Cardiovascular, immunosuppressant & anaesthetic drugs flashcards
19 high-yield MRCP Part 1 cards from the Intellect Medicos Clinical Pharmacology & Toxicology course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.
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By what mechanism does amiodarone cause hypothyroidism?
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The Wolff–Chaikoff effect: its large iodine load (about 37% iodine by weight) suppresses thyroid hormone synthesis.
Why? Amiodarone also inhibits peripheral 5'-deiodinase, reducing conversion of T4 to T3.
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How is amiodarone-induced hypothyroidism managed if amiodarone is still needed?
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Start levothyroxine and continue amiodarone.
Why? Hypothyroidism is easily corrected with replacement, so a useful antiarrhythmic does not need to be stopped.
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Type 1 amiodarone-induced thyrotoxicosis (iodine-driven excess synthesis in an abnormal gland) is treated with ______; type 2 (destructive thyroiditis in a normal gland) is treated with prednisolone.
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carbimazole (± potassium perchlorate)
Why? Type 1 is the Jod–Basedow phenomenon, with a goitre and increased vascularity on Doppler. Type 2 releases preformed hormone, with low vascularity and low uptake.
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Type 1 amiodarone-induced thyrotoxicosis (iodine-driven excess synthesis in an abnormal gland) is treated with carbimazole (± potassium perchlorate); type 2 (destructive thyroiditis in a normal gland) is treated with ______.
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prednisolone
Why? Type 1 is the Jod–Basedow phenomenon, with a goitre and increased vascularity on Doppler. Type 2 releases preformed hormone, with low vascularity and low uptake.
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Flecainide and propafenone are class ______ antiarrhythmics, whereas lidocaine and mexiletine are class IB.
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IC
Why? All class I drugs block sodium channels (phase 0). Class IA includes quinidine, procainamide and disopyramide.
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Flecainide and propafenone are class IC antiarrhythmics, whereas lidocaine and mexiletine are class ______.
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IB
Why? All class I drugs block sodium channels (phase 0). Class IA includes quinidine, procainamide and disopyramide.
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Which two cosmetic side effects are much more typical of ciclosporin than of tacrolimus?
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Gingival hyperplasia and hirsutism (hypertrichosis).
Why? Both are calcineurin inhibitors with similar nephrotoxicity, but these cosmetic effects point to ciclosporin.
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Name two electrolyte disturbances caused by calcineurin inhibitors.
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Hyperkalaemia and hypomagnesaemia.
Why? Calcineurin inhibitors affect renal tubular handling of potassium and magnesium; they are also nephrotoxic and cause hypertension.
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Which calcineurin inhibitor carries the higher risk of post-transplant diabetes?
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Tacrolimus.
Why? Tacrolimus is more toxic to pancreatic beta cells; it also causes more tremor than ciclosporin.
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Which electrolyte abnormality does suxamethonium cause, and in which patients is this dangerous?
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Hyperkalaemia — dangerous in burns, crush injury, denervation/neuromuscular disease and prolonged immobility.
Why? Depolarisation releases potassium from muscle; in these conditions there are extra (extrajunctional) receptors, so the rise can cause cardiac arrest.
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A 30-year-old man has a rapid sequence induction with suxamethonium for an appendicectomy. He remains paralysed and apnoeic for over 2 hours after surgery. What is the most likely cause?
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Inherited pseudocholinesterase (butyrylcholinesterase) deficiency.
Why? Plasma cholinesterase normally breaks suxamethonium down within minutes; without it, paralysis lasts hours. Treatment is ventilation and sedation until it wears off.
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What is the specific treatment for malignant hyperthermia?
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IV dantrolene (plus stopping the trigger and active cooling).
Why? Dantrolene blocks calcium release from the sarcoplasmic reticulum via the ryanodine receptor. The condition is autosomal dominant (usually RYR1) and triggered by suxamethonium and volatile anaesthetics.
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Which non-depolarising muscle relaxant is safe in both renal and hepatic failure, and why?
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Atracurium — it breaks down spontaneously in plasma (Hofmann elimination), independent of liver and kidney.
Why? Its main side effect is histamine release, causing flushing, hypotension and tachycardia.
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Which drug rapidly reverses rocuronium or vecuronium by encapsulating it?
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Sugammadex.
Why? It binds the steroid-based relaxant directly. Neostigmine reverses non-depolarising block indirectly by inhibiting acetylcholinesterase.
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The local anaesthetic of choice for IV regional anaesthesia (Bier's block) is ______; bupivacaine is contraindicated for this because of cardiotoxicity.
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prilocaine
Why? If the cuff fails, the drug enters the circulation; prilocaine is the least cardiotoxic. Prilocaine can cause methaemoglobinaemia.
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The local anaesthetic of choice for IV regional anaesthesia (Bier's block) is prilocaine; ______ is contraindicated for this because of cardiotoxicity.
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bupivacaine
Why? If the cuff fails, the drug enters the circulation; prilocaine is the least cardiotoxic. Prilocaine can cause methaemoglobinaemia.
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What is the specific treatment for cardiovascular collapse from local anaesthetic systemic toxicity (LAST)?
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IV 20% lipid emulsion (with standard resuscitation; benzodiazepines for seizures).
Why? The lipid acts as a 'sink' that draws the lipophilic anaesthetic out of the heart and brain.
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Which induction agent causes adrenal suppression by inhibiting 11-beta-hydroxylase?
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Etomidate.
Why? It is cardiovascularly stable, so it is useful in shock, but a single dose can suppress cortisol synthesis.
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Which induction agent is an NMDA antagonist that raises heart rate and blood pressure and causes emergence hallucinations?
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Ketamine.
Why? Its sympathomimetic effect and strong analgesia with little respiratory depression make it useful in haemodynamic instability.
More Clinical Pharmacology & Toxicology topics
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