AIM β’ KMU Exam Practice
KMU Past Paper Practice
Topic 9 β Disorders of Water Balance: Diabetes Insipidus, SIADH and Vasopressin Pharmacology
4th Year MBBS β’ 20 A-type Single Best Answer MCQs :contentReference[oaicite:0]{index=0}
MCQ 1
Question:
A 62-year-old man develops significant gastrointestinal blood loss. His plasma osmolality has not yet changed substantially, but vasopressin secretion increases. Which physiological stimulus best explains this response?
Options:
Increase in plasma osmolality
Reduction in serum sodium concentration
Increase in renal prostaglandin production
Reduction in effective circulating volume
Increase in aquaporin-2 removal
Correct Answer:
Reduction in effective circulating volume
Explanation: Vasopressin release is stimulated not only by increased osmolality but also by reduced effective circulating volume, helping conserve water during significant volume loss.
MCQ 2
Question:
A hypothalamic lesion selectively damages the supraoptic and paraventricular nuclei. Which physiological function is most directly impaired?
Options:
Synthesis of vasopressin
Secretion of aldosterone
Production of renal prostaglandins
Activation of epithelial sodium channels
Filtration of water at the glomerulus
Correct Answer:
Synthesis of vasopressin
Explanation: Vasopressin is synthesized mainly in the supraoptic and paraventricular nuclei of the hypothalamus before being transported to the posterior pituitary.
MCQ 3
Question:
A suprasellar lesion interrupts the pituitary stalk while leaving vasopressin-producing hypothalamic neurons intact. The patient subsequently develops excessive dilute urine. Which step has most likely been disrupted?
Options:
Renal sodium filtration
V1 receptor synthesis
Renal prostaglandin formation
Thirst-center activation
Axonal transport and posterior-pituitary release of vasopressin
Correct Answer:
Axonal transport and posterior-pituitary release of vasopressin
Explanation: Vasopressin synthesized in the hypothalamus travels down axons to the posterior pituitary. Stalk interruption can therefore prevent normal storage and release.
MCQ 4
Question:
A 29-year-old woman has persistent water diuresis. Imaging shows no pituitary mass or recent trauma. Further evaluation suggests immune-mediated damage to vasopressin-producing neurons. Which etiological category best fits her disorder?
Options:
Drug-induced nephrogenic diabetes insipidus
Autoimmune central diabetes insipidus
Pulmonary SIADH
Metabolic nephrogenic diabetes insipidus
Postoperative SIADH
Correct Answer:
Autoimmune central diabetes insipidus
Explanation: Autoimmune or idiopathic injury to vasopressin-producing neurons is a recognized cause of central diabetes insipidus when structural causes are absent.
MCQ 5
Question:
A boy has had marked polyuria and intense thirst since early childhood. Vasopressin production is preserved and the hypothalamic-pituitary region appears normal. A similar disorder is present in relatives. Which defect best explains the presentation?
Options:
Failure of posterior-pituitary development
Excessive V1 receptor activation
Inherited abnormality of the V2 receptor or aquaporin-2 pathway
Increased hypothalamic osmoreceptor sensitivity
Excess renal prostaglandin inhibition
Correct Answer:
Inherited abnormality of the V2 receptor or aquaporin-2 pathway
Explanation: Inherited nephrogenic DI may result from defects in the renal V2 receptor or aquaporin-2 system, causing poor renal response despite adequate hormone availability.
MCQ 6
Question:
A patient with persistent potassium depletion develops increasing thirst and large-volume dilute urine. Vasopressin secretion is appropriate for his plasma state. Which mechanism best accounts for the urinary abnormality?
Options:
Acquired reduction in renal concentrating responsiveness
Excess posterior-pituitary hormone release
Increased collecting-duct sensitivity to vasopressin
Reduced glomerular filtration of water
Persistent stimulation of hypothalamic thirst alone
Correct Answer:
Acquired reduction in renal concentrating responsiveness
Explanation: Hypokalemia can impair renal concentrating ability and produce acquired nephrogenic DI despite appropriate endogenous vasopressin secretion.
MCQ 7
Question:
A patient with chronic renal disease develops persistent water diuresis. Endogenous vasopressin is present, but urinary concentrating ability remains poor. Which abnormality is most likely responsible?
Options:
Excessive hypothalamic vasopressin synthesis
Increased posterior-pituitary storage
Enhanced renal sensitivity to V2 stimulation
Impairment of the renal concentrating mechanism
Reduced vascular V1 receptor activity
Correct Answer:
Impairment of the renal concentrating mechanism
Explanation: Renal disorders can cause nephrogenic DI by reducing the kidney’s ability to respond appropriately to vasopressin and concentrate urine.
MCQ 8
Question:
A man with untreated diabetes insipidus passes large amounts of dilute urine but maintains a near-normal serum sodium concentration while working at home. Which factor most likely prevents a major rise in serum sodium?
Options:
Increased aldosterone secretion
Reduced glomerular filtration
Enhanced V1-mediated vasoconstriction
Increased renal sodium retention
Thirst-driven water intake matching urinary losses
Correct Answer:
Thirst-driven water intake matching urinary losses
Explanation: Intact thirst and unrestricted access to water can compensate for urinary free-water losses and maintain near-normal plasma sodium in DI.
MCQ 9
Question:
A patient with established diabetes insipidus reports waking five to six times each night to pass urine. Which disturbance most directly explains this nocturnal symptom?
Options:
Intermittent nocturnal hyperglycemia
Persistent failure of renal water conservation
Transient nocturnal sodium retention
Excessive nocturnal V2 stimulation
Increased nighttime aldosterone secretion
Correct Answer:
Persistent failure of renal water conservation
Explanation: Impaired antidiuretic action continues during sleep, so high-volume dilute urine production persists and produces nocturia.
MCQ 10
Question:
A 36-year-old man presents with marked polyuria. Blood glucose is normal, urine contains no glucose, and the urine is very dilute. Which process best explains his excessive urine output?
Options:
Glucose-induced osmotic diuresis
Excess renal sodium filtration
Failure of normal renal free-water conservation
Increased aldosterone-mediated potassium loss
Excessive proximal glucose reabsorption
Correct Answer:
Failure of normal renal free-water conservation
Explanation: DI produces a water diuresis rather than glucose-driven osmotic diuresis; urine is characteristically dilute because renal water conservation is impaired.
MCQ 11
Question:
An 8-year-old child with persistent nocturnal enuresis is selected for desmopressin therapy after appropriate clinical assessment. Which therapeutic effect is being used in this setting?
Options:
Increasing nocturnal sodium excretion
Increasing bladder smooth-muscle tone
Suppressing nighttime thirst
Increasing glomerular water filtration
Reducing overnight urine production
Correct Answer:
Reducing overnight urine production
Explanation: Desmopressin enhances renal water reabsorption and can reduce nighttime urine production in appropriately selected patients with nocturnal enuresis.
MCQ 12
Question:
A patient with von Willebrand disease is given desmopressin before a planned procedure. Which pharmacological effect contributes to improved hemostasis?
Options:
Release of von Willebrand factor and factor VIII from endothelial stores
Direct activation of platelet cyclooxygenase
Inhibition of hepatic anticoagulant synthesis
Blockade of fibrinolytic enzymes
Direct stimulation of platelet aggregation
Correct Answer:
Release of von Willebrand factor and factor VIII from endothelial stores
Explanation: Desmopressin can increase circulating von Willebrand factor and factor VIII by promoting their release from endothelial stores in responsive patients.
MCQ 13
Question:
A patient receiving desmopressin has satisfactory control of urine output and normal serum sodium but develops mild headache and nausea shortly after treatment. Which interpretation is most appropriate?
Options:
The symptoms indicate hypercalcemia
The symptoms indicate renal V2 resistance
The symptoms indicate hypokalemic nephropathy
Headache and nausea can occur as adverse effects of desmopressin
Headache proves severe water intoxication
Correct Answer:
Headache and nausea can occur as adverse effects of desmopressin
Explanation: Headache and nausea are recognized adverse effects of desmopressin; normal sodium makes severe dilutional water intoxication less likely in this scenario.
MCQ 14
Question:
Indomethacin is being considered as adjunctive therapy for nephrogenic diabetes insipidus. Which feature most limits its prolonged routine use?
Options:
Marked suppression of posterior-pituitary function
Potential renal and gastrointestinal toxicity
Permanent V2 receptor downregulation
Severe stimulation of aldosterone release
Irreversible activation of aquaporin-2 channels
Correct Answer:
Potential renal and gastrointestinal toxicity
Explanation: NSAIDs such as indomethacin can reduce polyuria, but renal and gastrointestinal toxicity limits prolonged routine use.
MCQ 15
Question:
Vasopressin acts on a receptor subtype in the anterior pituitary and contributes to ACTH release. Which receptor mediates this effect?
Options:
V2 receptor
V1a receptor
V1b receptor
Alpha-1 receptor
Mineralocorticoid receptor
Correct Answer:
V1b receptor
Explanation: V1b receptors participate in vasopressin-mediated ACTH release from the anterior pituitary, whereas V2 receptors mainly mediate renal antidiuresis.
MCQ 16
Question:
A 44-year-old woman taking carbamazepine develops lethargy. Serum sodium and plasma osmolality are reduced, while urine remains more concentrated than expected. Which explanation best fits the clinical context?
Options:
Central diabetes insipidus
Inherited nephrogenic diabetes insipidus
Hypokalemia-induced water diuresis
Hypercalcemia-associated renal resistance
Drug-associated inappropriate vasopressin activity
Correct Answer:
Drug-associated inappropriate vasopressin activity
Explanation: Carbamazepine is a recognized drug-associated cause of SIADH, producing water retention with low plasma osmolality and inappropriate urine concentration.
MCQ 17
Question:
A patient admitted with a significant pulmonary disorder develops low serum sodium and low plasma osmolality without evidence of excessive renal water loss. Which endocrine disturbance should be considered?
Options:
Pulmonary disease-associated SIADH
Inherited central diabetes insipidus
Lithium-induced nephrogenic diabetes insipidus
Hypothalamic vasopressin deficiency
Aquaporin-2 deficiency causing water loss
Correct Answer:
Pulmonary disease-associated SIADH
Explanation: Pulmonary disorders can stimulate inappropriate vasopressin secretion and therefore form an important etiological group for SIADH.
MCQ 18
Question:
A patient develops hyponatremia following an inflammatory disorder affecting the central nervous system. There is no history of diuretic use or excessive gastrointestinal sodium loss. Which relationship best explains the endocrine abnormality?
Options:
Renal disease causes deficient vasopressin secretion
Hypokalemia increases posterior-pituitary release
V2 receptor loss causes free-water retention
Central nervous system disease disturbs regulation of vasopressin secretion
Aquaporin loss produces dilutional hyponatremia
Correct Answer:
Central nervous system disease disturbs regulation of vasopressin secretion
Explanation: CNS disorders can disrupt normal hypothalamic control of vasopressin, leading to inappropriate secretion and SIADH.
MCQ 19
Question:
A patient receiving cyclophosphamide develops progressive hyponatremia. Plasma is hypo-osmolar, yet renal water excretion remains inappropriately limited. Which explanation is most appropriate?
Options:
Acquired central vasopressin deficiency
Medication-related SIADH
Inherited aquaporin-2 deficiency
Hypercalcemia-induced nephrogenic diabetes insipidus
Primary failure of hypothalamic osmoreceptors
Correct Answer:
Medication-related SIADH
Explanation: Cyclophosphamide is among the drugs associated with SIADH, in which inappropriate antidiuretic activity prevents normal free-water excretion.
MCQ 20
Question:
A patient with SIADH develops a falling serum sodium concentration without a history suggesting major external sodium loss. Which process most directly produces the reduction in measured serum sodium?
Options:
Increased gastrointestinal sodium loss
Failure of glomerular sodium filtration
Dilution of extracellular sodium by retained free water
Loss of sodium through aquaporin-2 channels
Reduced sodium absorption caused by V1 receptors
Correct Answer:
Dilution of extracellular sodium by retained free water
Explanation: The characteristic hyponatremia of SIADH is primarily dilutional: inappropriate water retention increases body water relative to sodium concentration.