Drugs Flashcards
Erythromycin and Clindamycin:
MOA, Clinical, Adverse Effects,
MOA: It is a 50S subunit inhibitor, and is a bacteriostatic and inhibits protein synthesis.
Bacteriostatic.
Clindamycin causes pseudomembranous colitis
Benzoyl Peroxide
MOA: absorbed by skin –> benzoic acid –> metabolized by purine–> oxidize of bacterial proteins. Is
Clinical: acne rosacea.
Used in combo with antibiotics. Greater efficacy and decreased resistance.
Dapsone
MOA
Adverse Effects:
MOA: antibacterial and antibacterial
Adverse Effects: Methemoglobinemia and orange staining of skin benzoyl peroxide.
Azelaic Acid
MOA, Clinical Uses
MOA: anti comedome, anti-hyperproliferation, competitive inhibitor of mitochondrial oxidoreducatases and 5 alpha reductase, which lowers hyperpigmentation.
Clinical: Lightens post inflammatory hyperpigmentation, mild inflammatory acne, and comedonal acne.
Adverse Effects: Hypo-pigmentaton of the skin
Doxyxlycline, Minocycline, Tetracycline
MOA, Clinical Uses
MOA: 16rRNA of the 30s subunit, preventing binding of aminoacyl tRNA to the acceptor site
Clinical Uses: for inflammatory acne vulgaris
Clotrimazole and Miconazole.
MOA:
Adverse Effects:
MOA: Inhibit CYP450 14 alpha- demethylase (essential enzyme in ergosterol synthesis)
Clinical: Tinea Corporis, Tinea Cruris, tinea pedis, tine versicolor, Tina nigra.
Miconazole: is used for diaper dermatitis complicated by Candida albicans infection.
Adverse Effects: irritation, burning/ stinging,
Ketaconazole:
MOA:
Clinical Uses: (Topical)
Adverse Effects (oral)
Contraindications:
Do not use:
MOA: same as all azoles
Shampoo/ foam: seborrheic dermatitis, white and black piedra.
Clinical Uses:
Shampoo: Seborrheic Dermatitis
Topical: Tinea pedis, Tinea Cruris, Tinea Corporis
Clinical oral: chromomycosis, paracoccidioidimycosis, mucocutaneous candidiadis.
Do not use: if patient has achrohydria, is on bicarb, antacids, H2-blockers or PPIs
Itraconazole and Fluconazole
MOA
Clinical Aspects
MOA: CYP-450 14 alpha Demethylase needed for ergosterol synthesis.
Clinical Aspects: Used for onychomycosis.
Itraconzole: white pierdra, lobo mycosis, chromoblastomycosis
Terbinafine:
MOA
Clinical Use:
Oral Use:
Topical:
Side Effects:
MOA: It affects squalene epoxidase–> stops ergosterol synthesis
Clinical: first line for the dermatophytosis
Topical: tinea corporis, curries, versicolor and nigra
Oral: First choice for onychomycosis
Side Effects: Are change or loss of taste and smell. Not recommended in patients with renal or hepatic failure or in pregnant women.
Not recommended for renal or hepatic failure in women.
Naftinine:
MOA:
Clinical:
Adverse Effects:
MOA: same as any oral allylamine.
Clinical: tinea, corporis, pedis, curries.
Anti-inflammatory activity.
Adverse Effects:
Butenafine:
MOA:
Clinical
Adverse Effects
works as general allylamine
Griseolfulvin:
MOA:
Clinical:
Contraindications:
MOA: inhibition of mitotic spindle and inhibition of fungal mitosis
Clinical: Tinea Capitis , fungistatic and requires long time to be useful
Contraindications: pregnancy, patients with poryphria and hepatic failure
Ciclopirox Olamine
MOA: chelation of polyvalent cations resulting in stopping of metal dependent enzymes that are responsible for degradation of peroxides within fungal cell.
Clinical: Mild to moderate onychomycosis of fingernails and toenails. Seborrheic dermatitis, white piedra.
Imiquimod:
MOA:
Clinical:
Adverse Effects:
MOA: TLR7 agonist for immune cells and induces production of interferons alpha and gamma
Clinical: genital and perianal warts, common warts and cutaneous warts
Molluscum contagium
HSV off label.
Cimetidine:
MOA
Clinical
Adverse Effects:
MOA: immunoomdulatory effects by histamine induced T suppressor cell activity.
Clinical: warts in children, and molluscum contagious in small children
Lindane:
MOA:
Clinical Use
Contraindications:
MOA: It is directly absorbed by the parasites and ova through exoskeleton.
It activates the nervous system–> causes seizures and death of parasitic arthropods.
Clinical: scabies and lice.
Contra: potential for neurotoxicity and hematoxivity.
Crotamiton:
MOA:
MOA: scabicidal activity, and antipruritic effects.
Permethrin:
MOA:
Clinical:
MOA: inhibits sodium ion channel through sodium ion cell membranes channels. Paralysis and death of the parasite.
Clinical: head lice and nits (lotion and cream), and scabies
Ivermectin:
MOA:
Clinical:
- Glutamate gated chloride channel binding–> increases cl ions, and hyperpolarization of nerve of muscle cell and death of parasite
Clinical: topical heals lice and rosacea in adults, and immature onchocerciasis.
Praziquantel
MOA:
Clinical:
MOA: increases cell permeability to schistosomes, and causes there to be strong contractions and paralysis of worm musculature.
Clinical: Schistosoma adult forms
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Glucocorticoids
MOA:
Clinical Uses:
MOA: anti-inflammatory and immunosuppressive effects. Used for inflammatory and pruritic conditions.
MOA: bind to glucocorticoid response elements in DNA.
Adverse Effects: Tachyphylaxis
Hydrocortisone
Clinical:
Clinical: corticoid responsive dermatoses