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PH9.6 | PH9.6 | Dermatological Pharmacotherapy — SDL Guide — SDL Guide (Part 3)
Self-Assessment
Test your understanding of dermatological pharmacotherapy.
- A 16-year-old girl with comedonal acne (no inflammatory lesions) asks what topical drug will help most. Which class of drug and which specific agent would you recommend as first-line?
- A child with crusted (Norwegian) scabies and failure of two courses of permethrin cream. What systemic drug can be used, and at what dose?
- A 45-year-old man with moderate-severe plaque psoriasis is being considered for methotrexate. What is the correct dosing schedule, and what supplement must always be co-prescribed? What are the three parameters you will monitor monthly?
- Distinguish between the mechanisms of calcipotriol and topical corticosteroids in psoriasis treatment, and explain why they are often combined.
- Name two sunscreen types that are categorised as physical blockers, explain their mechanism, and state why they are preferred over chemical filters for infants.
SELF-CHECK
Permethrin is the first-line treatment for both scabies (5% cream) and head lice (1% lotion). What is its mechanism of action?
A. It inhibits acetylcholinesterase, causing paralysis and death of the mite or louse
B. It is a synthetic pyrethroid that prolongs voltage-gated sodium channel opening in the insect nervous system, causing prolonged depolarisation, paralysis, and death
C. It acts as an antifungal agent that disrupts the mite's cell wall ergosterol
D. It is an organophosphate insecticide that blocks ATP synthesis in the mite
Reveal Answer
Answer: B. It is a synthetic pyrethroid that prolongs voltage-gated sodium channel opening in the insect nervous system, causing prolonged depolarisation, paralysis, and death
Permethrin is a synthetic pyrethroid insecticide — it acts by binding to voltage-gated sodium channels in the peripheral nervous system of arthropods (mites, lice), holding the channels in their open state. This causes sustained depolarisation of nerve membranes, hyperexcitability followed by paralysis and death of the parasite. Permethrin has low mammalian toxicity because: (1) sodium channel recovery in mammals is rapid and (2) permethrin is rapidly metabolised by mammalian liver enzymes. Acetylcholinesterase inhibition is the mechanism of organophosphates (malathion); cell wall ergosterol is a fungal target; ATP synthesis disruption is not the permethrin mechanism.