Pharmacology
MBBS Pharmacology — high-yield long questions and short notes from K.D. Tripathi, covering general pharmacology, autonomic and cardiovascular drugs, CNS, autacoids, chemotherapy, endocrine and more, written to the marks with mechanisms, classification, clinical uses, adverse effects and pearls.
12chapters144questions99High-Yield
Definition
Antitubercular drugs treat tuberculosis using multidrug regimens to prevent resistance and eradicate persisting bacilli.
First-Line Drugs
- Isoniazid (H) — inhibits mycolic acid synthesis
- Rifampicin (R) — inhibits DNA-dependent RNA polymerase
- Pyrazinamide (Z) — acts in acidic environment
- Ethambutol (E) — inhibits arabinosyl transferase
Regimen (DOTS)
- Intensive phase — 2 months HRZE
- Continuation phase — 4 months HRE
- Directly observed therapy improves compliance
Second-Line
- Fluoroquinolones, aminoglycosides, bedaquiline, linezolid (for MDR-TB)
Multidrug therapy in two phases kills bacilli and prevents resistance. Drug Key toxicity Isoniazid Hepatitis, neuropathy Rifampicin Hepatitis, orange urine Ethambutol Optic neuritis Pyrazinamide Hyperuricaemia Applied
- Pyridoxine prevents isoniazid neuropathy
- Never add a single drug to a failing regimen
🔑KEY POINTS TO REMEMBER- First-line: isoniazid, rifampicin, pyrazinamide, ethambutol (HRZE).
- 2 months intensive + 4 months continuation (DOTS).
- Toxicities: hepatitis (H, R), optic neuritis (E), hyperuricaemia (Z).
📚SOURCES: Essentials of Medical Pharmacology (K.D. Tripathi); Goodman & Gilman’s The Pharmacological Basis of Therapeutics; Katzung’s Basic & Clinical Pharmacology.Definition
Antifungal drugs treat fungal infections by targeting ergosterol, the fungal cell membrane sterol, or the cell wall.
Classes & Mechanisms
- Polyenes — amphotericin B, nystatin (bind ergosterol → pores)
- Azoles — fluconazole, itraconazole, ketoconazole (inhibit ergosterol synthesis)
- Echinocandins — caspofungin (inhibit β-glucan cell-wall synthesis)
- Others — griseofulvin, terbinafine, flucytosine
Uses
- Superficial — candidiasis, dermatophytosis (topical azoles, terbinafine)
- Systemic — cryptococcal meningitis, invasive aspergillosis (amphotericin B, voriconazole)
Most antifungals attack ergosterol, absent from human membranes. Class Target Example Polyene Binds ergosterol Amphotericin B Azole Ergosterol synthesis Fluconazole Echinocandin Cell wall Caspofungin Applied
- Amphotericin B — nephrotoxic (‘ampho-terrible’)
- Azoles inhibit cytochrome P450 (interactions)
🔑KEY POINTS TO REMEMBER- Antifungals target ergosterol (polyenes, azoles) or cell wall (echinocandins).
- Amphotericin B for severe systemic mycoses — nephrotoxic.
- Azoles cause P450 drug interactions.
📚SOURCES: Essentials of Medical Pharmacology (K.D. Tripathi); Goodman & Gilman’s The Pharmacological Basis of Therapeutics; Katzung’s Basic & Clinical Pharmacology.Definition
Antiviral drugs inhibit specific steps of viral replication without seriously harming host cells.
Classes by Virus
- Herpes — aciclovir, valaciclovir, ganciclovir
- Influenza — oseltamivir (neuraminidase inhibitor)
- Hepatitis B/C — tenofovir, entecavir, sofosbuvir
- HIV — zidovudine, tenofovir, efavirenz, ritonavir, dolutegravir
Mechanisms
- Inhibit viral DNA polymerase (aciclovir)
- Inhibit reverse transcriptase (zidovudine)
- Inhibit protease / integrase
- Block viral release (oseltamivir)
Each drug halts a distinct stage of the viral replication cycle. Virus Drug Herpes Aciclovir Influenza Oseltamivir HIV Zidovudine, dolutegravir Applied
- HIV needs combination therapy (HAART)
- Antivirals are virustatic, not curative in most cases
🔑KEY POINTS TO REMEMBER- Antivirals inhibit specific replication steps.
- Aciclovir (herpes), oseltamivir (influenza), HAART (HIV).
- Combination therapy prevents resistance in HIV.
📚SOURCES: Essentials of Medical Pharmacology (K.D. Tripathi); Goodman & Gilman’s The Pharmacological Basis of Therapeutics; Katzung’s Basic & Clinical Pharmacology.Definition
Antimalarial drugs act on different stages of the malarial parasite to treat acute attacks, prevent relapse or provide prophylaxis.
Drugs by Action
- Blood schizonticides — chloroquine, artemisinin, quinine (clinical cure)
- Tissue schizonticide — primaquine (radical cure, prevents relapse)
- Gametocidal — primaquine
- Others — mefloquine, doxycycline (prophylaxis)
Current Treatment
- ACT (artemisinin-based combination therapy) for falciparum malaria
- Chloroquine for sensitive vivax malaria
- Primaquine added for vivax (14 days) to prevent relapse
- Severe malaria — IV artesunate
Blood-stage drugs cure the attack; primaquine clears the liver reservoir. Drug Stage Purpose Artemisinin Blood Clinical cure Chloroquine Blood Vivax malaria Primaquine Liver Radical cure Applied
- Primaquine causes haemolysis in G6PD deficiency
- Chloroquine resistance is widespread in falciparum malaria
🔑KEY POINTS TO REMEMBER- Blood schizonticides (ACT, chloroquine) treat the acute attack.
- Primaquine gives radical cure (kills liver hypnozoites).
- Severe malaria → IV artesunate; check G6PD before primaquine.
📚SOURCES: Essentials of Medical Pharmacology (K.D. Tripathi); Goodman & Gilman’s The Pharmacological Basis of Therapeutics; Katzung’s Basic & Clinical Pharmacology.Definition
Anthelmintic drugs eliminate parasitic worms by paralysing them or disrupting their metabolism.
Main Drugs
- Albendazole / mebendazole — inhibit microtubules (broad spectrum)
- Ivermectin — opens chloride channels → paralysis
- Praziquantel — ↑ calcium permeability (flukes, tapeworms)
- Diethylcarbamazine — filariasis
- Pyrantel pamoate — depolarising neuromuscular block
Uses
- Roundworm, hookworm, threadworm — albendazole
- Tapeworm, schistosomiasis — praziquantel
- Filariasis — diethylcarbamazine
- Strongyloidiasis, scabies — ivermectin
Paralysed or energy-starved worms detach and are passed out. Drug Worm Albendazole Roundworm, hookworm Praziquantel Tapeworm, fluke DEC Filaria Applied
- Mass deworming programmes (albendazole)
- Treat all family members in threadworm infection
🔑KEY POINTS TO REMEMBER- Albendazole/mebendazole inhibit microtubules — broad spectrum.
- Praziquantel for tapeworms and flukes; DEC for filariasis.
- Ivermectin for strongyloidiasis and scabies.
📚SOURCES: Essentials of Medical Pharmacology (K.D. Tripathi); Goodman & Gilman’s The Pharmacological Basis of Therapeutics; Katzung’s Basic & Clinical Pharmacology.Definition
Isoniazid (INH) is the most important first-line antitubercular drug, bactericidal against actively multiplying bacilli.
Mechanism & Features
- Inhibits mycolic acid synthesis (cell wall)
- Bactericidal to dividing bacilli
- Well absorbed orally; penetrates CSF
- Metabolised by acetylation (fast/slow acetylators)
Adverse Effects
- Peripheral neuropathy (pyridoxine deficiency)
- Hepatitis (age-related)
- Hypersensitivity, lupus-like syndrome
- Enzyme inhibitor
Without mycolic acid the mycobacterial wall cannot be built. Adverse effect Prevention Neuropathy Pyridoxine (B6) Hepatitis Monitor LFTs Applied
- Pyridoxine 10 mg daily prevents neuropathy
- Slow acetylators at higher risk of neuropathy
🔑KEY POINTS TO REMEMBER- Isoniazid inhibits mycolic acid synthesis — bactericidal.
- Adverse: peripheral neuropathy, hepatitis.
- Pyridoxine prevents neuropathy; slow acetylators at risk.
📚SOURCES: Essentials of Medical Pharmacology (K.D. Tripathi); Goodman & Gilman’s The Pharmacological Basis of Therapeutics; Katzung’s Basic & Clinical Pharmacology.Definition
Rifampicin is a bactericidal antitubercular drug that inhibits bacterial DNA-dependent RNA polymerase.
Mechanism & Features
- Inhibits DNA-dependent RNA polymerase → ↓ RNA synthesis
- Bactericidal to both dividing and dormant bacilli
- Excellent tissue and CSF penetration
- Potent enzyme inducer
Uses & Adverse Effects
- Tuberculosis, leprosy
- Meningococcal and H. influenzae prophylaxis
- Adverse: hepatitis, orange-red urine/secretions, flu-like syndrome
- Interactions: ↓ oral contraceptives, warfarin, antiretrovirals
Blocking RNA polymerase halts all bacterial protein production. Feature Detail Target RNA polymerase Marker effect Orange urine Interaction Enzyme inducer Applied
- Warn patients about orange urine (harmless)
- Oral contraceptive failure → advise alternative contraception
🔑KEY POINTS TO REMEMBER- Rifampicin inhibits DNA-dependent RNA polymerase — bactericidal.
- Orange-red urine and secretions are characteristic.
- Potent enzyme inducer → many drug interactions.
📚SOURCES: Essentials of Medical Pharmacology (K.D. Tripathi); Goodman & Gilman’s The Pharmacological Basis of Therapeutics; Katzung’s Basic & Clinical Pharmacology.Definition
Multidrug therapy (MDT) for leprosy uses a combination of drugs to cure infection and prevent resistance, as recommended by the WHO.
Drugs
- Dapsone — inhibits folate synthesis (bacteriostatic)
- Rifampicin — most potent bactericidal
- Clofazimine — binds DNA; also anti-inflammatory
WHO Regimens
- Paucibacillary — rifampicin (monthly) + dapsone (daily) for 6 months
- Multibacillary — rifampicin + clofazimine + dapsone for 12 months
- Rifampicin doses supervised
Combination therapy for a fixed duration cures leprosy and blocks resistance. Drug Key adverse effect Dapsone Haemolysis (G6PD) Clofazimine Skin pigmentation Rifampicin Hepatitis Applied
- Lepra reactions treated with steroids / thalidomide
- Free MDT under the national programme
🔑KEY POINTS TO REMEMBER- Leprosy MDT: rifampicin + dapsone ± clofazimine.
- Paucibacillary 6 months; multibacillary 12 months.
- Clofazimine causes skin pigmentation; dapsone causes haemolysis.
📚SOURCES: Essentials of Medical Pharmacology (K.D. Tripathi); Goodman & Gilman’s The Pharmacological Basis of Therapeutics; Katzung’s Basic & Clinical Pharmacology.Definition
Amphotericin B is a polyene antifungal, the drug of choice for severe systemic fungal infections.
Mechanism & Spectrum
- Binds ergosterol in the fungal membrane
- Forms pores → leakage of ions → fungal death
- Fungicidal, broadest antifungal spectrum
- Given IV (not absorbed orally)
Uses & Toxicity
- Cryptococcal meningitis, invasive aspergillosis, mucormycosis
- Visceral leishmaniasis (kala-azar)
- Adverse: nephrotoxicity, infusion fever/chills, hypokalaemia, anaemia
- Liposomal form is less toxic
Pore formation in the ergosterol-rich membrane kills the fungus. Feature Detail Target Ergosterol Main toxicity Nephrotoxicity Safer form Liposomal Applied
- Premedicate and hydrate to limit toxicity
- Monitor renal function and potassium
🔑KEY POINTS TO REMEMBER- Amphotericin B binds ergosterol → membrane pores → fungicidal.
- Used in severe systemic mycoses and kala-azar.
- Nephrotoxic; liposomal form is safer.
📚SOURCES: Essentials of Medical Pharmacology (K.D. Tripathi); Goodman & Gilman’s The Pharmacological Basis of Therapeutics; Katzung’s Basic & Clinical Pharmacology.Definition
Aciclovir is an antiviral nucleoside analogue selectively active against herpes viruses.
Mechanism (selective toxicity)
- Activated by viral thymidine kinase → aciclovir monophosphate
- Host enzymes complete phosphorylation
- Inhibits viral DNA polymerase + chain termination
- Active only in infected cells (highly selective)
Uses & Adverse Effects
- Herpes simplex — genital, labial, encephalitis
- Varicella zoster (chickenpox, shingles)
- Adverse: generally well tolerated; nephrotoxicity with rapid IV, neurotoxicity
Only virus-infected cells activate the drug, giving high selectivity. Feature Detail Activation Viral thymidine kinase Target Viral DNA polymerase Use Herpes, varicella zoster Applied
- IV aciclovir for herpes encephalitis (urgent)
- Maintain hydration during IV therapy
🔑KEY POINTS TO REMEMBER- Aciclovir is activated by viral thymidine kinase (selective).
- Inhibits viral DNA polymerase → chain termination.
- Drug of choice for herpes simplex and varicella zoster.
📚SOURCES: Essentials of Medical Pharmacology (K.D. Tripathi); Goodman & Gilman’s The Pharmacological Basis of Therapeutics; Katzung’s Basic & Clinical Pharmacology.Definition
Zidovudine (AZT) is a nucleoside reverse transcriptase inhibitor (NRTI) used in HIV infection.
Mechanism
- Thymidine analogue, phosphorylated intracellularly
- Inhibits reverse transcriptase
- Causes DNA chain termination
- ↓ Viral replication (virustatic)
Uses & Adverse Effects
- HIV infection (as part of combination therapy — HAART)
- Prevention of mother-to-child transmission
- Post-exposure prophylaxis
- Adverse: bone-marrow suppression (anaemia, neutropenia), myopathy, lactic acidosis
Blocking reverse transcription stops HIV converting RNA into DNA. Feature Detail Class NRTI Target Reverse transcriptase Main toxicity Marrow suppression Applied
- Never used alone (resistance develops quickly)
- Monitor haemoglobin and blood counts
🔑KEY POINTS TO REMEMBER- Zidovudine = NRTI inhibiting reverse transcriptase.
- Used in HAART and prevention of mother-to-child transmission.
- Main toxicity: bone-marrow suppression (anaemia).
📚SOURCES: Essentials of Medical Pharmacology (K.D. Tripathi); Goodman & Gilman’s The Pharmacological Basis of Therapeutics; Katzung’s Basic & Clinical Pharmacology.Definition
Diethylcarbamazine (DEC) is the drug of choice for lymphatic filariasis, active against microfilariae and adult worms.
Mechanism & Spectrum
- Alters microfilarial surface → enhanced phagocytosis
- Immobilises microfilariae
- Also partly macrofilaricidal (kills adult worms)
- Effective against Wuchereria bancrofti, Brugia malayi, loiasis
Uses & Adverse Effects
- Lymphatic filariasis (with albendazole in mass programmes)
- Tropical pulmonary eosinophilia
- Adverse: Mazzotti reaction (fever, itching, lymphadenitis) from dying parasites
- Headache, nausea
DEC exposes microfilariae so the host immune system can clear them. Feature Detail Use Lymphatic filariasis Reaction Mazzotti (dying parasites) Applied
- Mass drug administration for filariasis elimination
- Avoid in onchocerciasis (severe eye reaction)
🔑KEY POINTS TO REMEMBER- DEC is the drug of choice for lymphatic filariasis.
- Immobilises microfilariae → phagocytosis; partly kills adults.
- Mazzotti reaction from dying parasites; avoid in onchocerciasis.
📚SOURCES: Essentials of Medical Pharmacology (K.D. Tripathi); Goodman & Gilman’s The Pharmacological Basis of Therapeutics; Katzung’s Basic & Clinical Pharmacology.