NSG 5003 WEEK 5 ADVANCED
PATHOPHYSIOLOGY KNOWLEDGE
CHECK QUESTRIONS WITH
COMPLETE SOLUTION GUARANTEED
SUCCESS.
1. Which mechanism is primarily responsible for the development of metabolic acidosis in a
patient with Chronic Kidney Disease (CKD)?
A. Excessive loss of bicarbonate in the urine
B. Retention of carbon dioxide due to secondary respiratory failure
C. Overproduction of organic acids like lactic acid
D. Reduced excretion of hydrogen ions and impaired ammonia synthesis
Answer: D
Conceptual Explanation: In CKD, the kidneys lose the ability to excrete hydrogen ions and
regenerate bicarbonate effectively. Impaired synthesis of ammonia (which acts as a buffer)
further reduces the kidney’s ability to excrete the daily acid load, leading to metabolic
acidosis.
2. In the pathogenesis of Polycystic Kidney Disease (ADPKD), a mutation in which genes is
most commonly implicated?
A. VHL and TSC1
,B. COL4A3 and COL4A4
C. ACE and AGTR1
D. PKD1 and PKD2
Answer: D
Conceptual Explanation: Autosomal Dominant Polycystic Kidney Disease is primarily
caused by mutations in PKD1 (encoding polycystin-1) or PKD2 (encoding polycystin-2),
which affect ciliary function and calcium signaling in tubular epithelial cells.
3. Which hormone is responsible for the ‘shift’ of potassium into the intracellular space, and
is often used therapeutically to treat hyperkalemia?
A. Glucagon
B. Cortisol
C. Insulin
D. Aldosterone
Answer: C
Conceptual Explanation: Insulin stimulates the Na+/K+-ATPase pump, facilitating the
movement of potassium from the extracellular fluid into the intracellular compartment.
4. A patient presents with a TSH of 0.01 mU/L and elevated free T4. Which finding would
most specifically suggest Graves’ Disease rather than toxic multinodular goiter?
A. Exophthalmos and pretibial myxedema
, B. Presence of a palpable neck mass
C. Weight loss and heat intolerance
D. Tachycardia and palpitations
Answer: A
Conceptual Explanation: Exophthalmos (bulging eyes) and pretibial myxedema are
dermopathy and ophthalmopathy specific to Graves’ disease, caused by TSH receptor
antibodies reacting with orbital and dermal fibroblasts.
5. What is the primary pathophysiological trigger for the release of Renin from the
juxtaglomerular apparatus?
A. High levels of atrial natriuretic peptide
B. Increased sodium delivery to the macula densa
C. Parasympathetic nervous system stimulation
D. Decreased perfusion pressure in the afferent arteriole
Answer: D
Conceptual Explanation: Renin release is triggered by decreased renal perfusion pressure
(detected by baroreceptors in the afferent arteriole), sympathetic stimulation, or decreased
sodium delivery to the macula densa.
PATHOPHYSIOLOGY KNOWLEDGE
CHECK QUESTRIONS WITH
COMPLETE SOLUTION GUARANTEED
SUCCESS.
1. Which mechanism is primarily responsible for the development of metabolic acidosis in a
patient with Chronic Kidney Disease (CKD)?
A. Excessive loss of bicarbonate in the urine
B. Retention of carbon dioxide due to secondary respiratory failure
C. Overproduction of organic acids like lactic acid
D. Reduced excretion of hydrogen ions and impaired ammonia synthesis
Answer: D
Conceptual Explanation: In CKD, the kidneys lose the ability to excrete hydrogen ions and
regenerate bicarbonate effectively. Impaired synthesis of ammonia (which acts as a buffer)
further reduces the kidney’s ability to excrete the daily acid load, leading to metabolic
acidosis.
2. In the pathogenesis of Polycystic Kidney Disease (ADPKD), a mutation in which genes is
most commonly implicated?
A. VHL and TSC1
,B. COL4A3 and COL4A4
C. ACE and AGTR1
D. PKD1 and PKD2
Answer: D
Conceptual Explanation: Autosomal Dominant Polycystic Kidney Disease is primarily
caused by mutations in PKD1 (encoding polycystin-1) or PKD2 (encoding polycystin-2),
which affect ciliary function and calcium signaling in tubular epithelial cells.
3. Which hormone is responsible for the ‘shift’ of potassium into the intracellular space, and
is often used therapeutically to treat hyperkalemia?
A. Glucagon
B. Cortisol
C. Insulin
D. Aldosterone
Answer: C
Conceptual Explanation: Insulin stimulates the Na+/K+-ATPase pump, facilitating the
movement of potassium from the extracellular fluid into the intracellular compartment.
4. A patient presents with a TSH of 0.01 mU/L and elevated free T4. Which finding would
most specifically suggest Graves’ Disease rather than toxic multinodular goiter?
A. Exophthalmos and pretibial myxedema
, B. Presence of a palpable neck mass
C. Weight loss and heat intolerance
D. Tachycardia and palpitations
Answer: A
Conceptual Explanation: Exophthalmos (bulging eyes) and pretibial myxedema are
dermopathy and ophthalmopathy specific to Graves’ disease, caused by TSH receptor
antibodies reacting with orbital and dermal fibroblasts.
5. What is the primary pathophysiological trigger for the release of Renin from the
juxtaglomerular apparatus?
A. High levels of atrial natriuretic peptide
B. Increased sodium delivery to the macula densa
C. Parasympathetic nervous system stimulation
D. Decreased perfusion pressure in the afferent arteriole
Answer: D
Conceptual Explanation: Renin release is triggered by decreased renal perfusion pressure
(detected by baroreceptors in the afferent arteriole), sympathetic stimulation, or decreased
sodium delivery to the macula densa.
