Answer all these questions according to the heading mention on 2nd attachment
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Reading File
All 24 questions (Q.24-47) answered. Here's a quick reference summary of what was covered:
| Q# | Topic | Format Used |
|---|---|---|
| 24 | Antimicrobials inhibiting protein synthesis | Classification table |
| 25 | 3rd Gen Cephalosporins | Full short note |
| 26 | Drug Resistance | Mechanisms + types |
| 27 | Chloramphenicol | Full short note |
| 28 | Beta-Lactam Antibiotics | Full short note |
| 29 | Sulfamethoxazole + Trimethoprim | Full short note |
| 30 | Amoxicillin preferred over Ampicillin | Comparison table |
| 31 | Azithromycin once daily | PK explanation + short note |
| 32 | Classification of Cephalosporins | Generation-wise table |
| 33 | Narrow spectrum preferred | 7 reasons listed |
| 34 | Drugs for Pseudomonas | Drug groups + clinical table |
| 35 | Tuberculosis | HRZE regimen + ADR table |
| 36 | MDR-TB pharmacotherapy | WHO BPaL/BPaLM regimen |
| 37 | Artemisinin-based combination therapy | Full short note |
| 38 | Metronidazole | Full short note |
| 39 | Imipenem + Cilastatin | Why combined (DHP-I) |
| 40 | FDC advantages/disadvantages | Tables with examples |
| 41 | Penicillin G vs Ampicillin | Detailed comparison table |
| 42 | Drug therapy of anaerobic infections | Drug table + special cases |
| 43 | Superinfection | Definition, mechanism, treatment |
| 44 | Pharmacotherapy of typhoid fever | Drug table + resistance |
| 45 | Pharmacotherapy of pulmonary TB | HRZE with doses + special situations |
| 46 | E. coli-induced UTI | Uncomplicated vs complicated table |
| 47 | Pyridoxine with Isoniazid | Mechanism + who needs it most |
Every answer follows the 2nd attachment's format (Drug name, Disease, Class, MOA, P/K, Uses, Adverse Effects, C/I, Drug Interactions) where applicable, and descriptive/comparison questions are structured appropriately.
Create a comprehensive study guide PDF summarizing all 24 drug notes
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Antimicrobial Study Guide
PDF Document · PDF
What's inside the PDF:
| Feature | Details |
|---|---|
| Cover page | Title, format key, date |
| Table of contents | All 24 questions listed (Q24–Q47) |
| Format | Every drug uses the short note format from your 2nd attachment: Disease → Class → MOA → P/K → Uses → ADRs → C/I → Drug Interactions |
| Tables | Color-coded comparison tables throughout (cephalosporin generations, resistance mechanisms, TB drugs, ACT regimens, etc.) |
| Visual design | Navy/teal/orange color-coded question banners, alternating row shading, header/footer on every page |
| Special notes | ★ tip boxes with mnemonics and key clinical pearls |
| Topics covered | All 24 — from protein synthesis inhibitors and chloramphenicol through MDR-TB, metronidazole, imipenem-cilastatin, typhoid regimens, Pseudomonas drugs, and pyridoxine-INH rationale |
Answer all these questions according to the heading mention on 2nd attachment
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I can read both images clearly from the visual input. The 1st attachment lists questions 1-23, the 2nd attachment is the same short note format template. Let me compile all questions from image 1:
Questions (1-23) from attachment 1:
- MOA of Penicillins
- Diff b/w Ampicillin and Amoxicillin
- Penicillin is combined with Cilastin (Imipenem + Cilastin)
- Tetracycline is not preferred in children and pregnant women
- Describe advantages and disadvantages of antimicrobial fixed dose combination with suitable examples
- Amoxicillin and Clavulanic acid combined in bacterial infections
- Diff b/w Cefuroxime and Ceftriaxone
- Diff b/w Penicillin G and Amoxicillin (Diff)
- Beta-lactam antibiotics
- Cephalosporins
- Empirical and prophylactic therapy
- Remdesevir
- What is concentration dependent killing and time dependent killing?
- Antimalarial drugs classification
- Pharmacotherapy of category II TB
- Pharmacotherapy of UTI
- Ciprofloxacin
- Diff b/w Aminoglycosides and Macrolides
- Vancomycin
- Resistance to isoniazid produces cross-resistance to ethionamide
- Diff b/w macrolides and chloramphenicol
- Aminoglycosides (Gentamicin, Streptomycin)
- Urinary antiseptics
Now I'll answer all 23 questions using the Drug Short Note format from attachment 2: Disease | Class | MOA | P/K | Uses | Adverse Effects | C/I | Drug Interactions
Antimicrobials Study Notes (Q.1–23)
Format: Disease | Class | MOA (& Resistance) | P/K | Uses | Adverse Effects | C/I | Drug Interactions
Q.1 - MOA of Penicillins
Class: Beta-lactam antibiotics (natural and semi-synthetic)
Mechanism of Action (Detailed):
- Penicillins bind to Penicillin Binding Proteins (PBPs) - these are transpeptidase enzymes located on the bacterial cell membrane
- PBPs normally catalyse cross-linking (transpeptidation) of peptidoglycan chains in the bacterial cell wall
- Penicillin binding → inhibition of transpeptidase → prevents cross-linking → structurally weak cell wall
- Bacterial autolysins continue to break down existing peptidoglycan but new synthesis is blocked → net lysis → bactericidal
- Requires actively dividing bacteria (static bacteria have no active cell wall synthesis)
Resistance Mechanisms:
| Mechanism | Example |
|---|---|
| Beta-lactamase production | Destroys the beta-lactam ring (most common) |
| Altered PBPs (low affinity) | MRSA - acquires PBP2a via mecA gene |
| Reduced permeability | Gram-negatives reduce porin expression |
| Efflux pumps | Active export of drug from cell |
Selectivity: Human cells have no cell wall → no PBPs → penicillin has no toxicity to human cells (selective toxicity)
Q.2 - Difference Between Ampicillin and Amoxicillin
| Property | Ampicillin | Amoxicillin |
|---|---|---|
| Type | Aminopenicillin (semi-synthetic) | Aminopenicillin (semi-synthetic) |
| Oral bioavailability | ~40% (poor, variable) | ~90% (excellent) |
| Food effect | Absorption reduced by food (empty stomach) | Absorption NOT affected by food |
| Acid stability | Less acid stable | More acid stable |
| Serum levels | Lower | Higher (for same dose) |
| Dosing frequency | QID (4x/day) | TDS (3x/day) |
| GI side effects | More diarrhoea (unabsorbed drug irritates colon) | Less diarrhoea |
| Spectrum | Identical | Identical |
| Beta-lactamase | Susceptible (both destroyed) | Susceptible |
| Unique rash | Ampicillin rash (non-allergic, maculopapular) in EBV/CMV/CLL | Same rash possible |
| DOC for | Shigella (oral), IV therapy (Listeria meningitis), empirical sepsis | H. pylori (triple therapy), LRTI, otitis media, sinusitis, H. pylori |
| IV form | Yes (Ampicillin sodium IV) | Less common (Amoxicillin IV available) |
Conclusion: Amoxicillin is preferred for oral therapy due to better bioavailability, fewer GI side effects, and more convenient dosing. Ampicillin preferred IV and for Shigella.
Q.3 - Penicillin (Imipenem) Combined with Cilastatin
Drug: Imipenem-Cilastatin (trade name: Primaxin)
Disease: Hospital-acquired pneumonia, intra-abdominal infections, febrile neutropenia, complicated UTI, polymicrobial infections, ESBL-producing organisms
Class: Carbapenem beta-lactam antibiotic
Why Combined with Cilastatin?:
- Cilastatin is NOT an antibiotic - it is a specific inhibitor of the renal brush border enzyme Dehydropeptidase-I (DHP-I)
- Without cilastatin: DHP-I rapidly hydrolyses and inactivates imipenem in renal tubules → (1) urinary levels too low for UTI treatment, (2) hydrolysis product is nephrotoxic
- With cilastatin: DHP-I blocked → imipenem preserved in urine → adequate UTI treatment + nephrotoxicity prevented
- Combination ratio: Imipenem : Cilastatin = 1:1
- Note: Meropenem is stable to DHP-I and does NOT need cilastatin
MOA: Binds PBP1 and PBP2 → inhibits cell wall synthesis → bactericidal. Stable to most beta-lactamases including ESBLs; NOT active against MRSA, VRE, Stenotrophomonas maltophilia
P/K: IV only; good tissue distribution; renal excretion (of intact imipenem with cilastatin)
Adverse Effects: Seizures (lowers seizure threshold), nausea/vomiting, hypersensitivity, superinfection
C/I: Epilepsy (caution), hypersensitivity, dose reduce in renal failure
Drug Interactions: Valproate - imipenem dramatically reduces serum valproate levels → breakthrough seizures (avoid combination); Probenecid increases imipenem levels
Q.4 - Tetracycline is Not Preferred in Children and Pregnant Women
Drug: Tetracyclines (Tetracycline, Doxycycline, Minocycline)
Class: Broad-spectrum bacteriostatic antibiotic (30S ribosomal inhibitor)
Reasons for Avoidance:
In Children (< 8 years):
- Teeth discolouration: Tetracyclines chelate calcium → deposits in developing teeth → permanent yellow-brown-grey discolouration (enamel hypoplasia) - cosmetically and structurally damaging
- Bone growth retardation: Deposits in growing bones → chelates calcium in bone → reversible bone growth inhibition; can affect long bone development
- Permanent teeth develop up to age 8 → risk period is birth to 8 years
In Pregnant Women:
- Fetal teeth and bone effects: Crosses placenta freely → affects fetal teeth (all primary teeth form in utero) and bone development
- Maternal hepatotoxicity: Severe, potentially fatal acute fatty liver of pregnancy (especially IV tetracycline) - pregnant women more susceptible
- Fetal liver toxicity: Can cause hepatotoxicity in developing fetus
- Excreted in breast milk → affects nursing infant's teeth and bones
Additional General Contraindications:
- Renal failure (except doxycycline - hepatically eliminated)
- Outdated tetracycline: conversion to epitetracycline → nephrotoxic (Fanconi syndrome)
Q.5 - Advantages and Disadvantages of Antimicrobial Fixed Dose Combinations (FDCs)
Definition: Two or more drugs combined in fixed proportions in a single dosage form
ADVANTAGES:
| # | Advantage | Example |
|---|---|---|
| 1 | Synergism - enhanced killing | Co-trimoxazole (SMX+TMP) - sequential folate blockade → bactericidal |
| 2 | Reduced resistance | TB HRZE tablet - 4 drugs prevent resistance selection |
| 3 | Better compliance - fewer tablets | TB 4-in-1 tablet vs 4 separate tablets |
| 4 | Pharmacokinetic synergy | Augmentin - clavulanate protects amoxicillin from beta-lactamase |
| 5 | Prevents monotherapy in HIV | Atripla (TDF+FTC+EFV in 1 tablet) - ensures complete ART |
| 6 | Cost-effective | Single FDC cheaper than multiple drugs |
| 7 | Reduces pill burden | Critical in long-term HIV/TB therapy adherence |
DISADVANTAGES:
| # | Disadvantage | Example |
|---|---|---|
| 1 | Individual dose adjustment impossible | Cannot reduce rifampicin alone in hepatic disease (TB FDC) |
| 2 | ADR attribution difficult | Rash with Co-trimoxazole - sulfa or TMP? |
| 3 | Resistance to one component = ineffective FDC | SMX-resistant organism → TMP alone insufficient |
| 4 | Pharmacokinetic mismatch | Artemether (T½ 1-3h) vs Lumefantrine (T½ 3-6 days) in Coartem |
| 5 | C/I to one drug stops whole FDC | Ethambutol optic neuritis → all 4 TB drugs stopped |
| 6 | Formulation incompatibility | Chemical degradation or instability when mixed |
Key Examples: Co-trimoxazole | Augmentin (Amox+Clavulanate) | Pip-Tazo | TB HRZE tablet | Coartem (Artemether+Lumefantrine) | Kaletra (Lopinavir+Ritonavir)
Q.6 - Amoxicillin and Clavulanic Acid Combined in Bacterial Infections (Augmentin)
Drug: Amoxicillin + Clavulanic acid (Co-amoxiclav / Augmentin)
Disease: Respiratory tract infections (LRTI, sinusitis, otitis media), Skin/soft tissue infections, UTI, Diabetic foot, Animal bites, Dental infections, H. pylori
Class: Aminopenicillin + Beta-lactamase inhibitor combination
Rationale for Combination:
- Amoxicillin: Broad-spectrum aminopenicillin; susceptible to beta-lactamase destruction
- Clavulanic acid: Weak antibacterial alone (suicide inhibitor of beta-lactamase); binds irreversibly to beta-lactamase → inactivates it permanently → protects amoxicillin from destruction
- Together: covers beta-lactamase producing organisms that amoxicillin alone cannot treat
- Ratio: Amoxicillin : Clavulanate = 500:125 mg or 875:125 mg (tablets)
MOA: Clavulanate contains beta-lactam ring → suicide substrate for beta-lactamase → irreversible inhibition → amoxicillin restored to activity. Combined MOA: amoxicillin inhibits PBPs → bactericidal
P/K:
- Both well absorbed orally
- T½ amoxicillin ~1 hr; T½ clavulanate ~1 hr (matched)
- Renal excretion
- Take with food (reduces GI side effects; does not reduce amoxicillin absorption)
Uses: Beta-lactamase producing H. influenzae, Moraxella catarrhalis, S. aureus (MSSA), E. coli, Klebsiella; Polymicrobial infections (aspiration pneumonia, diabetic foot); Animal/human bites (Pasteurella); Dental abscesses; Sinusitis; Otitis media
Adverse Effects: Diarrhoea (most common - clavulanate causes GI motility effects); Nausea; Hypersensitivity; Cholestatic jaundice (hepatotoxicity) - more with co-amoxiclav than amoxicillin alone (clavulanate implicated); C. difficile colitis (with prolonged use)
C/I: Penicillin/cephalosporin hypersensitivity; Previous cholestatic jaundice with co-amoxiclav; Severe hepatic disease
Drug Interactions: Warfarin (may potentiate anticoagulation); Allopurinol (↑ rash frequency); Probenecid (↑ amoxicillin levels); Methotrexate toxicity (↓ renal excretion)
Q.7 - Difference Between Cefuroxime and Ceftriaxone
| Property | Cefuroxime | Ceftriaxone |
|---|---|---|
| Generation | 2nd generation cephalosporin | 3rd generation cephalosporin |
| Gram-positive coverage | Good (Staph, Strep) | Reduced compared to 2G |
| Gram-negative coverage | Extended (H. influenzae, E. coli, Klebsiella, Neisseria) | Excellent (broader than cefuroxime) |
| Anaerobic coverage | Limited | Limited |
| Pseudomonas | NO | NO (need ceftazidime/cefepime) |
| CSF penetration | Moderate (used for meningitis - 2G option) | Excellent - DOC for bacterial meningitis |
| Route | IV/IM and oral (cefuroxime axetil - prodrug) | IV/IM only (no oral form) |
| Half-life | ~1.3 hours (2-3x daily dosing) | ~8 hours (once daily dosing) |
| Protein binding | ~50% | ~95% (highest among cephalosporins) |
| Elimination | Renal | Biliary + Renal (dual excretion) |
| Biliary sludge | No | YES (pseudolithiasis - particularly in children/neonates) |
| Key Uses | Surgical prophylaxis, LRTI, UTI, Gonorrhoea, Lyme disease (mild), Otitis media | Meningitis (DOC), Typhoid fever, Gonorrhoea (single dose DOC), Septicaemia, Neonatal infections, MDR infections |
| Disulfiram reaction | No | No |
| Cost | Lower | Higher |
Q.8 - Difference Between Penicillin G and Amoxicillin
| Property | Penicillin G | Amoxicillin |
|---|---|---|
| Type | Natural penicillin | Aminopenicillin (semi-synthetic) |
| Spectrum | Narrow: gram-positive cocci (Staph-sensitive, Strep), Spirochetes, gram-negative cocci only (Neisseria) | Extended: gram-positives + gram-negatives (H. influenzae, E. coli, Proteus mirabilis, Salmonella, Listeria) |
| Oral route | NO - acid labile; IV/IM only | YES - acid stable; 90% oral bioavailability |
| Food effect | N/A (parenteral) | Not affected by food |
| Side chain | Benzyl side chain | Amino group side chain (broader spectrum) |
| Gram-negative coverage | N. meningitidis, N. gonorrhoeae only | H. influenzae, E. coli, Listeria, Salmonella, Shigella |
| Beta-lactamase | Susceptible | Susceptible (both need clavulanate to protect) |
| Antipseudomonal | No | No |
| DOC | Syphilis, GAS pharyngitis, Streptococcal endocarditis, Gas gangrene, Rheumatic fever prophylaxis, Actinomycosis, Tetanus | H. pylori (triple therapy), LRTI, Otitis media, Sinusitis, Listeria meningitis |
| Formulations | Pen G sodium/potassium (IV), Benzathine Pen G (IM depot - long-acting), Procaine Pen G (IM) | Oral capsules/suspension; IV amoxicillin (Amoxicillin trihydrate) |
Q.9 - Beta-Lactam Antibiotics (Short Note)
Disease: Wide range - gram-positive and gram-negative bacterial infections depending on the agent used
Class: Antibiotics containing a beta-lactam ring (4-membered cyclic amide)
Members:
| Group | Examples |
|---|---|
| Penicillins | Pen G, Amoxicillin, Ampicillin, Piperacillin, Oxacillin |
| Cephalosporins | Cefazolin (1G), Cefuroxime (2G), Ceftriaxone (3G), Cefepime (4G), Ceftaroline (5G) |
| Carbapenems | Imipenem-cilastatin, Meropenem, Ertapenem |
| Monobactams | Aztreonam (gram-negative only) |
| Beta-lactamase inhibitors | Clavulanic acid, Sulbactam, Tazobactam, Avibactam |
MOA: Bind PBPs (transpeptidases) → inhibit peptidoglycan cross-linking → bactericidal
Resistance: Beta-lactamase production, altered PBPs (MRSA), reduced permeability, efflux pumps
P/K: Most parenteral; some oral (amoxicillin, cephalexin, cefixime); mostly renal excretion; poor CNS penetration (except in meningitis with inflamed BBB)
Adverse Effects: Hypersensitivity (most common - rash to anaphylaxis); Diarrhoea; Seizures (imipenem, high-dose Pen G); Superinfection; Nephrotoxicity (rare); Electrolyte disturbances (Na+/K+ load with IV forms)
C/I: Hypersensitivity to that class (cross-allergy between penicillins and cephalosporins ~1-2%)
Drug Interactions: Probenecid blocks tubular secretion → ↑ levels; Aminoglycosides - synergistic but physically incompatible in same syringe; Warfarin may be potentiated
Q.10 - Cephalosporins (Short Note)
Disease: Varied by generation - gram-positive/negative infections, meningitis, typhoid, surgical prophylaxis
Class: Beta-lactam antibiotics - classified by generations 1-5
MOA: Bind PBPs → inhibit transpeptidation of peptidoglycan → bactericidal
Resistance: Beta-lactamases (ESBLs), altered PBPs, reduced permeability
| Gen | Key Drugs | Spectrum | Key Use |
|---|---|---|---|
| 1st | Cephalexin (PO), Cefazolin (IV) | Gram-positive > gram-negative | Surgical prophylaxis, Skin infections |
| 2nd | Cefuroxime, Cefaclor, Cefoxitin | Extended gram-negative + anaerobes (cefoxitin) | LRTI, Sinusitis, PID |
| 3rd | Ceftriaxone, Cefotaxime, Ceftazidime | Excellent gram-negative; Pseudomonas (ceftaz) | Meningitis, Typhoid, Gonorrhoea |
| 4th | Cefepime | Broad (gram+, gram-, Pseudomonas) | HAP, Febrile neutropenia |
| 5th | Ceftaroline | MRSA + gram-negative | MRSA infections |
P/K: Mostly IV/IM; some oral; mostly renal excretion (except cefoperazone - biliary)
Adverse Effects: Hypersensitivity (cross with penicillin 1-2%), diarrhoea, C. difficile, biliary sludge (ceftriaxone), disulfiram reaction (cefoperazone/cefotetan + alcohol)
C/I: Hypersensitivity; caution in penicillin allergy
Drug Interactions: Probenecid ↑ levels; alcohol + cefoperazone/cefotetan → disulfiram reaction; aminoglycosides (synergistic + nephrotoxic)
Q.11 - Empirical and Prophylactic Therapy
A) Empirical Therapy:
Definition: Treatment started before the causative organism is identified, based on clinical presentation and knowledge of likely pathogens.
Rationale: Delay in starting antibiotics while awaiting culture results can be life-threatening (sepsis, meningitis)
Principles:
- Choose drug based on clinical syndrome + likely pathogen + local resistance patterns
- Use broader spectrum initially, then de-escalate once C&S results available
- Always take cultures BEFORE starting antibiotics
Examples:
| Clinical Scenario | Empirical Regimen |
|---|---|
| Community-acquired pneumonia | Amoxicillin + Azithromycin |
| Bacterial meningitis | Ceftriaxone + Ampicillin (for Listeria) + Dexamethasone |
| Sepsis (hospital-acquired) | Pip-Tazo or Carbapenem + Vancomycin (if MRSA suspected) |
| Febrile neutropenia | Cefepime or Pip-Tazo |
| Pelvic inflammatory disease | Ceftriaxone + Doxycycline + Metronidazole |
B) Prophylactic Therapy:
Definition: Use of antibiotics to prevent infection before it occurs, in patients at high risk.
Types:
- Surgical prophylaxis: Single dose IV antibiotic 30-60 min before incision to prevent wound infection (e.g., cefazolin before most surgeries)
- Medical prophylaxis: Ongoing low-dose therapy to prevent recurrence/specific infections
- Rheumatic fever prophylaxis: Benzathine Pen G monthly for 5-10 years
- PCP prophylaxis in HIV: Co-trimoxazole (when CD4 <200 cells/μL)
- MAC prophylaxis in HIV: Azithromycin weekly (CD4 <50)
- Meningococcal contacts: Rifampicin or Ciprofloxacin
- Malaria prophylaxis: Chloroquine, Mefloquine, Doxycycline, Atovaquone-proguanil
- Post-exposure prophylaxis: After known exposure (e.g., anthrax, HIV occupational exposure)
Key Principle: Benefits must outweigh risks; use narrow-spectrum when possible; limited duration
Q.12 - Remdesivir (Short Note)
Disease: COVID-19 (SARS-CoV-2 infection), Ebola (investigated), Other RNA viral infections
Class: Nucleoside analogue - antiviral (adenosine analogue prodrug)
MOA:
- Remdesivir is a prodrug → metabolised intracellularly to active triphosphate form (GS-443902)
- Active form is an adenosine nucleoside triphosphate analogue
- Incorporated into viral RNA by RNA-dependent RNA polymerase (RdRp)
- Acts as a chain terminator → premature termination of viral RNA synthesis → prevents viral replication
- Uniquely causes delayed chain termination (3 nucleotides after incorporation - evades exonuclease proofreading)
P/K:
- IV infusion only (prodrug not orally bioavailable in original form)
- Rapidly converted to active metabolite in plasma and cells
- Distributed widely including lungs (high concentration at site of COVID-19 infection)
- Hepatic metabolism; renal excretion of metabolites
- T½ ~1 hour (prodrug); active metabolite T½ much longer intracellularly
Uses:
- COVID-19: Hospitalised adults and children requiring supplemental oxygen - reduces time to clinical improvement
- WHO/FDA approved for COVID-19 in adults and paediatric patients (≥28 days, ≥3 kg)
- Ebola virus disease (clinical trial use, not DOC)
Adverse Effects:
- Bradycardia (transient, within minutes of infusion - monitor heart rate)
- Elevated liver transaminases (ALT, AST) - hepatotoxicity
- Nausea, vomiting
- Hypersensitivity/infusion-related reactions (flushing, sweating, tachycardia during infusion)
- Hypotension
- Elevated serum creatinine (nephrotoxicity - related to vehicle sulfobutylether-β-cyclodextrin)
C/I:
- eGFR <30 mL/min (original IV formulation - cyclodextrin accumulates; newer oral form avoids this)
- Severe hepatic impairment (ALT >5x ULN)
- Hypersensitivity
Drug Interactions:
- Chloroquine/Hydroxychloroquine: Antagonises remdesivir activity (compete at RdRp) - avoid combination
- CYP3A4 inducers (rifampicin) reduce levels
- P-glycoprotein inducers reduce absorption
Q.13 - Concentration-Dependent vs Time-Dependent Killing
This is a pharmacodynamic (PD) concept describing how antibiotic efficacy relates to drug concentration and time.
A) Concentration-Dependent (Concentration-Dependent) Killing:
Definition: The rate and extent of bacterial killing increases as drug concentration rises above the MIC (Minimum Inhibitory Concentration). Higher peak = greater kill.
Key PD Parameter: Cmax/MIC ratio (peak concentration to MIC ratio) OR AUC/MIC (area under curve)
Characteristics:
- Maximum kill at peak concentrations
- Significant Post-Antibiotic Effect (PAE) - bacterial suppression continues even when drug levels fall below MIC
- Once-daily high-dose dosing is optimal (maximise Cmax)
Examples:
- Aminoglycosides (gentamicin, tobramycin) - once-daily extended interval dosing exploits this
- Fluoroquinolones (ciprofloxacin, levofloxacin) - higher doses achieve better kill
- Metronidazole
- Daptomycin
B) Time-Dependent (Time-Dependent) Killing:
Definition: Bacterial killing depends on how long drug concentration stays above MIC, not how high it goes. Raising concentration beyond 4x MIC provides no additional benefit.
Key PD Parameter: Time above MIC (T>MIC) - aim for 40-70% of dosing interval above MIC
Characteristics:
- Killing rate is saturated at moderate concentrations (4-5x MIC)
- Minimal PAE (bacteria regrow when levels fall)
- Frequent dosing or continuous infusion optimal
Examples:
- Beta-lactams (penicillins, cephalosporins, carbapenems) - continuous infusion or frequent dosing
- Vancomycin (AUC/MIC is actually the best predictor now)
- Clindamycin
- Macrolides
Summary Table:
| Feature | Concentration-Dependent | Time-Dependent |
|---|---|---|
| Key parameter | Cmax/MIC or AUC/MIC | Time above MIC |
| Optimal strategy | High peak doses, once daily | Frequent dosing or continuous infusion |
| PAE | Significant | Minimal to none |
| Examples | Aminoglycosides, Fluoroquinolones | Beta-lactams, Vancomycin, Clindamycin |
Q.14 - Antimalarial Drugs Classification
Disease: Malaria - caused by Plasmodium falciparum, P. vivax, P. malariae, P. ovale, P. knowlesi
Classification by Mechanism/Chemical Class:
A) By Chemical Class:
| Class | Drugs |
|---|---|
| Quinoline derivatives | Chloroquine, Quinine, Quinidine, Mefloquine, Primaquine, Tafenoquine, Amodiaquine |
| Aryl amino alcohols | Mefloquine, Lumefantrine, Halofantrine |
| Artemisinins | Artesunate, Artemether, Dihydroartemisinin (DHA) |
| Antifolates | Pyrimethamine, Proguanil, Sulfadoxine-Pyrimethamine (SP/Fansidar) |
| Antibiotics | Doxycycline, Clindamycin, Azithromycin |
| Naphthoquinone | Atovaquone (+ proguanil = Malarone) |
B) By Life Cycle Stage Targeted:
| Drug | Stage Targeted | Use |
|---|---|---|
| Chloroquine | Erythrocytic (blood) | Treatment + prophylaxis of sensitive P. vivax/malariae/ovale |
| Quinine/Artesunate | Erythrocytic | Treatment of severe/complicated falciparum malaria |
| Primaquine/Tafenoquine | Liver (hypnozoites) + Gametocytes | Radical cure of P. vivax/ovale (prevents relapse) |
| Proguanil | Pre-erythrocytic (liver) | Prophylaxis; combination with atovaquone (Malarone) |
| SP (Fansidar) | Erythrocytic | Intermittent preventive treatment in pregnancy (IPTp) |
C) ACT (Artemisinin-Based Combination Therapy) - Current Standard:
| ACT | Use |
|---|---|
| Artemether + Lumefantrine (Coartem) | Uncomplicated P. falciparum (global standard) |
| Artesunate + Mefloquine | SE Asia |
| Artesunate + Amodiaquine | Africa |
| Dihydroartemisinin + Piperaquine | Asia |
| Artesunate IV/IM | Severe malaria |
Chloroquine-resistant P. falciparum: Use ACT
Chloroquine-resistant P. vivax: Mefloquine or ACT + primaquine
Q.15 - Pharmacotherapy of Category II TB (Retreatment)
Category II TB: Retreatment cases - previously treated patients who have relapsed, failed, or defaulted from Category I treatment
WHO/RNTCP Category II Regimen (Older Classification):
- Intensive phase (3 months): HRZES - Isoniazid + Rifampicin + Pyrazinamide + Ethambutol + Streptomycin (first 2 months)
- Continuation phase (5 months): HRE - Isoniazid + Rifampicin + Ethambutol
- Total: 8 months
| Drug | Abbreviation | Dose | Mechanism |
|---|---|---|---|
| Isoniazid | H | 5 mg/kg (max 300 mg) | Inhibits mycolic acid synthesis (InhA) |
| Rifampicin | R | 10 mg/kg (max 600 mg) | Inhibits RNA polymerase |
| Pyrazinamide | Z | 25 mg/kg (max 2g) | Active at acidic pH; sterilising |
| Ethambutol | E | 15-20 mg/kg | Inhibits arabinosyl transferase |
| Streptomycin | S | 15 mg/kg IM (max 1g) | Binds 16S rRNA of 30S → protein synthesis inhibition |
Note - Current WHO 2022 Guidance: Category II regimen is no longer recommended by WHO for retreatment cases without susceptibility testing. Sputum culture + DST (Drug Susceptibility Testing) should be done before retreatment. If MDR confirmed → BPaL/BPaLM regimen.
Key ADRs of Streptomycin: Ototoxicity (vestibular - dizziness, ataxia > cochlear - hearing loss); Nephrotoxicity; Avoid in pregnancy (ototoxic to fetus); IM injection only
Q.16 - Pharmacotherapy of UTI
Organism: Most common - E. coli (80%), also Klebsiella, Staph saprophyticus, Proteus, Enterococcus
Classification:
- Uncomplicated lower UTI (cystitis) - women with normal urinary tract
- Complicated UTI - men, pregnancy, structural abnormality, catheter, diabetes
- Upper UTI (pyelonephritis) - kidney involvement
- Catheter-associated UTI (CAUTI)
Treatment by Type:
| Type | First-line Drug | Dose | Duration |
|---|---|---|---|
| Uncomplicated cystitis | Nitrofurantoin | 100 mg SR BD | 5 days |
| Uncomplicated cystitis | Fosfomycin | 3g single dose | Single dose |
| Uncomplicated cystitis | Co-trimoxazole | 960 mg BD | 3 days (if resistance <20%) |
| Pyelonephritis | Ciprofloxacin | 500 mg BD PO / 400 mg BD IV | 7-14 days |
| Pyelonephritis (severe/hospitalised) | Ceftriaxone | 1-2g OD IV | 10-14 days |
| ESBL-producing organisms | Ertapenem / Meropenem | IV | 10-14 days |
| Enterococcal UTI | Amoxicillin | 500 mg TDS | 7 days |
| CAUTI | Based on C&S results | - | 7-14 days |
| Pregnancy (treat asymptomatic bacteriuria!) | Cephalexin / Nitrofurantoin | - | 5-7 days |
Urinary Antiseptics (act specifically in urine):
- Nitrofurantoin: Reduced to reactive metabolites by bacterial enzymes → damages DNA; only UTI (not systemic infections)
- Fosfomycin: Inhibits MurA enzyme (first step in peptidoglycan synthesis); broad spectrum in urine
- Methenamine: Releases formaldehyde in acidic urine → bactericidal; prophylaxis only
Q.17 - Ciprofloxacin (Short Note)
Disease: UTI, respiratory tract infections (especially atypical/gram-negative), Pseudomonas infections, typhoid, gonorrhoea, anthrax (post-exposure), traveller's diarrhoea, osteomyelitis
Class: Fluoroquinolone (2nd generation quinolone)
MOA:
- Inhibits bacterial DNA gyrase (topoisomerase II) and topoisomerase IV
- DNA gyrase: Required for DNA supercoiling and replication in gram-negative bacteria (primary target)
- Topoisomerase IV: Required for chromosome segregation during cell division in gram-positive bacteria (primary target in gram-positives)
- Inhibition → DNA strand breaks → bacterial cell death → bactericidal
- Resistance: Mutations in gyrA/parC genes (altered target); efflux pumps (most common); reduced permeability
P/K:
- Excellent oral bioavailability (~70-80%) - one of best among antibiotics
- Widely distributed - penetrates tissues, bone, prostate, CSF (moderate)
- Volume of distribution very large (~2.5 L/kg)
- Metabolised in liver; renal + biliary excretion
- T½ ~4-6 hours; twice daily dosing
Uses:
- DOC: Anthrax (post-exposure prophylaxis + treatment), Typhoid (sensitive strains), Uncomplicated Pseudomonas UTI
- Gonorrhoea (if susceptible - widespread resistance now)
- Traveller's diarrhoea (empirical)
- Osteomyelitis and septic arthritis
- Complicated UTI and pyelonephritis
- Hospital-acquired infections (gram-negative)
- Febrile neutropenia (combination)
- Meningococcal prophylaxis (contacts)
Adverse Effects:
- Tendinopathy and tendon rupture (Achilles tendon most common - especially >60 yrs, steroids, renal failure) - black box warning
- Cartilage damage in growing animals → avoid in children <18 years (except anthrax, plague - risk-benefit)
- QT prolongation → Torsades de Pointes
- CNS: headache, dizziness, seizures (especially in elderly/epileptics)
- GI: nausea, diarrhoea, C. difficile
- Phototoxicity (sun sensitivity - especially sparfloxacin)
- Hepatotoxicity (rare)
- Blood glucose dysregulation (hypo- and hyperglycaemia)
C/I:
- Children and adolescents <18 years (cartilage toxicity - except specific indications)
- Pregnancy and lactation
- Known QT prolongation or concurrent QT-prolonging drugs
- Epilepsy (lowers seizure threshold)
- Hypersensitivity
Drug Interactions:
- Antacids, Calcium, Iron, Zinc → chelation → ↓ absorption by 50-90% (take ciprofloxacin 2 hrs before or 6 hrs after)
- Theophylline: Ciprofloxacin inhibits CYP1A2 → theophylline toxicity (tachycardia, seizures) - reduce dose by 50%
- Warfarin: ↑ anticoagulant effect (monitor INR)
- QT-prolonging drugs (antiarrhythmics, antipsychotics): ↑ risk of Torsades
- NSAIDs: ↑ CNS seizure risk
- Sucralfate: ↓ ciprofloxacin absorption
Q.18 - Difference Between Aminoglycosides and Macrolides
| Property | Aminoglycosides | Macrolides |
|---|---|---|
| Examples | Gentamicin, Tobramycin, Amikacin, Streptomycin, Neomycin | Erythromycin, Azithromycin, Clarithromycin, Roxithromycin |
| Chemical class | Amino sugars linked by glycosidic bonds | Large macrolactone ring (14, 15, or 16-membered) |
| Ribosomal target | 30S subunit (16S rRNA) | 50S subunit (23S rRNA) |
| Mechanism | Bind 30S → irreversible binding → mRNA misreading → faulty proteins inserted → bactericidal | Bind 23S rRNA → block translocation (peptide chain elongation) → bacteriostatic |
| Bactericidal/static | Bactericidal | Bacteriostatic |
| Killing type | Concentration-dependent (once-daily dosing optimal) | Time-dependent |
| Spectrum | Gram-negative (aerobic) - Pseudomonas, E. coli, Klebsiella; gram-positives (limited) | Gram-positive + atypical organisms (Mycoplasma, Chlamydia, Legionella, Bordetella); some gram-negatives |
| Anaerobic activity | None (require oxygen for drug uptake - oxygen-dependent active transport) | Limited; azithromycin has some activity |
| Oral bioavailability | Poor (polar, ionised) - IV/IM only (except neomycin topical) | Good oral bioavailability (especially azithromycin, clarithromycin) |
| CNS penetration | Poor | Moderate |
| Intracellular activity | Poor | Excellent (concentrate in cells/phagocytes) - ideal for atypicals |
| Key uses | Pseudomonas, Gram-negative sepsis, TB (streptomycin), Tularaemia, Plague, Endocarditis (synergy with beta-lactam) | CAP (atypical coverage), STIs (Chlamydia), H. pylori (clarithromycin), MAC in HIV, Whooping cough (erythromycin) |
| Toxicity | Ototoxicity (irreversible), Nephrotoxicity, Neuromuscular blockade | GI (most common), QT prolongation, Hepatotoxicity, Ototoxicity (azithromycin, reversible) |
| Monitoring | Drug levels (peak/trough), renal function, audiometry | QTc, LFTs |
Q.19 - Vancomycin (Short Note)
Disease: MRSA infections (DOC), C. difficile colitis (oral), severe gram-positive infections, Endocarditis (MRSA/Enterococcal), Febrile neutropenia (when MRSA suspected)
Class: Glycopeptide antibiotic
MOA:
- Binds to D-Ala-D-Ala terminal of peptidoglycan precursors (NAM-NAG) → physically blocks transglycosylase AND transpeptidase → prevents cell wall synthesis → bactericidal
- Mechanism is completely different from beta-lactams (different binding site) → active against MRSA (which has altered PBPs)
- Resistance (VRE - Vancomycin-Resistant Enterococci): VanA/VanB genes → change D-Ala-D-Ala to D-Ala-D-Lac → vancomycin cannot bind (1000x reduced affinity)
P/K:
- IV for systemic infections (very poor oral absorption)
- Oral vancomycin acts ONLY in the gut (not absorbed) → used only for C. difficile colitis
- Vd ~0.7 L/kg; ~50% protein binding
- Eliminated entirely by kidneys (GFR-dependent) → dose reduction in renal failure
- T½ ~6 hours (normal renal function); prolonged in renal failure
- TDM (Therapeutic Drug Monitoring) is mandatory: Monitor AUC/MIC (target AUC 400-600 mg·h/L for MRSA) or trough levels (target 15-20 mg/L for serious infections)
Uses:
- MRSA infections (DOC for all serious MRSA: pneumonia, bacteraemia, endocarditis, osteomyelitis)
- C. difficile colitis (oral): moderate-severe (or when metronidazole fails)
- Gram-positive endocarditis (when penicillin allergic)
- Febrile neutropenia (MRSA coverage)
- CNS infections (MRSA meningitis - with rifampicin)
- Surgical prophylaxis (in penicillin-allergic patients)
Adverse Effects:
- Nephrotoxicity (dose-dependent - concentration-related; additive with aminoglycosides)
- Ototoxicity (high serum levels - tinnitus, hearing loss)
- "Red Man Syndrome" (not true allergy) - rapid IV infusion → mast cell degranulation → histamine release → flushing, erythema, pruritus, hypotension over face/neck/upper torso. Prevented by: slow infusion (>60 min), premedication with antihistamines
- Thrombophlebitis at infusion site
- Neutropenia (prolonged use)
- Hypersensitivity (rare true IgE-mediated)
C/I: Severe hypersensitivity; reduce dose in renal failure; caution with other nephrotoxic/ototoxic drugs
Drug Interactions:
- Aminoglycosides: Synergistic antibacterial effect + synergistic nephrotoxicity and ototoxicity (monitor closely)
- Loop diuretics (furosemide): ↑ ototoxicity risk
- Other nephrotoxins (amphotericin, NSAIDs, contrast): Additive nephrotoxicity
- Neuromuscular blocking agents: Vancomycin may enhance neuromuscular blockade
Q.20 - Resistance to Isoniazid Produces Cross-Resistance to Ethionamide
Explanation:
Isoniazid (INH) Mechanism:
- INH is a prodrug → activated by mycobacterial enzyme KatG (catalase-peroxidase)
- Activated INH binds to InhA (enoyl-ACP reductase) → inhibits mycolic acid synthesis → bactericidal
Ethionamide Mechanism:
- Ethionamide is also a prodrug → activated by EthA (monooxygenase)
- Activated ethionamide also binds InhA (same target as activated INH)
- Both inhibit the same enzyme InhA
Why Cross-Resistance Occurs:
- Most INH resistance is due to mutations in the inhA gene (encoding InhA) or its promoter
- These mutations reduce InhA's affinity for both activated INH AND activated ethionamide
- Therefore, inhA mutations confer resistance to BOTH drugs simultaneously
- Resistance can also occur via KatG mutations (reduced INH activation) - these do NOT produce ethionamide cross-resistance (since ethionamide is activated by a different enzyme EthA)
Clinical Implication:
- Before prescribing ethionamide for MDR-TB, check the mechanism of INH resistance
- If resistance is due to inhA mutation → ethionamide will also be ineffective
- If resistance is due to katG mutation → ethionamide may still work
- DST (Drug Susceptibility Testing) or molecular testing (GenoType MTBDRplus) should guide therapy
Q.21 - Difference Between Macrolides and Chloramphenicol
| Property | Macrolides | Chloramphenicol |
|---|---|---|
| Examples | Erythromycin, Azithromycin, Clarithromycin | Chloramphenicol |
| Chemical class | Macrolactone ring (14/15/16-membered) | Nitrobenzene derivative |
| Target on 50S | 23S rRNA (binding blocks translocation) | 23S rRNA (inhibits peptidyl transferase) |
| Mechanism | Block translocation step → peptide chain cannot move forward | Inhibit peptide bond formation step (peptidyl transferase) |
| Bactericidal/static | Bacteriostatic | Bacteriostatic (bactericidal for some: H. influenzae, N. meningitidis, S. pneumoniae) |
| Spectrum | Gram-positive + atypical organisms; H. influenzae; limited gram-negative | Broad spectrum: gram-positive, gram-negative, anaerobes, rickettsiae, Salmonella |
| Intracellular penetration | Excellent (concentrates in phagocytes) | Excellent (crosses BBB) |
| CSF penetration | Moderate (azithromycin limited) | Excellent (45-90% of plasma levels) |
| Oral bioavailability | Good (azithromycin, clarithromycin) | Excellent (~100%) |
| Key Uses | Atypical pneumonia, CAP, STIs, H. pylori, MAC, Whooping cough | Meningitis, Typhoid, Rickettsial infections, Brain abscess, Anaerobic infections |
| Key Toxicity | GI, QT prolongation, Hepatotoxicity, mild ototoxicity | Aplastic anaemia (idiosyncratic, 1:25,000-40,000), Grey Baby Syndrome (neonates), Dose-related bone marrow suppression |
| Resistance mechanism | Methylation of 23S rRNA (erm genes - most common); efflux; esterases | Acetyltransferase (CAT enzyme) destroys drug; efflux |
| Enzyme inhibition | CYP3A4 inhibitors (erythromycin, clarithromycin strong; azithromycin mild) | Inhibits CYP2C9 and CYP3A4 → warfarin, phenytoin toxicity |
| Pregnancy | Generally safe (avoid erythromycin estolate) | Avoid (Grey baby risk; fetal hepatotoxicity) |
Q.22 - Aminoglycosides: Gentamicin and Streptomycin (Short Note)
GENTAMICIN
Disease: Gram-negative sepsis, Pseudomonas infections, Endocarditis (synergy), Plague, Tularaemia, Pelvic inflammatory disease
Class: Aminoglycoside antibiotic
MOA: Enters bacteria via oxygen-dependent active transport → binds irreversibly to 30S ribosomal subunit (16S rRNA) → causes misreading of mRNA → faulty proteins inserted into cell membrane → increased membrane permeability → more drug enters → accelerated kill → bactericidal (concentration-dependent)
Resistance: Aminoglycoside-modifying enzymes (acetyltransferases, phosphotransferases, nucleotidyltransferases); efflux; reduced uptake (anaerobes - no oxygen-dependent uptake)
P/K: IV/IM only (not absorbed orally). Distributed extracellularly (hydrophilic). Poor CNS/intracellular penetration. Renal excretion (GFR-dependent). T½ ~2 hours. Therapeutic Drug Monitoring essential (peak 5-10 mg/L; trough <2 mg/L for conventional dosing).
Uses: Hospital-acquired gram-negative infections, Septicaemia, Pseudomonas (+ pip-tazo), Endocarditis (synergy with penicillin for Enterococcus/Streptococcus), Neonatal sepsis, PID (+ clindamycin), Burns, Topical (ear/eye drops)
Adverse Effects:
- Nephrotoxicity: Proximal tubular damage (acute tubular necrosis); reversible if detected early; accumulates in proximal tubular cells
- Ototoxicity: Cochlear (hearing loss - high frequency first) and vestibular (dizziness, ataxia); often irreversible - hair cell destruction in organ of Corti
- Neuromuscular blockade: Blocks presynaptic Ca²⁺-dependent ACh release → apnoea in myasthenia gravis, post-anaesthesia
- Avoid in pregnancy (fetal ototoxicity)
C/I: Renal failure (reduce dose/extend interval); Myasthenia gravis; Pregnancy; Prior ototoxicity
Drug Interactions: Loop diuretics (↑ ototoxicity); Vancomycin (↑ nephrotoxicity + ototoxicity); NSAIDs (↑ nephrotoxicity); Neuromuscular blockers (enhanced blockade); Penicillins - synergistic (don't mix in same syringe - physically incompatible)
STREPTOMYCIN
Disease: TB (first-line - Category II), Plague (DOC), Tularaemia (DOC), Brucellosis (+ doxycycline), Endocarditis (synergy)
Class: Aminoglycoside antibiotic (first discovered antibiotic in this class)
MOA: Binds irreversibly to 30S ribosomal subunit (specifically protein S12 of 16S rRNA) → misreading of mRNA → wrong amino acids inserted → bactericidal. Also active against Mycobacterium tuberculosis (used in TB regimen).
Resistance: Methylation of 16S rRNA; mutations in rpsL/rrs genes (encoding S12 protein); aminoglycoside-modifying enzymes
P/K: IM injection only. Not absorbed orally. Poor CNS penetration. Renal excretion. T½ ~2-3 hours. TDM recommended.
Uses:
- TB (Category II retreatment regimen; or when other drugs contraindicated)
- Plague (Yersinia pestis) - DOC
- Tularaemia (Francisella tularensis) - DOC
- Brucellosis (+ doxycycline - synergistic)
- Streptococcal endocarditis (synergy with penicillin)
Adverse Effects:
- Vestibular ototoxicity more than cochlear (unlike other aminoglycosides which cause more cochlear toxicity first)
- Nephrotoxicity (less than gentamicin)
- Neuromuscular blockade
- Optic neuritis (rare)
C/I: Pregnancy (ABSOLUTE - causes congenital deafness); Renal failure; Myasthenia gravis; Prior ototoxicity
Drug Interactions: Same as gentamicin (loop diuretics, vancomycin, NMBs)
Q.23 - Urinary Antiseptics (Short Note)
Definition: Drugs that achieve high concentrations specifically in urine and are used to treat or prevent urinary tract infections. They are NOT used for systemic infections (insufficient blood/tissue levels).
1. Nitrofurantoin
Disease: Uncomplicated lower UTI (cystitis), recurrent UTI prophylaxis
Class: Nitrofuran antibiotic
MOA: Reduced by bacterial nitroreductase enzymes (present in E. coli) → reactive intermediates → damage DNA, ribosomes, and metabolic enzymes simultaneously → bactericidal. Concentrates in urine (acidic urine enhances activity)
P/K: Oral only. Rapidly absorbed. Rapidly excreted in urine (high urinary levels). Blood levels negligible (hence only useful for lower UTI, NOT pyelonephritis). T½ ~20 min (plasma), but active in urine for hours
Uses: Uncomplicated UTI (E. coli, S. saprophyticus); Recurrent UTI prophylaxis (50-100 mg at bedtime); Safe in pregnancy (avoid at term)
Adverse Effects: Nausea, vomiting (take with food); Pulmonary toxicity (acute: hypersensitivity pneumonitis; chronic: pulmonary fibrosis with long-term use); Peripheral neuropathy (prolonged); Haemolytic anaemia (G6PD deficiency); Brown urine discolouration (harmless); Hepatotoxicity (rare)
C/I: eGFR <30 mL/min (drug does not concentrate in urine adequately + accumulates → toxicity); Near-term pregnancy (neonatal haemolysis); G6PD deficiency; Infants <1 month
Drug Interactions: Antacids ↓ absorption; Probenecid/Sulfinpyrazone ↓ urinary excretion → ↓ efficacy
2. Fosfomycin
Disease: Uncomplicated UTI (including ESBL-producing E. coli)
Class: Phosphonic acid antibiotic
MOA: Inhibits MurA (UDP-N-acetylglucosamine enolpyruvyl transferase) - the first enzyme in peptidoglycan synthesis → bactericidal. Concentrates in urine. Active against many beta-lactam and fluoroquinolone-resistant strains
Uses: Single 3g oral dose for uncomplicated cystitis. Increasingly used for ESBL-producing E. coli and VRE UTI
Adverse Effects: Diarrhoea, nausea (generally well-tolerated)
C/I: Severe renal failure
3. Methenamine (Methenamine Mandelate / Hippurate)
Disease: Recurrent UTI prophylaxis (not for acute treatment)
Class: Formaldehyde-releasing prodrug
MOA: In acidic urine (pH <6) → decomposes to release formaldehyde → non-specific bactericidal (denatures proteins, DNA) → prevents bacterial colonisation
Uses: Long-term UTI prophylaxis (especially post-urological procedures, neurogenic bladder); NOT for treatment of acute UTI
C/I: Sulfonamide concurrent use (formaldehyde + sulfa → precipitates in urine → haematuria); Renal failure; Liver failure; Metabolic acidosis cannot be induced (requires acid urine)
4. Trimethoprim (alone) & Co-trimoxazole
Already covered in Q.29 of previous session. Trimethoprim 100 mg BD × 7 days used for uncomplicated UTI; Co-trimoxazole 960 mg BD × 3 days if local resistance <20%.
5. Fluoroquinolones (Norfloxacin/Ciprofloxacin for UTI)
- Norfloxacin: Older fluoroquinolone with highest urinary concentration relative to serum - used specifically for UTI (poor systemic tissue levels compared to ciprofloxacin)
- Ciprofloxacin: Used for complicated UTI, pyelonephritis (also achieves systemic levels for upper UTI)
Summary Table - Urinary Antiseptics:
| Drug | Route | Dose | Best Use | Caution |
|---|---|---|---|---|
| Nitrofurantoin | Oral | 100mg SR BD ×5d | Uncomplicated cystitis; prophylaxis | eGFR <30; near-term pregnancy |
| Fosfomycin | Oral | 3g single dose | Uncomplicated cystitis (incl. ESBL) | Severe renal failure |
| Methenamine | Oral | 1g QID | Long-term prophylaxis only | Sulfonamides; alkaline urine |
| Norfloxacin | Oral | 400mg BD ×3-7d | UTI (use sparingly - reserve) | Children, pregnancy, resistance |
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Antimicrobial StudyGuide Set2
PDF Document · PDF
What's inside:
| Feature | Details |
|---|---|
| Cover page | Title, topic list, date, format key |
| Table of contents | All 23 questions indexed |
| Questions covered | Q1–Q23 in full |
| Format | Every answer uses the short note structure from your 2nd attachment: Disease → Class → MOA (& Resistance) → P/K → Uses → ADRs → C/I → Drug Interactions |
| Special topics | Comparison tables for Q2 (Ampicillin vs Amoxicillin), Q7 (Cefuroxime vs Ceftriaxone), Q8 (Pen G vs Amoxicillin), Q13 (Concentration vs Time-dependent killing), Q18 (Aminoglycosides vs Macrolides), Q21 (Macrolides vs Chloramphenicol) |
| Design | Color-coded banners per question, alternating row shading, navy header/gold footer on every page |
| Key highlights | ★ tip boxes — Red Man Syndrome prevention, INH/ethionamide cross-resistance mechanism, streptomycin absolute CI in pregnancy, Augmentin cholestatic jaundice warning |
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