NSG530 Final Exam V2 | NSG 530
Advanced Pathophysiology | Wilkes
University
1. Which of the following compensatory mechanisms is primarily responsible for the long-
term maladaptive remodeling seen in chronic heart failure?
A. Parasympathetic nervous system activation
B. Activation of the renin-angiotensin-aldosterone system (RAAS)
C. Increased release of atrial natriuretic peptide
D. Decreased production of antidiuretic hormone
Answer: B
Rationale: The RAAS system is activated in response to decreased cardiac output and renal
perfusion. While initially helpful to maintain blood pressure, chronic activation leads to
excessive vasoconstriction and fluid retention. This prolonged stress results in cardiac
hypertrophy and fibrotic remodeling of the ventricular wall.
2. A patient presents with sudden shortness of breath and wheezing after exposure to an
allergen. Which immunoglobulin is primarily involved in this Type I hypersensitivity reaction?
A. IgG
B. IgM
C. IgA
,D. IgE
Answer: D
Rationale: Type I hypersensitivity is an immediate allergic reaction mediated by IgE
antibodies. These antibodies bind to high-affinity receptors on mast cells and basophils.
Upon re-exposure to the allergen, cross-linking occurs, triggering the release of
inflammatory mediators like histamine.
3. In the pathophysiology of Type 2 Diabetes Mellitus, what is the primary mechanism leading
to hyperglycemia?
A. Absolute deficiency of insulin due to beta-cell destruction
B. Increased peripheral insulin sensitivity
C. Insulin resistance and relative insulin deficiency
D. Decreased hepatic glucose production
Answer: C
Rationale: Type 2 Diabetes involves a combination of insulin resistance in peripheral
tissues and an inadequate secretory response by pancreatic beta cells. Initially, the body
compensates by producing more insulin, but eventually, the beta cells fail to keep up with
the demand. This leads to persistent elevated blood glucose levels and associated metabolic
complications.
, 4. Which pathophysiological change characterizes the early stage of chronic obstructive
pulmonary disease (COPD)?
A. Reversible airway constriction
B. Inflammation of the central airways and increased mucus production
C. Complete destruction of the alveolar septa
D. Increased elastic recoil of the lung tissue
Answer: B
Rationale: The early stages of COPD involve chronic inflammation of the airways caused
by irritants like cigarette smoke. This inflammation leads to goblet cell hyperplasia and
excessive mucus secretion. Over time, this progresses to fixed airway obstruction and
permanent alveolar damage.
5. What is the hallmark pathological finding in the brains of patients with Alzheimer’s
Disease?
A. Demyelination of peripheral nerves
B. Extracellular amyloid-beta plaques and intracellular tau tangles
C. Depletion of dopamine in the substantia nigra
D. Loss of motor neurons in the spinal cord
Answer: B
Advanced Pathophysiology | Wilkes
University
1. Which of the following compensatory mechanisms is primarily responsible for the long-
term maladaptive remodeling seen in chronic heart failure?
A. Parasympathetic nervous system activation
B. Activation of the renin-angiotensin-aldosterone system (RAAS)
C. Increased release of atrial natriuretic peptide
D. Decreased production of antidiuretic hormone
Answer: B
Rationale: The RAAS system is activated in response to decreased cardiac output and renal
perfusion. While initially helpful to maintain blood pressure, chronic activation leads to
excessive vasoconstriction and fluid retention. This prolonged stress results in cardiac
hypertrophy and fibrotic remodeling of the ventricular wall.
2. A patient presents with sudden shortness of breath and wheezing after exposure to an
allergen. Which immunoglobulin is primarily involved in this Type I hypersensitivity reaction?
A. IgG
B. IgM
C. IgA
,D. IgE
Answer: D
Rationale: Type I hypersensitivity is an immediate allergic reaction mediated by IgE
antibodies. These antibodies bind to high-affinity receptors on mast cells and basophils.
Upon re-exposure to the allergen, cross-linking occurs, triggering the release of
inflammatory mediators like histamine.
3. In the pathophysiology of Type 2 Diabetes Mellitus, what is the primary mechanism leading
to hyperglycemia?
A. Absolute deficiency of insulin due to beta-cell destruction
B. Increased peripheral insulin sensitivity
C. Insulin resistance and relative insulin deficiency
D. Decreased hepatic glucose production
Answer: C
Rationale: Type 2 Diabetes involves a combination of insulin resistance in peripheral
tissues and an inadequate secretory response by pancreatic beta cells. Initially, the body
compensates by producing more insulin, but eventually, the beta cells fail to keep up with
the demand. This leads to persistent elevated blood glucose levels and associated metabolic
complications.
, 4. Which pathophysiological change characterizes the early stage of chronic obstructive
pulmonary disease (COPD)?
A. Reversible airway constriction
B. Inflammation of the central airways and increased mucus production
C. Complete destruction of the alveolar septa
D. Increased elastic recoil of the lung tissue
Answer: B
Rationale: The early stages of COPD involve chronic inflammation of the airways caused
by irritants like cigarette smoke. This inflammation leads to goblet cell hyperplasia and
excessive mucus secretion. Over time, this progresses to fixed airway obstruction and
permanent alveolar damage.
5. What is the hallmark pathological finding in the brains of patients with Alzheimer’s
Disease?
A. Demyelination of peripheral nerves
B. Extracellular amyloid-beta plaques and intracellular tau tangles
C. Depletion of dopamine in the substantia nigra
D. Loss of motor neurons in the spinal cord
Answer: B
