Answer the following questions in very proper, for exam writing , easy medium sized with well described . ANTIMICROBIAL, ANTIVIRAL DRUGS 1. Classification of antibiotics by the mechanism of action. 2. Mechanism of bacterial resistance to antibiotics, methods of control and preventions of resistance. 3. Penicillins. Mechanism of action, antibacterial spectrum, classification, therapeutic use, resistance, adverse effects. 4. Cephalosporins. Mechanism of action, antibacterial spectrum, classification, therapeutic use, resistance, adverse effects. 5. Carbapenems. Mechanism of action, antibacterial spectrum, classification, therapeutic use, resistance, adverse effects. 6. Tetracyclines. Mechanism of action, antibacterial spectrum, classification, therapeutic use, resistance, adverse effects. 7. Aminoglycosides. Mechanism of action, antibacterial spectrum, classification, therapeutic use, resistance, adverse effects. 8. Macrolides. Mechanism of action, antibacterial spectrum, classification, therapeutic use, resistance, adverse effects. 9. Quinolones. Mechanism of action, antibacterial spectrum, classification, therapeutic use, resistance, adverse effects. 10.Sulfonamides. Mechanism of action, antibacterial spectrum, classification, therapeutic use, resistance, adverse effects. 11.Antimycobacterial drugs (Drugs used to treat tuberculosis). Mechanisms of action, classification, therapeutic use, resistance, adverse effects. 12.Antifungal drugs. Classification, antifungal spectrum, therapeutic use, resistance, adverse effects. 13.Antiviral drugs for the treatment of herpes virus infection. Mechanisms of action, classification, therapeutic use, adverse reactions 14.Antiviral drugs for the treatment of HIV. Mechanisms of action, classification, therapeutic use, adverse effects. 15.Antiseptics. Classification, mechanisms of action, therapeutic and practice use, resistance, adverse effects.

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Its kind of long answer, i want in short and well described

Here are all 15 questions answered in a concise, exam-ready format:

ANTIMICROBIAL & ANTIVIRAL DRUGS — Exam Answers


Q1. Classification of Antibiotics by Mechanism of Action

MechanismDrug ClassesExamples
Cell wall synthesis inhibitionBeta-lactams, GlycopeptidesPenicillin, Cephalosporins, Vancomycin
Cell membrane disruptionPolymyxins, LipopeptidesColistin, Daptomycin
Protein synthesis inhibition (30S)Aminoglycosides, TetracyclinesGentamicin, Doxycycline
Protein synthesis inhibition (50S)Macrolides, Chloramphenicol, LincosamidesAzithromycin, Clindamycin
DNA/RNA synthesis inhibitionFluoroquinolones, RifampicinCiprofloxacin, Rifampin
Metabolic pathway inhibitionSulfonamides, TrimethoprimSulfamethoxazole, TMP
Nucleic acid structure disruptionNitroimidazolesMetronidazole

Q2. Bacterial Resistance to Antibiotics

Mechanisms of Resistance:

  1. Enzymatic inactivation - Beta-lactamases destroy beta-lactam ring; acetyltransferases inactivate aminoglycosides
  2. Altered target site - Modified PBPs (MRSA); altered 23S rRNA (macrolide resistance)
  3. Reduced permeability - Loss of outer membrane porins in gram-negative bacteria
  4. Efflux pumps - Active transport of drug out of the cell (tetracyclines, fluoroquinolones)
  5. Bypass pathways - Bacteria acquire alternative metabolic routes (e.g., MRSA acquires mecA gene)

Types:

  • Intrinsic resistance - Natural, always present (e.g., gram-negatives to vancomycin)
  • Acquired resistance - Via mutation or horizontal gene transfer (plasmids, transposons)

Control & Prevention:

  • Rational antibiotic prescribing (avoid overuse/misuse)
  • Use narrow-spectrum agents when possible
  • Complete full course of therapy
  • Antibiotic stewardship programs in hospitals
  • Infection control - hand hygiene, barrier precautions
  • Avoid antibiotics in agriculture/animal husbandry
  • Combination therapy to prevent resistance emergence
  • Development of new antibiotics and alternative therapies

Q3. Penicillins

Mechanism of Action:

Bind to Penicillin-Binding Proteins (PBPs) - enzymes that catalyze cross-linking (transpeptidation) of peptidoglycan in the bacterial cell wall. This inhibits cell wall synthesis, causing osmotic lysis. They are bactericidal.

Classification:

ClassExamplesSpectrum
Natural penicillinsPenicillin G (IV), Penicillin V (oral)Streptococci, Treponema, Neisseria
Penicillinase-resistantNafcillin, Oxacillin, DicloxacillinMSSA (Staph aureus)
AminopenicillinsAmpicillin, AmoxicillinExtended gram-positive + Haemophilus, E. coli
Anti-pseudomonalPiperacillin, TicarcillinPseudomonas + gram-negatives
Beta-lactam/inhibitorAmoxicillin-Clavulanate, Piperacillin-TazobactamBroad spectrum

Antibacterial Spectrum:

  • Gram-positive: Streptococcus, Enterococcus, Listeria
  • Gram-negative (broad spectrum): E. coli, Haemophilus, Klebsiella (with inhibitors)
  • Spirochetes: Treponema pallidum
  • Anaerobes: Clostridium, Bacteroides (with inhibitors)

Therapeutic Use:

  • Streptococcal pharyngitis, pneumococcal pneumonia, syphilis (Pen G)
  • Skin/soft tissue infections (ampicillin/amoxicillin)
  • Hospital-acquired infections, intra-abdominal infections (pip-tazo)
  • MSSA infections (nafcillin/oxacillin)

Resistance:

  • Beta-lactamase production (most common) - cleaves beta-lactam ring
  • Altered PBPs - e.g., PBP2a in MRSA (mecA gene)
  • Reduced permeability via porin changes
  • Efflux pumps

Adverse Effects:

  • Hypersensitivity (most important) - urticaria, anaphylaxis (0.05%), rash
  • GI - nausea, diarrhea; pseudomembranous colitis (ampicillin)
  • CNS - seizures at very high doses
  • Interstitial nephritis (methicillin - now withdrawn)
  • Hematologic - Coombs-positive hemolytic anemia, neutropenia (with high doses)
  • Ampicillin causes maculopapular rash in patients with EBV infection

Q4. Cephalosporins

Mechanism of Action:

Same as penicillins - bind PBPs and inhibit cell wall synthesis (transpeptidation of peptidoglycan). Bactericidal. More resistant to beta-lactamases than most penicillins.

Classification (Generations):

GenerationExamplesKey Spectrum
1stCephalexin (oral), Cefazolin (IV)Gram-positives, basic gram-negatives (E. coli, Klebsiella, Proteus)
2ndCefuroxime, Cefoxitin, CefaclorExtended gram-negatives, anaerobes (cefoxitin)
3rdCeftriaxone, Cefotaxime, CeftazidimeBroad gram-negatives, CNS penetration; Ceftazidime covers Pseudomonas
4thCefepimeGram-positives + gram-negatives + Pseudomonas
5thCeftarolineMRSA + broad gram-negatives

Antibacterial Spectrum:

  • As generations increase, gram-negative coverage improves; gram-positive coverage relatively decreases
  • 3rd/4th generation: CNS penetration; useful for meningitis
  • 5th generation: covers MRSA

Therapeutic Use:

  • 1st gen: Surgical prophylaxis, skin/soft tissue, UTI
  • 2nd gen: Respiratory infections, intra-abdominal (cefoxitin)
  • 3rd gen: Meningitis (ceftriaxone), gonorrhea, serious gram-negative infections, typhoid
  • 4th gen: Febrile neutropenia, hospital-acquired infections
  • 5th gen: MRSA infections, CAP with MRSA risk

Resistance:

  • Extended-spectrum beta-lactamases (ESBLs) - destroy 3rd generation cephalosporins
  • AmpC beta-lactamases - encoded chromosomally in Enterobacter, Citrobacter
  • Modified PBPs
  • Efflux pumps, reduced porins

Adverse Effects:

  • Hypersensitivity - ~1-2% cross-reactivity with penicillin allergy
  • GI - nausea, diarrhea
  • Bleeding - some 3rd gen (cefoperazone) inhibit Vitamin K-dependent clotting factors
  • Disulfiram-like reaction (with alcohol - MTT side chain drugs)
  • Ceftriaxone - biliary sludging, pseudocholelithiasis in children

Q5. Carbapenems

Mechanism of Action:

Bind PBPs and inhibit transpeptidation of peptidoglycan cell wall synthesis. Bactericidal. Have highest stability against beta-lactamases (including ESBLs) - broadest beta-lactam spectrum.

Classification:

DrugKey Feature
Imipenem-CilastatinImipenem degraded by renal dehydropeptidase-I; cilastatin inhibits this enzyme
MeropenemMore stable to dehydropeptidase, better CNS penetration
ErtapenemOnce-daily dosing; NO Pseudomonas/Acinetobacter coverage
DoripenemCovers Pseudomonas

Antibacterial Spectrum:

Broadest of all antibiotics - covers:
  • Gram-positives (including Enterococcus - imipenem)
  • Gram-negatives including Pseudomonas (except ertapenem)
  • Anaerobes (Bacteroides fragilis)
  • ESBL-producing organisms
  • NOT active against MRSA, VRE, Stenotrophomonas

Therapeutic Use:

  • Polymicrobial infections, intra-abdominal sepsis
  • Hospital-acquired pneumonia, ventilator-associated pneumonia
  • Febrile neutropenia
  • Infections due to ESBL-producing organisms
  • Meningitis (meropenem preferred - less seizurogenic)
  • Last-resort therapy for multi-drug resistant organisms

Resistance:

  • Carbapenemases - KPC (Klebsiella pneumoniae carbapenemase), NDM-1 (New Delhi Metallo-beta-lactamase), OXA-type
  • Loss of porins (OmpK35/36 in Klebsiella) combined with ESBL production
  • Efflux pumps (in Pseudomonas)

Adverse Effects:

  • CNS: Seizures (imipenem more than meropenem - lower seizure threshold)
  • GI: Nausea, vomiting, diarrhea
  • Hypersensitivity: Cross-reactivity with penicillins (~1%)
  • C. difficile colitis - disrupts normal flora
  • Elevated liver transaminases (transient)

Q6. Tetracyclines

Mechanism of Action:

Bind 30S ribosomal subunit - block attachment of aminoacyl-tRNA to the A-site of the ribosome, thereby inhibiting protein synthesis. Bacteriostatic. Enter bacteria via active transport.

Classification:

GenerationExamples
Short-actingTetracycline, Oxytetracycline
Intermediate-actingDemeclocycline
Long-actingDoxycycline, Minocycline
Newer (glycylcycline)Tigecycline (overcomes efflux resistance)

Antibacterial Spectrum:

  • Gram-positives and gram-negatives (broad spectrum)
  • Atypicals: Chlamydia, Mycoplasma, Rickettsia, Coxiella, Brucella
  • Spirochetes (Lyme disease - Borrelia)
  • Some protozoa (malaria prophylaxis - doxycycline)
  • Acne (Propionibacterium acnes)

Therapeutic Use:

  • Chlamydia (drug of choice), Mycoplasma pneumonia
  • Rickettsia (Rocky Mountain spotted fever)
  • Lyme disease (early stages)
  • Acne vulgaris (long-term, low-dose doxycycline)
  • Cholera, Brucellosis, Q fever
  • SIADH (demeclocycline - causes nephrogenic DI)
  • Malaria prophylaxis (doxycycline)

Resistance:

  • Efflux pumps (tet genes) - most common mechanism
  • Ribosomal protection proteins - protect 30S subunit from drug
  • Tigecycline is less affected because it is a poor substrate for efflux pumps

Adverse Effects:

  • Tooth discoloration and enamel hypoplasia (children < 8 years, pregnancy) - CONTRAINDICATED
  • Photosensitivity (especially demeclocycline)
  • GI: Nausea, vomiting, esophageal ulceration (take with water upright)
  • Hepatotoxicity (high doses in pregnancy)
  • Renal: Fanconi syndrome (outdated/degraded tetracycline)
  • Vestibular effects - dizziness, vertigo (minocycline)
  • Chelate divalent cations (Ca2+, Mg2+, Fe2+) - impaired absorption with dairy/antacids

Q7. Aminoglycosides

Mechanism of Action:

  • Bind 30S ribosomal subunit (specifically 16S rRNA)
  • Cause misreading of mRNA - incorporation of wrong amino acids
  • Also cause membrane disruption - cell death
  • Concentration-dependent bactericidal - killing depends on peak concentration (Cmax/MIC ratio)
  • Require oxygen for uptake - therefore INACTIVE against anaerobes

Classification:

DrugKey Use
GentamicinGram-negative sepsis, synergy
TobramycinPseudomonas (especially in CF)
AmikacinResistant gram-negatives, MDR TB
StreptomycinTB, plague, tularemia
NeomycinTopical use, bowel prep, hepatic encephalopathy
SpectinomycinGonorrhea (alternative)

Antibacterial Spectrum:

  • Gram-negatives (primary): Pseudomonas, E. coli, Klebsiella, Enterobacter
  • Synergy with beta-lactams against gram-positives (Enterococcus, Streptococcus)
  • Mycobacteria (streptomycin, amikacin)
  • NOT anaerobes

Therapeutic Use:

  • Serious gram-negative infections (bacteremia, sepsis, UTI)
  • Pseudomonal infections (esp. tobramycin)
  • Combination therapy for Enterococcal endocarditis (synergy)
  • TB (streptomycin, amikacin - second-line)
  • Topical (neomycin) - skin infections, ophthalmology
  • Inhaled tobramycin - cystic fibrosis

Resistance:

  • Enzymatic modification (most common) - acetyltransferases, phosphotransferases, adenylyltransferases modify drug
  • Ribosomal mutation - altered 30S subunit
  • Reduced uptake - loss of membrane transport
  • Amikacin is least susceptible to enzymatic inactivation

Adverse Effects:

  • Nephrotoxicity (dose-dependent, reversible) - proximal tubular damage; monitor creatinine
  • Ototoxicity (cochlear + vestibular, often irreversible) - deafness, tinnitus, vertigo
  • Neuromuscular blockade - can worsen myasthenia gravis; use Ca2+ as antidote
  • Risk factors: prolonged use, high doses, renal failure, concurrent nephrotoxic drugs
  • Therapeutic drug monitoring is essential (peak and trough levels)

Q8. Macrolides

Mechanism of Action:

Bind 50S ribosomal subunit (23S rRNA) - block translocation step of protein synthesis (prevent movement of ribosome along mRNA). Bacteriostatic (bactericidal at high doses against susceptible organisms).

Classification:

DrugRouteKey Feature
ErythromycinOral/IVOriginal; GI prokinetic effect (motilin agonist)
ClarithromycinOralBetter bioavailability; H. pylori triple therapy
AzithromycinOral/IVLong half-life (68 hrs), tissue concentrations; once-daily; Z-pack
RoxithromycinOralSimilar to erythromycin
TelithromycinOralKetolide; covers macrolide-resistant strains

Antibacterial Spectrum:

  • Gram-positives: Streptococcus, Staphylococcus (not MRSA)
  • Atypicals: Mycoplasma, Chlamydia, Legionella, Bordetella, Campylobacter
  • Mycobacteria (clarithromycin - MAC prophylaxis/treatment in HIV)
  • Spirochetes (early Lyme disease)
  • H. pylori (clarithromycin component of triple therapy)

Therapeutic Use:

  • Community-acquired pneumonia (CAP) - drug of choice for atypical coverage
  • Streptococcal infections in penicillin-allergic patients
  • Pertussis (whooping cough)
  • STIs: Chlamydia, Ureaplasma (azithromycin 1g single dose)
  • MAC prophylaxis/treatment in HIV (clarithromycin/azithromycin)
  • H. pylori eradication (clarithromycin + amoxicillin + PPI)
  • GI prokinetic (erythromycin)

Resistance:

  • Methylation of 23S rRNA (erm genes) - most common; also confers cross-resistance to lincosamides and streptogramin B (MLS resistance)
  • Efflux pumps (mef genes)
  • Ribosomal mutations

Adverse Effects:

  • GI (most common): Nausea, vomiting, diarrhea, abdominal cramps (especially erythromycin)
  • QT prolongation - risk of arrhythmias (torsades de pointes); avoid with other QT-prolonging drugs
  • Hepatotoxicity - cholestatic jaundice (erythromycin estolate)
  • Drug interactions - potent CYP3A4 inhibitors (erythromycin, clarithromycin)
  • Ototoxicity - rare, high doses of erythromycin
  • Telithromycin - hepatotoxicity, visual disturbances

Q9. Quinolones (Fluoroquinolones)

Mechanism of Action:

Inhibit bacterial DNA gyrase (topoisomerase II) and topoisomerase IV - enzymes required for DNA supercoiling, replication, and repair. This causes DNA strand breaks. Concentration-dependent bactericidal.
  • DNA gyrase: primary target in gram-negatives
  • Topoisomerase IV: primary target in gram-positives

Classification:

GenerationExamplesKey Coverage Added
1stNalidixic acidGram-negatives (UTI only)
2ndCiprofloxacin, Norfloxacin, OfloxacinEnhanced gram-negatives, Pseudomonas (cipro)
3rdLevofloxacin+ Gram-positives, atypicals (respiratory)
4thMoxifloxacin, Gemifloxacin+ Anaerobes, enhanced gram-positives

Antibacterial Spectrum:

  • Gram-negatives (excellent): Enterobacteriaceae, Pseudomonas (ciprofloxacin)
  • Gram-positives (3rd/4th gen): Pneumococcus, Streptococcus
  • Atypicals: Mycoplasma, Chlamydia, Legionella
  • Mycobacteria (moxifloxacin - 2nd line TB)
  • Anaerobes (moxifloxacin)

Therapeutic Use:

  • UTIs and complicated UTIs (ciprofloxacin, norfloxacin)
  • Respiratory infections/CAP (levofloxacin, moxifloxacin - "respiratory quinolones")
  • Typhoid fever, traveler's diarrhea
  • Anthrax (ciprofloxacin - drug of choice)
  • STIs: Gonorrhea (but resistance increasing)
  • TB - 2nd line (moxifloxacin, levofloxacin)
  • Bone and joint infections

Resistance:

  • Mutations in DNA gyrase (gyrA) and topoisomerase IV (parC) genes
  • Efflux pumps - most common in Pseudomonas
  • Plasmid-mediated resistance (qnr genes) - protect topoisomerases
  • Resistance can develop rapidly during therapy (step-wise mutations)

Adverse Effects:

  • Tendinopathy and tendon rupture (Achilles tendon) - especially in elderly + corticosteroids; BLACK BOX WARNING
  • CNS: Headache, dizziness, insomnia; rarely seizures (lower seizure threshold)
  • QT prolongation - risk of arrhythmias
  • Photosensitivity (especially sparfloxacin)
  • GI: Nausea, diarrhea
  • Cartilage damage - CONTRAINDICATED in children < 18 years and pregnancy
  • Peripheral neuropathy - may be irreversible
  • Drug interactions: chelation with antacids, Mg2+, Fe2+

Q10. Sulfonamides

Mechanism of Action:

Structural analogs of PABA (para-aminobenzoic acid) - competitively inhibit dihydropteroate synthase, blocking bacterial folate synthesis. Bacteria cannot use exogenous folate (unlike humans), making this selectively toxic. Bacteriostatic.
Trimethoprim (often combined) blocks the next step - inhibits dihydrofolate reductase - producing sequential blockade of folate synthesis (synergistic combination = TMP-SMX / Co-trimoxazole).

Classification:

TypeExamples
Short-acting (systemic)Sulfamethoxazole (used with TMP), Sulfisoxazole
Long-actingSulfadoxine (with pyrimethamine - malaria)
TopicalSilver sulfadiazine (burns), Sulfacetamide (eye drops)
IntestinalSulfasalazine (IBD, RA)

Antibacterial Spectrum:

  • Gram-positives and gram-negatives (broad spectrum)
  • Nocardia, Pneumocystis jirovecii (PCP)
  • Toxoplasma (with pyrimethamine)
  • Malaria (sulfadoxine-pyrimethamine)

Therapeutic Use:

  • TMP-SMX: UTIs (first-line), PCP (treatment and prophylaxis in HIV)
  • PCP treatment (high-dose TMP-SMX = drug of choice)
  • Toxoplasmosis prophylaxis in HIV (TMP-SMX)
  • Nocardiosis
  • Traveler's diarrhea
  • Sulfadoxine-pyrimethamine: Malaria (Fansidar)
  • Silver sulfadiazine: Burn wound infections
  • Sulfasalazine: Ulcerative colitis, Crohn's, rheumatoid arthritis

Resistance:

  • Mutation in dihydropteroate synthase (reduced drug binding)
  • Overproduction of PABA by bacteria
  • Plasmid-mediated resistance acquisition

Adverse Effects:

  • Hypersensitivity: Rash, Stevens-Johnson syndrome (severe - life-threatening)
  • Hematologic: Hemolytic anemia (in G6PD deficiency), agranulocytosis, thrombocytopenia
  • Renal: Crystalluria and nephrotoxicity (maintain good hydration)
  • Kernicterus - displace bilirubin from albumin - CONTRAINDICATED in neonates/late pregnancy
  • Drug interactions: Displace warfarin, methotrexate from albumin
  • Photosensitivity

Q11. Antimycobacterial Drugs (Treatment of Tuberculosis)

First-Line Drugs (RIPE):

DrugMechanismKey Feature
Rifampicin (R)Inhibits DNA-dependent RNA polymerase - blocks transcriptionBactericidal; penetrates CSF, macrophages
Isoniazid (I)Inhibits mycolic acid synthesis (InhA enzyme) - requires activation by KatGBactericidal; best drug for TB
Pyrazinamide (P/Z)Disrupts membrane energetics at acidic pH (in macrophage lysosomes)Bactericidal; kills dormant intracellular bacteria
Ethambutol (E)Inhibits arabinosyl transferase - blocks arabinogalactan cell wall synthesisBacteriostatic; added to prevent resistance

Standard Regimen:

  • Intensive phase (2 months): RIPE (all four drugs)
  • Continuation phase (4 months): RI (Rifampicin + Isoniazid)
  • Total: 6 months for drug-sensitive TB

Second-Line Drugs (for MDR-TB and XDR-TB):

  • Fluoroquinolones (Moxifloxacin, Levofloxacin)
  • Injectable agents (Amikacin, Streptomycin, Capreomycin)
  • Newer drugs: Bedaquiline (inhibits ATP synthase), Linezolid, Delamanid

Resistance:

  • MDR-TB: Resistant to at least Rifampicin + Isoniazid
  • XDR-TB: MDR-TB + resistant to fluoroquinolones and injectable agents
  • Mechanisms: Mutations in rpoB (rifampicin), katG/inhA (isoniazid), pncA (pyrazinamide), embB (ethambutol)
  • Poor adherence is the most common cause of acquired resistance

Adverse Effects:

DrugKey Adverse Effects
RifampicinOrange-red discoloration of body fluids; hepatotoxicity; induces CYP450 (many drug interactions); flu-like syndrome
IsoniazidPeripheral neuropathy (give pyridoxine/B6 prophylactically); hepatotoxicity; drug-induced lupus; sideroblastic anemia
PyrazinamideHyperuricemia/gout; hepatotoxicity
EthambutolOptic neuritis (dose-dependent, reversible if stopped) - check visual acuity regularly

Q12. Antifungal Drugs

Classification:

ClassDrugsMechanism
PolyenesAmphotericin B, NystatinBind ergosterol in fungal membrane - form pores - cell lysis
AzolesFluconazole, Itraconazole, Voriconazole, Posaconazole, KetoconazoleInhibit CYP51 (lanosterol 14-alpha-demethylase) - block ergosterol synthesis
EchinocandinsCaspofungin, Micafungin, AnidulafunginInhibit beta-1,3-glucan synthase - block cell wall synthesis
Pyrimidine analogsFlucytosine (5-FC)Converted to 5-FU intracellularly - inhibits DNA/RNA synthesis
AllylaminesTerbinafineInhibit squalene epoxidase - block ergosterol synthesis
TopicalClotrimazole, Miconazole, NystatinLocal fungal infections

Antifungal Spectrum & Therapeutic Use:

DrugKey Uses
Amphotericin BGold standard for severe systemic fungal infections (Aspergillus, Cryptococcus, Mucor, Candida); liposomal form reduces toxicity
FluconazoleCandidiasis (oropharyngeal, vaginal, systemic); Cryptococcal meningitis maintenance
VoriconazoleDrug of choice for Aspergillosis; also covers Fusarium
PosaconazoleProphylaxis in neutropenic patients; Mucormycosis
ItraconazoleHistoplasmosis, Blastomycosis, Sporotrichosis, onychomycosis
CaspofunginInvasive Candidiasis, Aspergillus (second-line), febrile neutropenia
FlucytosineCryptococcal meningitis (combined with Amphotericin B)
TerbinafineDermatophytes (tinea), onychomycosis (nail fungus)

Resistance:

  • Azoles: Mutations in CYP51 (ERG11), efflux pump upregulation (CDR genes in Candida)
  • Echinocandins: Mutations in FKS1/FKS2 (glucan synthase genes)
  • Amphotericin B: Reduced ergosterol content in membrane (rare resistance)

Adverse Effects:

  • Amphotericin B: Infusion reactions ("shake and bake" - fever, rigors, chills); nephrotoxicity (dose-limiting); hypokalemia, hypomagnesemia; anemia
  • Azoles: Hepatotoxicity; CYP450 inhibition (major drug interactions); QT prolongation (voriconazole); visual disturbances (voriconazole); teratogenic (CONTRAINDICATED in pregnancy)
  • Echinocandins: Well-tolerated; hepatotoxicity (mild); histamine release (caspofungin)
  • Flucytosine: Bone marrow suppression; GI toxicity; monitor blood levels

Q13. Antiviral Drugs for Herpes Virus Infections

Classification & Mechanism of Action:

DrugMechanismSpectrum
AcyclovirNucleoside analog - phosphorylated by viral thymidine kinase (TK) to acyclovir-triphosphate - inhibits viral DNA polymerase and causes chain terminationHSV-1, HSV-2, VZV
ValacyclovirProdrug of acyclovir; better oral bioavailabilityHSV-1, HSV-2, VZV, EBV
FamciclovirProdrug of penciclovir; similar to acyclovirHSV-1, HSV-2, VZV
GanciclovirSimilar mechanism to acyclovir; phosphorylated by viral UL97 kinaseCMV (primary drug)
ValganciclovirProdrug of ganciclovir; better oral bioavailabilityCMV
FoscarnetDirectly inhibits viral DNA polymerase (pyrophosphate analog) - does NOT require viral kinase activationHSV (TK-deficient resistant), CMV, VZV
CidofovirNucleotide analog; inhibits viral DNA polymerase; requires only host cell kinaseCMV, resistant HSV
TrifluridineInhibits viral DNA polymeraseHSV keratitis (topical)

Therapeutic Use:

  • HSV-1/HSV-2 (genital herpes, cold sores): Acyclovir, Valacyclovir, Famciclovir
  • HSV encephalitis: IV Acyclovir (drug of choice)
  • Herpes Zoster (shingles/VZV): Valacyclovir, Famciclovir (better for VZV)
  • Neonatal herpes: IV Acyclovir
  • CMV retinitis/colitis (in HIV): Ganciclovir/Valganciclovir (first-line)
  • CMV resistant to ganciclovir: Foscarnet, Cidofovir
  • Acyclovir-resistant HSV: Foscarnet

Adverse Effects:

  • Acyclovir: Generally well tolerated; nephrotoxicity (crystalluria - maintain hydration); encephalopathy (high IV doses); phlebitis
  • Ganciclovir: Myelosuppression (neutropenia, thrombocytopenia - dose-limiting); teratogenic/carcinogenic; avoid with zidovudine (additive myelosuppression)
  • Foscarnet: Nephrotoxicity (major); hypocalcemia (chelates Ca2+) - causes seizures, arrhythmias; electrolyte imbalances
  • Cidofovir: Severe nephrotoxicity (give with probenecid and IV saline for protection)

Q14. Antiviral Drugs for HIV (Antiretroviral Therapy - ART)

Mechanism of Action & Classification:

ClassDrugsMechanism
NRTIs (Nucleoside Reverse Transcriptase Inhibitors)Zidovudine (AZT), Lamivudine (3TC), Emtricitabine, Tenofovir, Abacavir, StavudineIncorporated into viral DNA - cause chain termination; competitively inhibit reverse transcriptase
NNRTIs (Non-Nucleoside Reverse Transcriptase Inhibitors)Efavirenz, Nevirapine, Rilpivirine, EtravirineBind allosterically to reverse transcriptase (different site than NRTIs) - conformational change - inhibit enzyme
Protease Inhibitors (PIs)Ritonavir, Lopinavir, Atazanavir, Darunavir, SaquinavirInhibit HIV protease - prevent cleavage of polyprotein precursors - produce immature, non-infectious virions
Integrase Inhibitors (INSTIs)Raltegravir, Dolutegravir, Bictegravir, ElvitegravirInhibit HIV integrase - prevent insertion of viral DNA into host genome
Fusion InhibitorsEnfuvirtide (T-20)Bind gp41 - prevent conformational change needed for fusion of viral envelope with cell membrane
CCR5 AntagonistsMaravirocBlock CCR5 co-receptor on host CD4+ cell - prevent HIV entry
Post-Attachment InhibitorsIbalizumabBind CD4 receptor - block viral attachment

Current Standard Regimen:

2 NRTIs + 1 INSTI (preferred - e.g., Tenofovir/Emtricitabine + Dolutegravir = TLD)

Therapeutic Use:

  • Treatment of HIV infection (reduce viral load to undetectable, preserve CD4 count)
  • Prevention of opportunistic infections
  • PrEP (Pre-Exposure Prophylaxis): Tenofovir/Emtricitabine (Truvada)
  • PEP (Post-Exposure Prophylaxis): 3-drug ART within 72 hours
  • Prevention of mother-to-child transmission (PMTCT)
  • Goal: Undetectable viral load = untransmittable (U=U)

Resistance:

  • High mutation rate of reverse transcriptase (no proofreading)
  • NRTI: M184V mutation (lamivudine/emtricitabine); K65R (tenofovir)
  • NNRTI: K103N (efavirenz/nevirapine) - single mutation causes high-level resistance
  • PI: Multiple mutations needed; boosting with ritonavir compensates
  • Prevention: Combination therapy (HAART) - multiple simultaneous mutations required

Adverse Effects:

Drug/ClassKey Toxicity
Zidovudine (AZT)Bone marrow suppression (anemia, neutropenia), mitochondrial toxicity, lactic acidosis
TenofovirNephrotoxicity, Fanconi syndrome, bone demineralization
AbacavirHypersensitivity reaction (HLA-B*5701 allele - screen before use)
NNRTIsHepatotoxicity (nevirapine); CNS effects - vivid dreams, dizziness (efavirenz); rash
Protease InhibitorsLipodystrophy, dyslipidemia, hyperglycemia/diabetes, GI intolerance; ritonavir - major CYP3A4 inhibitor
INSTIsGenerally well tolerated; weight gain; insomnia
EnfuvirtideInjection site reactions (subcutaneous injection)
MaravirocHepatotoxicity; requires tropism testing (only for CCR5-tropic virus)

Q15. Antiseptics

Definition:

Antiseptics are antimicrobial agents applied to living tissue (skin/mucous membranes) to reduce or eliminate microorganisms. They differ from disinfectants (used on inanimate objects) and antibiotics (systemic agents).

Classification & Mechanisms of Action:

ClassExamplesMechanism
HalogensIodine (Povidone-iodine), Chlorine compounds (hypochlorite)Oxidize sulfhydryl groups of proteins; disrupt cell membrane; denature proteins
AlcoholsEthanol (70%), IsopropanolProtein denaturation, lipid dissolution, membrane disruption
BiguanidesChlorhexidineDisrupts bacterial cell membrane - causes lysis; binds to skin (residual activity)
Quaternary Ammonium CompoundsBenzalkonium chloride, CetrimideDisrupt cell membrane, denature proteins
Oxidizing agentsHydrogen peroxide, Potassium permanganateGenerate free radicals that oxidize cellular components
Heavy metal compoundsSilver nitrate, Silver sulfadiazinePrecipitate proteins; silver ions inhibit bacterial enzymes
Phenolic compoundsPhenol, Chloroxylenol (Dettol)Denature proteins, disrupt cell membranes
AldehydesGlutaraldehyde, FormaldehydeCross-link proteins and nucleic acids (mainly disinfectants, some topical use)
Acridine dyesAcriflavineIntercalate into DNA, inhibit replication

Therapeutic & Practical Use:

  • Povidone-iodine: Wound antisepsis, surgical scrub, mucosal disinfection, vaginal infections
  • Chlorhexidine: Surgical hand scrub, wound care, oral rinse (gingivitis), catheter site care, neonatal eye care; has residual activity (adsorbs to skin)
  • Ethanol 70%: Hand sanitization, skin preparation before injection
  • Hydrogen peroxide: Wound cleaning (mechanical debridement via oxygen release), ear wax
  • Silver sulfadiazine: Burns (antibacterial + antifungal coverage)
  • Benzalkonium chloride: Eye drops, wound care, skin antisepsis
  • Potassium permanganate: Fungal skin infections, eczema (wet dressings)

Resistance:

  • Intrinsic resistance in some organisms (e.g., spores, mycobacteria resist alcohols)
  • Biofilm formation - significant protective barrier
  • Efflux pumps - e.g., qac genes (quaternary ammonium compound resistance) in Staphylococcus
  • Cross-resistance between antiseptics and antibiotics (e.g., qac gene expression associated with MRSA efflux pumps)
  • Generally, resistance is less problematic than with antibiotics

Adverse Effects:

  • Iodine: Skin irritation; iodine allergy; systemic absorption causing thyroid dysfunction (prolonged use)
  • Chlorhexidine: Rare hypersensitivity (anaphylaxis possible); ototoxic (do NOT use in the ear canal); staining of teeth and tongue (oral use)
  • Alcohols: Skin drying, dermatitis; flammable; ineffective against spores
  • Hydrogen peroxide: Tissue damage at high concentrations; gas embolism (in deep wounds)
  • Silver compounds: Argyria (blue-grey skin discoloration with prolonged use)
  • Phenols: Skin irritation, necrosis; systemic absorption causes CNS toxicity
  • Quaternary ammonium compounds: Skin irritation; anaphylaxis (rare)

Key Exam Tips:
  • Beta-lactams (penicillins, cephalosporins, carbapenems) all inhibit cell wall synthesis via PBPs
  • Aminoglycosides and tetracyclines both target 30S; macrolides target 50S
  • Fluoroquinolones = concentration-dependent; beta-lactams = time-dependent
  • TB treatment: RIPE x 2 months + RI x 4 months = 6 months total
  • HIV standard regimen: 2 NRTIs + 1 INSTI
  • Foscarnet does NOT need viral kinase activation (used for acyclovir/ganciclovir-resistant infections)

Re write it same to same , without altering any single word - 1. Classification of Antibiotics by Mechanism of Action 1. Inhibitors of Cell Wall Synthesis Penicillins Cephalosporins Carbapenems Vancomycin 2. Inhibitors of Protein Synthesis Aminoglycosides (30S) Tetracyclines (30S) Macrolides (50S) Chloramphenicol (50S) 3. Inhibitors of Nucleic Acid Synthesis Quinolones (DNA replication) Rifampicin (RNA synthesis) Metronidazole 4. Antimetabolites Sulfonamides Trimethoprim 5. Cell Membrane Disruptors Polymyxins Daptomycin --- 2. Mechanisms of Bacterial Resistance to Antibiotics Mechanisms Enzymatic destruction of drug (β-lactamases). Alteration of target site. Decreased permeability of bacterial cell wall. Active efflux pumps. Bypass of metabolic pathway. Prevention and Control Rational antibiotic use. Culture and sensitivity testing. Complete treatment course. Avoid unnecessary prescriptions. Combination therapy when indicated. Hospital infection-control measures. Surveillance of resistant strains. --- 3. Penicillins Mechanism of Action Inhibit bacterial cell wall synthesis by binding penicillin-binding proteins (PBPs). Antibacterial Spectrum Mainly Gram-positive bacteria. Some Gram-negative organisms. Classification Natural: Penicillin G, Penicillin V. Penicillinase-resistant: Oxacillin, Cloxacillin. Aminopenicillins: Ampicillin, Amoxicillin. Antipseudomonal: Piperacillin, Ticarcillin. Therapeutic Uses Streptococcal infections. Syphilis. Meningitis. Respiratory and urinary tract infections. Resistance β-lactamase production. Altered PBPs. Reduced permeability. Adverse Effects Hypersensitivity reactions. Rash. Diarrhea. Anaphylaxis. --- 4. Cephalosporins Mechanism of Action Inhibit bacterial cell wall synthesis. Antibacterial Spectrum Broad-spectrum activity. Later generations have greater Gram-negative coverage. Classification 1st: Cefazolin, Cephalexin. 2nd: Cefuroxime. 3rd: Ceftriaxone, Ceftazidime. 4th: Cefepime. 5th: Ceftaroline. Therapeutic Uses Pneumonia. Meningitis. Sepsis. Urinary tract infections. Resistance β-lactamases. Altered PBPs. Adverse Effects Allergy. Diarrhea. Superinfection. Rare nephrotoxicity. --- 5. Carbapenems Mechanism of Action Inhibit bacterial cell wall synthesis. Classification Imipenem. Meropenem. Ertapenem. Doripenem. Antibacterial Spectrum Very broad spectrum. Effective against Gram-positive, Gram-negative and anaerobic bacteria. Therapeutic Uses Severe hospital-acquired infections. Sepsis. Complicated intra-abdominal infections. Resistance Carbapenemase enzymes. Efflux pumps. Porin mutations. Adverse Effects Nausea. Diarrhea. Rash. Seizures (especially imipenem). --- 6. Tetracyclines Mechanism of Action Bind 30S ribosomal subunit and inhibit protein synthesis. Classification Tetracycline. Doxycycline. Minocycline. Antibacterial Spectrum Broad spectrum. Effective against atypical organisms. Therapeutic Uses Acne. Cholera. Rickettsial infections. Chlamydia. Lyme disease. Resistance Efflux pumps. Ribosomal protection proteins. Adverse Effects Gastrointestinal irritation. Photosensitivity. Teeth discoloration. Hepatotoxicity. --- 7. Aminoglycosides Mechanism of Action Irreversibly bind 30S ribosomal subunit causing defective protein synthesis. Classification Gentamicin. Amikacin. Tobramycin. Streptomycin. Antibacterial Spectrum Mainly aerobic Gram-negative bacilli. Therapeutic Uses Severe systemic infections. Tuberculosis (streptomycin). Sepsis. Resistance Drug-inactivating enzymes. Ribosomal mutations. Adverse Effects Nephrotoxicity. Ototoxicity. Neuromuscular blockade. --- 8. Macrolides Mechanism of Action Bind 50S ribosomal subunit and inhibit protein synthesis. Classification Erythromycin. Clarithromycin. Azithromycin. Antibacterial Spectrum Gram-positive cocci. Atypical organisms. Therapeutic Uses Respiratory tract infections. Mycoplasma pneumonia. Chlamydial infections. Resistance Ribosomal modification. Efflux pumps. Adverse Effects Nausea. Diarrhea. QT prolongation. Cholestatic hepatitis. --- 9. Quinolones Mechanism of Action Inhibit DNA gyrase and topoisomerase IV. Classification Ciprofloxacin. Levofloxacin. Moxifloxacin. Ofloxacin. Antibacterial Spectrum Broad-spectrum activity. Excellent Gram-negative coverage. Therapeutic Uses UTIs. Gastrointestinal infections. Respiratory infections. Resistance DNA gyrase mutations. Efflux pumps. Adverse Effects Tendon rupture. QT prolongation. Gastrointestinal upset. CNS effects. --- 10. Sulfonamides Mechanism of Action Inhibit folic acid synthesis by blocking dihydropteroate synthase. Classification Sulfamethoxazole. Sulfadiazine. Sulfisoxazole. Antibacterial Spectrum Broad-spectrum bacteriostatic agents. Therapeutic Uses Urinary tract infections. Pneumocystis jirovecii pneumonia. Toxoplasmosis. Resistance Altered enzyme. Increased PABA production. Adverse Effects Hypersensitivity. Stevens–Johnson syndrome. Hemolysis in G6PD deficiency. Crystalluria. --- 11. Antimycobacterial Drugs (Tuberculosis) First-Line Drugs Isoniazid (INH) Rifampicin Pyrazinamide Ethambutol Streptomycin Mechanisms of Action INH: inhibits mycolic acid synthesis. Rifampicin: inhibits RNA polymerase. Pyrazinamide: disrupts membrane function. Ethambutol: inhibits cell wall synthesis. Streptomycin: inhibits protein synthesis. Therapeutic Use Pulmonary and extrapulmonary tuberculosis. Resistance Gene mutations due to inadequate therapy. Adverse Effects INH: peripheral neuropathy, hepatitis. Rifampicin: hepatotoxicity, orange secretions. Ethambutol: optic neuritis. Pyrazinamide: hyperuricemia. Streptomycin: ototoxicity. --- 12. Antifungal Drugs Classification Polyenes: Amphotericin B, Nystatin. Azoles: Fluconazole, Ketoconazole. Echinocandins: Caspofungin. Antimetabolite: Flucytosine. Allylamines: Terbinafine. Spectrum and Uses Candidiasis. Aspergillosis. Cryptococcosis. Dermatophyte infections. Resistance Altered ergosterol synthesis. Efflux pumps. Adverse Effects Amphotericin B: nephrotoxicity. Azoles: hepatotoxicity. Flucytosine: bone marrow suppression. --- 13. Antiviral Drugs for Herpes Virus Infection Classification and Mechanism Acyclovir, Valacyclovir, Famciclovir: Inhibit viral DNA polymerase. Ganciclovir: Active against CMV. Therapeutic Uses Herpes simplex virus (HSV). Varicella-zoster virus (VZV). Cytomegalovirus (CMV). Adverse Effects Nausea. Headache. Nephrotoxicity (acyclovir). Bone marrow suppression (ganciclovir). --- 14. Antiviral Drugs for HIV Classification and Mechanism NRTIs Zidovudine, Lamivudine, Tenofovir. Inhibit reverse transcriptase. NNRTIs Efavirenz, Nevirapine. Directly inhibit reverse transcriptase. Protease Inhibitors Ritonavir, Atazanavir. Inhibit viral protease. Integrase Inhibitors Dolutegravir, Raltegravir. Prevent integration of viral DNA. Entry/Fusion Inhibitors Enfuvirtide, Maraviroc. Therapeutic Use Combination therapy (HAART/ART) for HIV infection. Adverse Effects Hepatotoxicity. Lipodystrophy. Metabolic abnormalities. Gastrointestinal disturbances. --- 15. Antiseptics Definition Chemical agents applied to living tissues to prevent or inhibit microbial growth. Classification Alcohols: Ethanol, Isopropanol. Halogens: Iodine, Povidone-iodine. Oxidizing agents: Hydrogen peroxide. Biguanides: Chlorhexidine. Phenolic compounds. Mechanism of Action Protein denaturation. Oxidation. Cell membrane disruption. Enzyme inhibition. Therapeutic and Practical Uses Hand disinfection. Surgical skin preparation. Wound cleansing. Prevention of infection. Resistance Rare but may occur through efflux mechanisms and biofilm formation. Adverse Effects Skin irritation. Allergic reactions. Chemical burns with improper use.

ANTIMICROBIAL & ANTIVIRAL DRUGS


1. Classification of Antibiotics by Mechanism of Action

1. Inhibitors of Cell Wall Synthesis
  • Penicillins
  • Cephalosporins
  • Carbapenems
  • Vancomycin
2. Inhibitors of Protein Synthesis
  • Aminoglycosides (30S)
  • Tetracyclines (30S)
  • Macrolides (50S)
  • Chloramphenicol (50S)
3. Inhibitors of Nucleic Acid Synthesis
  • Quinolones (DNA replication)
  • Rifampicin (RNA synthesis)
  • Metronidazole
4. Antimetabolites
  • Sulfonamides
  • Trimethoprim
5. Cell Membrane Disruptors
  • Polymyxins
  • Daptomycin

2. Mechanisms of Bacterial Resistance to Antibiotics

Mechanisms
  • Enzymatic destruction of drug (β-lactamases).
  • Alteration of target site.
  • Decreased permeability of bacterial cell wall.
  • Active efflux pumps.
  • Bypass of metabolic pathway.
Prevention and Control
  • Rational antibiotic use.
  • Culture and sensitivity testing.
  • Complete treatment course.
  • Avoid unnecessary prescriptions.
  • Combination therapy when indicated.
  • Hospital infection-control measures.
  • Surveillance of resistant strains.

3. Penicillins

Mechanism of Action Inhibit bacterial cell wall synthesis by binding penicillin-binding proteins (PBPs).
Antibacterial Spectrum
  • Mainly Gram-positive bacteria.
  • Some Gram-negative organisms.
Classification
  • Natural: Penicillin G, Penicillin V.
  • Penicillinase-resistant: Oxacillin, Cloxacillin.
  • Aminopenicillins: Ampicillin, Amoxicillin.
  • Antipseudomonal: Piperacillin, Ticarcillin.
Therapeutic Uses
  • Streptococcal infections.
  • Syphilis.
  • Meningitis.
  • Respiratory and urinary tract infections.
Resistance
  • β-lactamase production.
  • Altered PBPs.
  • Reduced permeability.
Adverse Effects
  • Hypersensitivity reactions.
  • Rash.
  • Diarrhea.
  • Anaphylaxis.

4. Cephalosporins

Mechanism of Action Inhibit bacterial cell wall synthesis.
Antibacterial Spectrum
  • Broad-spectrum activity.
  • Later generations have greater Gram-negative coverage.
Classification
  • 1st: Cefazolin, Cephalexin.
  • 2nd: Cefuroxime.
  • 3rd: Ceftriaxone, Ceftazidime.
  • 4th: Cefepime.
  • 5th: Ceftaroline.
Therapeutic Uses
  • Pneumonia.
  • Meningitis.
  • Sepsis.
  • Urinary tract infections.
Resistance
  • β-lactamases.
  • Altered PBPs.
Adverse Effects
  • Allergy.
  • Diarrhea.
  • Superinfection.
  • Rare nephrotoxicity.

5. Carbapenems

Mechanism of Action Inhibit bacterial cell wall synthesis.
Classification
  • Imipenem.
  • Meropenem.
  • Ertapenem.
  • Doripenem.
Antibacterial Spectrum
  • Very broad spectrum.
  • Effective against Gram-positive, Gram-negative and anaerobic bacteria.
Therapeutic Uses
  • Severe hospital-acquired infections.
  • Sepsis.
  • Complicated intra-abdominal infections.
Resistance
  • Carbapenemase enzymes.
  • Efflux pumps.
  • Porin mutations.
Adverse Effects
  • Nausea.
  • Diarrhea.
  • Rash.
  • Seizures (especially imipenem).

6. Tetracyclines

Mechanism of Action Bind 30S ribosomal subunit and inhibit protein synthesis.
Classification
  • Tetracycline.
  • Doxycycline.
  • Minocycline.
Antibacterial Spectrum
  • Broad spectrum.
  • Effective against atypical organisms.
Therapeutic Uses
  • Acne.
  • Cholera.
  • Rickettsial infections.
  • Chlamydia.
  • Lyme disease.
Resistance
  • Efflux pumps.
  • Ribosomal protection proteins.
Adverse Effects
  • Gastrointestinal irritation.
  • Photosensitivity.
  • Teeth discoloration.
  • Hepatotoxicity.

7. Aminoglycosides

Mechanism of Action Irreversibly bind 30S ribosomal subunit causing defective protein synthesis.
Classification
  • Gentamicin.
  • Amikacin.
  • Tobramycin.
  • Streptomycin.
Antibacterial Spectrum Mainly aerobic Gram-negative bacilli.
Therapeutic Uses
  • Severe systemic infections.
  • Tuberculosis (streptomycin).
  • Sepsis.
Resistance
  • Drug-inactivating enzymes.
  • Ribosomal mutations.
Adverse Effects
  • Nephrotoxicity.
  • Ototoxicity.
  • Neuromuscular blockade.

8. Macrolides

Mechanism of Action Bind 50S ribosomal subunit and inhibit protein synthesis.
Classification
  • Erythromycin.
  • Clarithromycin.
  • Azithromycin.
Antibacterial Spectrum
  • Gram-positive cocci.
  • Atypical organisms.
Therapeutic Uses
  • Respiratory tract infections.
  • Mycoplasma pneumonia.
  • Chlamydial infections.
Resistance
  • Ribosomal modification.
  • Efflux pumps.
Adverse Effects
  • Nausea.
  • Diarrhea.
  • QT prolongation.
  • Cholestatic hepatitis.

9. Quinolones

Mechanism of Action Inhibit DNA gyrase and topoisomerase IV.
Classification
  • Ciprofloxacin.
  • Levofloxacin.
  • Moxifloxacin.
  • Ofloxacin.
Antibacterial Spectrum
  • Broad-spectrum activity.
  • Excellent Gram-negative coverage.
Therapeutic Uses
  • UTIs.
  • Gastrointestinal infections.
  • Respiratory infections.
Resistance
  • DNA gyrase mutations.
  • Efflux pumps.
Adverse Effects
  • Tendon rupture.
  • QT prolongation.
  • Gastrointestinal upset.
  • CNS effects.

10. Sulfonamides

Mechanism of Action Inhibit folic acid synthesis by blocking dihydropteroate synthase.
Classification
  • Sulfamethoxazole.
  • Sulfadiazine.
  • Sulfisoxazole.
Antibacterial Spectrum Broad-spectrum bacteriostatic agents.
Therapeutic Uses
  • Urinary tract infections.
  • Pneumocystis jirovecii pneumonia.
  • Toxoplasmosis.
Resistance
  • Altered enzyme.
  • Increased PABA production.
Adverse Effects
  • Hypersensitivity.
  • Stevens-Johnson syndrome.
  • Hemolysis in G6PD deficiency.
  • Crystalluria.

11. Antimycobacterial Drugs (Tuberculosis)

First-Line Drugs
  • Isoniazid (INH)
  • Rifampicin
  • Pyrazinamide
  • Ethambutol
  • Streptomycin
Mechanisms of Action
  • INH: inhibits mycolic acid synthesis.
  • Rifampicin: inhibits RNA polymerase.
  • Pyrazinamide: disrupts membrane function.
  • Ethambutol: inhibits cell wall synthesis.
  • Streptomycin: inhibits protein synthesis.
Therapeutic Use Pulmonary and extrapulmonary tuberculosis.
Resistance Gene mutations due to inadequate therapy.
Adverse Effects
  • INH: peripheral neuropathy, hepatitis.
  • Rifampicin: hepatotoxicity, orange secretions.
  • Ethambutol: optic neuritis.
  • Pyrazinamide: hyperuricemia.
  • Streptomycin: ototoxicity.

12. Antifungal Drugs

Classification
  • Polyenes: Amphotericin B, Nystatin.
  • Azoles: Fluconazole, Ketoconazole.
  • Echinocandins: Caspofungin.
  • Antimetabolite: Flucytosine.
  • Allylamines: Terbinafine.
Spectrum and Uses
  • Candidiasis.
  • Aspergillosis.
  • Cryptococcosis.
  • Dermatophyte infections.
Resistance
  • Altered ergosterol synthesis.
  • Efflux pumps.
Adverse Effects
  • Amphotericin B: nephrotoxicity.
  • Azoles: hepatotoxicity.
  • Flucytosine: bone marrow suppression.

13. Antiviral Drugs for Herpes Virus Infection

Classification and Mechanism
  • Acyclovir, Valacyclovir, Famciclovir:
    • Inhibit viral DNA polymerase.
  • Ganciclovir:
    • Active against CMV.
Therapeutic Uses
  • Herpes simplex virus (HSV).
  • Varicella-zoster virus (VZV).
  • Cytomegalovirus (CMV).
Adverse Effects
  • Nausea.
  • Headache.
  • Nephrotoxicity (acyclovir).
  • Bone marrow suppression (ganciclovir).

14. Antiviral Drugs for HIV

Classification and Mechanism
NRTIs - Zidovudine, Lamivudine, Tenofovir.
  • Inhibit reverse transcriptase.
NNRTIs - Efavirenz, Nevirapine.
  • Directly inhibit reverse transcriptase.
Protease Inhibitors - Ritonavir, Atazanavir.
  • Inhibit viral protease.
Integrase Inhibitors - Dolutegravir, Raltegravir.
  • Prevent integration of viral DNA.
Entry/Fusion Inhibitors - Enfuvirtide, Maraviroc.
Therapeutic Use Combination therapy (HAART/ART) for HIV infection.
Adverse Effects
  • Hepatotoxicity.
  • Lipodystrophy.
  • Metabolic abnormalities.
  • Gastrointestinal disturbances.

15. Antiseptics

Definition Chemical agents applied to living tissues to prevent or inhibit microbial growth.
Classification
  • Alcohols: Ethanol, Isopropanol.
  • Halogens: Iodine, Povidone-iodine.
  • Oxidizing agents: Hydrogen peroxide.
  • Biguanides: Chlorhexidine.
  • Phenolic compounds.
Mechanism of Action
  • Protein denaturation.
  • Oxidation.
  • Cell membrane disruption.
  • Enzyme inhibition.
Therapeutic and Practical Uses
  • Hand disinfection.
  • Surgical skin preparation.
  • Wound cleansing.
  • Prevention of infection.
Resistance Rare but may occur through efflux mechanisms and biofilm formation.
Adverse Effects
  • Skin irritation.
  • Allergic reactions.
  • Chemical burns with improper use.
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