Chamberlain
University
NR-283:
Pathophysiology
Comprehensive Final Exam
Instructions: Read each question carefully and select the best answer. The correct
answer is bolded and followed by a rationale.
1. A patient presents with a deep, aching pain in their left arm and jaw. An ECG
and cardiac enzymes confirm a myocardial infarction (MI). The patient's pain is an
example of:
a. Somatic pain
b. Visceral pain
c. Referred pain
d. Neuropathic pain
,Rationale: Referred pain is pain perceived at a site distant from the actual source of the
stimulus. This occurs because visceral and somatic afferent neurons converge on the
same second-order neurons in the spinal cord. The heart's ischemic pain signals
(visceral) are interpreted by the brain as coming from the arm and jaw (somatic) because
those areas share the same spinal cord pathways (T1-T5).
2. A patient with chronic kidney disease has a glomerular filtration rate (GFR) of 25
mL/min. Which of the following lab values would the nurse expect to see?
a. Decreased serum creatinine and increased BUN
b. Decreased BUN and increased serum creatinine
c. Increased BUN and increased serum creatinine
d. Decreased BUN and decreased serum creatinine
Rationale: A decreased GFR indicates a reduced ability of the kidneys to filter waste
products. As a result, both Blood Urea Nitrogen (BUN) and serum creatinine, which are
normally excreted by the kidneys, will accumulate in the blood, leading to elevated
levels.
3. Which of the following is the primary pathophysiologic change in asthma that
leads to airflow obstruction?
a. Destruction of alveolar walls
b. Fibrosis and stiffening of the lung tissue
c. Bronchoconstriction, airway inflammation, and mucus production
d. Excessive production of surfactant
Rationale: Asthma is a chronic inflammatory disorder of the airways. The key
pathophysiologic features are bronchoconstriction (smooth muscle constriction),
inflammation and edema of the bronchial mucosa, and increased mucus secretion.
These factors combined lead to reversible airflow obstruction.
,4. A patient is diagnosed with Syndrome of Inappropriate Antidiuretic Hormone
(SIADH). The nurse should anticipate which of the following electrolyte
imbalances?
a. Hypernatremia
b. Hyponatremia
c. Hyperkalemia
d. Hypokalemia
Rationale: In SIADH, excessive ADH secretion leads to water retention by the kidneys.
This dilutional effect on the blood causes a decrease in serum sodium concentration,
resulting in hyponatremia. The urine will be concentrated (high specific gravity) despite
the low serum osmolality.
5. A patient with a history of deep vein thrombosis (DVT) is at risk for a pulmonary
embolism (PE). The most common pathophysiologic consequence of a PE is:
a. Increased alveolar compliance
b. Bronchodilation and decreased airway resistance
c. Impaired gas exchange due to ventilation-perfusion (V/Q) mismatch
d. Increased surfactant production
Rationale: A pulmonary embolism obstructs pulmonary blood flow. This creates a
mismatch between ventilation (air reaching the alveoli) and perfusion (blood flow to the
alveoli). The embolus prevents blood from reaching the alveoli that are still being
ventilated, creating dead space and leading to impaired gas exchange, hypoxemia, and
potentially right heart failure.
6. A patient with type 1 diabetes mellitus is experiencing polyuria, polydipsia, and
polyphagia. These classic symptoms are a direct result of:
a. Excessive insulin production
b. Hyperglycemia and the resulting osmotic diuresis
, c. Hypoglycemia
d. Decreased glucagon production
Rationale: In type 1 diabetes, lack of insulin leads to severe hyperglycemia. When blood
glucose exceeds the renal threshold, the kidneys cannot reabsorb all the filtered
glucose. This glucose remains in the urine, creating an osmotic force that draws water
into the urine (polyuria). The resulting fluid loss leads to dehydration and excessive thirst
(polydipsia). Since cells cannot use glucose for energy, the body breaks down fat and
protein, leading to weight loss and increased hunger (polyphagia).
7. A patient is admitted with an acute exacerbation of heart failure. Which of the
following pathophysiologic mechanisms is primarily responsible for the
development of peripheral edema?
a. Decreased capillary hydrostatic pressure
b. Decreased capillary permeability
c. Increased capillary hydrostatic pressure and sodium/water retention
d. Increased plasma oncotic pressure
Rationale: In heart failure, the heart's reduced pumping ability leads to decreased
cardiac output and increased venous pressure (venous congestion). This increased
venous pressure is transmitted back to the capillaries, raising capillary hydrostatic
pressure and forcing fluid into the interstitial space. Additionally, decreased renal
perfusion activates the RAAS system, causing sodium and water retention, which further
increases blood volume and hydrostatic pressure.
8. The primary pathophysiologic defect in osteoarthritis is:
a. Systemic inflammation of the synovial membrane
b. Autoimmune destruction of the synovium
c. Progressive loss of articular cartilage
d. Deposition of uric acid crystals in the joint
University
NR-283:
Pathophysiology
Comprehensive Final Exam
Instructions: Read each question carefully and select the best answer. The correct
answer is bolded and followed by a rationale.
1. A patient presents with a deep, aching pain in their left arm and jaw. An ECG
and cardiac enzymes confirm a myocardial infarction (MI). The patient's pain is an
example of:
a. Somatic pain
b. Visceral pain
c. Referred pain
d. Neuropathic pain
,Rationale: Referred pain is pain perceived at a site distant from the actual source of the
stimulus. This occurs because visceral and somatic afferent neurons converge on the
same second-order neurons in the spinal cord. The heart's ischemic pain signals
(visceral) are interpreted by the brain as coming from the arm and jaw (somatic) because
those areas share the same spinal cord pathways (T1-T5).
2. A patient with chronic kidney disease has a glomerular filtration rate (GFR) of 25
mL/min. Which of the following lab values would the nurse expect to see?
a. Decreased serum creatinine and increased BUN
b. Decreased BUN and increased serum creatinine
c. Increased BUN and increased serum creatinine
d. Decreased BUN and decreased serum creatinine
Rationale: A decreased GFR indicates a reduced ability of the kidneys to filter waste
products. As a result, both Blood Urea Nitrogen (BUN) and serum creatinine, which are
normally excreted by the kidneys, will accumulate in the blood, leading to elevated
levels.
3. Which of the following is the primary pathophysiologic change in asthma that
leads to airflow obstruction?
a. Destruction of alveolar walls
b. Fibrosis and stiffening of the lung tissue
c. Bronchoconstriction, airway inflammation, and mucus production
d. Excessive production of surfactant
Rationale: Asthma is a chronic inflammatory disorder of the airways. The key
pathophysiologic features are bronchoconstriction (smooth muscle constriction),
inflammation and edema of the bronchial mucosa, and increased mucus secretion.
These factors combined lead to reversible airflow obstruction.
,4. A patient is diagnosed with Syndrome of Inappropriate Antidiuretic Hormone
(SIADH). The nurse should anticipate which of the following electrolyte
imbalances?
a. Hypernatremia
b. Hyponatremia
c. Hyperkalemia
d. Hypokalemia
Rationale: In SIADH, excessive ADH secretion leads to water retention by the kidneys.
This dilutional effect on the blood causes a decrease in serum sodium concentration,
resulting in hyponatremia. The urine will be concentrated (high specific gravity) despite
the low serum osmolality.
5. A patient with a history of deep vein thrombosis (DVT) is at risk for a pulmonary
embolism (PE). The most common pathophysiologic consequence of a PE is:
a. Increased alveolar compliance
b. Bronchodilation and decreased airway resistance
c. Impaired gas exchange due to ventilation-perfusion (V/Q) mismatch
d. Increased surfactant production
Rationale: A pulmonary embolism obstructs pulmonary blood flow. This creates a
mismatch between ventilation (air reaching the alveoli) and perfusion (blood flow to the
alveoli). The embolus prevents blood from reaching the alveoli that are still being
ventilated, creating dead space and leading to impaired gas exchange, hypoxemia, and
potentially right heart failure.
6. A patient with type 1 diabetes mellitus is experiencing polyuria, polydipsia, and
polyphagia. These classic symptoms are a direct result of:
a. Excessive insulin production
b. Hyperglycemia and the resulting osmotic diuresis
, c. Hypoglycemia
d. Decreased glucagon production
Rationale: In type 1 diabetes, lack of insulin leads to severe hyperglycemia. When blood
glucose exceeds the renal threshold, the kidneys cannot reabsorb all the filtered
glucose. This glucose remains in the urine, creating an osmotic force that draws water
into the urine (polyuria). The resulting fluid loss leads to dehydration and excessive thirst
(polydipsia). Since cells cannot use glucose for energy, the body breaks down fat and
protein, leading to weight loss and increased hunger (polyphagia).
7. A patient is admitted with an acute exacerbation of heart failure. Which of the
following pathophysiologic mechanisms is primarily responsible for the
development of peripheral edema?
a. Decreased capillary hydrostatic pressure
b. Decreased capillary permeability
c. Increased capillary hydrostatic pressure and sodium/water retention
d. Increased plasma oncotic pressure
Rationale: In heart failure, the heart's reduced pumping ability leads to decreased
cardiac output and increased venous pressure (venous congestion). This increased
venous pressure is transmitted back to the capillaries, raising capillary hydrostatic
pressure and forcing fluid into the interstitial space. Additionally, decreased renal
perfusion activates the RAAS system, causing sodium and water retention, which further
increases blood volume and hydrostatic pressure.
8. The primary pathophysiologic defect in osteoarthritis is:
a. Systemic inflammation of the synovial membrane
b. Autoimmune destruction of the synovium
c. Progressive loss of articular cartilage
d. Deposition of uric acid crystals in the joint
