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Antidepressants drugs
- 2. What is depression Depression is a common mental disorder, characterized by low mood, loss of interest, feelings of guilt or worthlessness, disturbed sleep or appetite, feelings of tiredness, poor concentration and suicidal ideation.
- 3. A major cause of disability and premature death. Approximately 10-15% of those with severe depression attempt suicide. Females are affected more frequently than male.
- 4. Types of depression • The mood changes are always in the same direction Unipolar depression • Depression alternates with Mania • Usually in elderly Bipolar Depression
- 5. Symptoms of depression Emotional symptoms • Apathy • hopeless • Guilt • Lack of motivation Biological symptoms • Retarded thought and activity • loss of libido • sleep disturbance • loss of appetite.
- 8. Theories of Depression The Monoamine Theory The neuroendocrine mechanisms Trophic effects and neuroplasticity
- 9. The Monoamine Theory 0The main biochemical theory of depression 0Functional deficit of monoamine transmitters - NE and/or 5-HT in certain sites of brain.
- 11. Drugs Principal action Effect in depressed patients Tricyclic antidepressants Block NA and 5-HT reuptake Mood ↑ Monoamine oxidase (MAO) inhibitors Increase stores of NA and 5- HT Mood↑ Reserpine Inhibits NA and 5-HT storage Mood ↓ Alpha - methyldopa Inhibits NA synthesis Mood ↓ Methyldopa Inhibits NA synthesis Mood ↓ Electroconvulsive therapy ?increase CNS response to NA and 5-HT Mood↑ Pharmacological evidence supporting monoamine hypothesis
- 12. Neuroendocrine hypothesis 0Stress causes increase in CRF- produce behavior changes similar to depression. 0CRF regulate tyrosine hydroxylase link of monoamine hypothesis 0Increase in ACTH 0Weak response of plasma cortisol to exogenous steroids (dexamethasone suppression test) 0 (CRF antagonist CP-154,526, R-121919)
- 14. Trophic effect and neuroplasticity 0 Lowered levels of BDNF or malfunction of its receptor, TrkB, plays a significant role in the pathology of depression. 0 Changes in glutamatergic neurotransmission Antidepressant treatment may reduce glutamate release and depress NMDA receptor function 0 major depression is associated with neuronal loss in the hippocampus and prefrontal cortex, and that antidepressant therapies of different kinds act by inhibiting or actually reversing this loss by stimulating neurogenesis
- 16. CLASSIFICATION 1.) Reversible inhibitors of MAO-A (RIMAs) 0 Moclobemide, Clorgyline 2.) Tricyclic antidepressants (TCAs) A. ) NA + 5-HT reuptake inhibitors - Imipramine, Amitriptyline, Trimipramine, Doxepin, Dothiepin, Clomipramine B.) Predominantly NA reuptake inhibitors Desipramine, Nortriptyline, protriptyline (TCA) Amoxapine, Reboxetine, Maprotiline (NEWER)
- 17. cont……. 3.) Selective serotonin reuptake inhibitors (SSRIs) 0Fluoxetine, Fluvoxamine, Paroxetine, Sertraline, Citalopram, Escitalopram, Dapoxetine 4.) Serotonin And Norepinephrine Reuptake Inhibitors (SNRIs)- Duloxetine, Venlafaxine 5.) Atypical antidepressants - Trazodone, Mianserin, Mirtazapine, Bupropion, Nefazodone, Atomoxetine , Tianeptine
- 18. GENERATION 0 First Generation Antidepressants – MAO inhibitors, TCA 0 Second Generation Antidepressants – SSRIs, SNRIs, Atypical antidepressants.
- 20. MAOIs MOA Clinical indication S/E Moclobemide, Clorgyline Blockade of MAO-A & MAO-B Irreversible selective MAO-B inhibition Major depression unresponsive to other drugs Hypotesion Insomnia Serotonin syndrome with serotonergic agents Hypertensive crisis with tyramine
- 21. TCAs MOA Effects Clinical application S/E Imipramine Amitriptyline Doxepine Chlomipramine Amoxepine Desipramine etc. Mixed & variable inhibition of NET & SERT Like SNRIs+ significant blockade of ANS & histamine receptor Major depression not responding to other drugs Chronic pain disorder Incontinence OCD Anticholinergic α-blocking effect Sedation Weight gain Arrhythmias Seizures in overdose
- 22. Subclass SSRIs MOA Effects Clinical application PK & S/E Fluoxetine Citralopram Escitalopram Paroxetine Sertraline Highly selective blockade of SERT, little effect on NET Acute increase of serotonergic synaptic activity & neurotrophic activity Major depression & anxiety disorder, OCD, PTSD, & eating disorder t1/2 15-75h Oral activity Well tolerated causes sexual dysfunction
- 23. SNRIs MOA Effects Clinical application S/E Duloxetine Venlafaxine Moderately selective blockade of NET & SERT Acute increase in serotonergic & adrenergic activity Major depression, chronic pain disorder, fibromyalgia & peri- menopausal symptoms Anticholinergic sedation HT
- 24. Tricyclic, unicyclic antidepressa nt MOA Effects Clinical application PK & S/E Bupropion Amoxipine Maprotiline Mirtazapine Increased DA & NE activity Increased release of NE & 5-HT (mirtazapine) Presynaptic release of catecholamine s Major depression Smoking cessation Sedation (amoxipine) Extensive metabolized in liver Lower seizure threshold Sedation & weight gain
- 25. THANK YOU
Editor's Notes
- depression is
- 79% of suicide is due to depression in US. 75% of pts develop major depression episode in 10yr As depression often complicate the management of other medical condotions female to male 5.2%
- Multifactorial – genetic, neurotrasmitter dysfunction, psychosocial stress , chronic illness
- Extensively distributed through the network of Limbic, striatal and PFC and also visceral manifestation of mood disorder
- R-121919 halted in phase IIa due to hepatotaxicity, it hs promised antidepressnt effcicay, NBI pharma, CRF –regulate tyrosine hydroxylase link of monoamine hypothesis
- Corticotropic relaesing factor- administration-produced behaviour changes,
- Implications for the developnemt of novel treatment