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Pharmacology Flashcards

6 cards from real MFDS practice questions. Tap to flip, then mark Knew It or Still Learning — missed cards come back until you master them.

Read the first 6 Pharmacology flashcards as text
  1. Which corticosteroid preparation is most appropriate for topical treatment of oral mucosal lesions?

    Answer: All are appropriate depending on severity

    Hydrocortisone pellets suit localised lesions, betamethasone mouthwash is ideal for widespread lesions, and clobetasol is used for severe resistant cases, selected by lesion extent and severity.

  2. Carbamazepine is the drug of first choice for management of:

    Answer: Trigeminal neuralgia

    Carbamazepine, a sodium channel blocker, is the first-line treatment for trigeminal neuralgia due to its demonstrated efficacy in reducing the frequency and intensity of attacks.

  3. The mechanism of action of chlorhexidine as an antiseptic mouthwash is:

    Answer: Disruption of bacterial cell membranes

    Chlorhexidine is a cationic bisbiguanide that adsorbs onto negatively charged bacterial cell walls, disrupting membrane integrity and causing cytoplasmic precipitation.

  4. Erythromycin achieves its antibacterial effect by binding to the:

    Answer: 50S ribosomal subunit

    Erythromycin (and other macrolides) bind to the 50S ribosomal subunit, blocking translocation and inhibiting bacterial protein synthesis.

  5. Which drug is used prophylactically to prevent infective endocarditis before high-risk dental procedures?

    Answer: NICE guidelines no longer recommend routine antibiotic prophylaxis

    NICE guideline CG64 (2008, maintained in reviews) concludes there is insufficient evidence that antibiotic prophylaxis prevents IE and recommends against routine prophylaxis for dental procedures.

  6. Prednisolone, a synthetic glucocorticoid, suppresses inflammation primarily by:

    Answer: Inducing lipocortin which inhibits phospholipase A2

    Glucocorticoids induce synthesis of annexin-1 (lipocortin), which inhibits phospholipase A2, blocking arachidonic acid release and thus the entire downstream inflammatory cascade.