AIM • KMU EXAM PRACTICE
KMU Past Paper Practice
Topic 2. Electrolyte & Acid–Base Disorders
Final Year MBBS • 20 A-Type Single Best Answer MCQs • Renal Module
MCQ 1
A 70-year-old man with profuse diarrhea is admitted with dizziness, dry mucous membranes and hypotension. Serum sodium is 126 mmol/L. Which mechanism most appropriately explains the sodium abnormality?
Loss of sodium and water with proportionally greater sodium loss
Pure free-water retention without volume depletion
Reduced intracellular potassium uptake
Excess renal phosphate retention
Primary carbon dioxide retention
Correct Answer: Loss of sodium and water with proportionally greater sodium loss
Explanation: Gastrointestinal loss with clinical hypovolemia can produce hypovolemic hyponatremia when sodium loss is proportionally greater than water loss.
MCQ 2
A hospitalized patient has hyponatremia but appears clinically euvolemic. There is no history of vomiting or diarrhea. Which mechanism should be considered as an important cause?
Excessive potassium loss
Reduced phosphate absorption
Inappropriate antidiuretic hormone activity
Primary magnesium retention
Chronic carbon dioxide retention
Correct Answer: Inappropriate antidiuretic hormone activity
Explanation: Excess antidiuretic hormone effect causes inappropriate water retention and is an important mechanism of euvolemic hyponatremia.
MCQ 3
An unconscious patient is found to have hypernatremia and very high urine output. Despite marked dehydration, the urine remains unusually dilute. Which process best explains this pattern?
Failure to conserve water appropriately
Excessive sodium loss through diarrhea
Excess bicarbonate retention
Intracellular phosphate depletion
Respiratory carbon dioxide retention
Correct Answer: Failure to conserve water appropriately
Explanation: Hypernatremia with polyuria and inappropriately dilute urine points toward renal free-water loss, as occurs in diabetes insipidus.
MCQ 4
A patient with marked hypernatremia is hypotensive and clinically volume depleted. Which management priority is most appropriate before complete correction of the water deficit?
Immediate phosphate replacement
Restore effective circulating volume
Restrict all fluids
Give potassium before assessing circulation
Induce respiratory alkalosis
Correct Answer: Restore effective circulating volume
Explanation: Hemodynamic instability takes priority. Circulatory volume must be restored before gradual correction of the free-water deficit.
MCQ 5
A patient with extensive tissue injury develops a rising serum potassium level despite no potassium supplementation. Which mechanism best explains this abnormality?
Release of intracellular potassium into extracellular fluid
Movement of extracellular potassium into cells
Loss of potassium through stool
Increased renal potassium excretion
Reduced sodium absorption from the intestine
Correct Answer: Release of intracellular potassium into extracellular fluid
Explanation: Most body potassium is intracellular. Major cellular injury can release potassium into plasma and produce hyperkalemia.
MCQ 6
A patient with renal failure and hyperkalemia receives therapy that temporarily lowers serum potassium. Which additional management principle remains necessary?
Prevent all intracellular potassium uptake
Ensure excess potassium is ultimately removed from the body
Increase serum phosphate concentration
Maintain metabolic acidosis
Induce hypernatremia
Correct Answer: Ensure excess potassium is ultimately removed from the body
Explanation: Intracellular shifting is temporary. Definitive control requires removal of excess potassium, especially when renal excretion is impaired.
MCQ 7
A patient with prolonged vomiting has weakness and a low serum potassium. Which combination most strongly explains the persistence of the potassium deficit?
Gastrointestinal loss with ongoing renal potassium loss
Phosphate retention with potassium release
Magnesium excess with reduced potassium loss
Hypernatremia with increased potassium intake
Respiratory acidosis with cellular potassium uptake
Correct Answer: Gastrointestinal loss with ongoing renal potassium loss
Explanation: Vomiting produces volume and chloride depletion and may be accompanied by continued renal potassium wasting, sustaining hypokalemia.
MCQ 8
A patient receiving treatment for severe hyperkalemia has an initially improved serum potassium, but the level rises again several hours later. Which explanation is most appropriate?
The initial therapy only redistributed potassium temporarily
Potassium was converted into phosphate
Renal sodium excretion caused cerebral edema
Magnesium replacement caused permanent potassium retention
Respiratory alkalosis increased potassium absorption
Correct Answer: The initial therapy only redistributed potassium temporarily
Explanation: Potassium-shifting therapy lowers plasma potassium transiently but does not reduce total body potassium, so rebound may occur.
MCQ 9
A patient with severe renal impairment has persistently elevated serum phosphate. Which management principle directly addresses the mechanism of the abnormality?
Increase phosphate intake
Reduce phosphate burden and address impaired excretion
Induce respiratory alkalosis
Give potassium supplementation routinely
Increase magnesium exposure
Correct Answer: Reduce phosphate burden and address impaired excretion
Explanation: Hyperphosphatemia in renal failure results mainly from reduced phosphate excretion, so therapy aims to reduce phosphate load and burden.
MCQ 10
A critically ill patient develops severe hypophosphatemia followed by generalized weakness. Which additional complication would be most clinically important to anticipate?
Respiratory muscle weakness
Increased deep tendon reflexes from magnesium excess
Cerebral swelling from hypernatremia
Peaked T waves from phosphate deficiency
Persistent respiratory alkalosis from renal phosphate loss
Correct Answer: Respiratory muscle weakness
Explanation: Severe phosphate deficiency reduces cellular energy availability and can weaken skeletal and respiratory muscles.
MCQ 11
A patient with chronic diarrhea develops tremor, muscle cramps and low magnesium. Which physiological change best explains these manifestations?
Increased neuromuscular excitability
Profound neuromuscular depression
Reduced extracellular sodium tonicity
Suppression of all cardiac conduction
Increased phosphate deposition
Correct Answer: Increased neuromuscular excitability
Explanation: Hypomagnesemia increases neuromuscular excitability, producing tremor, cramps, tetany and sometimes seizures or arrhythmias.
MCQ 12
A patient with severe hypermagnesemia has hypotension, bradycardia and marked hyporeflexia. Which treatment principle is most appropriate for significant neuromuscular and cardiac toxicity?
Intravenous calcium for physiological antagonism
Immediate potassium loading
Free-water restriction alone
Induced respiratory alkalosis
Phosphate supplementation as sole treatment
Correct Answer: Intravenous calcium for physiological antagonism
Explanation: Calcium can counter important cardiac and neuromuscular effects of magnesium toxicity while measures are taken to reduce magnesium burden.
MCQ 13
A patient has pH 7.28, low bicarbonate and an appropriately reduced PaCO₂. Which statement best describes the role of the respiratory response?
It eliminates the underlying metabolic disorder
It partially limits the fall in pH by reducing carbon dioxide
It raises bicarbonate immediately to normal
It converts metabolic acidosis into metabolic alkalosis
It prevents renal hydrogen-ion excretion
Correct Answer: It partially limits the fall in pH by reducing carbon dioxide
Explanation: Hyperventilation lowers PaCO₂ and therefore reduces the severity of acidemia, but compensation does not correct the primary metabolic process.
MCQ 14
A patient has metabolic acidosis with an increased anion gap. Which interpretation is most appropriate?
There is likely accumulation of unmeasured acids
There is necessarily isolated gastrointestinal bicarbonate loss
The patient has primary respiratory alkalosis
The bicarbonate concentration must be increased
The PaCO₂ must be elevated as compensation
Correct Answer: There is likely accumulation of unmeasured acids
Explanation: A raised anion gap indicates that additional unmeasured anions are present, commonly reflecting accumulation of fixed acids.
MCQ 15
A patient with diarrhea has metabolic acidosis but a normal anion gap. Which mechanism best explains this pattern?
Bicarbonate loss with compensatory increase in chloride
Massive retention of unmeasured organic acids
Primary carbon dioxide retention
Excess magnesium absorption
Loss of sodium without bicarbonate loss
Correct Answer: Bicarbonate loss with compensatory increase in chloride
Explanation: Gastrointestinal bicarbonate loss can produce a normal-anion-gap metabolic acidosis in which chloride increases as bicarbonate falls.
MCQ 16
A patient has pH 7.52, elevated bicarbonate and elevated PaCO₂ following several days of vomiting. Which interpretation is most appropriate?
Metabolic alkalosis with respiratory compensation
Respiratory acidosis with renal compensation
Metabolic acidosis with respiratory compensation
Respiratory alkalosis with metabolic compensation
Normal acid–base physiology
Correct Answer: Metabolic alkalosis with respiratory compensation
Explanation: Elevated bicarbonate is the primary abnormality producing alkalemia; the raised PaCO₂ reflects compensatory hypoventilation.
MCQ 17
Two patients have the same degree of elevated PaCO₂. Patient A developed hypoventilation 30 minutes ago, while Patient B has had chronic ventilatory failure. Which finding is more likely in Patient B?
Greater increase in serum bicarbonate
Lower bicarbonate than Patient A
Complete absence of renal compensation
Primary metabolic acidosis
Severe hypernatremia caused by PaCO₂
Correct Answer: Greater increase in serum bicarbonate
Explanation: Chronic respiratory acidosis allows time for renal adaptation, producing greater bicarbonate retention than occurs in an acute episode.
MCQ 18
A patient with chronic hyperventilation has low PaCO₂. Compared with an acute episode of respiratory alkalosis, which additional change is expected after renal compensation develops?
A greater reduction in serum bicarbonate
A progressive increase in PaCO₂ above normal
A rise in bicarbonate caused by renal retention
Development of primary respiratory acidosis
No change in bicarbonate concentration
Correct Answer: A greater reduction in serum bicarbonate
Explanation: With persistent respiratory alkalosis, the kidneys reduce bicarbonate retention, so bicarbonate falls more than in an acute episode.
MCQ 19
A patient has pH 7.20, low bicarbonate and a PaCO₂ that is lower than normal but not as low as expected for the degree of metabolic acidosis. Which interpretation is most appropriate?
Metabolic acidosis with superimposed respiratory acidosis
Pure metabolic acidosis with ideal compensation
Metabolic alkalosis with respiratory compensation
Pure respiratory alkalosis
Normal acid–base physiology
Correct Answer: Metabolic acidosis with superimposed respiratory acidosis
Explanation: PaCO₂ should fall predictably in metabolic acidosis. A value higher than the expected compensation indicates additional ventilatory failure.
MCQ 20
A patient has alkalemia, markedly reduced PaCO₂ and a bicarbonate concentration that has fallen by the amount expected in chronic respiratory alkalosis. Which interpretation best fits the findings?
Chronic respiratory alkalosis with appropriate renal compensation
Acute respiratory acidosis with renal compensation
Primary metabolic alkalosis
Metabolic acidosis with inadequate respiratory compensation
Mixed respiratory acidosis and metabolic alkalosis
Correct Answer: Chronic respiratory alkalosis with appropriate renal compensation
Explanation: A primary fall in PaCO₂ with the expected chronic reduction in bicarbonate indicates appropriately compensated chronic respiratory alkalosis.
