Controlled Hypertension, and a Moment of Lightheadedness

Correct answer: C. Stop, place him supine with the legs slightly elevated, and monitor

• A. Aromatic ammonia is an adjunct AFTER positioning, not instead of it, and continuing treatment through the episode remains inappropriate.
• B. Reassurance alone does not restore cerebral perfusion, and continuing while the patient is symptomatic risks a full faint with the airway unprotected and instruments in the mouth.
• C. CORRECT. Lightheadedness with pallor and moist skin is PRESYNCOPE. The management is the same whatever the cause: stop treatment, place the patient SUPINE with the legs slightly elevated to restore cerebral perfusion, ensure a patent airway, give oxygen, and monitor vital signs. Most episodes resolve within a minute or two in that position. Only when he is fully recovered and stable do you decide whether to continue.
• D. Dismissing the symptom is unsafe. It also forecloses on the differential — orthostatic hypotension from his antihypertensives, hypoglycaemia, or an arrhythmia.

Note: ⚑ FLAG FOR THE GROUP. The recall recorded 'reassure and continue' as the chosen answer. Positioning is the standard first response to presyncope and should be your default. Note also the specific relevance of his medication: both an ACE inhibitor and a thiazide predispose to orthostatic hypotension, so raise him SLOWLY at the end of the appointment.

Correct answer: B. Maculopapular rash

• A. This IS characteristic, and it is the commonest reason patients stop the drug — a dry, tickling, non-productive cough affecting roughly 5–20% of users. It arises because ACE also degrades BRADYKININ; inhibiting the enzyme lets bradykinin accumulate in the airways.
• B. CORRECT — this is the EXCEPTION. Rash is not among the characteristic adverse effects of ACE inhibitors. It can occur with almost any drug, but it is not what this class is known for and it is not what the question is testing.
• C. This IS characteristic. Reduced angiotensin II means reduced aldosterone, which means potassium retention. It is why potassium-sparing diuretics and potassium supplements are used cautiously with ACE inhibitors.
• D. This IS characteristic and it is the dangerous one. ACE-inhibitor angioedema is bradykinin-mediated, so it does NOT respond to antihistamines or corticosteroids, and it can present as sudden swelling of the lips, tongue or larynx years into therapy. It is a genuine airway emergency.

Note: Lisinopril is an ANGIOTENSIN-CONVERTING ENZYME INHIBITOR — it blocks the conversion of angiotensin I to angiotensin II. ⚑ It is NOT a diuretic. That miskeying recurs across several files in this series; correct it wherever you see it.

Correct answer: A. Hypokalaemia

• A. CORRECT. HYPOKALAEMIA is the signature adverse effect of thiazide diuretics. By blocking the sodium-chloride symporter in the DISTAL CONVOLUTED TUBULE, more sodium reaches the collecting duct, where it is exchanged for potassium — which is then lost in the urine. Thiazides also cause hyponatraemia, hyperuricaemia (gout), hyperglycaemia, hypercalcaemia and photosensitivity, and dry mouth is a common patient complaint.
• B. Ototoxicity belongs to the LOOP diuretics — furosemide in particular, especially given rapidly by intravenous route or with an aminoglycoside.
• C. Dry cough belongs to the ACE inhibitors, through bradykinin accumulation.
• D. Hyperkalaemia is the opposite, and belongs to the potassium-SPARING diuretics (spironolactone, amiloride, triamterene) and to ACE inhibitors and ARBs.

Note: ⚑ RECURRING SOURCE ERROR ACROSS THIS SERIES: hydrochlorothiazide is a THIAZIDE acting on the distal convoluted tubule, NOT a loop diuretic. Loop diuretics (furosemide, bumetanide) act on the thick ascending limb of the loop of Henle. Both waste potassium, but they are different classes with different potencies and different toxicities.