WBR0216
| Author | PageAuthor::Vendhan Ramanujam |
|---|---|
| Exam Type | ExamType:: |
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| Prompt | [[Prompt::A 46 year old female complains of increased polyuria and polydipsia along with muscle weakness and abdominal cramps. She has been smoking 2 packs a day for the past 24 years along with history of alcohol intake for the past 22 years. She is a also a known diabetic who is on metformin. On physical examination, the PMI is found at the sixth intercostal space. Further examinations reveal normal neck veins without any peripheral edema. Her blood pressure recording comes out as 148/98 mmHg. Standing from behind and examining reveals a mild scoliosis. She was taking licorice in the past, but denies taking them recently. Her lab works are pending, but which will be the most specific lab finding that will correlate with the patient’s clinical condition?]] |
| Answer A | AnswerA::Low serum potassium level |
| Answer A Explanation | AnswerAExp:: |
| Answer B | AnswerB::High anion gap metabolic acidosis |
| Answer B Explanation | AnswerBExp:: |
| Answer C | AnswerC::High serum sodium level |
| Answer C Explanation | AnswerCExp:: |
| Answer D | AnswerD::Metabolic alkalosis |
| Answer D Explanation | AnswerDExp:: |
| Answer E | AnswerE::High aldosterone/renin ratio |
| Answer E Explanation | AnswerEExp:: |
| Right Answer | RightAnswer::E |
| Explanation | [[Explanation::The patient has hypertension associated with hypokalemia that manifests as muscle weakness and abdominal cramps. Along with worsening symptoms of diabetes like polyuria, primary hyperaldosteronism should be suspected in 30 to 50 year age group individuals in the absence of secondary causes like CHF. Excessive aldosterone production increases distal tubular exchange of sodium for potassium, leading to hypertension following increased sodium absorption and hypokalemia following progressive depletion of body potassium. Worsening of polyuria is due to the resistance to ADH at the level of kidney and glucose levels might also rise due to impaired insulin excretion. Following increased plasma sodium, plasma renin levels fall low and fail to increase even with appropriate stimulus such as volume depletion. Along with elevated aldosterone levels due to hypersecretion, the diagnosis of primary hyperaldosteronism can be made. Suppressed renin activity alone can even occur in about 25% of hypertensive patients with essential hypertension. But lack of suppression of aldosterone is also necessary to diagnose primary hyperaldosteronism. High aldosterone levels that are not suppressed by salt loading will prove that there is a primary inappropriate secretion of aldosterone. Adrenal adenoma is the commonest cause, followed by bilateral adrenal hyperplasia and unilateral adrenal hyperplasia for primary hyperaldosteronism. Educational Objective: |
| Approved | Approved::No |
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| Linked Question | Linked:: |
| Order in Linked Questions | LinkedOrder:: |