Paper I
2017 February (2010 Scheme) · 40 marks · 120 min

Question

A patient suffering from schizophrenia was being treated with haloperidol for the last four weeks. Now he developed rigidity, tremors, hypokinesia and classical gait. Answer the following:

  • (a) What is the cause of these symptoms in this patient. 1 mark(s)
  • (b) How will you treat this problem. 2 mark(s)
  • (c) Why levodopa is combined with carbidopa in parkinsonism and mention its dose 3 mark(s)
Q26 marksEssays

Answer

(a) Cause of symptoms

  • Drug-induced (pseudo)parkinsonism due to haloperidol — a typical (high-potency) antipsychotic that blocks D2 receptors in the nigrostriatal pathway, producing extrapyramidal symptoms (rigidity, tremor, hypokinesia, shuffling/festinant gait) resembling idiopathic Parkinson’s disease

(b) Treatment

  • Reduce the dose of haloperidol, or switch to an atypical antipsychotic with lower extrapyramidal risk (e.g., olanzapine, risperidone)
  • Add an anticholinergic drug (e.g., Trihexyphenidyl) to control the extrapyramidal symptoms
  • (Levodopa is generally NOT effective/appropriate here, since the problem is receptor blockade, not dopamine deficiency, and it can worsen the underlying psychosis)

(c) Levodopa-carbidopa combination and dose

  • Carbidopa is a peripheral dopa-decarboxylase inhibitor that does not cross the blood-brain barrier
  • It blocks peripheral conversion of levodopa to dopamine, increasing the amount of levodopa available to cross into the brain (increasing CNS bioavailability and allowing a lower levodopa dose)
  • It also markedly reduces peripheral dopamine-mediated adverse effects (nausea, vomiting, hypotension, arrhythmias)
  • Dose: Typically combined in a fixed ratio (e.g., 10:100 or 25:250 carbidopa:levodopa), started at a low dose (e.g., levodopa 100–300 mg/day in divided doses) and titrated gradually to clinical response

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