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.
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Definition
Sedative-hypnotics depress the CNS — sedatives calm, hypnotics induce sleep, and anxiolytics relieve anxiety.
Classification
- Benzodiazepines — diazepam, lorazepam, alprazolam
- Barbiturates — phenobarbitone (obsolete as hypnotics)
- Non-benzodiazepines (Z drugs) — zolpidem, zopiclone
- Buspirone, melatonin agonists
Mechanism
- Benzodiazepines — ↑ frequency of GABA-A chloride channel opening
- Barbiturates — ↑ duration of channel opening
- → CNS depression
Enhancing GABA lets chloride in, quieting neuronal firing. Drug GABA effect Safety Benzodiazepine ↑ Frequency Safer Barbiturate ↑ Duration Narrow margin Applied
- Insomnia, anxiety, preanaesthetic medication
- Flumazenil reverses benzodiazepines
🔑KEY POINTS TO REMEMBER- Benzodiazepines ↑ frequency, barbiturates ↑ duration of GABA-A opening.
- Benzodiazepines are safer (wider margin, antidote available).
- Flumazenil is the benzodiazepine antidote.
📚SOURCES: Essentials of Medical Pharmacology (K.D. Tripathi); Goodman & Gilman’s The Pharmacological Basis of Therapeutics; Katzung’s Basic & Clinical Pharmacology.Definition
Antiepileptic drugs prevent seizures by reducing neuronal excitability through ion channels or GABA enhancement.
Mechanisms
- Sodium-channel blockade — phenytoin, carbamazepine, lamotrigine
- Calcium-channel (T-type) blockade — ethosuximide
- GABA enhancement — valproate, benzodiazepines, phenobarbitone
- Multiple mechanisms — sodium valproate, levetiracetam
Drug of Choice
- Generalised tonic-clonic — valproate, carbamazepine
- Partial (focal) — carbamazepine, levetiracetam
- Absence — ethosuximide, valproate
- Status epilepticus — IV lorazepam / diazepam
Drugs either damp excitation through channels or boost inhibition. Seizure Drug of choice Tonic-clonic Valproate Absence Ethosuximide Status epilepticus IV lorazepam Applied
- Valproate is teratogenic (neural tube defects)
- Monotherapy preferred; withdraw gradually
🔑KEY POINTS TO REMEMBER- Mechanisms: Na⁺ block, T-type Ca²⁺ block, GABA enhancement.
- Tonic-clonic → valproate; absence → ethosuximide.
- Status epilepticus → IV benzodiazepine.
📚SOURCES: Essentials of Medical Pharmacology (K.D. Tripathi); Goodman & Gilman’s The Pharmacological Basis of Therapeutics; Katzung’s Basic & Clinical Pharmacology.Definition
Antipsychotic (neuroleptic) drugs treat schizophrenia and psychosis mainly by blocking dopamine D2 receptors.
Classification
- Typical (first generation) — chlorpromazine, haloperidol
- Atypical (second generation) — risperidone, olanzapine, clozapine, quetiapine
Mechanism & Differences
- Typical — strong D2 blockade → more extrapyramidal effects
- Atypical — D2 + 5-HT2 blockade → fewer extrapyramidal effects
- Atypicals better for negative symptoms
Blocking dopamine relieves psychosis but risks movement side effects. Group Example Main problem Typical Haloperidol Extrapyramidal Atypical Olanzapine Weight gain, diabetes Atypical Clozapine Agranulocytosis Applied
- Clozapine for resistant schizophrenia (monitor white cells)
- Neuroleptic malignant syndrome is a rare emergency
🔑KEY POINTS TO REMEMBER- Antipsychotics block dopamine D2 receptors.
- Typicals → extrapyramidal effects; atypicals → metabolic effects.
- Clozapine: resistant cases, causes agranulocytosis.
📚SOURCES: Essentials of Medical Pharmacology (K.D. Tripathi); Goodman & Gilman’s The Pharmacological Basis of Therapeutics; Katzung’s Basic & Clinical Pharmacology.Definition
Antidepressants relieve depression by increasing serotonin and/or noradrenaline at central synapses.
Classification
- SSRIs — fluoxetine, sertraline, escitalopram (first-line)
- SNRIs — venlafaxine, duloxetine
- Tricyclics — amitriptyline, imipramine
- MAO inhibitors — phenelzine, moclobemide
- Atypical — mirtazapine, bupropion
Key Points
- Effect takes 2–4 weeks
- SSRIs preferred (safer in overdose)
- Tricyclics — anticholinergic, cardiotoxic in overdose
- MAO inhibitors + tyramine → hypertensive crisis
Blocking reuptake raises transmitter levels; benefit takes weeks. Class Example Note SSRI Fluoxetine First-line TCA Amitriptyline Cardiotoxic MAOI Phenelzine Cheese reaction Applied
- Serotonin syndrome if SSRIs combined with MAO inhibitors
- Amitriptyline also used in neuropathic pain
🔑KEY POINTS TO REMEMBER- SSRIs first-line (fluoxetine, sertraline); take 2–4 weeks.
- Tricyclics cardiotoxic in overdose.
- MAO inhibitors + tyramine → hypertensive crisis.
📚SOURCES: Essentials of Medical Pharmacology (K.D. Tripathi); Goodman & Gilman’s The Pharmacological Basis of Therapeutics; Katzung’s Basic & Clinical Pharmacology.Definition
Anti-Parkinsonian drugs restore the dopamine-acetylcholine balance in the basal ganglia, which is lost in Parkinson’s disease.
Dopaminergic Drugs
- Levodopa + carbidopa — most effective
- Dopamine agonists — bromocriptine, pramipexole, ropinirole
- MAO-B inhibitors — selegiline
- COMT inhibitors — entacapone
- Amantadine
Anticholinergics
- Trihexyphenidyl, benztropine
- Useful for tremor and drug-induced parkinsonism
Levodopa replaces dopamine; carbidopa keeps it from being wasted peripherally. Drug Action Levodopa Dopamine precursor Carbidopa Peripheral decarboxylase inhibitor Selegiline MAO-B inhibitor Applied
- Long-term levodopa → on-off phenomenon, dyskinesias
- Anticholinergics for drug-induced parkinsonism
🔑KEY POINTS TO REMEMBER- Levodopa + carbidopa is the most effective therapy.
- Carbidopa prevents peripheral conversion (↓ side effects).
- Long-term levodopa → on-off phenomenon and dyskinesias.
📚SOURCES: Essentials of Medical Pharmacology (K.D. Tripathi); Goodman & Gilman’s The Pharmacological Basis of Therapeutics; Katzung’s Basic & Clinical Pharmacology.Definition
Benzodiazepines are CNS depressants that enhance GABA-A action, producing anxiolytic, hypnotic, anticonvulsant and muscle-relaxant effects.
Mechanism
- Bind the GABA-A receptor benzodiazepine site
- ↑ Frequency of chloride channel opening
- Neuronal hyperpolarisation → CNS depression
Uses & Adverse Effects
- Anxiety, insomnia, status epilepticus
- Muscle spasm, alcohol withdrawal, preanaesthetic medication
- Adverse: sedation, dependence, tolerance, respiratory depression (IV)
Facilitating GABA hyperpolarises neurons and calms the CNS. Drug Duration Use Diazepam Long Status epilepticus Lorazepam Intermediate Anxiety, seizures Alprazolam Short Panic disorder Applied
- Flumazenil is the specific antidote
- Avoid abrupt withdrawal (seizures)
🔑KEY POINTS TO REMEMBER- Benzodiazepines ↑ frequency of GABA-A chloride channel opening.
- Uses: anxiety, insomnia, status epilepticus, alcohol withdrawal.
- Antidote = flumazenil; risk of dependence.
📚SOURCES: Essentials of Medical Pharmacology (K.D. Tripathi); Goodman & Gilman’s The Pharmacological Basis of Therapeutics; Katzung’s Basic & Clinical Pharmacology.Definition
Morphine is a natural opioid analgesic acting mainly on μ (mu) receptors to relieve severe pain.
Actions
- Potent analgesia (μ receptor agonist)
- Euphoria, sedation
- Respiratory depression (main danger)
- Miosis (pinpoint pupils), constipation
- Histamine release → itching
Uses & Adverse Effects
- Severe pain — myocardial infarction, cancer, trauma
- Acute pulmonary oedema
- Adverse: respiratory depression, constipation, dependence, vomiting
Mu-receptor activation blocks pain but also depresses respiration. Effect Detail Analgesia Severe pain Pupils Pinpoint miosis Danger Respiratory depression Applied
- Naloxone reverses overdose
- Triad of overdose: coma, pinpoint pupils, respiratory depression
🔑KEY POINTS TO REMEMBER- Morphine = μ receptor agonist → potent analgesia.
- Adverse: respiratory depression, miosis, constipation, dependence.
- Overdose triad reversed by naloxone.
📚SOURCES: Essentials of Medical Pharmacology (K.D. Tripathi); Goodman & Gilman’s The Pharmacological Basis of Therapeutics; Katzung’s Basic & Clinical Pharmacology.Definition
Phenytoin is an antiepileptic that blocks voltage-gated sodium channels, stabilising neuronal membranes.
Mechanism & Kinetics
- Blocks sodium channels (use-dependent)
- Prolongs the inactivated state
- Zero-order kinetics at therapeutic doses
- Narrow therapeutic index; enzyme inducer
Uses & Adverse Effects
- Generalised tonic-clonic and partial seizures
- Status epilepticus (IV fosphenytoin)
- Adverse: gum hypertrophy, hirsutism, ataxia, nystagmus, megaloblastic anaemia
- Teratogenic (fetal hydantoin syndrome)
Sodium-channel blockade prevents the rapid firing that drives seizures. Feature Detail Kinetics Zero-order Classic adverse Gum hypertrophy Enzyme Inducer Applied
- Small dose increase → toxicity (zero-order)
- Monitor serum levels
🔑KEY POINTS TO REMEMBER- Phenytoin blocks sodium channels (use-dependent).
- Zero-order kinetics → toxicity with small dose rises.
- Adverse: gum hypertrophy, hirsutism, ataxia; teratogenic.
📚SOURCES: Essentials of Medical Pharmacology (K.D. Tripathi); Goodman & Gilman’s The Pharmacological Basis of Therapeutics; Katzung’s Basic & Clinical Pharmacology.Definition
Lithium is a mood stabiliser used in bipolar disorder, with a very narrow therapeutic index.
Mechanism & Uses
- Interferes with inositol phosphate signalling
- Modifies neurotransmitter action
- Uses: acute mania, prophylaxis of bipolar disorder
- Excreted unchanged by the kidney
Toxicity
- Therapeutic range 0.6–1.2 mEq/L (narrow)
- Early: tremor, nausea, diarrhoea
- Toxic: ataxia, confusion, seizures, coma
- Chronic: hypothyroidism, diabetes insipidus
Lithium steadies mood but demands close blood-level monitoring. Feature Detail Range 0.6–1.2 mEq/L Excretion Renal Chronic effect Hypothyroidism Applied
- Diuretics and NSAIDs ↑ lithium levels (toxicity)
- Maintain hydration and sodium intake
🔑KEY POINTS TO REMEMBER- Lithium = mood stabiliser for bipolar disorder.
- Narrow range 0.6–1.2 mEq/L; renally excreted.
- Diuretics/NSAIDs → toxicity; chronic use → hypothyroidism.
📚SOURCES: Essentials of Medical Pharmacology (K.D. Tripathi); Goodman & Gilman’s The Pharmacological Basis of Therapeutics; Katzung’s Basic & Clinical Pharmacology.Definition
Naloxone is a pure opioid antagonist used as the specific antidote for opioid overdose.
Mechanism & Features
- Competitive antagonist at μ, κ, δ opioid receptors
- No agonist activity of its own
- Given IV — acts within 1–2 minutes
- Short duration (may need repeat doses)
Uses
- Opioid overdose (reverses respiratory depression)
- Reversal of opioid effect after anaesthesia
- Neonatal respiratory depression from maternal opioids
Naloxone competes opioids off their receptors, restoring breathing. Feature Detail Type Pure antagonist Onset 1–2 minutes IV Duration Short Applied
- Precipitates withdrawal in dependent patients
- Repeat doses needed (opioids outlast naloxone)
🔑KEY POINTS TO REMEMBER- Naloxone = pure opioid antagonist (μ, κ, δ).
- Antidote in opioid overdose; acts within minutes IV.
- Short-acting — repeat doses often required.
📚SOURCES: Essentials of Medical Pharmacology (K.D. Tripathi); Goodman & Gilman’s The Pharmacological Basis of Therapeutics; Katzung’s Basic & Clinical Pharmacology.Definition
Status epilepticus is a continuous seizure lasting over 5 minutes, or repeated seizures without recovery of consciousness — a medical emergency.
Immediate Management
- Airway, breathing, circulation; oxygen
- Check blood glucose; IV access
- IV lorazepam (or diazepam) — first-line
- If persists: IV fosphenytoin / phenytoin or valproate
- Refractory: general anaesthesia (thiopentone, midazolam infusion)
Treatment escalates stepwise from benzodiazepine to anaesthesia. Step Drug First-line IV lorazepam Second-line Fosphenytoin/valproate Refractory Midazolam/thiopentone Applied
- Commonest cause: antiepileptic withdrawal
- High mortality if untreated
🔑KEY POINTS TO REMEMBER- Status epilepticus = seizure >5 min or repeated without recovery.
- First-line IV lorazepam/diazepam; then phenytoin.
- Refractory cases need general anaesthesia.
📚SOURCES: Essentials of Medical Pharmacology (K.D. Tripathi); Goodman & Gilman’s The Pharmacological Basis of Therapeutics; Katzung’s Basic & Clinical Pharmacology.Definition
Extrapyramidal side effects (EPS) are movement disorders caused by dopamine D2 blockade in the nigrostriatal pathway by antipsychotics.
Types (by time of onset)
- Acute dystonia — hours–days (spasm, torticollis, oculogyric crisis)
- Akathisia — days–weeks (motor restlessness)
- Parkinsonism — weeks–months (tremor, rigidity, bradykinesia)
- Tardive dyskinesia — months–years (often irreversible)
Management
- Anticholinergics (trihexyphenidyl) for dystonia and parkinsonism
- β blockers for akathisia
- Switch to an atypical antipsychotic
- Tardive dyskinesia — stop or change drug (poor response)
Dopamine blockade in the nigrostriatal tract produces staged movement effects. Effect Onset Treatment Dystonia Hours Anticholinergic Akathisia Days β blocker Tardive dyskinesia Years Change drug Applied
- Atypical antipsychotics cause fewer EPS
- Tardive dyskinesia may be permanent
🔑KEY POINTS TO REMEMBER- EPS from D2 blockade in the nigrostriatal pathway.
- Sequence: dystonia → akathisia → parkinsonism → tardive dyskinesia.
- Atypicals cause fewer EPS; tardive dyskinesia often irreversible.
📚SOURCES: Essentials of Medical Pharmacology (K.D. Tripathi); Goodman & Gilman’s The Pharmacological Basis of Therapeutics; Katzung’s Basic & Clinical Pharmacology.