinical manifestations of hyperthyroidism and goiter.


4. In the renin-angiotensin-aldosterone system (RAAS), what is the direct effect of

Angiotensin II on blood vessels?

A. Systemic vasodilation to lower pressure.

, B. Potent systemic vasoconstriction.


C. Increased permeability of the endothelium.


D. Inhibition of smooth muscle contraction.


Correct Answer: B


Expert Explanation: Angiotensin II is a powerful vasoconstrictor that acts directly on

vascular smooth muscle to increase systemic vascular resistance. This action rapidly raises

blood pressure in response to low renal perfusion. Additionally, it stimulates the adrenal

cortex to release aldosterone for long-term volume regulation.


5. What is the primary cause of Pernicious Anemia?

A. Lack of intrinsic factor for Vitamin B12 absorption.


B. Chronic blood loss from the GI tract.


C. Deficiency of dietary iron intake.


D. Bone marrow suppression from chemotherapy.


Correct Answer: A


Expert Explanation: Pernicious anemia is an autoimmune condition where the body

attacks parietal cells or intrinsic factor itself. Intrinsic factor is essential for the absorption

of Vitamin B12 in the terminal ileum. Without adequate B12, DNA synthesis in red blood

cells is impaired, leading to megaloblastic anemia.

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