Flashcards: Sulphonamides: History, Chemistry, and Clinical Use — 24 cards

Introduction — significance?

First effective antimicrobials against pyogenic bacteria.

Sulphonamide core — structure?

Derived from sulphanilamide with N¹ and N⁴ substitutions.

N¹ substitution — role?

Affects solubility, pharmacokinetics.

N⁴ substitution — role?

Determines antibacterial activity.

Classification — basis?

Chemical structure and pharmacokinetics.

Prototype sulphonamide — example?

Sulfadiazine.

Spectrum — activity?

Bacteriostatic against gram-positive and negative bacteria.

Bacterial resistance — mechanism?

Increased PABA, reduced enzyme affinity, alternative pathways.

Mechanism — target enzyme?

Dihydropteroate synthase in folate synthesis.

Mode of action — process?

Competitive inhibition of PABA binding.

Bacteria unaffected?

Anaerobic bacteria resistant.

Urinary activity — significance?

Bactericidal concentrations in urine treat UTIs.

Pharmacokinetics — absorption?

Rapid, complete from GIT.

Metabolism — process?

Acetylation at N⁴ in liver.

Crystalluria — cause?

Precipitation of insoluble metabolites in urine.

Adverse effect — hypersensitivity?

Stevens-Johnson syndrome in long-acting sulphonamides.

Hemolysis risk — in?

G6PD deficiency.

Hepatitis — cause?

Drug-induced liver inflammation.

Uses — main application?

Urinary infections, topical burn treatment, ocular infections.

Cotrimoxazole — components?

Sulfamethoxazole and trimethoprim.

Trimethoprim — action?

Inhibits bacterial dihydrofolate reductase.

Synergism — effect?

Bactericidal by blocking sequential folate steps.

Spectrum — expanded?

Includes Salmonella typhi and others.

Current role —?

Limited; mainly in combination and topical applications.