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Pharmacotherapy of anxiety disorder
- 1. Pharmacotherapy of Anxiety disorder
- 2. Contents Introduction Symptoms Pathophysiology Serotonin system • Cognitive Behavioral Therapy • Pharmacotherapy Treatment
- 3. Introduction Anxiety • Most common mental illness • Normal human emotion that serves an adaptive function from a psychobiological perspective.
- 4. • Generalized anxiety disorder • Obsessive – compulsive disoreder • Panic disorder • Acute stress disorder • PTSD • Separation anxiety disorder • Social phobia • Specific phobias Constellation of symptoms
- 5. Pathophysiology GABA system: In GAD reduced temporal lobe benzodiazepine receptor are observed. In PTSD, cortical benzodiazepine receptor are reduced In PANIC decreased GABAA binging is noted
- 6. Serotonin System • 5 HT is involved in the pathophysiology of anxiety disorders • Abnormal regulation of serotonin release and reuptake or abnormal responsiveness to 5-HT signals
- 7. Treatment • Cognitive Behavioral Therapy • Pharmacotherapy
- 8. Treatment Cognitive Behavioral Therapy • Calm and diminish hyperarousal • Correcting cognitive distortions • Progressive exposure method for phobias • Tracking of behavior with daily diary 8
- 9. Treatment • Pharmacotherapy • Benzodiazepines • SSRIs • SNRIs • TCAs • Azapirone • Beta-adrenergic blockers
- 10. Benzodiazepines • Widely used anxiolytics • Though commonly used, they are not necessarily the best choice.
- 12. Benzodiazepines Pharmacokinetics: • Absorption: • Rapidly and completely absorbed after oral administration • DOA • Roughly divided into short- , intermediate- and long-acting groups. • Fate • Metabolized by hepatic microsomal system. • Excreted in urine as glucuronides or oxidized metabolites. • Not recommended for use during pregnancy as can cross placenta.
- 13. Benzodiazepines • ADRs • Drowsiness, confusion (most common) • Ataxia • Cognitive impairment
- 14. Selective Serotonin Reuptake Inhibitors: • Citalopram • Escitalopram • Fluvoxamine • Fluoxetine (prototypic drug) • Paroxetine • Sertraline 14
- 15. SSRIs MOA 15
- 16. SSRIs Pharmacokinetics: • Absorption • Orally active • Food has little effect on absorption • DOA • Once daily dosing possible • Plasma half lives ranging between 16 and 36 hours. • Fate • Metabolized by cytochrome P450 • Dosages to be reduced in patients with hepatic impairment 16
- 17. ADRs: • From excessive stimulation of brain 5HT2 and 5HT3 receptors • Nausea • Insomnia • Irritability • Decreased libido • Ejaculatory delay • Paroxetine causes Congenital Cardiac malformation, must be avoided in pregnancy • Suicidal ideation 17
- 18. Drug Interactions: • Increase in TCA exposure observed during coadministration of TCAs and SSRIs. • SSRIs and MAOI Serotonin syndrome
- 19. Serotonin-Norepinephrine Reuptake Inhibitors • Venlafaxine • Desvenlafaxine • Levomilnacipran • Duloxetine 19
- 20. SNRIs MOA
- 21. SNRIs Pharmacokinetics: • Absorption • Orally active • Both immediate release and extended release preparations are available. • DOA • Fate • Eliminated by hepatic metabolism and renal excretion.
- 22. ADRs • Similar to that of SSRIs • Venlafaxine can induce sustained diastolic hypertension
- 23. Drug interactions • 14 days period recommended between ending MAOI therapy and SNRIs (7 days is considered safe).
- 24. Tricyclic antidepressants • Imipramine (prototype drug) • Clomipramine • Amitriptyline • Doxepin • Trimipramine • Desipramine • Nortriptyline 24
- 25. TCAs MOA
- 26. TCAs Pharmacokinetics: • Absorption • Well absorbed orally • Lipophilic readily penetrate into CNS • DOA • Plasma half lives of 8-80 hours • Once daily dosing possible • Fate • Metabolized by hepatic microsomal system • Excreted as inactive metabolite via kidneys
- 27. TCAs ADRs Blockade of muscarinic receptors • Blurred vision • Xerostomia • Urinary retention • Constipation • Aggravation of angle-closure glaucoma Block alpha- adrenergic receptors • Orthostatic hypotension • Dizziness • Reflex tachycardia
- 28. Azapirone • Buspirone • Gepirone • Ipsapirone 28
- 29. Azapirone • MoA: • Ennhances noradrenergic and dopaminergic neurotransmission via inhibition of reuptake by NET and DAT • Presynaptic release of NE and DA and effects on VMAT2
- 30. Azapirone Pharmacokinetic • DOA • T1/2 21 hrs • Fate • Elimination involves both hepatic and renal routes
- 31. Azapirone ADRs • Tachycardia • Hypertension • Irritability • Tremor • Headache • Nausea • Dry mouth
- 32. Beta-adrenergic blocker • Propranolol MOA • Interacts with beta 1 and beta 2 receptors with equal affinity • Does not block alpha receptors
- 33. Beta – adrenergic blocker Pharmacokinetic • Absorption • Highly lipophilic almost completely absorbed after oral administration • DOA • T1/2 – 4 hours • Single dose of 10-20 mg may be administered 20-30 minutes before the event. • Fate • Clearance is by liver
- 34. Beta – adrenergic blockers • ADRs • Nausea • Vomiting • Diarrhea • bradycardia
- 35. Conclusion • A thorough history should be elicited to find role of exogenous factors in Anxiety development • Multiple modalities may have to be considered for resolution of the issue 35
- 36. Thank you!
Editor's Notes
- Absorption – except sertraline food increases its absorption Fluoxetine has half life of 50 hrs, and that of its active metabolite S-norfluoxetine averages around 10 days.
- MDD
- Pts with severe hepatic cirrhosis should receive max dose of 150 mg every other day; consideration for decreased dose should also be made in cases of renal impairment.
- Acute panic symptoms Not useful for people with general social phobia who are anxious in most social situations; instead may be useful for people who are anxious about specific performance situations, such as presenting a speech before an audience.