NR 507 Final Exam Actual Exam V1 | NR 507 Advanced
Pathophysiology (NR507 Final Exam) [PDF] | Chamberlain University
1. A 55-year-old male with chronic hypertension presents with left ventricular hypertrophy.
What is the primary cellular mechanism driving this adaptation?
A. Increased number of myocytes
B. Programmed cell death via caspases
C. Conversion of one mature cell type to another
D. Increase in cellular size and protein synthesis
Answer: D
Rationale: Hypertrophy involves an increase in the size of cells rather than the number of
cells. In the heart, mechanical stress from hypertension activates signaling pathways that
increase protein synthesis and the number of sarcomeres. This process is a compensatory
mechanism to handle increased afterload but can eventually lead to heart failure.
2. Following a myocardial infarction, tissue undergoes reperfusion. Why can this lead to
additional cell injury?
A. Excessive accumulation of glycogen within the cytoplasm
B. Restoration of the sodium-potassium pump activity
C. Massive influx of calcium and production of reactive oxygen species
D. Inhibition of the mitochondrial transition pore
Answer: C
Rationale: Reperfusion injury occurs when the return of oxygen leads to the formation of
reactive oxygen species that damage cell membranes. The influx of calcium into the
mitochondria further triggers the opening of the mitochondrial permeability transition
pore, leading to ATP depletion. This phenomenon explains why restoration of blood flow
can sometimes exacerbate cellular damage initially.
3. A patient is diagnosed with Huntington disease, an autosomal dominant disorder. If one
parent has the disease (heterozygous) and the other does not, what is the probability that
their child will inherit the condition?
A. 25%
B. 50%
C. 75%
D. 100%
,Answer: B
Rationale: Autosomal dominant disorders require only one copy of the mutated gene for
the phenotype to be expressed. Since the affected parent is heterozygous (Aa) and the
other is homozygous recessive (aa), the offspring have a 50 percent chance of inheriting the
‘A’ allele. There is no carrier status for autosomal dominant conditions; an individual either
has the disease or does not.
4. During an inflammatory response, which plasma protein system is responsible for the
formation of a fibrinous meshwork at an injured or inflamed site?
A. The complement system
B. The coagulation system
C. The kinin system
D. The fibrinolytic system
Answer: B
Rationale: The coagulation (clotting) system forms a fibrinous meshwork at an injured or
inflamed site to prevent the spread of infection. It traps microorganisms and foreign bodies
at the site of the greatest inflammatory activity for removal. This process also provides a
framework for future repair and healing.
5. A child presents with severe allergic reaction after bee sting, characterized by
bronchospasm and hypotension. What type of hypersensitivity reaction is occurring?
A.
B. Type II (Tissue-specific)
C. Type III (Immune complex-mediated)
D. Type IV (Cell-mediated)
E. Type I (IgE-mediated)
Answer: E
Rationale: Type I hypersensitivity reactions are mediated by IgE antibodies that bind to
mast cells. Upon re-exposure to the antigen, mast cells degranulate and release histamine
and other vasoactive substances. This results in the rapid onset of systemic symptoms such
as vasodilation and airway constriction.
6. A 60-year-old smoker presents with a chronic cough and dyspnea. Testing reveals a
deficiency in alpha-1 antitrypsin. Which condition is most likely developing?
A. Chronic Bronchitis
B. Emphysema
, C. Bronchial Asthma
D. Pulmonary Edema
Answer: B
Rationale: Alpha-1 antitrypsin is a protease inhibitor that protects the lungs from
neutrophil elastase. A deficiency in this enzyme allows elastase to break down the alveolar
walls, leading to emphysema. This destruction results in permanent enlargement of gas-
exchange airways and loss of elastic recoil.
7. A patient with a history of chronic kidney disease presents with low serum calcium and
high serum phosphate. What is the underlying cause of the secondary hyperparathyroidism?
A. Excessive intake of Vitamin D supplements
B. Reduced synthesis of 1,25-dihydroxyvitamin D3 by the kidneys
C. Decreased secretion of parathyroid hormone from the parathyroid glands
D. Primary tumor of the parathyroid gland
Answer: B
Rationale: In chronic kidney disease, the kidneys fail to activate vitamin D into its
functional form, 1,25-dihydroxyvitamin D3. This lead to impaired calcium absorption from
the gut and subsequent hypocalcemia. The parathyroid glands respond to low calcium by
increasing PTH secretion, causing secondary hyperparathyroidism and bone resorption.
8. A patient is found to have a high level of thyroid-stimulating immunoglobulins (TSI) and a
low TSH level. Which clinical manifestation is most likely?
A. Weight gain and bradycardia
B. Cold intolerance and lethargy
C. Myxedema and dry skin
D. Exophthalmos and heat intolerance
Answer: D
Rationale: Graves disease is an autoimmune condition where TSI mimics TSH, leading to
hyperthyroidism. The excess thyroid hormone increases the metabolic rate, causing heat
intolerance and weight loss. Exophthalmos is a unique feature caused by orbital fat
accumulation and inflammation behind the eyes.
9. In the early stages of septic shock, what is the primary reason for the observed
hypotension?
A. Massive systemic vasodilation due to inflammatory mediators
B. Severe dehydration and low blood volume
Pathophysiology (NR507 Final Exam) [PDF] | Chamberlain University
1. A 55-year-old male with chronic hypertension presents with left ventricular hypertrophy.
What is the primary cellular mechanism driving this adaptation?
A. Increased number of myocytes
B. Programmed cell death via caspases
C. Conversion of one mature cell type to another
D. Increase in cellular size and protein synthesis
Answer: D
Rationale: Hypertrophy involves an increase in the size of cells rather than the number of
cells. In the heart, mechanical stress from hypertension activates signaling pathways that
increase protein synthesis and the number of sarcomeres. This process is a compensatory
mechanism to handle increased afterload but can eventually lead to heart failure.
2. Following a myocardial infarction, tissue undergoes reperfusion. Why can this lead to
additional cell injury?
A. Excessive accumulation of glycogen within the cytoplasm
B. Restoration of the sodium-potassium pump activity
C. Massive influx of calcium and production of reactive oxygen species
D. Inhibition of the mitochondrial transition pore
Answer: C
Rationale: Reperfusion injury occurs when the return of oxygen leads to the formation of
reactive oxygen species that damage cell membranes. The influx of calcium into the
mitochondria further triggers the opening of the mitochondrial permeability transition
pore, leading to ATP depletion. This phenomenon explains why restoration of blood flow
can sometimes exacerbate cellular damage initially.
3. A patient is diagnosed with Huntington disease, an autosomal dominant disorder. If one
parent has the disease (heterozygous) and the other does not, what is the probability that
their child will inherit the condition?
A. 25%
B. 50%
C. 75%
D. 100%
,Answer: B
Rationale: Autosomal dominant disorders require only one copy of the mutated gene for
the phenotype to be expressed. Since the affected parent is heterozygous (Aa) and the
other is homozygous recessive (aa), the offspring have a 50 percent chance of inheriting the
‘A’ allele. There is no carrier status for autosomal dominant conditions; an individual either
has the disease or does not.
4. During an inflammatory response, which plasma protein system is responsible for the
formation of a fibrinous meshwork at an injured or inflamed site?
A. The complement system
B. The coagulation system
C. The kinin system
D. The fibrinolytic system
Answer: B
Rationale: The coagulation (clotting) system forms a fibrinous meshwork at an injured or
inflamed site to prevent the spread of infection. It traps microorganisms and foreign bodies
at the site of the greatest inflammatory activity for removal. This process also provides a
framework for future repair and healing.
5. A child presents with severe allergic reaction after bee sting, characterized by
bronchospasm and hypotension. What type of hypersensitivity reaction is occurring?
A.
B. Type II (Tissue-specific)
C. Type III (Immune complex-mediated)
D. Type IV (Cell-mediated)
E. Type I (IgE-mediated)
Answer: E
Rationale: Type I hypersensitivity reactions are mediated by IgE antibodies that bind to
mast cells. Upon re-exposure to the antigen, mast cells degranulate and release histamine
and other vasoactive substances. This results in the rapid onset of systemic symptoms such
as vasodilation and airway constriction.
6. A 60-year-old smoker presents with a chronic cough and dyspnea. Testing reveals a
deficiency in alpha-1 antitrypsin. Which condition is most likely developing?
A. Chronic Bronchitis
B. Emphysema
, C. Bronchial Asthma
D. Pulmonary Edema
Answer: B
Rationale: Alpha-1 antitrypsin is a protease inhibitor that protects the lungs from
neutrophil elastase. A deficiency in this enzyme allows elastase to break down the alveolar
walls, leading to emphysema. This destruction results in permanent enlargement of gas-
exchange airways and loss of elastic recoil.
7. A patient with a history of chronic kidney disease presents with low serum calcium and
high serum phosphate. What is the underlying cause of the secondary hyperparathyroidism?
A. Excessive intake of Vitamin D supplements
B. Reduced synthesis of 1,25-dihydroxyvitamin D3 by the kidneys
C. Decreased secretion of parathyroid hormone from the parathyroid glands
D. Primary tumor of the parathyroid gland
Answer: B
Rationale: In chronic kidney disease, the kidneys fail to activate vitamin D into its
functional form, 1,25-dihydroxyvitamin D3. This lead to impaired calcium absorption from
the gut and subsequent hypocalcemia. The parathyroid glands respond to low calcium by
increasing PTH secretion, causing secondary hyperparathyroidism and bone resorption.
8. A patient is found to have a high level of thyroid-stimulating immunoglobulins (TSI) and a
low TSH level. Which clinical manifestation is most likely?
A. Weight gain and bradycardia
B. Cold intolerance and lethargy
C. Myxedema and dry skin
D. Exophthalmos and heat intolerance
Answer: D
Rationale: Graves disease is an autoimmune condition where TSI mimics TSH, leading to
hyperthyroidism. The excess thyroid hormone increases the metabolic rate, causing heat
intolerance and weight loss. Exophthalmos is a unique feature caused by orbital fat
accumulation and inflammation behind the eyes.
9. In the early stages of septic shock, what is the primary reason for the observed
hypotension?
A. Massive systemic vasodilation due to inflammatory mediators
B. Severe dehydration and low blood volume
