BIO 322 Exam 2 V3 | BIO 322 Applied
Pathophysiology | Actual Q&A with Rationale
(BIO322 Exam 2) | Grand Canyon University
1. A patient presents with acute inflammation following an injury. Which of the following
findings are considered cardinal signs of the inflammatory process? (Select all that apply)
A. Rubor (Redness)
B. Calor (Heat)
C. Tumor (Swelling)
D. Dolor (Pain)
E. Functio laesa (Loss of function)
F. Pallor (Paleness)
Correct Answer: A, B, C, D, E
Explanation: Acute inflammation is characterized by five classic cardinal signs: redness,
heat, swelling, pain, and loss of function. These signs result from increased blood flow,
increased capillary permeability, and the release of chemical mediators at the site of injury.
Pallor is not a sign of inflammation but rather often associated with shock or anemia.
2. Which physiological mechanism is primarily responsible for the development of edema in a
patient with right-sided heart failure?
A. Decreased capillary oncotic pressure
,B. Lymphatic obstruction
C. Increased capillary permeability
D. Increased capillary hydrostatic pressure
Correct Answer: D
Explanation: Right-sided heart failure leads to backflow of blood into the systemic venous
circulation, which increases venous pressure. This elevation in venous pressure translates
to increased capillary hydrostatic pressure, forcing fluid out of the vessels into the
interstitial space. Decreased oncotic pressure is typically associated with liver failure or
protein loss, not primary heart failure.
3. A 55-year-old male is diagnosed with Chronic Obstructive Pulmonary Disease (COPD).
Which of the following pathological changes are characteristic of emphysema? (Select all that
apply)
A. Permanent enlargement of gas-exchange airways
B. Destruction of alveolar walls
C. Hypersecretion of mucus in large airways
D. Loss of elastic recoil
E. Formation of bullae
Correct Answer: A, B, D, E
,Explanation: Emphysema involves the destruction of alveolar septa and loss of elastic
recoil, leading to air trapping and airway collapse during expiration. The enlargement of
airways and destruction of walls result in decreased surface area for gas exchange. Mucus
hypersecretion is more characteristic of chronic bronchitis than pure emphysema.
4. In the pathophysiology of Type 1 Diabetes Mellitus, what is the primary cause of insulin
deficiency?
A. Insulin resistance in peripheral tissues
B. Autoimmune destruction of pancreatic beta cells
C. Excessive glucagon secretion by alpha cells
D. Downregulation of insulin receptors
Correct Answer: B
Explanation: Type 1 Diabetes Mellitus is characterized by an absolute insulin deficiency
resulting from the T-cell mediated autoimmune destruction of beta cells in the islets of
Langerhans. This leads to a total lack of insulin, necessitating lifelong exogenous insulin
replacement. Peripheral insulin resistance is the hallmark of Type 2 Diabetes, not Type 1.
5. A patient is admitted with a serum potassium level of 6.8 mEq/L. Which electrocardiogram
(ECG) changes should the nurse anticipate?
A. Prominent U waves
B. Shortened PR interval
C. ST-segment depression
, D. Tall, peaked T waves
Correct Answer: D
Explanation: Hyperkalemia (serum potassium > 5.0 mEq/L) typically manifests on an ECG
as tall, peaked T waves due to rapid repolarization of the ventricles. As levels rise further,
the PR interval lengthens and the QRS complex widens, eventually leading to a sine-wave
pattern or cardiac arrest. U waves and ST depression are more commonly associated with
hypokalemia.
6. Which of the following describes the pathophysiology of Myasthenia Gravis?
A. Demyelination of central nervous system neurons
B. Degeneration of dopamine-producing neurons in the substantia nigra
C. Compression of spinal nerves due to herniated discs
D. Autoimmune destruction of acetylcholine receptors at the neuromuscular junction
Correct Answer: D
Explanation: Myasthenia Gravis is an autoimmune disorder where antibodies block or
destroy acetylcholine receptors at the postsynaptic neuromuscular junction. This leads to
impaired transmission of nerve impulses to the muscles, causing fluctuating muscle
weakness and fatigue. Treatment often focuses on increasing acetylcholine availability
through anticholinesterase medications.
Pathophysiology | Actual Q&A with Rationale
(BIO322 Exam 2) | Grand Canyon University
1. A patient presents with acute inflammation following an injury. Which of the following
findings are considered cardinal signs of the inflammatory process? (Select all that apply)
A. Rubor (Redness)
B. Calor (Heat)
C. Tumor (Swelling)
D. Dolor (Pain)
E. Functio laesa (Loss of function)
F. Pallor (Paleness)
Correct Answer: A, B, C, D, E
Explanation: Acute inflammation is characterized by five classic cardinal signs: redness,
heat, swelling, pain, and loss of function. These signs result from increased blood flow,
increased capillary permeability, and the release of chemical mediators at the site of injury.
Pallor is not a sign of inflammation but rather often associated with shock or anemia.
2. Which physiological mechanism is primarily responsible for the development of edema in a
patient with right-sided heart failure?
A. Decreased capillary oncotic pressure
,B. Lymphatic obstruction
C. Increased capillary permeability
D. Increased capillary hydrostatic pressure
Correct Answer: D
Explanation: Right-sided heart failure leads to backflow of blood into the systemic venous
circulation, which increases venous pressure. This elevation in venous pressure translates
to increased capillary hydrostatic pressure, forcing fluid out of the vessels into the
interstitial space. Decreased oncotic pressure is typically associated with liver failure or
protein loss, not primary heart failure.
3. A 55-year-old male is diagnosed with Chronic Obstructive Pulmonary Disease (COPD).
Which of the following pathological changes are characteristic of emphysema? (Select all that
apply)
A. Permanent enlargement of gas-exchange airways
B. Destruction of alveolar walls
C. Hypersecretion of mucus in large airways
D. Loss of elastic recoil
E. Formation of bullae
Correct Answer: A, B, D, E
,Explanation: Emphysema involves the destruction of alveolar septa and loss of elastic
recoil, leading to air trapping and airway collapse during expiration. The enlargement of
airways and destruction of walls result in decreased surface area for gas exchange. Mucus
hypersecretion is more characteristic of chronic bronchitis than pure emphysema.
4. In the pathophysiology of Type 1 Diabetes Mellitus, what is the primary cause of insulin
deficiency?
A. Insulin resistance in peripheral tissues
B. Autoimmune destruction of pancreatic beta cells
C. Excessive glucagon secretion by alpha cells
D. Downregulation of insulin receptors
Correct Answer: B
Explanation: Type 1 Diabetes Mellitus is characterized by an absolute insulin deficiency
resulting from the T-cell mediated autoimmune destruction of beta cells in the islets of
Langerhans. This leads to a total lack of insulin, necessitating lifelong exogenous insulin
replacement. Peripheral insulin resistance is the hallmark of Type 2 Diabetes, not Type 1.
5. A patient is admitted with a serum potassium level of 6.8 mEq/L. Which electrocardiogram
(ECG) changes should the nurse anticipate?
A. Prominent U waves
B. Shortened PR interval
C. ST-segment depression
, D. Tall, peaked T waves
Correct Answer: D
Explanation: Hyperkalemia (serum potassium > 5.0 mEq/L) typically manifests on an ECG
as tall, peaked T waves due to rapid repolarization of the ventricles. As levels rise further,
the PR interval lengthens and the QRS complex widens, eventually leading to a sine-wave
pattern or cardiac arrest. U waves and ST depression are more commonly associated with
hypokalemia.
6. Which of the following describes the pathophysiology of Myasthenia Gravis?
A. Demyelination of central nervous system neurons
B. Degeneration of dopamine-producing neurons in the substantia nigra
C. Compression of spinal nerves due to herniated discs
D. Autoimmune destruction of acetylcholine receptors at the neuromuscular junction
Correct Answer: D
Explanation: Myasthenia Gravis is an autoimmune disorder where antibodies block or
destroy acetylcholine receptors at the postsynaptic neuromuscular junction. This leads to
impaired transmission of nerve impulses to the muscles, causing fluctuating muscle
weakness and fatigue. Treatment often focuses on increasing acetylcholine availability
through anticholinesterase medications.
