Explain definition, classification, pharmacodynamics, pharmacokinetics, indica, contraindications, adverse effect, side effects, of anticonvulsant in PharmacologyExplain definition, classification, pharmacodynamics, pharmacokinetics, indica, contraindications, adverse effect, side effects, of antipsychotic in Pharmacology
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PART 1: ANTICONVULSANTS (Antiepileptic / Antiseizure Medications)
Source: Katzung's Basic and Clinical Pharmacology, 16th Edition
1. Definition
Anticonvulsants (also called antiepileptic drugs, AEDs, or antiseizure medications, ASMs) are agents that prevent or reduce the frequency, severity, and duration of seizures in patients with epilepsy and other conditions associated with abnormal neuronal discharges. They act by suppressing the initiation or spread of epileptiform electrical activity in the CNS without necessarily eliminating the underlying cause.
A seizure is a transient occurrence of signs and/or symptoms resulting from abnormal excessive or synchronous neuronal activity in the brain. Epilepsy is defined as a disorder characterized by recurrent unprovoked seizures.
2. Classification
By Seizure Type (International League Against Epilepsy - ILAE Classification)
| Seizure Category | Type |
|---|---|
| Focal onset | Focal aware (formerly simple partial), Focal impaired awareness (formerly complex partial), Focal-to-bilateral tonic-clonic |
| Generalized onset | Tonic-clonic (grand mal), Absence (petit mal), Myoclonic, Atonic (drop seizure), Epileptic spasms (e.g., West syndrome) |
| Unknown onset | Unclassified |
By Drug Class / Mechanism
| Class | Examples |
|---|---|
| Sodium channel blockers | Phenytoin, Carbamazepine, Oxcarbazepine, Lamotrigine, Lacosamide, Valproate (partial) |
| Calcium channel modulators (T-type) | Ethosuximide, Valproate |
| GABA enhancers | Phenobarbital, Benzodiazepines (diazepam, clonazepam, lorazepam), Valproate, Gabapentin, Pregabalin, Vigabatrin, Tiagabine |
| Glutamate (NMDA/AMPA) antagonists | Perampanel, Felbamate, Topiramate (partial) |
| SV2A ligands (synaptic vesicle) | Levetiracetam, Brivaracetam |
| Multiple mechanisms | Valproate, Topiramate, Zonisamide, Felbamate |
| Newer/novel agents | Cenobamate, Fenfluramine (Dravet syndrome), Cannabidiol |
By Generation
- Older (1st generation): Phenobarbital, Phenytoin, Carbamazepine, Ethosuximide, Valproate, Primidone
- Newer (2nd/3rd generation): Lamotrigine, Levetiracetam, Topiramate, Oxcarbazepine, Gabapentin, Pregabalin, Lacosamide, Perampanel, Cenobamate
3. Pharmacodynamics (Mechanism of Action)
A. Sodium Channel Blockade
Phenytoin, Carbamazepine, Lamotrigine, Oxcarbazepine - These drugs bind to the inactivated state of voltage-gated Na+ channels, prolonging their inactivated state. This is called use-dependent (frequency-dependent) blockade - they act more on rapidly firing neurons. Result: stabilization of the neuronal membrane, preventing repetitive firing.
B. Calcium Channel Blockade (T-type)
Ethosuximide, Valproate - Inhibit low-threshold T-type calcium currents (IT) in thalamic neurons, which are responsible for the 3-Hz spike-and-wave discharge of absence seizures. Thalamic neurons are the pacemakers for absence epilepsy.
C. Enhancement of GABA-mediated Inhibition
- Benzodiazepines (diazepam, clonazepam) - Bind to the GABA-A receptor, increasing the frequency of Cl⁻ channel opening → hyperpolarization
- Barbiturates (phenobarbital) - Bind to GABA-A receptor at a different site, increasing the duration of Cl⁻ channel opening; also directly activate the channel at high doses
- Vigabatrin - Irreversibly inhibits GABA transaminase (the enzyme that breaks down GABA), increasing synaptic GABA
- Tiagabine - Blocks the GABA reuptake transporter (GAT-1), increasing synaptic GABA
- Gabapentin, Pregabalin - Bind to the α2δ subunit of voltage-gated Ca²⁺ channels, reducing glutamate, noradrenaline, and substance P release (despite the name, they do NOT directly act on GABA receptors)
D. Glutamate Antagonism
- Perampanel - Selective, non-competitive AMPA receptor antagonist
- Felbamate - Blocks NMDA receptors and enhances GABA activity
E. SV2A Modulation
- Levetiracetam - Binds to synaptic vesicle protein SV2A, modulating synaptic vesicle exocytosis and reducing neurotransmitter release - a unique mechanism
F. Carbonic Anhydrase Inhibition
- Acetazolamide, Topiramate, Zonisamide - Inhibit carbonic anhydrase, contributing to anticonvulsant effects
4. Pharmacokinetics
General Principles
Most antiseizure medications follow linear (first-order) kinetics - a constant fraction per unit time is eliminated. Two important exceptions:
- Phenytoin - Exhibits zero-order (Michaelis-Menten, saturable) kinetics at therapeutic doses. As dose increases, hepatic metabolism saturates, causing disproportionately large rises in plasma levels from small dose increases. Half-life ranges from 12-36 hours (average ~24 hours in mid-therapeutic range), but extends significantly at higher concentrations.
- Gabapentin - Absorption via gut is saturation-limited (large neutral amino acid transporter system L), so bioavailability paradoxically falls at high doses.
Key Pharmacokinetic Parameters
| Drug | Route | Protein Binding | Half-life | Metabolism / Elimination |
|---|---|---|---|---|
| Phenytoin | Oral/IV | ~90% | 12-36 h (dose-dependent) | Hepatic CYP2C9/2C19; zero-order at high doses |
| Carbamazepine | Oral | 75-80% | 12-17 h (autoinduction) | Hepatic CYP3A4; active epoxide metabolite |
| Valproate | Oral/IV | 80-90% | 8-16 h | Hepatic glucuronidation + mitochondrial β-oxidation |
| Ethosuximide | Oral | Negligible | 40-50 h (adults) | Hepatic (CYP3A4), renal (25% unchanged) |
| Phenobarbital | Oral/IV/IM | 40-60% | 4-5 days | Hepatic CYP2C9; 25% renal unchanged |
| Lamotrigine | Oral | 55% | 24-35 h (alone); 12 h (+ enzyme inducers) | Hepatic glucuronidation (UGT1A4) |
| Levetiracetam | Oral/IV | <10% | 6-8 h | Hydrolysis; 66% renal elimination unchanged |
| Gabapentin | Oral | Negligible | 5-9 h | Renal elimination unchanged; NOT metabolized |
| Topiramate | Oral | 15-41% | 20-30 h | 70% renal elimination; some hepatic |
| Oxcarbazepine | Oral | 40% | 8-10 h (active MHD metabolite) | Hepatic; renal excretion of metabolite |
Enzyme-inducing ASMs (phenytoin, carbamazepine, phenobarbital, primidone) stimulate CYP450 enzymes, reducing levels of many co-administered drugs including other ASMs, oral contraceptives, warfarin, and immunosuppressants.
5. Indications
| Drug | Primary Indication |
|---|---|
| Phenytoin / Fosphenytoin | Focal seizures, tonic-clonic seizures, status epilepticus (IV) |
| Carbamazepine | Focal seizures, trigeminal neuralgia, bipolar disorder |
| Valproate | Broad-spectrum: all seizure types esp. generalized (absence, myoclonic, tonic-clonic), migraine prophylaxis, bipolar |
| Ethosuximide | Absence seizures (drug of choice for pure absence) |
| Phenobarbital | Tonic-clonic, focal, neonatal seizures, status epilepticus |
| Lamotrigine | Focal, tonic-clonic, absence, Lennox-Gastaut, bipolar depression |
| Levetiracetam | Focal, myoclonic, tonic-clonic, adjunctive; status epilepticus (IV) |
| Gabapentin | Focal seizures (adjunctive), neuropathic pain, postherpetic neuralgia |
| Topiramate | Focal, tonic-clonic, Lennox-Gastaut, migraine prophylaxis |
| Diazepam / Lorazepam | Acute seizures, status epilepticus |
| Clonazepam | Absence, myoclonic, atonic seizures, panic disorder |
Other indications shared by some anticonvulsants:
- Neuropathic pain (gabapentin, pregabalin, carbamazepine)
- Bipolar disorder (valproate, lamotrigine, carbamazepine)
- Migraine prophylaxis (valproate, topiramate)
- Trigeminal neuralgia (carbamazepine, oxcarbazepine)
6. Contraindications
| Drug | Contraindications |
|---|---|
| Phenytoin | Sinus bradycardia, SA/AV block, Adams-Stokes syndrome; hypersensitivity; IV formulation: extravasation risk |
| Carbamazepine | History of bone marrow depression; MAO inhibitor use; hypersensitivity (cross-reactivity with other tricyclics); HLA-B*1502 allele (risk of SJS in Asian populations) |
| Valproate | Hepatic disease/dysfunction; mitochondrial disease (Alpers syndrome); pregnancy (Category X for neural tube defects); urea cycle disorders |
| Ethosuximide | Hypersensitivity to succinimides |
| Phenobarbital | Respiratory depression; hepatic impairment; porphyria |
| Lamotrigine | Hypersensitivity |
| Levetiracetam | Hypersensitivity (relatively few absolute contraindications) |
| Topiramate | Metabolic acidosis (relative); kidney stones history (relative); hypersensitivity; pregnancy (teratogenic) |
| Benzodiazepines | Acute narrow-angle glaucoma; severe hepatic impairment; concurrent use of strong CNS depressants (relative) |
7. Adverse Effects and Side Effects
Common CNS Effects (Class-wide)
- Sedation, drowsiness, fatigue
- Dizziness, ataxia, nystagmus (especially phenytoin, carbamazepine)
- Cognitive impairment, memory problems
- Diplopia, blurred vision
- Behavioral changes (mood disturbance, irritability - especially levetiracetam)
Drug-Specific Adverse Effects
| Drug | Key Adverse Effects |
|---|---|
| Phenytoin | Nystagmus, ataxia, diplopia (dose-related toxicity); gingival hyperplasia (chronic use); hirsutism; coarsening of facial features; peripheral neuropathy; teratogenicity (fetal hydantoin syndrome); rash; lymphadenopathy; osteomalacia; Purple Glove Syndrome (IV extravasation) |
| Carbamazepine | Diplopia, ataxia, nausea; aplastic anemia, agranulocytosis (rare but serious); Stevens-Johnson Syndrome (SJS)/TEN (especially HLA-B*1502); hyponatremia (SIADH); hepatotoxicity; teratogenicity |
| Valproate | Hepatotoxicity (especially children < 2 years; potentially fatal); pancreatitis; weight gain; hair loss (alopecia, sometimes with curly regrowth); tremor; teratogenicity (neural tube defects, spina bifida - 2-4% risk); thrombocytopenia; hyperammonemia |
| Ethosuximide | Nausea, hiccups, drowsiness; rare: SLE-like syndrome; blood dyscrasias |
| Phenobarbital | Sedation; cognitive impairment; dependence; tolerance; withdrawal seizures; osteoporosis (long-term); folate deficiency; teratogenicity; respiratory depression (overdose) |
| Lamotrigine | Rash (potentially life-threatening SJS/TEN - esp. with rapid dose titration or combined with valproate); diplopia; ataxia; headache; insomnia |
| Levetiracetam | Behavioral problems (agitation, aggression, irritability, psychosis); somnolence; fatigue - generally very well tolerated |
| Gabapentin | Somnolence, dizziness, ataxia, weight gain, edema; rare: respiratory depression (in combination with opioids) |
| Topiramate | Word-finding difficulty/cognitive slowing ("Dopamax"); weight loss (anorexia); kidney stones (nephrolithiasis); metabolic acidosis; paresthesias; teratogenicity (cleft lip/palate) |
| Vigabatrin | Irreversible visual field defects (peripheral vision loss) - limits use |
| Benzodiazepines | Tolerance; dependence; withdrawal; respiratory depression (IV); anterograde amnesia |
PART 2: ANTIPSYCHOTICS (Neuroleptics)
Source: Katzung's Basic and Clinical Pharmacology, 16th Edition
1. Definition
Antipsychotics (also called neuroleptics or major tranquilizers) are drugs that reduce psychotic symptoms - including hallucinations, delusions, disorganized thinking, and severe agitation - in a wide variety of psychiatric conditions. They are able to reduce psychotic symptoms in schizophrenia, bipolar disorder, psychotic depression, psychoses associated with dementia, and drug-induced psychoses.
A neuroleptic is a subtype of antipsychotic that produces a high incidence of extrapyramidal side effects (EPS) at clinically effective doses, or catalepsy in laboratory animals. The term distinguishes first-generation (typical) from second-generation (atypical) antipsychotics.
Psychosis is characterized by: inability to distinguish what is real from what is not; presence of delusions (false beliefs); hallucinations (usually auditory/visual); and grossly disorganized thinking in a clear sensorium.
2. Classification
A. First-Generation (Typical / Conventional) Antipsychotics
High D2/5-HT2A ratio - predominantly D2 blockers with high EPS risk.
| Chemical Class | Prototype Drug | Potency |
|---|---|---|
| Phenothiazines - Aliphatic | Chlorpromazine | Low potency |
| Phenothiazines - Piperazine | Fluphenazine, Trifluoperazine | High potency |
| Phenothiazines - Piperidine | Thioridazine | Low potency |
| Thioxanthenes | Thiothixene, Flupentixol | Medium potency |
| Butyrophenones | Haloperidol, Droperidol | High potency |
| Diphenylbutylpiperidines | Pimozide | High potency |
B. Second-Generation (Atypical) Antipsychotics
Low D2/5-HT2A ratio - combined D2 and 5-HT2A blockade; much lower EPS risk.
| Chemical Class | Drug |
|---|---|
| Dibenzodiazepine | Clozapine (prototype), Quetiapine |
| Benzisoxazole | Risperidone, Paliperidone, Iloperidone |
| Thienobenzodiazepine | Olanzapine |
| Dihydroindolone | Ziprasidone |
| Dihydrocarbostyril | Aripiprazole, Brexpiprazole, Cariprazine (partial D2 agonists) |
| Dibenzothiazepine | Quetiapine |
| Benzamide | Amisulpride |
| Other | Lurasidone, Asenapine, Lumateperone |
C. Third-Generation / Selective Agents
- Pimavanserin - Selective serotonin (5-HT2A) inverse agonist; NO dopamine antagonism; approved for Parkinson's disease psychosis
- Aripiprazole, Brexpiprazole, Cariprazine - Partial D2 agonists ("dopamine stabilizers")
3. Pharmacodynamics (Mechanism of Action)
The Dopamine Hypothesis
The cornerstone of antipsychotic action is D2 receptor blockade, particularly in the mesolimbic pathway (positive symptoms). Evidence:
- All effective antipsychotics block postsynaptic D2 receptors (or act as partial agonists)
- Drugs increasing dopamine (levodopa, amphetamines) worsen or induce psychosis
- D2 receptor density is increased postmortem in untreated schizophrenic brains
- Imaging shows increased striatal dopamine synthesis and release in schizophrenia
Dopamine Pathways & Clinical Relevance
| Pathway | Block Result | Clinical Effect |
|---|---|---|
| Mesolimbic | Reduces excess DA | Reduces positive symptoms (hallucinations, delusions) - desired |
| Mesocortical | Reduces DA | Worsens negative/cognitive symptoms - unwanted |
| Nigrostriatal | Reduces DA | Extrapyramidal side effects (EPS) - unwanted |
| Tuberoinfundibular | Reduces DA | Elevated prolactin (hyperprolactinemia) - unwanted |
The Serotonin Hypothesis (Atypical Antipsychotics)
5-HT2A receptor blockade is the key factor distinguishing atypical from typical antipsychotics. Atypical antipsychotics are inverse agonists at 5-HT2A receptors, blocking their constitutive activity. These receptors modulate the release of dopamine, norepinephrine, glutamate, GABA, and acetylcholine in cortex, limbic region, and striatum. The combination of D2 + 5-HT2A blockade is why atypicals treat negative symptoms better and cause fewer EPS.
5-HT2C inverse agonism - Many atypicals (clozapine, asenapine, olanzapine) also block 5-HT2C receptors, contributing to antipsychotic and metabolic effects.
Additional Receptor Profiles of Specific Drugs
- Clozapine - D1/D4 antagonism, 5-HT2A/2C inverse agonist, muscarinic M1 antagonist, H1 antagonist, α1 antagonist
- Aripiprazole/Cariprazine/Brexpiprazole - Partial agonists at D2 and D3 receptors (act as agonists when DA is low, antagonists when DA is high)
- Haloperidol - Highly selective D2 blocker; very high EPS, minimal sedation
- Chlorpromazine - D2 blocker + H1 + M1 + α1 antagonism → sedative, anticholinergic, hypotensive profile
4. Pharmacokinetics
General Principles
- Most antipsychotics are well-absorbed orally
- Undergo extensive first-pass hepatic metabolism
- High lipophilicity - distribute widely into tissues
- Highly protein-bound (90-99%)
- Long half-lives allow once-daily dosing for most
- Many have active metabolites (risperidone → paliperidone; thioridazine → mesoridazine)
- Available in long-acting injectable (LAI / depot) formulations for compliance: haloperidol decanoate, fluphenazine decanoate, risperidone microspheres, paliperidone palmitate, aripiprazole lauroxil
| Drug | Half-life | Active Metabolite | Notable PK Feature |
|---|---|---|---|
| Chlorpromazine | 8-35 h | Multiple | Significant first-pass; erratic absorption IM |
| Haloperidol | 18-40 h | Reduced haloperidol | CYP3A4/2D6 metabolism |
| Clozapine | 12 h | Norclozapine | CYP1A2 (smoking induces); requires blood monitoring |
| Risperidone | 3-24 h | Paliperidone (9-OH-risperidone) | CYP2D6 poor metabolizers have prolonged action |
| Olanzapine | 21-54 h | None active | CYP1A2 + 2D6; smoking lowers levels |
| Quetiapine | 6-7 h | Norquetiapine (active) | Twice-daily dosing |
| Aripiprazole | 75-146 h | Dehydro-aripiprazole | Very long half-life; once daily |
| Ziprasidone | 7 h | None | Must be taken with food (2x bioavailability) |
| Lurasidone | 18-40 h | Active metabolites | Must be taken with food (≥350 kcal) |
5. Indications
Primary
- Schizophrenia (acute and maintenance therapy) - all antipsychotics
- Bipolar disorder - manic episodes - approved: olanzapine, risperidone, quetiapine, aripiprazole, ziprasidone, asenapine, cariprazine
- Bipolar depression - quetiapine, lurasidone, cariprazine, lumateperone, olanzapine+fluoxetine
- Schizoaffective disorder
- Acute agitation (IM formulations) - haloperidol, lorazepam+haloperidol, ziprasidone IM, olanzapine IM, aripiprazole IM
- Psychotic depression (with antidepressant)
- Major depressive disorder - adjunctive - aripiprazole, quetiapine, brexpiprazole, olanzapine+fluoxetine
Secondary / Other
- Tourette syndrome - haloperidol, pimozide, aripiprazole
- Autism spectrum disorder (irritability) - risperidone, aripiprazole (FDA approved)
- Parkinson's disease psychosis - pimavanserin (no dopamine blockade), quetiapine (low EPS)
- Antiemetic - prochlorperazine, metoclopramide (D2 blockade)
- Delirium/ICU agitation - haloperidol (long-standing use)
- Chorea in Huntington's disease - haloperidol, tetrabenazine
6. Contraindications
| Category | Contraindications |
|---|---|
| All antipsychotics | CNS depression/coma; hypersensitivity to the specific agent |
| Typical antipsychotics | Parkinson's disease (worsen motor symptoms); Lewy body dementia (severe sensitivity reactions) |
| Clozapine | History of clozapine-induced agranulocytosis/granulocytopenia; severe CNS depression; uncontrolled epilepsy; myeloproliferative disorders; concurrent use of drugs causing agranulocytosis |
| Thioridazine | QTc prolongation; concurrent use of QT-prolonging drugs; reduced CYP2D6 metabolism |
| Ziprasidone | QTc prolongation; recent MI or uncompensated heart failure |
| Elderly with dementia | All antipsychotics carry an FDA Black Box Warning for increased mortality in elderly patients with dementia-related psychosis (both typical and atypical) |
| Pimavanserin | Drugs that prolong QT interval (relative) |
7. Adverse Effects and Side Effects
A. Extrapyramidal Side Effects (EPS)
These result from D2 blockade in the nigrostriatal pathway. Higher with typical (high-potency) antipsychotics.
| EPS Type | Onset | Features | Treatment |
|---|---|---|---|
| Acute dystonia | Hours to days | Sustained muscle contractions, oculogyric crisis, torticollis | Anticholinergics (benztropine, diphenhydramine) IM |
| Akathisia | Days to weeks | Subjective restlessness, inability to sit still | Propranolol, benzodiazepines, dose reduction |
| Parkinsonism (pseudo-parkinsonism) | Weeks | Bradykinesia, rigidity, tremor, masked facies | Anticholinergics (benztropine), dose reduction |
| Tardive Dyskinesia (TD) | Months to years | Involuntary oro-facial movements (lip smacking, grimacing, tongue protrusion), trunk/limb movements | VMAT2 inhibitors (valbenazine, deutetrabenazine); prevention by lowest effective dose |
B. Neuroleptic Malignant Syndrome (NMS)
A rare but life-threatening reaction: hyperthermia, muscle rigidity (lead-pipe), autonomic instability, altered consciousness, and elevated CK. Management: discontinue antipsychotic immediately, dantrolene, bromocriptine, supportive care.
C. Metabolic Effects (Mainly Atypicals)
- Weight gain: Most severe with clozapine and olanzapine; moderate with quetiapine and risperidone; least with aripiprazole, ziprasidone, lurasidone
- Hyperglycemia / Type 2 diabetes: Especially clozapine, olanzapine
- Dyslipidemia: Elevated triglycerides (olanzapine, clozapine)
- Metabolic syndrome
D. Endocrine - Hyperprolactinemia
D2 blockade in tuberoinfundibular pathway → elevated prolactin → galactorrhea, amenorrhea, gynecomastia, sexual dysfunction, decreased bone density. Most common with typical antipsychotics, risperidone, and paliperidone. Aripiprazole (partial agonist) does not raise prolactin.
E. Cardiovascular
- QTc prolongation and risk of torsades de pointes: especially thioridazine, ziprasidone, droperidol, haloperidol IV
- Orthostatic hypotension (α1 blockade): chlorpromazine, clozapine, quetiapine
- Myocarditis/cardiomyopathy (clozapine - rare but serious)
F. Anticholinergic Effects (from M1 blockade)
Dry mouth, constipation, urinary retention, blurred vision, tachycardia, confusion. Worst with clozapine, chlorpromazine, olanzapine.
G. Hematologic
- Agranulocytosis - clozapine carries a 1-2% risk; requires mandatory weekly CBC monitoring (REMS program). Other antipsychotics carry low but real risk.
- Leukopenia/neutropenia - clozapine, chlorpromazine
H. Sedation
From H1 (histamine) blockade: most sedating are clozapine, olanzapine, chlorpromazine, quetiapine. Least sedating: haloperidol, aripiprazole.
I. Seizure Threshold Lowering
Clozapine dose-dependently lowers seizure threshold and causes EEG changes.
J. Other Effects
- Photosensitivity and skin pigmentation (chlorpromazine, long-term)
- Cholestatic jaundice (phenothiazines)
- Pigmentary retinopathy (thioridazine at high doses > 800 mg/day)
- Corneal and lens deposits (chlorpromazine, high doses)
- Sexual dysfunction - most antipsychotics
- Venous thromboembolism - clozapine, low-potency typicals
Summary Comparison Table
| Feature | Anticonvulsants | Antipsychotics |
|---|---|---|
| Primary target | CNS neuronal excitability | Dopamine/serotonin receptors |
| Key mechanism | Na⁺/Ca²⁺ channel blockade, GABA enhancement, glutamate antagonism | D2 receptor blockade (±5-HT2A) |
| Main use | Epilepsy, neuropathic pain, bipolar (some) | Schizophrenia, bipolar, agitation |
| Serious toxicity | Teratogenicity (valproate, phenytoin), SJS (carbamazepine, lamotrigine), hepatotoxicity (valproate) | NMS, agranulocytosis (clozapine), QT prolongation, tardive dyskinesia |
| Monitoring | Serum drug levels (phenytoin, valproate, carbamazepine), LFTs, CBC | CBC (clozapine), metabolic panel, QTc, EPS assessment |
Source: Katzung's Basic and Clinical Pharmacology, 16th Edition; Goodman & Gilman's The Pharmacological Basis of Therapeutics, 14th Edition; Katzung's Basic and Clinical Pharmacology, 16th Edition
explain definition, classification, pharmacodynamics, pharmacokinetics, indica, contraindications, adverse effect, side effects, of hypnotic and sedative in pharmacolog
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