angiotensin II in the pathophysiology of hypertension?
A) Increased renal sodium excretion
B) Vasoconstriction and aldosterone release
C) Decreased sympathetic nervous system activity
D) Inhibition of renin secretion
Answer: B) Vasoconstriction and aldosterone release
Rationale: Angiotensin II primarily causes vasoconstriction, which
increases systemic vascular resistance. It also stimulates the release of
aldosterone from the adrenal glands, leading to sodium retention,
which in turn increases blood volume and blood pressure. These actions
contribute significantly to the pathophysiology of hypertension.
2. In the context of diabetes mellitus, what is the major
pathophysiological cause of microvascular complications like
retinopathy and nephropathy?
A) Increased blood glucose leading to the formation of advanced
glycation end-products (AGEs)
B) Overactivity of the sympathetic nervous system
C) Autoimmune destruction of pancreatic beta cells
D) Decreased insulin sensitivity in peripheral tissues
Answer: A) Increased blood glucose leading to the formation of
advanced glycation end-products (AGEs)
Rationale: Chronic hyperglycemia leads to the formation of AGEs, which
are involved in the pathogenesis of microvascular complications. AGEs
accumulate in tissues like the retina and kidneys, promoting
,inflammation, fibrosis, and endothelial dysfunction, contributing to
conditions such as diabetic retinopathy and nephropathy.
3. Which of the following is a primary pathophysiological feature of
chronic obstructive pulmonary disease (COPD)?
A) Hyperplasia of bronchial goblet cells and increased mucus production
B) Decreased production of surfactant
C) Enhanced ciliary movement and airway clearance
D) Overexpression of interleukin-10 (IL-10)
Answer: A) Hyperplasia of bronchial goblet cells and increased mucus
production
Rationale: COPD is characterized by airflow limitation and
inflammation, which lead to structural changes in the airways. The
hyperplasia of goblet cells and subsequent increased mucus production
contribute to the chronic cough and sputum production seen in COPD.
This impairs airflow and increases the risk of infections and
exacerbations.
4. In the pathophysiology of atherosclerosis, which of the following is
a key event in the formation of atherosclerotic plaques?
A) Endothelial injury leading to increased permeability
B) Decreased low-density lipoprotein (LDL) levels
C) Decreased platelet aggregation
D) Increased nitric oxide production by smooth muscle cells
Answer: A) Endothelial injury leading to increased permeability
Rationale: The pathogenesis of atherosclerosis begins with endothelial
injury, which increases the permeability of the endothelium, allowing
, LDL cholesterol to enter the arterial wall. This sets off an inflammatory
response, attracting monocytes that transform into macrophages and
accumulate foam cells, leading to plaque formation and the thickening
of arterial walls.
5. Which of the following is a primary mechanism by which bacterial
endotoxins cause septic shock?
A) Increased production of interleukins that enhance immunity
B) Excessive activation of the sympathetic nervous system
C) Release of pro-inflammatory cytokines, leading to vasodilation and
hypotension
D) Decreased nitric oxide production
Answer: C) Release of pro-inflammatory cytokines, leading to
vasodilation and hypotension
Rationale: Bacterial endotoxins activate immune cells, which release
pro-inflammatory cytokines such as TNF-α and interleukins. This leads
to widespread vasodilation, increased vascular permeability, and
hypotension, which are key features of septic shock. These cytokines
also contribute to organ dysfunction in severe cases.
6. In the pathogenesis of heart failure with reduced ejection fraction
(HFrEF), which of the following mechanisms plays a key role in cardiac
remodeling?
A) Inhibition of aldosterone secretion
B) Activation of the renin-angiotensin-aldosterone system (RAAS)
C) Decreased sympathetic nervous system activation
D) Reduced myocardial contractility without fibrosis