PSYCH DRUGS Flashcards
Haloperidol
First-generation antipsychotics (FGAs)
High-potency antipsychotics
Mechanism:
Dopamine-specific antagonism (D2 receptor) (potency of a substance is directly related to the degree of its D2 antagonism)
Clinical Use: Schizophrenia Bipolar disorder Acute psychosis Delirium Acute agitated states (e.g., patients who are agitated and aggressive due to alcohol and/or illicit drug use) Tourette syndrome OCD (concomitant therapy) Huntington disease
Adverse Effects:
Extrapyramidal symptoms most common in high-potency FGAs
Prolonged QT interval
Neuroleptic malignant syndrome
Lipid soluble –> stored in body fat –> slow to be removed from body.
Dopamine receptor antagonism –> hyperprolactinemia –> galactorrhea, oligomenorrhea, gynecomastia.
Dyslipidemia, weight gain, hyperglycemia.
Antimuscarinic (dry mouth, constipation)
Antihistamine (sedation)
α1-blockade (orthostatic hypotension)
Neuroleptic malignant syndrome.
Hyperthermia or hypothermia (believed to be due to the drug’s effect on the hypothalamus, which leads to inappropriate responses to heat (e.g., lack of sweating/peripheral vasodilation) or cold (e.g., lack of shivering))
Fluphenazine
First-generation antipsychotics (FGAs)
High-potency antipsychotics
Mechanism:
Dopamine-specific antagonism (D2 receptor) (potency of a substance is directly related to the degree of its D2 antagonism)
Clinical Use: Schizophrenia Bipolar disorder Acute psychosis Delirium Acute agitated states (e.g., patients who are agitated and aggressive due to alcohol and/or illicit drug use) Tourette syndrome OCD (concomitant therapy) Huntington disease
Adverse Effects:
Extrapyramidal symptoms most common in high-potency FGAs
Prolonged QT interval
Neuroleptic malignant syndrome
Lipid soluble –> stored in body fat –> slow to be removed from body.
Dopamine receptor antagonism –> hyperprolactinemia –> galactorrhea, oligomenorrhea, gynecomastia.
Dyslipidemia, weight gain, hyperglycemia.
Antimuscarinic (dry mouth, constipation)
Antihistamine (sedation)
α1-blockade (orthostatic hypotension)
Neuroleptic malignant syndrome.
Hyperthermia or hypothermia (believed to be due to the drug’s effect on the hypothalamus, which leads to inappropriate responses to heat (e.g., lack of sweating/peripheral vasodilation) or cold (e.g., lack of shivering))
Perphenazine
First-generation antipsychotics (FGAs)
High-potency antipsychotics
Mechanism:
Dopamine-specific antagonism (D2 receptor) (potency of a substance is directly related to the degree of its D2 antagonism)
Clinical Use: Schizophrenia Bipolar disorder Acute psychosis Delirium Acute agitated states (e.g., patients who are agitated and aggressive due to alcohol and/or illicit drug use) Tourette syndrome OCD (concomitant therapy) Huntington disease
Adverse Effects:
Extrapyramidal symptoms most common in high-potency FGAs
Prolonged QT interval
Neuroleptic malignant syndrome
Lipid soluble –> stored in body fat –> slow to be removed from body.
Dopamine receptor antagonism –> hyperprolactinemia –> galactorrhea, oligomenorrhea, gynecomastia.
Dyslipidemia, weight gain, hyperglycemia.
Antimuscarinic (dry mouth, constipation)
Antihistamine (sedation)
α1-blockade (orthostatic hypotension)
Neuroleptic malignant syndrome
Hyperthermia or hypothermia (believed to be due to the drug’s effect on the hypothalamus, which leads to inappropriate responses to heat (e.g., lack of sweating/peripheral vasodilation) or cold (e.g., lack of shivering))
Trifluoperazine
First-generation antipsychotics (FGAs)
High-potency antipsychotics
Mechanism:
Dopamine-specific antagonism (D2 receptor) (potency of a substance is directly related to the degree of its D2 antagonism)
Clinical Use: Schizophrenia Bipolar disorder Acute psychosis Delirium Acute agitated states (e.g., patients who are agitated and aggressive due to alcohol and/or illicit drug use) Tourette syndrome OCD (concomitant therapy) Huntington disease
Adverse Effects:
Extrapyramidal symptoms most common in high-potency FGAs
Prolonged QT interval
Neuroleptic malignant syndrome
Lipid soluble –> stored in body fat –> slow to be removed from body.
Dopamine receptor antagonism –> hyperprolactinemia –> galactorrhea, oligomenorrhea, gynecomastia.
Dyslipidemia, weight gain, hyperglycemia.
Antimuscarinic (dry mouth, constipation)
Antihistamine (sedation)
α1-blockade (orthostatic hypotension)
Hyperthermia or hypothermia (believed to be due to the drug’s effect on the hypothalamus, which leads to inappropriate responses to heat (e.g., lack of sweating/peripheral vasodilation) or cold (e.g., lack of shivering))
Pimozide
First-generation antipsychotics (FGAs)
High-potency antipsychotics
Mechanism:
Dopamine-specific antagonism (D2 receptor) (potency of a substance is directly related to the degree of its D2 antagonism)
Clinical Use: Schizophrenia Bipolar disorder Acute psychosis Delirium Acute agitated states (e.g., patients who are agitated and aggressive due to alcohol and/or illicit drug use) Tourette syndrome OCD (concomitant therapy) Huntington disease
Adverse Effects:
Extrapyramidal symptoms most common in high-potency FGAs
Prolonged QT interval
Neuroleptic malignant syndrome
Lipid soluble –> stored in body fat –> slow to be removed from body.
Dopamine receptor antagonism –> hyperprolactinemia –> galactorrhea, oligomenorrhea, gynecomastia.
Dyslipidemia, weight gain, hyperglycemia.
Antimuscarinic (dry mouth, constipation)
Antihistamine (sedation)
α1-blockade (orthostatic hypotension)
Hyperthermia or hypothermia (believed to be due to the drug’s effect on the hypothalamus, which leads to inappropriate responses to heat (e.g., lack of sweating/peripheral vasodilation) or cold (e.g., lack of shivering))
First-generation antipsychotics (FGAs)
High-potency antipsychotics Haloperidol Fluphenazine Perphenazine Trifluoperazine Pimozide
Low-potency antipsychotics
Chlorpromazine
Thioridazine
High-Potency First-Generation Antipsychotics (FGAs)
Haloperidol Fluphenazine Perphenazine Trifluoperazine Pimozide
Mechanism:
Dopamine-specific antagonism (D2 receptor) (potency of a substance is directly related to the degree of its D2 antagonism)
Clinical Use: Schizophrenia Bipolar disorder Acute psychosis Delirium Acute agitated states (e.g., patients who are agitated and aggressive due to alcohol and/or illicit drug use) Tourette syndrome OCD (concomitant therapy) Huntington disease
Adverse Effects:
Extrapyramidal symptoms most common in high-potency FGAs
Prolonged QT interval
Neuroleptic malignant syndrome
Lipid soluble –> stored in body fat –> slow to be removed from body.
Dopamine receptor antagonism –> hyperprolactinemia –> galactorrhea, oligomenorrhea, gynecomastia.
Dyslipidemia, weight gain, hyperglycemia.
Antimuscarinic (dry mouth, constipation)
Antihistamine (sedation)
α1-blockade (orthostatic hypotension)
Neuroleptic malignant syndrome.
Low-Potency First-Generation Antipsychotics (FGAs)
Chlorpromazine
Thioridazine
Mechanism:
Dopamine antagonism
Anticholinergic
Antihistaminergic (primarily sedative, due to H1 antagonism)
Clinical Use:
Acute agitation
Delirium
Adverse Effects: Anticholinergic effects, sympatholytic effects, metabolic effects, and sedation dominate EPS less common Corneal deposits (chlorpromazine) Retinal deposits (thioridazine) Neuroleptic malignant syndrome.
Chlorpromazine
Low-Potency First-Generation Antipsychotics (FGAs)
Mechanism:
Dopamine antagonism
Anticholinergic
Antihistaminergic (primarily sedative, due to H1 antagonism)
Clinical Use:
Acute agitation
Delirium
Adverse Effects:
Lipid soluble –> stored in body fat –> slow to be removed from body.
Dopamine receptor antagonism –> hyperprolactinemia –> galactorrhea, oligomenorrhea, gynecomastia.
Dyslipidemia, weight gain, hyperglycemia.
Antimuscarinic (dry mouth, constipation)
Antihistamine (sedation)
α1-blockade (orthostatic hypotension)
QT prolongation.
EPS less common
Lenticular and corneal deposits
Neuroleptic malignant syndrome
Thioridazine
Low-Potency First-Generation Antipsychotics (FGAs)
Mechanism:
Dopamine antagonism
Anticholinergic
Antihistaminergic (primarily sedative, due to H1 antagonism)
Clinical Use:
Acute agitation
Delirium
Adverse Effects:
Lipid soluble –> stored in body fat –> slow to be removed from body.
Dopamine receptor antagonism –> hyperprolactinemia –> galactorrhea, oligomenorrhea, gynecomastia.
Dyslipidemia, weight gain, hyperglycemia.
Antimuscarinic (dry mouth, constipation)
Antihistamine (sedation)
α1-blockade (orthostatic hypotension)
QT prolongation.
EPS less common
Retinal deposits
Carries the highest risk of retinitis pigmentosa.
Neuroleptic malignant syndrome
Second-generation antipsychotics (SGAs)
Clozapine Olanzapine Risperidone Quetiapine Amisulpride Ziprasidone Aripiprazole Lurasidone Asenapine Iloperidone Paliperidone
Clozapine
Second-generation antipsychotics (SGAs)
Mechanism:
D2 receptor antagonism (less pronounced than that of FGAs)
5-HT2A receptor antagonism
Interaction with several other receptors (i.e., D3, D4, α-adrenergic, and H1 receptors)
Clinical Use:
Clozapine is used for treatment-resistant psychotic disorders or those with persistent suicidality
Acute therapy for psychotic symptoms caused by medication for Parkinson disease (dopamine agonists)
Adverse Effects: Metabolic effects (usually weight gain, hyperglycemia, dyslipidemia) most prominent Prolonged QT interval Hyperprolactinemia (less pronounced than in FGAs) Neuroleptic malignant syndrome Clozapine can cause agranulocytosis, and lowers the seizure threshold Myocarditis Cardiomyopathy Sinus tachycardia Sedation, somnolence EPS less common Anticholinergic and sympatholytic effect
Monitoring guidelines –> fasting glucose and lipids, blood pressure and waist circumference
Olanzapine
Second-generation antipsychotics (SGAs)
Mechanism:
D2 receptor antagonism (less pronounced than that of FGAs)
5-HT2A receptor antagonism
Interaction with several other receptors (i.e., D3, D4, α-adrenergic, and H1 receptors)
Clinical Use: Schizophrenia Bipolar disorder Acute psychosis Postpartum psychosis MDD with psychotic features OCD (concomitant medication) Tourette syndrome Anxiety disorders Huntington disease
Adverse Effects: Metabolic effects (usually weight gain, hyperglycemia, dyslipidemia) most prominent Prolonged QT interval Hyperprolactinemia (less pronounced than in FGAs) Neuroleptic malignant syndrome Sedation, somnolence EPS less common Anticholinergic and sympatholytic effect Asymptomatic increase of liver enzymes.
Monitoring guidelines –> fasting glucose and lipids, blood pressure and waist circumference
Risperidone
Second-generation antipsychotics (SGAs)
Mechanism:
D2 receptor antagonism (less pronounced than that of FGAs)
5-HT2A receptor antagonism
Interaction with several other receptors (i.e., D3, D4, α-adrenergic, and H1 receptors)
Clinical Use: Schizophrenia Bipolar disorder Acute psychosis Postpartum psychosis MDD with psychotic features OCD (concomitant medication) Tourette syndrome Anxiety disorders Huntington disease Acute therapy for dementia (should be reserved for severe symptoms only)
Adverse Effects: Metabolic effects (usually weight gain, hyperglycemia, dyslipidemia) most prominent Prolonged QT interval Hyperprolactinemia (less pronounced than in FGAs) Neuroleptic malignant syndrome Sedation, somnolence EPS less common Anticholinergic and sympatholytic effect
Monitoring guidelines –> fasting glucose and lipids, blood pressure and waist circumference
Quetiapine
Second-generation antipsychotics (SGAs)
Mechanism:
D2 receptor antagonism (less pronounced than that of FGAs)
5-HT2A receptor antagonism
Interaction with several other receptors (i.e., D3, D4, α-adrenergic, and H1 receptors)
Clinical Use: Schizophrenia Bipolar disorder Acute psychosis Postpartum psychosis MDD with psychotic features OCD (concomitant medication) Tourette syndrome Anxiety disorders Huntington disease
Adverse Effects: Metabolic effects (usually weight gain, hyperglycemia, dyslipidemia) most prominent Prolonged QT interval Hyperprolactinemia (less pronounced than in FGAs) Neuroleptic malignant syndrome Sedation, somnolence EPS less common Anticholinergic and sympatholytic effect
Monitoring guidelines –> fasting glucose and lipids, blood pressure and waist circumference
Amisulpride
Second-generation antipsychotics (SGAs)
Mechanism:
D2 receptor antagonism (less pronounced than that of FGAs)
5-HT2A receptor antagonism
Interaction with several other receptors (i.e., D3, D4, α-adrenergic, and H1 receptors)
Clinical Use: Schizophrenia Bipolar disorder Acute psychosis Postpartum psychosis MDD with psychotic features OCD (concomitant medication) Tourette syndrome Anxiety disorders Huntington disease
Adverse Effects: Metabolic effects (usually weight gain, hyperglycemia, dyslipidemia) most prominent Prolonged QT interval Hyperprolactinemia (less pronounced than in FGAs) Neuroleptic malignant syndrome Sedation, somnolence EPS less common Anticholinergic and sympatholytic effect
Monitoring guidelines –> fasting glucose and lipids, blood pressure and waist circumference
Ziprasidone
Second-generation antipsychotics (SGAs)
Mechanism:
D2 receptor antagonism (less pronounced than that of FGAs)
5-HT2A receptor antagonism
Interaction with several other receptors (i.e., D3, D4, α-adrenergic, and H1 receptors)
Clinical Use: Schizophrenia Bipolar disorder Acute psychosis Postpartum psychosis MDD with psychotic features OCD (concomitant medication) Tourette syndrome Anxiety disorders Huntington disease
Adverse Effects: Metabolic effects (usually weight gain, hyperglycemia, dyslipidemia) most prominent Prolonged QT interval Hyperprolactinemia (less pronounced than in FGAs) Neuroleptic malignant syndrome Sedation, somnolence EPS less common Anticholinergic and sympatholytic effect
Monitoring guidelines –> fasting glucose and lipids, blood pressure and waist circumference
Aripiprazole
Second-generation antipsychotics (SGAs)
Mechanism:
Aripiprazole is a partial D2 agonist
5-HT2A receptor antagonism
Interaction with several other receptors (i.e., D3, D4, α-adrenergic, and H1 receptors)
Clinical Use: Schizophrenia Bipolar disorder Acute psychosis Postpartum psychosis MDD with psychotic features OCD (concomitant medication) Tourette syndrome Anxiety disorders Huntington disease
Adverse Effects: Metabolic effects (usually weight gain, hyperglycemia, dyslipidemia) most prominent Prolonged QT interval Hyperprolactinemia (less pronounced than in FGAs) Neuroleptic malignant syndrome Sedation, somnolence EPS less common Anticholinergic and sympatholytic effect
Monitoring guidelines –> fasting glucose and lipids, blood pressure and waist circumference
Lurasidone
Second-generation antipsychotics (SGAs)
Mechanism:
D2 receptor antagonism (less pronounced than that of FGAs)
5-HT2A receptor antagonism
Interaction with several other receptors (i.e., D3, D4, α-adrenergic, and H1 receptors)
Clinical Use: Schizophrenia Bipolar disorder Acute psychosis Postpartum psychosis MDD with psychotic features OCD (concomitant medication) Tourette syndrome Anxiety disorders Huntington disease
Adverse Effects: Metabolic effects (usually weight gain, hyperglycemia, dyslipidemia) most prominent Prolonged QT interval Hyperprolactinemia (less pronounced than in FGAs) Neuroleptic malignant syndrome Sedation, somnolence EPS less common Anticholinergic and sympatholytic effect
Monitoring guidelines –> fasting glucose and lipids, blood pressure and waist circumference
Asenapine
Second-generation antipsychotics (SGAs)
Mechanism:
D2 receptor antagonism (less pronounced than that of FGAs)
5-HT2A receptor antagonism
Interaction with several other receptors (i.e., D3, D4, α-adrenergic, and H1 receptors)
Clinical Use: Schizophrenia Bipolar disorder Acute psychosis Postpartum psychosis MDD with psychotic features OCD (concomitant medication) Tourette syndrome Anxiety disorders Huntington disease
Adverse Effects: Metabolic effects (usually weight gain, hyperglycemia, dyslipidemia) most prominent Prolonged QT interval Hyperprolactinemia (less pronounced than in FGAs) Neuroleptic malignant syndrome Sedation, somnolence EPS less common Anticholinergic and sympatholytic effect
Monitoring guidelines –> fasting glucose and lipids, blood pressure and waist circumference
Iloperidone
Second-generation antipsychotics (SGAs)
Mechanism:
D2 receptor antagonism (less pronounced than that of FGAs)
5-HT2A receptor antagonism
Interaction with several other receptors (i.e., D3, D4, α-adrenergic, and H1 receptors)
Clinical Use: Schizophrenia Bipolar disorder Acute psychosis Postpartum psychosis MDD with psychotic features OCD (concomitant medication) Tourette syndrome Anxiety disorders Huntington disease
Adverse Effects: Metabolic effects (usually weight gain, hyperglycemia, dyslipidemia) most prominent Prolonged QT interval Hyperprolactinemia (less pronounced than in FGAs) Neuroleptic malignant syndrome Sedation, somnolence EPS less common Anticholinergic and sympatholytic effect
Monitoring guidelines –> fasting glucose and lipids, blood pressure and waist circumference
Paliperidone
Second-generation antipsychotics (SGAs)
Mechanism:
D2 receptor antagonism (less pronounced than that of FGAs)
5-HT2A receptor antagonism
Interaction with several other receptors (i.e., D3, D4, α-adrenergic, and H1 receptors)
Clinical Use: Schizophrenia Bipolar disorder Acute psychosis Postpartum psychosis MDD with psychotic features OCD (concomitant medication) Tourette syndrome Anxiety disorders Huntington disease
Adverse Effects: Metabolic effects (usually weight gain, hyperglycemia, dyslipidemia) most prominent Prolonged QT interval Hyperprolactinemia (less pronounced than in FGAs) Neuroleptic malignant syndrome Sedation, somnolence EPS less common Anticholinergic and sympatholytic effect
Monitoring guidelines –> fasting glucose and lipids, blood pressure and waist circumference
Tiapride
First-generation antipsychotic drug (although it is sometimes classified as an SGA drug without antipsychotic effects)
Mainly used for tic disorders and Huntington disease
Lithium
Mechanism:
Not established; possibly related to inhibition of phosphoinositol cascade.
Steady state is usually reached 4–5 days after initiation or a change in dosage
95% of lithium is excreted by the kidneys. The remaining part is excreted via sweat and feces.
It is freely filtered at the glomerulus and mostly reabsorbed in the proximal convoluted tubule via sodium channels.
Clinical Use:
First-line therapy for bipolar disorder
Treats acute manic episodes and prevents relapse.
Maintenance therapy
Augmentation in treatment-resistant depression (lithium monotherapy or augmentation (with an antidepressant) is effective in preventing suicide in individuals with unipolar depression and suicidal ideation)
Adverse Effects:
Adverse effects occur at therapeutic levels (0.4–1.0 mEq/L) but tend to be more severe at peak serum concentration of the drug.
Nausea, diarrhea
Weight gain (due to dysregulation of appetite in the hypothalamus)
Dry oral mucosa
Leukocytosis
Nonprogessive, symmetric, fine postural tremor in the distal ends of upper extremities. Often decreases spontaneously over time. Treat with beta blockers (e.g., propranolol) if persistent or severe
Muscle weakness
Acne
Worsening psoriasis
Hair thinning
T-wave depressions (most common), U waves, repolarization abnormalities
Sinus node dysfunction (most commonly sinus bradycardia)
Hypothyroidism
Hyperparathyroidism causing hypercalcemia
Goiter (particularly in second and third trimester of pregnancy)
Nephrogenic diabetes insipidus (lithium interferes with ADH signaling → ↓ aquaporins (water channels) on the collecting duct cell’s surface → ↓ water molecules are reabsorbed and kidneys are unable to concentrate urine → ↑ free water excretion) (polyuria, nocturia, and polydipsia → ↑ risk of dehydration and subsequent lithium toxicity) Treat with amiloride (blocks ENaC channels, reducing urine volume and lithium uptake in the kidneys)
Chronic interstitial nephritis (lithium-associated nephropathy) → interstitial fibrosis, focal nephron atrophy, tubular cysts with chronic use. Risk correlates with the cumulative dose and duration of lithium use. Often occurs in the setting of nephrogenic DI. Can progress to chronic kidney disease
Ebstein anomaly
Thiazides (and other nephrotoxic agents) are implicated in lithium toxicity.
LiTHIUM: Low Thyroid (hypothyroidism) Heart (Ebstein anomaly) Insipidus (nephrogenic diabetes insipidus) Unwanted Movements (tremor)
Absolute contraindications:
Advanced renal failure (creatinine clearance < 30 mL/min)
Severe cardiovascular disease
Relative contraindications:
Concurrent diuretic use
Dehydration, sodium depletion
First trimester of pregnancy if lithium is needed during pregnancy, aim for the minimum effective dose and monitor serum levels regularly.
Monitoring guidelines –> BUN, creatinine and thyroid function
Long-term treatment reduce the risk of suicide attempts and deaths.
Lithium Toxicity
Occurs at serum levels > 1.5 mEq/L.
Causes
Increase in dosage (lithium has a narrow therapeutic window)
Renal impairment from any cause
Low effective circulating volume (e.g., due to dehydration, loop diuretic use, cirrhosis, congestive heart failure)
Medications that can precipitate lithium toxicity by increasing renal absorption of lithium:
- Thiazide diuretics
- NSAIDs (except aspirin)
- ACE inhibitors
- Tetracyclines
- Cyclosporines
Clinical Features:
Gastrointestinal symptoms dominate in acute poisoning. Neuromuscular symptoms may develop as the intoxication progresses.
Nausea, vomiting, and diarrhea (further fluid loss may exacerbate lithium toxicity)
Altered mental status, confusion
Somnolence, coma
Delirium, encephalopathy, psychomotor impairment
Coarse tremors, seizures, fasciculations, myoclonic jerks,
Ataxia, slurred speech, nystagmus
Hyperreflexia
Acute renal failure
Treatment:
Discontinuation of lithium
Hydration with isotonic fluid (0.9% NaCl solution) and electrolyte correction to promote lithium clearance
Hemodialysis is the first-line treatment for severe lithium toxicity
Buspirone
Mechanism:
Stimulates 5-HT1A receptors
Clinical Use:
Generalized anxiety disorder.
Does not cause sedation, addiction, or tolerance.
Takes 1–2 weeks to take effect.
Does not interact with alcohol (vs barbiturates, benzodiazepines).
SSRIs
Fluoxetine, fluvoxamine, paroxetine, sertraline, escitalopram, citalopram.
Mechanism:
Inhibition of serotonin reuptake in synaptic cleft → ↑ serotonin levels in cortico-amygdala pathways
It normally takes 4–8 weeks for antidepressants to have an effect.
Clinical Use: Major depressive disorder (first-line therapy) Generalized anxiety disorder (GAD) Obsessive-compulsive disorder (OCD) Post-traumatic stress disorder (PTSD) Panic disorder Premature ejaculation Premenstrual dysphoric disorder Binge-eating disorder Bulimia nervosa Social anxiety disorder Gambling disorder Somatic symptom disorder Irritable bowel syndrome
Adverse Effects:
Fewer than TCAs.
Sexual dysfunction (e.g., anorgasmia, ↓ libido, erectile or ejaculatory dysfunction)
Diarrhea, nausea, vomiting (because serotonin receptors are located in the area postrema, the stimulation of which causes nausea and vomiting)
Agitation
Insomnia
SIADH
Headache
Increased risk of serotonin syndrome if used concomitantly with other serotonergic drugs (e.g., MAOIs, linezolid, St. John’s wort, dextromethorphan, meperidine, methylene blue)
In the first trimester of pregnancy, paroxetine increases the risk of fetal cardiovascular malformations; in the third trimester, it increases the risk of pulmonary hypertension in the fetus.
Fluoxetine
SSRIs
Mechanism:
Inhibition of serotonin reuptake in synaptic cleft → ↑ serotonin levels in cortico-amygdala pathways
It normally takes 4–8 weeks for antidepressants to have an effect.
Clinical Use: Major depressive disorder (first-line therapy) Generalized anxiety disorder (GAD) Obsessive-compulsive disorder (OCD) Post-traumatic stress disorder (PTSD) Panic disorder Premature ejaculation Premenstrual dysphoric disorder Binge-eating disorder Bulimia nervosa Social anxiety disorder Gambling disorder Somatic symptom disorder Irritable bowel syndrome
Adverse Effects:
Fewer than TCAs.
Sexual dysfunction (e.g., anorgasmia, ↓ libido, erectile or ejaculatory dysfunction)
Diarrhea, nausea, vomiting (because serotonin receptors are located in the area postrema, the stimulation of which causes nausea and vomiting)
Agitation
Insomnia
SIADH
Headache
Increased risk of serotonin syndrome if used concomitantly with other serotonergic drugs (e.g., MAOIs, linezolid, St. John’s wort, dextromethorphan, meperidine, methylene blue)
