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Thyrotoxic periodic paralysis is a rare but potentially life‐threatening complication of thyrotoxicosis characterised by hypokalaemia‐induced flaccid paralysis due to an intracellular potassium shift rather than total body depletion. We report a male in his early 40s of Filipino origin who awoke with acute bilateral lower‐limb weakness after he had consumed a large carbohydrate meal and performed strenuous exercise within the preceding 12 hours. Venous blood gas was normal; initial serum potassium was 1.7 mmol/L with phosphate 1.07 mmol/L. The ECG showed sinus tachycardia, first‐degree atrioventricular block and prominent U‐waves with QTc 388 ms. Urine potassium/creatinine ratio was 1.7 mmol/mmol (expected <2.0 in hypokalaemia), indicating appropriate renal conservation. A point‐of‐care thyroid panel did not include thyroid-stimulating hormone (TSH); the laboratory TSH was reported later as suppressed (0.001 mIU/L) with elevated FT4/FT3. There was no diuretic, insulin or β‐agonist use. The patient received potassium chloride totalling 80 mEq (≤10 mEq/hour peripherally with continuous ECG monitoring) with serum potassium checks every 1–2 hour, and supplementation was stopped once K+ reached 4.0 mmol/L; propranolol 40 mg orally every 8 hours and methimazole 10 mg orally every 8 hours were started. Muscle strength normalised within 24 hours. This case underscores the diagnostic triad of hypokalaemia without an acid–base disorder, appropriate renal K+ conservation and characteristic ECG changes, and highlights pragmatic dosing/monitoring plus the need for definitive control of thyrotoxicosis to prevent recurrence.