Antidepressant drugs

Dr. Satabdi Ghosh

MBBS, MD
Assistant Professor
Department of Pharmacology & Therapeutics
Depression
 Depression is one kind of mood disorder which is characterized
by
1. Feeling of intense sadness and despair (loss of hope)
2. Mental slowing and loss of concentration
3. Pessimistic worry (always expect bad things to happen)
4. Lack of pleasure
5. Self-deprecation
6. Variable agitation and hostility
7. Some physical changes in severe depression
 Cont….
- Insomnia or hypersomnia
- Altered eating pattern with anorexia and weight loss or something
overeating
- Decreased energy and libido
- Disruption of the normal circadian rhythms of activity, body
temperature and many endocrine function.
Mood disorder
 Clinically significant depression is major depression disorder
1. Unipolar depression: The patient suffers one or more episodes of
lowered mood.

2. Bipolar depression: The patient also experiences episodes of

elevated mood, usually but not always interspersed with episodes
of depression.

3. Dysthymia: describes a particularly chronic low-grade depression.

Depression
 Major depressive disorder (MDD) is characterized by depressed
mood most of the time for at least 2 weeks and/
or loss of interest
or pleasure in most activities.
 In addition, depression is characterized by disturbances in sleep
and appetite as well as deficits in cognition and energy. Thoughts of
guilt, worthlessness and suicide are common.
 Coronary artery disease,diabetes and stroke appear to be
more common, in depressed patients and depression may
considerably worsen the prognosis for patients with a variety of co-
morbid medical conditions.
Chemical basis of depression
 Histologic studies, structural and functional brain imaging

research, genetic findings, and steroid research all suggest a

complex pathophysiology for MDD with important implications
for drug treatment.

 In addition to monoamine hypothesis,there is evidence that

neurotrophic and endocrine factors play a major role (the
neurotrophichypothesis)in depression.
 Cont……
 Monoamine hypothesis:

In depression, there is a deficit in function or amount of

monoamines (like amine neurotransmitter, noradrenaline and
serotonin) in the brain which stands central to the biology of
depression.
 Cont…..
 Neurotrophichypothesis:

There is substantial evidence that nerve growth factors such as

brain-derived neurotrophic factor (BDNF) are critical in the
regulation of neural plasticity,resilience,and neurogenesis.
 The evidence suggests that depression is associated with the loss
of neurotrophic support and that effective antidepressant
therapies increase neurogenesis and synaptic connectivity in
cortical areas such as the hippocampus.
 Cont…..

 BDNF is thought to exert its influence on neuronal survival and

growth effects by activating tyrosine kinase receptor B in both
neurons and glia.

 Neuro-endocrine mechanism: Depression is associated a

number of hormonal abnormalities such as - cortisol, ACTH,
thyroid, sex steroid.
Anti-depressant takes 2-3 weeks to produce effect/W hy
onset of action of antidepressant is delayed?************
1. The time required to synthesize neurotrophic factor has been
proposed as an explanation for this delay of antidepressant effect.
BDNF (brain derived neurotrophic factor) typically takes 2 weeks
or longer and coincides with the clinical course of antidepressant
treatment.
2. They act by receptor down regulation, for this it takes time to
down regulation. So, delayed in onset of action.
Amine neurotransmitter
 Epinephrine or adrenaline
 Nor epinephrine or noradrenaline (NA)
 Serotonin (5HT)
 Dopamine
Classification of anti-depressant drugs
1. TCA (Tri-cyclic antidepressant)
- Imipramine
- Desipramine
- Amitriptyline
- Nortriptyline
- Clomipramine
2. Selective serotonin reuptake inhibitors (SSRI)
- Fluoxetine - Citalopram
- Paroxetine - Fluvoxamine
- Sertraline
- Escitalopram
 Cont……

3. Selective serotonin nor-epinephrine reuptake inhibitors (SNRI)

- Venlafaxine
- Duloxetine
- Desvenlafaxine

4. 5HT2 antagonist
- Trazodone
- Nefazodone
 Cont……

5. Tetracyclic and unicyclic antidepressants (Newer)

- Bupropion
- Mirtazapine
- Amoxapine
- Maprotiline
- Velazodone
6. Monoamine oxidase inhibitors
a. Irreversible non-competitive – Phenelzine, Isocarboxazid
b. Reversible selective – Moclobemide
Atypical anti-depressants
 Atypical anti-depressants are mixed group of agents having
actions at several different sites. They are not more efficacious than
TCA or SSRIs, but their side effect profiles are different.
Example
 Bupropion Tetracyclic and unicyclic anti-depressant
 Mirtazapine
 Nefazodone 5HT2 antagonist
 Trazodone
 Duloxetine
 Reboxetine SNRI
 Atomoxetine
Background
• Antidepressants were first developed in the 1950s (TCA) and
have been extensively used since then.
• The two most valuable classes are Selective Serotonin
Reuptake Inhibitors (SSRIs) and Tricyclic Antidepressants
(TCAs).
• The first SSRI, fluoxetine was released in 1987.
Tricyclicantidepressant (TCA)
- Widely used
- Closely related in structure to the phenothiazines
- Initially synthesized as potential antipsychotic drugs
- They all have imino di benzyl (tricyclic core)
- Prototype is imipramine
Pharmacokinetics
 Absorption
All are rapidly absorbed when given orally.
 Distribution
- Binds strongly to plasma albumin
- Binds to extra-vascular tissues which accounts for the generally
very large volume distribution.
 Metabolism
- In the liver by two main routes, N-methylation and ring
hydroxylation
- undergoes first pass metabolism
 Cont…..

- both the desmethyl and hydroxylated metabolites common retain

biological activity
Imipramine – Desmethyl imipramine
Amitryptyline – Nortriptyline
Imipramine – Desipramine
- Inactivation of the drugs occurs by glucuronide conjugation of the
hydroxylated metabolites.

 Excretion
- Glucuronides being excreted in the urine
- 5% TCA are excreted unchanged in the urine
 Cont……
 Half life
- generally long
- 10 – 12 hours (Imipramine, Desipramine)
- 80 hours (Protriptyline)
- Even longer in elderly patients
- Therefore gradual accumulation is possible, leading to slowly
developing side effects.

Tertiary amine: Amitriptyline, Imipramine, Clomipramine

Secondary amine: Desipramine, Nortriptyline, Protriptyline
Mechanism of action TCA/Imipramine/Amitriptyline
1. TCA block the uptake of amines by nerve terminals by
competition for the binding site of amine transporters

increase concentration of noradrenaline and 5HT

More neurotransmitter is available to action on specific receptor

Antidepresssant action
 Cont…..
 Enhancement of 5HT mediated transmission

Improve emotional symptoms

 Enhancement of nor-adrenergic transmission

Relief of biological symptoms

2. TCA also blocks cholinergic, adrenergic and histaminergic

receptors
 Cont……
Due to blocking different receptors Effects
a) Due to blocking muscarinic -Tachycardia - Blurred vision
receptors (Atropine like action) - Urine retention - Constipation
- Dry mouth and skin

b) Block α1 adrenergic receptors - Postural hypotension - Ejaculatory failure

- Reflex tachycardia - Constipation

c)Block pre-synaptic α2 receptor no - Tachycardia

auto inhibitory effect of noradrenaline - Tremor
- Insomnia
increase nor-adrenaline release
from pre-synaptic nerve endings
d) Block central H1 receptors - Sedation
- Weight gain
Indications of TCA/Amitriptyline
1. Major depressive disorder (MDD)
2. Anxiety disorders
3. Attention deficit hyperactivity disorder (ADHD)
4. Bipolar disorder
5. Nocturnal enuresis (Imipramine)
6. Obsessive compulsive disorders
7. Prevention of migraine
8. Treatment of neuropathic pain such as fibromyalgia, postherpetic
neuralgia
9. Less commonly insomnia
 Adverse effects of TCA
Due to blocking different receptors Adverse Effects
1. Due to blocking muscarinic -Tachycardia - Blurred vision
receptors (Atropine like action) - Urine retention - Constipation
- Dry mouth and skin

2. Block α1 adrenergic receptors - Postural hypotension - Ejaculatory failure

- Reflex tachycardia - Constipation

3.Block pre-synaptic α2 receptor no - Tachycardia

auto inhibitory effect of noradrenaline - Tremor
- Insomnia
increase nor-adrenaline release
from pre-synaptic nerve endings
4. Block central H1 receptors - Sedation
- Weight gain
 Cont……
Mechanism of causing adverse Adverse effects
effects
5. Neurologic adverse effects - Seizures

6. Psychiatric adverse effects - Aggravation of psychosis

- Withdrawal syndrome
7. Metabolic-endocrine adverse effects - Sexual disturbance
- Weight gain
Imipramine is used in nocturnal enuresis *********
 Imipramine has a vasopressin independent anti-diuretic effect.

Antidiuretic effect of imipramine can be attributed primarily to

increased α adrenergic stimulation in PCT with a secondary
increased urea and water reabsorption more distally in the
nephron.
Contraindications of TCA
1. History of MI, IHD, cardiac arrhythmias
2. Old age
3. Pregnancy, lactation
4. Following MAOI
5. Severe hepatic damage
6. Obese person
Advantages of TCA
1. Sedation may be beneficial. A severely depressed person who
has a disrupted sleep pattern or agitation
2. Long half life
3. Used in patient unresponsive to SSRI or SNRI
4. Used in treatment of anuresis, insomnia, pain
Drug interactions of TCA (pharmacokineticinteraction)
• TCA + dopaminergic drug (entacapone, Selegiline for treatment of
parkinsonism) = CNS toxicity
• TCA + adrenaline (in local anesthetics) = Serious rise in blood
pressure due to potentiation of catecholamines
• TCA + antihypertensive = Severe hypotension
• TCA + opioid analgesics, H1 receptor antihistamines, anxiolytics,
hypnotics, alcohol, anesthetics excessive drowsiness, daytime
somnolence, respiratory depression
Drug interactions of TCA (pharmacodynamicinteraction)
 TCA + antiepileptic drug (carbamazepine) = Acceleration of
metabolism of TCA decrease therapeutic efficacy require
adjustment of dose

• TCA + Enzyme inhibitors (Fluoxetine, paroxetine, cimetidine,

haloperidol) = increase concentration of TCA

• TCA + Enzyme inducer (phenobarbital, rifampicin) = decrease

concentration of TCA
Selective serotonin reuptake inhibitors (SSRIs)
- Most commonly prescribed

- Less likely than TCAs to cause anti-cholinergicside effects and are less
dangerous in overdose.

- They do not cause cheese reactions

- Effective as TCAs and MAOI in treating depression of moderate degree,

but probably less effective than TCAs in treating severe depression.

- Used to treat anxiety disorders.

Pharmacokinetics of SSRIs
 Long plasma half life
 High plasma protein binding
 Long plasma half life 18–24hours
 Fluoxetine is metabolized to a active product norfluoxetine
(half life 24-96hour).
 Once daily dosing
 Cont…
• Absorption
Peak plasma time: 5.2-8.1 hr
Peak plasma concentration: 61.7 ng/ml
• Distribution
Protein bound: 93-95%
Vd: 8.7 l/kg
• Metabolism
Metabolism: Hepatic P450 enzyme CYP2D6
Enzymes inhibited: CYP2D6
Metabolites: Inactive
• Elimination
Half-life: 21 hour
Excretion: Urine (64%), feces (36%)
 Mechanism of action of SSRI
• The selective serotonin reuptake inhibitors (SSRIs) cause
inhibition of the serotonin transporter (SERT) at presynaptic
nerve terminal.

• High affinity for monoamine receptors but lacked the affinity for
histamine, acetylcholine, and α adrenoceptors.
Anti-depressant effect of SSRI
Fluoxetine/ Paroxetine/ SSRIs

Selectively block the reuptake of serotonin by blocking serotonin

transporter (SERT)

Decrease transport of serotonin along with Na+ and cl- into the nerve cell

Subsequent increase conc. of serotonin in the synaptic cleft

Greater post-synaptic neuronal activity

Anti-depressant effect
 Fig: Site of
action of
SSRI:
SSRI
increase
serotonergic
neurotransm
ission by
blocking the
serotonergic
transporter
at
presynaptic
terminals
(SERT).
Source: Goodman & Gilman’s The Pharmacological Basis of THERAPEUTICS,12th edition
Indications of SSRI
1. Depression
2. Anxiety Disorder: Obsessive compulsive disorder
Social anxiety disorder
Panic disorder
Generalized anxiety disorder
Post traumatic Stress Disorder
3. Premenstrual dysphoric disorder
4. Eating disorder (Bulimia nervosa, anorexia nervosa)
5. Fibromyalgia
Adverse effects
1) Due to serotonergic activity in the gut
• Nausea
• GI upset
• Diarrhoea
• Anorexia
2) Due to serotonergic activity at the level of spinal cord
• Loss of libido
• Delayed orgasm
3) Headache, insomnia or hypersomnia
4) Weight gain (paroxetine)
5) Discontinuation Syndrome
• Dizziness
• Paresthesia
(Begins 1-2 days after stopping the therapy and persists for 1
week or longer)
6) Teratogenicity
- Cardiac septal defects (Paroxetine)
Advantage of SSRIs over TCAs and others
1. Selective
2. Well tolerated as a starting dose
3. More efficacy
4. Less toxicity
5. Generally free of sedative effects
6. Less likely to induce mania
7. Less dangerous in overdose
8. Relatively safe
9. Can be used in anxiety disorder
10. Less likely to cause anti-cholinergic effects
11. No interaction with food
12. Single daily dose
Disadvantages of SSRIs
1. High cost
2. Less effective than TCAs in treating severe depression
3. Increase suicidal or aggressive ideation – fluoxetine
4. Dangerous serotonin syndrome
5. More chance of sexual dysfunction
6. Teratogenic effect
7. Transient nausea, insomnia
Drug interaction of SSRI
• SSRI + MAOI = Serotonin syndrome
• Paroxetine, fluoxetine potent CYP2D6 inhibitor 
decreases metabolism of other drugs and increases toxicity.
 Serotonin syndrome *********
• Combination of an MAOI and a serotonergic agent (SSRI,
SNRI, meperidine, tramadol, triptans) may result in life
threatening serotonin syndrome.
• Rare but dangerous.
• Caused by over stimulation of 5HT receptors in the central
gray nuclei and the medulla.
 Cont……

 Combination of SSRI with antimigraine triptan, tramadol

serotonin syndrome

 SSRIs inhibit the metabolism of tramadol to its active metabolite

Unmetabolised tramadol has sufficient serotonergic activity itself to

interact with the SSRIs and enhance the risk of serotonin syndrome
Sign and symptoms of serotonin syndrome
 Triad of
A)Somatic– myoclonus, hyper-reflexia, tremor, shivering,
restlessness
B)Autonomic– HTN, tachycardia
C)Cognitive – Delirium, coma
Treatment
1. Stopping all serotonergic drugs.
2. Administration of nonselective serotonin antagonist
3. Supportive measures.
Precautions
 Most serotonergic antidepressants should be discontinued
2 weeks before starting MAO inhibitors to avoid serotonin
syndrome.

 Fluoxetine because of its long half life should be

discontinuous for 4-5 weeks before an MAO inhibitors is
initiated.
Contraindications of SSRI
• Hypersensitivity
• Concomitant pimozide
• Co-administration with serotonergic drugs
• Concomitant use or within 14 days of MAOIs increases risk
of serotonin syndrome
• Pregnancy
Black boxwarning
The FDA has issued “black box” warning regarding the use of
SSRIs and a number of other antidepressants in children and
adolescent, particularly in the early phase of treatment, due to
possibility of an association between antidepressant treatment and
suicide.
Superiority of SSRIover other antidepressant drug
• Selective
• More efficacious
• Well tolerated
• Safety in overdose
• Less toxicity
• No interaction with food
• Less likely to cause anticholinergic side effect
• Single daily dose
Difference between TCA and SSRI
Points TCA/ Amitriptyline/ SSRI/Sertraline/
Fluoxetine
Nortriptyline
1. Chemistry Tricyclic . There is 3 benzene Dicyclic. There is 2 benzene
ring ring
2. Mechanism of Blocks both NA and 5 HT Blocks only serotonin
action receptors and noradrenaline transporters.
and serotonin transporters.
3. Bioavailability Relatively less bioavailability Bioavailabity is more.
(40-50%) Sertraline 45%
Amitriptyline: 45% Fluoxetine 70%
4. Absorption Incompletely absorbed Well absorbed than TCAs.
5. First pass Significant first pass No first pass metabolism
metabolism metabolism occurs.
 Cont……
Points TCA/ Amitriptyline/ SSRI/
Nortriptyline Sertraline/
Fluoxetine
6. Half-life Relatively short Long
7. Effects on Blocks and has adverse effects Does not block
muscarinic, α like Atropine like side effects,
receptor, pre sympathomimetic effects and
synaptic α2 receptor, sedation.
central H1 receptor
8. Effcets on libido No effects Decrease libido
9. Increase suicidal No Yes
tendency
10. Weight gain Yes No
Monoamine oxidase inhibitors (MAOI)
There are two form of monoamine oxidase
i) MAO-A
ii) MAO-B

MAO-A:
 Present in dopamine and nor-epinephrine neuron and is found
primarily in the brain, gut, placenta, liver .
 Moclobemide is a reversible and selective inhibitor of MAO-
A.
 Cont…..
MAO -B
 Found primarily in serotonergic and histaminergic neurons and is

distributed in the brain, liver, placenta

 Selegilline is an irreversible MAO-B inhibitor at low doses. It is

useful in the treatment of parkinson’s diseases at low doses. But
at higher doses it becomes a non-selective MAOI similar to other
agents.

Note: Both MAO-A and MAO-B metabolize tyramine and dopamine.

Pharmacokinetics
- Well absorbed from the GIT
- Because of the prominent first pass effects and their tendency to
inhibit MAO in gut.
M/A of MAOI
MAOI

Inhibits MAO

decrease break down of noradrenaline, 5HT, Dopamine

increase noradrenaline, 5HT, dopamine

Antidepressant action
Indications of MAOI
- Depression (
MDD)
Note: Much less used because of their adverse effects and serious
indications, indicated for major depression in patients who have
not responded to other drugs.
Adverse effects
1. Orthostatic hypotension (dopamine accumulate within peripheral
sympathetic nerve terminals and displace noradrenaline from
storage vesicles, thus reducing noradrenaline release associated
with sympathetic activity)
2. Tremor
3. Excitement due to excessive central stimulation
4. Insomnia
5. Convulsion
6. Weight gain (due to increase appetite)
7. Dry mouth
8. Blurred vision Atropine like side effects
 Cont…..
9. Urinary retention (atropine like side effects)
10. Hepatotoxicity
11. Sexual dysfunction
12. Sedation
13. Confusion (higher doses, due to blockade of tyramine
metabolism)
14. Sudden discontinuation syndrome
- delirium like presentation
- Psychosis
- Excitement
- Confusion
Disadvantage of MAOI
1. Orthostatic hypotension
2. Excessive central stimulation
Tremor
Excitement
Insomnia
3. Atropine like side effect
Dry mouth
Constipation
Urinary retention
Blurring of vision
Drug Interaction of MAOI

MAOI + TCA = Hypertensive crisis

MAOI + tyramine = Cheese reaction
MAOI + SSRI = Serotonin syndrome
MAOI+ TCA = W hat occurs?
 TCA inhibit uptake of NE and 5HT.
 MAOI inhibit breakdown of NE. So, increase concentration of nor-
epinephrine.
 As a result hypertensive crisis occurs due to sympathetic over
activity. It is complicated by CNS excitation with hyperreflexia,
rigid hyperpyrexia.
 MAOI+ tyramine = W hat occurs?
Cheese reaction: When a patient is treated with MAOI and
consumes food rich in tyramine  tyramine reaches systemic
circulation and is taken up by adrenergic nerve ending, because it
escapes degradation  release of nor-adrenaline from store and
increase nor-adrenaline  hypertensive crisis.

S: - Sudden severe throbbing headache

S/
- Palpitation - Nausea, vomiting
- Flushing - Severe hypertension
- visual disturbance
 Cont…..
Treatment
- Phentolamine (α –adrenoceptor blocker) 5 mg I/V
- Β – adrenoceptor later added incase of excessive tachycardia.

** At least 10 mg of tyramine needs to be ingested to produce cheese

reaction.
** Moclebemide, a specific MAO-A inhibitor does not cause cheese
reaction, probably because tyramine can still be metabolized by
MAO-B.
Comparison between TCA and MAOI
Points TCA MAOI

1. Mechanism of action Block the reuptake of Irreversible inhibition of

NE and 5HT MAO enzyme
2. Sedation More Less

3. Weight gain Less More

4. Interaction with No Yes

tyramine containing
food
5. Hypertensive crisis No Yes
Comparison between TCA and quadricycliccompound
Points TCA Quadricyclic

1. Chemistry Tricyclic Tetracyclic

2. α1 receptor block Yes No

3. α2 receptor block No Yes

4. Cardiac patient Cannot use Can be used

5. Sedation More Less

6. Acute toxicity More Less

 Advantages of newer antidepressants (Venlafaxine,
Mirtazapine,Nefazodone)
1. Less anti-muscarinic effect
2. Less CVS effect
3. Safe in overdose
4. Greater therapeutic efficacy
5. Risk of drug interaction is less
6. Effective in patient unresponsive to TCA or MAOI
7. Retain some antipsychotic action thus it is suitable drug for
depression in psychotic patient.
Selective serotonin-norepinephrine reuptake inhibitor (SSNRIs)
 Pharmacokinetics
 Metabolized in liver by CYP 450
 Plasma protein binding: Venlafaxine, desvenlafaxine – 27 -30%
Duloxetine – 97%
 Half life – 11 -12 hours
 Once daily dosing

M/A
Inhibition of both serotonin and nor-epinephrine transporters
Indication of SNRIs
1. MDD
2. Neuropathic pain
3. Fibromyalgia
4. Generalized anxiety
5. Stress urinary incontinence
6. Vasomotor symptoms of menopause

Adverse effects
1. Sedation
2. Nausea
3. Dizziness
4. Sexual dysfunction
Contraindications of SNRIs
- In combinations with MAOIs

Advantages of SNRIs
1. Rapid onset of action
2. Work better in treatment resistant patient
3. No anti-histamine, α adrenergic blocking and anti-cholinergic
effects
4. Better tolerability
Mirtazapine
 Pharmacokinetics
- Demethylated followed by hydroxylation and glucoronide
conjugation.
- Several isoenzymes are involved in metabolism.
- Half life 20-40 hour.
- Usually dosed once in the evening because of its sedating effects.

M/A
- Antagonize the presynaptic α2 autoreceptor enhances the release
of both noradrenaline and 5HT
- Antagonize the 5HT2 and 5HT3 receptor
- Antagonize the 5HT1 receptor
 Cont….
[α2 presynaptic membrane inhibition of release of NA from
adrenergic nerve ending]
Adverse effects
- Dry mouth
- Sedation
- Weight gain
Advantage *********
- Act more rapidly than other antidepressants
- Causes less nausea and sexual dysfunction than SSRIs
- No serious drug interactions (Mirtazapine + alcohol/BDZ = CNS
depression)
Bupropion
 Pharmacokinetics
- Rapidly absorbed
- Plasma protein binding of 85%
- Undergoes extensive hepaticmetabolism
- It has 3 active metabolites including hydroxybupropion
(antidepressant agent)
- Has a biphasic elimination with the first phase lasting about one hour
and second phase lasting 14 hours.

M/A
- Inhibits both noradrenaline and dopamine (but not 5HT) reuptake,
enhances presynaptic release of cathecholamine.
 Cont……
Indication
- Effective as nicotine patches in smoking cessation.
(may mimic’s effects on dopamine and nor-adrenaline and may
antagonize nicotinic receptors)

Adverse effect
- Agitation
- Insomnia
- Anorexia

Precautions
Should be avoided in patients taking MAOI.
Questions
1. Define depression. What are the mood or affective disorders?
2. Briefly discuss about biological basis of depression.
3. Classify antidepressants.
4. What are atypical anti-depressants? Why are they called so?
5. Why onset of action of anti-depressant is delayed?
6. Enlist pharmacokinetic properties of TCA.
7. Write down the mechanism of TCA
8. Write down indication and adverse effects of TCA.
9. Why imipramine is used in nocturnal enuresis?
10.Write down contraindications and advantages of TCA.
 Cont…..
11. Write about pharmacokinetics and pharmacodynamic drug
interactions of TCA.
12. Enlist pharmacokintic properties of SSRI.
13. How does fluoxetine produce anti-depressant effect?
14. Write down indication and adverse effects of SSRI.
15. Write about advantages and disadvantages of SSRI over TCA and
others.
16. What is serotonin syndrome? Write about sign and symptoms.
What are precautions taken to avoid serotonin syndrome?
17. Contraindications of SSRI.
18. What is black box warning?
19. Difference between TCA and SSRI.
 Cont….
20. Mechanism of action of MAOI.
21. Indication and adverse effects of MAOI.
22. What happens?
MAOI + TCA = ?
MAOI + Tyramine = ?
MAOI + SSRI = ?
23. Comparison between TCA and MAOI.
24. Comparison between TCA and quadricyclic compound.
25. Advantages of newer antidepressants.
26. Write short note on – SNRI
- Mirtazepine
- Bupropion
Prof questions
1. Mention five antidepressant drugs from different group. Write
down the advantages of escitalopram over amitriptyline. (Nov
22)
2. Short note: Escitalopram (Nov 19)
3. Name the selective serotonin reuptake inhibitors with their
indication. Mention the advantages of atypical antipsychotics. (July
18)
4. Name the commonly used antidepressant drugs. Compare and
contrast between TCAs and SSRIs. (Nov 18)
5. Name the SSRIs with indications. Compare between SSRIs with
TCAs. (Nov 17)
THANK YOU