1. Which of the following is most characteristic of acute inflammation?
A. Increased vascular permeability
B. Tissue fibrosis
C. Immune tolerance
D. Chronic cell death
Answer: A. Increased vascular permeability
Rationale: Acute inflammation is primarily characterized by increased
vascular permeability, which allows immune cells, proteins, and
nutrients to reach the site of injury. This leads to the classic signs of
inflammation, such as redness, heat, and swelling. Fibrosis and chronic
cell death are more associated with chronic inflammation, not acute
inflammation.
2. The primary mechanism of action of non-steroidal anti-
inflammatory drugs (NSAIDs) is inhibition of which enzyme?
A. Cyclooxygenase (COX)
B. Phospholipase A2
C. 5-Lipoxygenase
D. Myeloperoxidase
Answer: A. Cyclooxygenase (COX)
Rationale: NSAIDs inhibit the cyclooxygenase (COX) enzymes, COX-1
and COX-2. These enzymes are responsible for converting arachidonic
acid into prostaglandins, which are involved in the inflammatory
process. Inhibition of COX reduces pain, fever, and inflammation.
,3. Which of the following pathophysiological mechanisms is most
commonly associated with chronic obstructive pulmonary disease
(COPD)?
A. Increased mucous production and bronchoconstriction
B. Alveolar wall destruction and airflow limitation
C. Increased production of surfactant
D. Pulmonary vasodilation and hypertension
Answer: B. Alveolar wall destruction and airflow limitation
Rationale: COPD is primarily characterized by progressive airflow
limitation caused by chronic inflammation that leads to the destruction
of alveolar walls (emphysema) and thickening of airway walls (chronic
bronchitis). This leads to decreased oxygen exchange and difficulty
breathing.
4. In the pathophysiology of diabetes mellitus type 2, which of the
following is a key factor?
A. Autoimmune destruction of pancreatic beta cells
B. Insulin resistance at the cellular level
C. Impaired production of glucagon
D. Increased insulin production from the pancreas
Answer: B. Insulin resistance at the cellular level
Rationale: In type 2 diabetes, the body's cells become resistant to the
effects of insulin, leading to impaired glucose uptake and elevated
blood glucose levels. This is a key feature of type 2 diabetes, unlike type
1 diabetes, where autoimmune destruction of pancreatic beta cells
occurs.
, 5. Which of the following is a classic sign of hypovolemic shock?
A. Cyanosis
B. Tachycardia
C. Hyperthermia
D. Edema
Answer: B. Tachycardia
Rationale: Hypovolemic shock is caused by a significant loss of blood
volume, such as from hemorrhage or dehydration. The body
compensates by increasing the heart rate (tachycardia) to maintain
cardiac output and perfusion to vital organs.
6. In the pathophysiology of heart failure, which of the following
mechanisms occurs to compensate for decreased cardiac output?
A. Activation of the renin-angiotensin-aldosterone system (RAAS)
B. Decreased secretion of atrial natriuretic peptide (ANP)
C. Decreased sympathetic nervous system activity
D. Decreased aldosterone secretion
Answer: A. Activation of the renin-angiotensin-aldosterone system
(RAAS)
Rationale: In heart failure, the body activates compensatory
mechanisms such as the RAAS to try to increase blood volume and
maintain blood pressure. This system increases sodium and water
retention, which may worsen heart failure over time if the underlying
cause is not addressed.
7. A deficiency of which vitamin is most commonly associated with the
development of pernicious anemia?
A. Increased vascular permeability
B. Tissue fibrosis
C. Immune tolerance
D. Chronic cell death
Answer: A. Increased vascular permeability
Rationale: Acute inflammation is primarily characterized by increased
vascular permeability, which allows immune cells, proteins, and
nutrients to reach the site of injury. This leads to the classic signs of
inflammation, such as redness, heat, and swelling. Fibrosis and chronic
cell death are more associated with chronic inflammation, not acute
inflammation.
2. The primary mechanism of action of non-steroidal anti-
inflammatory drugs (NSAIDs) is inhibition of which enzyme?
A. Cyclooxygenase (COX)
B. Phospholipase A2
C. 5-Lipoxygenase
D. Myeloperoxidase
Answer: A. Cyclooxygenase (COX)
Rationale: NSAIDs inhibit the cyclooxygenase (COX) enzymes, COX-1
and COX-2. These enzymes are responsible for converting arachidonic
acid into prostaglandins, which are involved in the inflammatory
process. Inhibition of COX reduces pain, fever, and inflammation.
,3. Which of the following pathophysiological mechanisms is most
commonly associated with chronic obstructive pulmonary disease
(COPD)?
A. Increased mucous production and bronchoconstriction
B. Alveolar wall destruction and airflow limitation
C. Increased production of surfactant
D. Pulmonary vasodilation and hypertension
Answer: B. Alveolar wall destruction and airflow limitation
Rationale: COPD is primarily characterized by progressive airflow
limitation caused by chronic inflammation that leads to the destruction
of alveolar walls (emphysema) and thickening of airway walls (chronic
bronchitis). This leads to decreased oxygen exchange and difficulty
breathing.
4. In the pathophysiology of diabetes mellitus type 2, which of the
following is a key factor?
A. Autoimmune destruction of pancreatic beta cells
B. Insulin resistance at the cellular level
C. Impaired production of glucagon
D. Increased insulin production from the pancreas
Answer: B. Insulin resistance at the cellular level
Rationale: In type 2 diabetes, the body's cells become resistant to the
effects of insulin, leading to impaired glucose uptake and elevated
blood glucose levels. This is a key feature of type 2 diabetes, unlike type
1 diabetes, where autoimmune destruction of pancreatic beta cells
occurs.
, 5. Which of the following is a classic sign of hypovolemic shock?
A. Cyanosis
B. Tachycardia
C. Hyperthermia
D. Edema
Answer: B. Tachycardia
Rationale: Hypovolemic shock is caused by a significant loss of blood
volume, such as from hemorrhage or dehydration. The body
compensates by increasing the heart rate (tachycardia) to maintain
cardiac output and perfusion to vital organs.
6. In the pathophysiology of heart failure, which of the following
mechanisms occurs to compensate for decreased cardiac output?
A. Activation of the renin-angiotensin-aldosterone system (RAAS)
B. Decreased secretion of atrial natriuretic peptide (ANP)
C. Decreased sympathetic nervous system activity
D. Decreased aldosterone secretion
Answer: A. Activation of the renin-angiotensin-aldosterone system
(RAAS)
Rationale: In heart failure, the body activates compensatory
mechanisms such as the RAAS to try to increase blood volume and
maintain blood pressure. This system increases sodium and water
retention, which may worsen heart failure over time if the underlying
cause is not addressed.
7. A deficiency of which vitamin is most commonly associated with the
development of pernicious anemia?
