ANTIDEPRESSANTS|PPT|PPTX|slides available

This document provide information about Anti depressants which play an important role in treatment of depression. It also provide information about depression ,its symptoms, causes and types. Depression is a mood disorder which affect mood,thoughts , behaviour and overall health of a person. It causes can be due to factors effecting genetic,psychological or environmental and social.and there are many type of depressions.
This document also provide information about how these Drugs or Anti depressants are divided into 5 classes -SSRIs,SNRIs,TCAs,maoI and atypical anti depressants..and their MOA,ADR and USES.

1. DONE BY: kahkashan sultana MPharm (PHARMACOLOGY) ANTIDEPRESSANTS

2. I ntroduction D epression R ole of neurotransmitters in depression S ymptoms of depression C auses of depression T ypes of depression M echanism of action C lassification of antidepressants C onclusion TABLE OF CONTENT

3. INTRODUCTION Antidepressants are medications that can help relieve the symptoms of depression and they were first developed in the 1950s .antidepressant significantly improved quality of life, it’s important to note that they often take several weeks to reach full effectiveness. Additionally, finding the right medication and dosage can be a process of trial and adjustment,which should always be managed under the care of a healthcare professional.

4. Depression is an illness that affect mood, thoughts, behaviour and overall health. it is a mood disorder that causes persistent feeling of sadness and loss of interest in things and activities you once enjoyed .it can also causes difficulty with thinking ,memory, eating and sleeping. DEPRESSION

5. ROLE OF NEUROTRANSMITTER IN DEPRESSION Neurotransmitters play a crucial role in depression, as they regulate mood, emotions, and cognitive functions. The most relevant neurotransmitters in depression include serotonin (5-HT), norepinephrine (NE), and dopamine (DA), along with glutamate, gamma-aminobutyric acid (GABA), and brain-derived neurotrophic factor (BDNF).

6. SYMPTOMS OF DEPRESSION excessive guilty sleep disturbances change in weights suicidal thoughts difficuty in concentration fatigue feeling of worthlessness persistent sadness social withdrawal

7. CAUSES OF DEPRESSION 1- BIOLOGICAL FACTORS Genetics – A family history of depression increases the risk. Brain Chemistry Imbalance – Low levels of neurotransmitters like serotonin, dopamine, and norepinephrine are linked to depression. Hormonal Changes – Hormonal imbalances (e.g., thyroid disorders, pregnancy, menopause) can trigger depression. Chronic Illness & Inflammation – Conditions like diabetes, cancer, heart disease, and chronic inflammation are associated with depression. 3- ENVIRONMENTAL AND SOCIAL FACTORS Lack of Social Support – Isolation, loneliness, or unhealthy relationships can contribute to depression. Substance Abuse – Alcohol and drug misuse can cause or worsen depression. Chronic Stress – Work stress, academic pressure, or financial problems may trigger depression. Unhealthy Lifestyle – Poor diet, lack of exercise, and inadequate sleep can increase the risk. 2. PSYCHOLOGICAL FACTORS Trauma & Stress – Early childhood trauma, abuse, or highly stressful events (e.g., loss of a loved one, financial crisis) can lead to depression. Negative Thinking Patterns – Pessimistic thinking, self-criticism, and low self-esteem contribute to depression. Personality Traits – Perfectionism, dependency, and high sensitivity to stress may increase vulnerability.

8. TYPES OF DEPRESSION Major Depressive Disorder (MDD) Also called clinical depression. Symptoms include persistent sadness, loss of interest in activities, sleep disturbances, fatigue, and suicidal thoughts. Must last at least two weeks for diagnosis. Persistent Depressive Disorder (PDD) (Dysthymia) Chronic form of depression lasting at least two years. Symptoms are milder than MDD but persistent. Can have periods of major depression (double depression Bipolar Disorder (Manic Depression) Alternating episodes of depression and mania/hypomania. Bipolar I: Severe manic episodes, often requiring hospitalization. Bipolar II: Hypomanic episodes (less severe) and major depressive episodes. 01 02 03

9. TYPES OF DEPRESSION Seasonal Affective Disorder (SAD) Depression that occurs seasonally, usually in winter. Linked to reduced sunlight exposure. Treated with light therapy, antidepressants, and vitamin D. Postpartum Depression (PPD) Occurs after childbirth due to hormonal changes, stress, and sleep deprivation. More severe than "baby blues" and requires treatment. Premenstrual Dysphoric Disorder (PMDD) Severe mood disturbances before menstruation. Includes irritability, depression, and physical symptoms like bloating. Related to hormonal fluctuations. 04 05 06

10. TYPES OF DEPRESSION Atypical Depression Mood improves in response to positive events (unlike MDD). Symptoms include increased appetite, weight gain, excessive sleep, and sensitivity to rejection. Psychotic Depression Major depression with psychotic symptoms (hallucinations or delusions). Requires antipsychotics and antidepressants. Situational Depression (Adjustment Disorder with Depressed Mood) Short-term depression triggered by life stressors (e.g., job loss, divorce). Symptoms usually resolve when the stressor is managed. 07 08 09

11. MECHANISM OF ACTION how they work? increase neurotransmitter levels by preventing their breakdown or reuptake or enchance receptor sensitivity overtime, leading to improved mood

12. TYPES OF ANTIDEPRESSANTS SELECTIVE SEROTONIN REUPTAKE INHITBITORS(SSRI) - fluoxetne,fluvoxamine,paroxetine,serterline,citalopram,escitalopram SEROTONIN-NOREPINEPHIRINE REUPTAKE INHIBITORS (SNRIs)- venalafaxine , duloxetine TRICYCLIC ANTIDEPRESSANT- Amitriptyline,Imipramine,Nortriptyline,Desipramine , Clomipramine,Doxepin,Trimipramine MONOAMINE OXIDASE INHIBITORS- seligiline,phenelzine ATYPICAL ANTIDEPRESSANTS- buproin,trazodone ,

13. example- citalopram,flueoxteine,paraxetine MAO-1. Normal Serotonin Transmission: Serotonin (5-HT) is released from the presynaptic neuron into the synaptic cleft.It binds to postsynaptic serotonin receptors,transmitting mood-regulating signals.The serotonin transporter (SERT) reabsorbs serotonin back into the presynaptic neuron. 2. Action of SSRIs: SSRIs block the SERT transporter, preventing serotonin reuptake. More serotonin remains in the synaptic cleft, enhancing neurotransmission. Over time, postsynaptic receptor sensitivity changes, leading to therapeutic effects. less side effects than tricyclic antidepressants safe even at overdose take 2 weeks to show effects. ADR-decreased libido,serotonin syndrome(excessive serotonin accumulation),risk of arrthymia,sleep disturbance etc USES-aniexty disorders,migraineetc . SELECTIVE SEROTONIN REUPTAKE INHIBITORS(SSRI)

14. example- venlafaxine,duloxetine MAO-1. Normal Neurotransmission: Serotonin (5-HT) and norepinephrine (NE) are released from the presynaptic neuron into the synaptic cleft.They bind to postsynaptic receptors, transmitting signals for mood regulation and pain perception.The serotonin transporter (SERT) and norepinephrine transporter (NET) normally reabsorb these neurotransmitter 2. Action of SNRIs: SNRIs inhibit SERT and NET, preventing serotonin and norepinephrine reuptake.This increases their concentration in the synaptic cleft, enhancing neurotransmission more cardiovascular effects due to ne action like increase bp and heart rate ADR-decreased libido,serotonin syndrome(excessive serotonin accumulation),increase bp,liver toxicity,hyponatremia USES-psychiatric disorders,migraine,diabetic neuropathy etc . SEROTONIN AND NE REUPTAKE INHIBITORS

15. example- bupropion,trazodone Atypical antidepressants are a diverse group of antidepressants that do not fit into the conventional classes like SSRIs, SNRIs, TCAs, or MAOIs. Their mechanisms of action vary widely, but they generally target multiple neurotransmitter systems to improve mood and alleviate depressive symptoms. :1. Bupropion (Wellbutrin) Mechanism: Norepinephrine-Dopamine Reuptake Inhibitor (NDRI) Action: Inhibits the reuptake of norepinephrine (NE) and dopamine (DA), increasing their levels in the synaptic cleft. Unique Features: No significant serotonergic activity, making it useful for patients who do not tolerate SSRI-related side effects like sexual dysfunction. ADR -seizures, hypertension,hallucinations etc 2. Trazodone Mechanism: Serotonin Antagonist and Reuptake Inhibitor (SARI) Action: Weak serotonin reuptake inhibition. Blocks 5-HT2A receptors, leading to anxiolytic and antidepressant effects. H1 histamine receptor blockade, causing sedation. α1-adrenergic receptor antagonism, which can lead to orthostatic hypotension. Unique Features: Commonly used as a sedative at lower doses. ADR-sedation,orthostatic hypotension,dry mouth etc USES-insomia ,major depressive disorder . ATYPICAL ANTIDEPRESSANT

16. example: Imipramine,Nortriptyline,Desipramine,Clomipramine,Doxepine,Trimipramine,amitriptyline MOA Inhibition of Neurotransmitter Reuptake: Serotonin and Norepinephrine: TCAs block the presynaptic reuptake transporters for serotonin (5-HT) and norepinephrine (NE), leading to increased concentrations of these neurotransmitters in the synaptic cleft. This enhancement in neurotransmission is thought to contribute significantly to their antidepressant effects. Receptor Blockade: Muscarinic (Cholinergic) Receptors: Blockade leads to anticholinergic effects. Histamine H1 Receptors: Blockade results in sedation and weight gain. Alpha1-Adrenergic Receptors: Blockade can cause orthostatic hypotension (a drop in blood pressure on standing). ADR-Orthostatic hypotension (due to α1-adrenergic blockade),arrthymia,dry mouth etc USES- nocturnal enuresis,ocd,migraine etc . TRICYCLIC ANTIDEPRESSANT

17. example: 1)Non-Selective (Inhibit Both MAO-A & MAO-B) IrreversiblePhenelzine,Tranylcypromine,Isocarboxazide . 2)Selective MAO-A Inhibitors (Reversible) Moclobemide (Used in depression, fewer dietary restrictions) 3.)Selective MAO-B Inhibitors (Used in Parkinson’sDisease ) Selegiline,Rasagiline,Safinamide (Reversible) MAOIs inhibit the enzyme monoamine oxidase (MAO), which exists in two forms: MAO-A: Primarily metabolizes serotonin (5-HT), norepinephrine (NE), and dopamine (DA). Inhibition of MAO-A increases levels of these neurotransmitters, leading to antidepressant effects. MAO-B: Primarily metabolizes dopamine and phenylethylamine . Inhibition of MAO-B increases dopamine levels, which is useful in Parkinson’s disease. By inhibiting these enzymes, MAOIs increase the levels of neurotransmitters in the synaptic cleft, leading to improved mood and cognitive function. ADR-Hypertensive crisis (if taken with tyramine-rich foods like aged cheese, cured meats, and alcohol) USES- parkison disease,ptsd,aniextyetc . MONOAMINE OXIDASE INHIBITORS

18. CONCLUSION Antidepressants play a vital role in the treatment of depression and other mood disorders, helping to regulate brain chemistry and improve overall well-being. While they are effective for many individuals, they are not a one-size-fits-all solution and may require time to find the right medication and dosage. Additionally, they work best when combined with therapy, lifestyle changes, and a strong support system.Although antidepressants can have side effects and withdrawal challenges, medical supervision can help manage these risks. Ongoing research continues to improve their effectiveness, offering hope for more personalized treatments in the future. Ultimately, antidepressants remain a crucial tool in mental health care, providing relief and stability for those struggling with depression.

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