What are antibiotics?
Chemicals (natural or synthetic) that suppress or destroy bacteria; can be bacteriostatic (inhibit growth) or bactericidal (kill bacteria).
What makes bacterial cells different from human cells?
Bacteria have a peptidoglycan cell wall, absent in human cells; provides shape and prevents lysis.
What’s the difference between Gram-positive and Gram-negative bacteria?
Gram-positive: Thick peptidoglycan layer, no outer membrane (e.g. Staphylococcus)
Gram-negative: Thin peptidoglycan + outer membrane (e.g. E. coli)
How can antibiotics be classified by spectrum?
Narrow spectrum: Targets specific species (e.g. Penicillin G)
Broad spectrum: Targets wide range (e.g. Tetracyclines)
How can antibiotics be classified by mechanism?
Cell wall synthesis inhibitors – Penicillin
DNA synthesis inhibitors – Fluoroquinolones
Protein synthesis inhibitors – Tetracyclines, Macrolides
Metabolic inhibitors – Sulfonamides, Trimethoprim
How do penicillins work?
Mimic D-alanyl-D-alanine → block transpeptidase enzyme → weak wall → cell lysis.
What are the main types of penicillins and their uses?
Penicillin G – Gram+ (pneumonia, syphilis)
Methicillin – penicillinase-resistant
Amoxicillin/Ampicillin – broader (Gram–)
Amoxicillin + Clavulanic acid – combats resistance
What are common adverse effects of penicillins?
GI upset, rash, fever, anaphylaxis (rare).
What are cephalosporins?
Penicillin-like drugs, more penicillinase-resistant, divided into five generations.
What do fluoroquinolones do?
Inhibit bacterial DNA replication (e.g. Ciprofloxacin); work against many Gram+ and Gram– bacteria.
How do tetracyclines work and what are key cautions?
Bind 30S ribosome → block amino acid addition; avoid in pregnancy/kids <12; causes tooth discoloration and GI upset.
What are macrolides used for?
Bind 50S ribosome → block peptide bond formation; used if penicillin allergy (e.g. Erythromycin).
What do antifolate (metabolic inhibitor) drugs do?
Block folate synthesis (needed by bacteria).
Sulfonamides: Block PABA → dihydropteroic acid
Trimethoprim: Blocks dihydrofolate reductase
Co-trimoxazole: Combines both → synergistic effect.
Why are antibiotic combinations used?
For unknown/mixed infections, severe infections, TB, or synergy.
Disadvantages: Cost, toxicity, resistance, flora destruction.
What causes antibiotic resistance?
Mutations
Overuse/misuse
Agricultural use
Mechanisms: Decreased uptake, target modification, enzyme inactivation (penicillinase), efflux pumps.
How can antibiotic resistance be prevented?
Use only when needed, complete full course, never share/hoard antibiotics.
What are the main classes of antifungals and how do they work?
Echinocandins: Inhibit fungal cell wall synthesis (e.g. Micafungin)
Azoles (Imidazoles): Inhibit fungal P450 → ↓ ergosterol (e.g. Fluconazole)
What are the main antiviral targets in a virus’s life cycle?
Attachment, entry, replication, assembly, release.
How does Oseltamivir (Tamiflu) work?
Neuraminidase inhibitor → prevents viral spread (influenza).
How does Acyclovir work and what is it used for?
Activated by viral enzymes → inhibits viral DNA replication; treats HSV, VZV.
Difference between antivirals and vaccines?
Antivirals: Treat infection after onset
Vaccines: Prevent infection by priming immune system.
How do hormonal contraceptives work?
Inhibit GnRH → no FSH/LH → no ovulation
Thicken cervical mucus
Make endometrium unsuitable for implantation
What are the types of oral contraceptives?
Fixed combination: Same dose 21/28 days
Multiphasic: Varying doses, fewer side effects
Progestin-only (mini-pill): Daily; irregular bleeding common
What are mild, moderate, and serious side effects of OCPs?
Mild: Nausea, headache
Moderate: Acne, breakthrough bleeding
Serious: Blood clots, stroke, heart attack (esp. smokers >35)
