1. AFFECTIVE DISORDERS
From of psychosis characterized by the charge in mood &
behavior.
CNS SITES LINKED WITH MOOD & BEHAVIORS.
LIMBIC SYSTEM.
Hypothalamus.
Ant. Thalamic nuclei. Rich in
Singular gyros. Monoamines.
Hippocampus
Amygdale & septum.
2. MAMILLARY BODY.
For nix.
AFFECTIVE DISORDERS INCLUDE;
MANIA:
• Opposite of depression, exceberance & enthusiasm.
• Rapid flow of though
• Talkativeness.
• Ed self confidence.
• Hyperactivity & improved judgment.
b) Depression:
Manifested by:-
*Vague somatic symptoms (Aches & pains)
* General feelings of misery, Apathy, hopelessness & despaired.
* Intense feelings of sadness.
* Inability to experience please urine usual activities.
Psycho mooted showing, retardation.
• Feeling of guilt & inadequacy.
• Disturbance of body system of sleeps hunger & appetite.
& Indecisiveness.
• Inductiveness.
• Anxiety & agitation.
• Loss of libido & sexual drive.

2. INCIDENCE.
• Most common psychiatric disorders.
• Hereditary link.
• 5-6 of population at a given moment.
• 10% may suffers during thert lifetime.
TYPES OF DEPRESSION:
a) Uni- Polar.
• Do not swing in to bout of mania
• Hereditary link.
• Specific genes have been identified.
I RECTIVE DEPRESION (SECOBDARY OR NEUROTIC).
• Most common type.
• 60% of all depression.
• Exaggerated & distorted response to depressing circumstance.
Common precipitations. Factors R.
• Adveese life events loss, grief etc.
• Physical illness self or relatives.
• Drughs (Anti- HTN, alcohol, hormones)
• Others psychiatric disorders.
• Women are affected more than men.
• Incidence es with age.
ii. ENDOGENOUS (Major,)
Melancholic depression.
25% of all & 1-2 of population
Result of genetically determined biochemical disorders.
Inability to cope with ordinary strees.
Usually start in early adulthood but may affect any age gp.
Affect both sexes equally
Precipitated by ordinary life events
Usually associated with bipolar.
PATHOPHYSIOLOGY.
Monoaminbe (biogentic amine recory):

3. Ist proposed by schild kraut in 1965 functional deficit of NA &/or 5ht at
certain sites of brain.
Drughs:-
Potentate activity of NA. DA/or 5.HT directly or indirectly.
a) Points in favor.
Deughs TCA & MAO inhibitors armine transmission.
Rescipine cause depression..
b) Poinks Against.
• Amphetamine & cocaine amine tramnsmission but have no
antidepressant effect.
• Anti depressant eff is late & does not correspond to transmission.
• Some anti depressants have no action on amine transmission.
• Several studies show biochemical changes in depression which are
similar to mamia.
Latest View
Mania Fxnal Excess
ERIC HASELINS.
Have you ever experience any of the sympatoms every or nearly
every day in 2 weeks period.
• Difficulity in cons.
• Loss of interest in activities you normally enjoys.
• Changes in apetite and wt.
• Insomnia or oversleeping.
• Feeling of sadness.
• Physical showing.
• Agitation or Anxiety.
• Presistent thoughts of death or suicide.
More than 5 years means.
You had a mazjor depreisvie epoisdie & potential cnadiatres for RX.
If depression strikes to you or someone close to you Good new.
Medication & psychotherapy more than 80% effective as RX.
ANTI DEPRESSANTS (THYMOEPETICS.)
A. Amine uptake Inhibitors: (Non selctive)

4. Tricyclics (Ist genecation antidepresants)
a) Dibenzapine gp.
• Imipramine for nocturial enuresis class I a for anythomia.
• Dessipraminbe.
• Inimepramine.
• Clomipramine.
• Iofepramine.
B) Dibenzocycloptane gp.
* Amitriptyline.
* Nortiriptycine.
* Protriptycine.
* Butriptyline.
C) Other tricyclics. (Not used now, for peptic ulcer previuously.
* Doxepin
* Dotherpin.
2. HETERO CYCLICS. (2ND GENERFATION).
* Amoxapine.
* Maprotiline (tetrfacyclic)
* Bupropion.
Trazodone (More prominent effeit on 5HT reuptake.)
3 THIRD GENERATION DRUGHS:
Venla faxine
Duloxetine.
Nefazodone.
Selective NA reuptake inhibitors.
Reboxitine.
Desipramine
Nortripthyliner.
Maprotilaine.
4). SELECTIVER SEROTONIN REUPTAKE INNIBITORS. (SSRI)
Flurxatine.
Paroxetine

5. Sertaline.
Fluroxamine.
Citalopram
Escitaloprin.
B. ATYPICAL (AGENTS)
Mianserin (No effect on Amines)
Iprindole.
MAO INHIBITORS
Inhibit crptcike pump of amine NT by competition with carrier of memb
transport system some TCA NT release by. Pre- synaptic blockade.
More effect on NA & 5ht
Much less effect on DA
Which effect is morer prominenet?
Not clear.
But.
Imp0rovement of mood 5ht psychotomotor stimulation & motor activity
NA recept blockade X-adr X2
Inhibit release blockade release.
Histaminegic.
Muscarnic
Down regulartion:-
Effect non NT is manifested 2 hrs. but antidepressant eff 2 weeks.
So not sos use.
So, it goes against biogenic amine theory.
POST SYNAPTIC EFFECT (ADAPTIRC CHANGES)
As a result of cone of NT at synaptic site post syhnaptic & receptor
effects are:
i. CAMP
ii. Down regulation of X2 receptors.
iii. Down regulation of B- receptors
iv. Activity of SHT receptors with SSR.
Seen with.
Selective NA reuptate.
Both NA & SHT block

6. MAO I block..
ECT
To a leser extent with
SSRI
X2 antaganist
B-against.
Even after ECT these occur and they remain stopped.
Time couse of these alterones in recap fxn (adaptive changes).
Correspond more with clinical improvement.
Actions: Of TRICYCLIC ANTIDEPESSANTS.
1cns;
Normal inclividual.
No. CNS stimulationb
No mood elevation.
Sedation & confusion so no addiction potention.
Motor in coordination esp.
Skilled performance
Instead they depress themnsels.
b/c they actually depress the depressive idealization idisinhibitory. Effect.
Per antiniuscacinic
Per suympathomirretic specific on CVS.
Anti depression effect.
Mood election.
Mental alertness.
Physical activity
Improved sleep
Anxiety agitation & apathy.
Phacmacokinetics.
Rapidly obsorbed vaciable.
Like phenothiazines. Buthyrophonones. Halopecidol etc.
Ist pass effect vacialble B.A.
Protein binding 90-95%
Extravascrilas tissue bnding large
Volume of distribution 10-50 kg
High clipid solubility

7. Metabolism N-demthylation active Glucronidati
Ring hydroxylation active. Oxidation
Clearance mostly hepatic.
Clinical uses of tri cyclic antidepcessants
None of antidepressants are CNS
Stirmulatory.
Not useful in drugs induced
CNS depression.
1. Depression SP endogenous only 2/3 pts respond
2. Bipolar with Li
3. Psychotic depression with anti psychotics or amoxapine.
4. Obsersive compulsive disorders
SSRI clomipramine. Both anti depressant & antipsychotic effect
5. Enuccesis Imipramine but risk of caediotoxicity.
6.Acute panic symptoms imipramine but
Benzodiaq z Preferred.
7. Cata plexy associated with narrolepsy loss of tone.
8. Chonic pain syndrome tricyclics
e.g. like migraine.
14 Sleep aprea also used amine thyuine.
15. Fibromyeilgia & promyalgia
IBS also in depression so antidepression mixed with other peptic ulcer.
Doxepin.
A/E TEICYCLIC ANTIDEPRESSANTS.
1. CNS:- Secation CH1 block
Max Amitriptyline & doxpin
Min protriptyline.
Convnlsions aggravation of epilepsy or seizure threshold. In low doses:
Tolecasnce after few wks.
In high doses themselves cause convulsion.
2) Anticholinergic:
More with Amitryptline.
Dry mouth difficulty in chewing swelling.
Bhusing of vision.
Aggrevation of glansoma
Inhibition of gut & blodder
Tacchycardia arrythmias.

8. 2. CVS:
3. Postur/ hypotension
Reflex HR
Cardia conanction difects
Cardiac assythmics may lead to MT
Symp activity.
b/c B-recep, are not blocked.
4) Metabolic & encdocrine:
WT gain & sexual distue bances
Appetite pactially
By & blockade libido in made.
DRUG INTERACTIONS.
1. Protein binding so displaccd aspirin, phentyl butazone so, free once of
this drugh and as they are low safety margin drughs so toxicity.
2. Alcohol (NS depressants, anasesthetics. Opiods, barbiturates, they
will pllentiate their depressant effect.
3. Block antity pertensdive effect of gannethin methyldopa. Clonidine.
B/C their carried for entesing neucon is blocked.
It entries the neown by reuptake which is blocked.
It entries the Newton by reuptake which blocked.
Clonidine is clonidine as x2 are blocked and down regulated so its eff.
4. Hepatic metabolism of TCA competitively inhibited by some stecoids,
neuroleptics b/c they are also mety by some cyp 450 microsomal
enzymes.
5. MAO Inhibition Mutual potwentiation they are breakdown of NJ in
the stored from TC release so, both pokntiate each other effect.
Anti conorinergic.
Anti- Convulsives asntagonism
b/c TCA conirulsive threshold.
Directly acting sympatha mimetics.
Potentiation.
ICA are post syneptic.
Conoluction.
Indriectly effect.
B/C ICA their entry into neve terminal.
Precaution.
Cartdiac arrythimias.

9. Epilespsy.
Glaucoma.
CI.
TCA POISNING:
Frequenct method for attempted suicide so, drughs are given to relatives.
SYSMPTOMS:
CNS: initial excitement, delirium N.M imitability, jcomulsion, followed
by coma shock resp depress & acidosis.
ATROPINE LIKE EFFECT.
Flusining ,dryness of mouks & skin.
Hypespyrexia.
Inhibition of gut & bladder.
CARDIAC:
Atrial & venticulkar fibrillation.
Ventriculars, fibrillation, sudden death.
TREATMENT
NO specific antidote so, symptomatic therapy.
Physostigmine for CNS effect.
For accythmias
Lidosaine.
Phenytion.
Propranorl.
Electric pacing.
IN NAHCO3 KCL
Dialysis to remove from
Tissues+ supportive therapy.
OTHERAMINE UPTAKE BLOCKERS:
MAPROTILINE.
2ND generation TCA.
Selective NE uptake block
Few seda & anti cholinesgic effective.
Longer acting +1/2 40 hrs.
A/E
Scizeure threshold.
Allergic reaction.
Mayt be even anaphylaxis.
NAMIFENSINE.
NA & DA uptake blocker

10. NO effect on sit
NO sedation.
NO atropine like effect.
No post hypotension.
NO cardiotoxicity
Safe in over dose.
Short acting BD doses.
A/E
Behgaviousal strimulation restlessness
Insomina
Dyskinesa
Allergic RXNA
AMOXAPINE.
2nd generation.
Methaboltic of loxapine (Anti posychotic)
Inhibition uptake of NA SHT & DA.
Sedative.
Anti muscaeinic
Has some DA antagonistic effect. CNS effect.
BUROPION.
Alters NA output.
Resemble to amphetamine skilkled activity.Block uptake of DA by
occupying 25% pump in brain
Maqy canse seizures.
VENLA FEXINE:
Inhibits uptake of NA SHT (+++)
& DA (++)
No sedation
No sedation
Not antimuscairnic
Behave like SSRI in low doses.
MIRTAZEPINES:
X2 5HT2 5HT3 BLOCKES

11. Potent H1 blokers
WT gain appetite
Useful in pts who do not respond well to sssri
ATYPICAL AGENTS.
1.MICMSECIN:
A TETRACY6CLIC COMP.
No effect on amine uptake
Inhibit presymaptic x2 recorptor
Intribit SHT, H1 receptors
No Cardiotoxicity.
A/E.
Sedation, sizurces, Hy7per- Sensitivity RXN
IPRINDOL:
No effect on amine uptaske
No side effect.
MOA hot knows.
MONOAMINE OXIDASE:-
MAO Mitoctondrtial enz
DISTRIBUTIONS:
Neural tissue.
All others tissue including gut & lives here destrong ingested indirectly
acting mono amines e.g in cough syrup etc.
FUNCTIONS.
Oxidative deamination of safety value function in neuron jhust like in gut
& lives.
Inactrvtion endogenous & ingested amines (Tyramine.)
Here it degrades any NT entering newon outsides the vesides.
TYPES & SELECTIVITY:

12. TYPE-A
Preferred substrate NA & 5HT
Selective inhibitor clorgyline moclobarinde.
Type- B
Prefessed substrate- Ptienylethanine. Benzylamin. Dopamine.
Selective inhibition selegillone
Rasagelline.
Non- Specific substrfate of both enz.
Tyr amine, phenyle propylamine.
Non specific inhibitors of both enz.
Pargyline
Tranylycpromine.
Iproniazid.
CLINICAL USES OF TRICYILIC ANTIDEPRESSANTS.
None of antidepressants CNS stimulant
Not useful in drugs induced CNS depressor.
1. Depression SP endogenous only 2/3 pts respond
2. Bipolar with lithium
3. Psychotic depression jwith antipsychoticsor Amoxapine.
4. Obsessive compulsive jdisodress (SSR)&
5. Clonipramine
Enurcsis. Imipramine. But risk of cardiotoxicity.
6. Acute panic symptoms. Imi pramine but benzoliazipenes
preferred.7. Caraplexy associated with Narcdepsy loss of tone.
7. Ch. Pain syndeone. Ticyclics,
8. Venlafaxine, duloxetnine.
9. * Migrainbe.
10.Trigeninal neuralgia
11.Assojciated with deprecession.
9. Phobic states eg. Soial phobias
SSRI Not go in duloxitine Social gatyherting
Venlafaxine.

13. Benezodiazepine.
Phofia of height
Hydrophobia
Hydrtophobia
Henrophjobia
Phobia of open spaces.
10. School jphobias & attention & attention defgicit hyperkinetic disjorsders
in ehilkren
I mipramme.
Desipramie.
Atomoxetine.
12.certaing caediac arrythmiasimipramine
12 Eatinbg disjorders amorexia nervbosa& bulinaia nervosa over
wt. SSRI wt anorexia
13. Prem anstural dysphoric disordes SSRI.
14 Sleep apnoca
15.Fibro myalgia promeflagia.
16. IBS
17. P.U idoxepin vsed for Rx of depression.
A/E of TCA
1. CNS
2. sedation coz of h1 blockade
Max amitriptytline & doxipin
Min protriyline.
• tolecance after few weeks
• convulsion aggravation of
• epilepsy. Conulsive threshold.
• In trigh doses. Themselves cause. Coniulsions.
3. ANTICHOLINERGIC: (Max with Amitriptyline.)
Dry mounth difficulty in swallowing.
Blurring of vision talking due dilatation of pupil
Agg. Glaricome
Inhibition of gut & bladder
Retention.
3 CVS: Posturl hypotension (X-block)
Eff on HR

14. Cardiac conduction defect more with irritrameine as it is also a Nat
channel blockers.
Cardic arrythmics
VMC. Adaptive change.
Receptors doun regulation
Transmission inhibitory effect. Due to adaptive syrup outflow
Adrenergic transmission should in case of CNS receptors involve
in rtclease of NT are postsynaptic not pre-synaptic.
4. METBOLIC & ENDOCRINE.
5. Wt gain & secual disturbances. Libido, penile cretion.
DRUG INTERACTIONS:-
Protcin binding displacement, asprin, ph, butazone, p.kinetic interaction.
Highly pr. Binding drug 90-99%
Alchol CNS depressants & anesthetics potentiation.
Block anti HTNSIVE eff of
Guanethgedine, methyl dopa & clowdine.
TCA block update system, anti HTN.
Effect is lost as depleting effect is lost.
M. Dopa:
Enter newon from circulation by carrier system, carrier system blocked.
Clonidine X2 recep stimulation
X2 recep down rtegulation and clockade.
Hepatic metabolish of TCA, competitively inhibitled by some sleroids,
newoleptics. Other drugs not tabolished by eiver, so some metabolizeing
sites are occupied by steroids etc. So their metabolism is ed.
MAO-I mutual potentiation, breakdown of amires storage.
TCA block rcuptake, so both.
Anti cholinergic___ polentiation
Anti conulsants___ antagonism
As themselves___ convulsion.
Threshold.
Dosage req.
Directly acting sympathetics, potentiation.
TCA ing transmission post synaptically.
Indirectly acting. Effect as they enter by carriers systems which are blocked.
PRECAUTIONS.
Cardiac arrythmias.
Glaucoma Anti cholinergic acitivity.
Epilepsy.

15. TCA POISONING.
Frequent menthod for attempted suicide.
As deprersive pt. being considered himself useless person, so have suicide
thoughts.
In antipsychotics initial stages, no suijcidal jidealization.
Relatives are advised jto give time drugs instead of himself.
CNS:
Initial excitement, delirium NM irritability, convulsions followed by coma,
shock. Resp depression & Acidosis.
ATROPINE LIKE EFFECTS.
Flushing, dryness of mouth, & skin, Hyperprexia, Heat loss meeh in loss.
Inhibition of gut & bladdes.
CARDIAC
Atr & ventricul are fibrillation vent fibrillation sudden death.
TREATMENT.
No specific antidotc, so supportive & symptomatic therapy.
1. Physostigmine for CNS effects
2. For arrythmias:
Lidocaine.
Phenytoin
Propranolol.
Electric pacing.
3. I/V Nattco3 & KCL + dialysis+ supportive.
4. Diuretics not useful
5. petunia dialysis.
:- OTHER AMINE UPTAKE BLOCKERS:-
MAPROTILINE:-
2nd generation drug
A tetracylic comp.
Selective NA uptake bloker.
Few sedative & ant cholinergic eff.
Longer acting (+1/2 40 hrs)
A/E
Seizure in higher dose range. Allergic rxn skin rashes urticasria.
ANOFNIFENSINE:-
 NA & DA uptake blockers.
 No effect on SHT.
 No sedation.

16.  No alropine like eff.
 No car diotoxicity.
 Safe in over dose.
 Short acting BD dose.
A/E:-
B chaviowal of loxapine (anti psychotic).
Inhibit reuptake of NA, SHT & Sedative.
 Anti muscarinics.
 Has some DA antagonistic eff CVS symptoms less common.
Buproprion:
Alless NA output
Resembile to arrphetamine
Blocks reuptake of DA by occuping 25 % pump in brain may course
sciues.
Fine movements mental performance at the jcost of jmist5akes.
VENLAFAXINE:
Inhibit uptake of NA (++) SHT (+++) & DA (++)
No sedation.
No antinuscacinic effect behave like SSRI inb low doses as more effect
on serotonin recap).
Don’t caves sedation.
Useful in phobias & (TCA not soi effect.)
Compulsive. Disorders effective.
MIRTAZEPINE:
X2 BLOCKER
Sht2 & 5TH3 BLOCKER
Potent H1 blockers sedation appetite wt gain. Useful in pts who do not
respond well to SSRI.
ATYPICAL DRUGS:
No effect on re-transmission
MIANSERIN:
A tetracylic comp
No effect on amine uptake
Inhibit pre-synaptic X2 receptors also block SHT2 H1 receptors No
cardiotoxicity. Sedation.

17. A/E
Sedation due to H1 recep blockade seizure,
Hypersensitivity REXN.
IPRINDOLE:
No effect amine uptake.
No side effect.
MOA not known.
MJONOAMINE JOXIDEAS INHIBITORS.
(MAO1)
M.A.O
Mitochondria enz
Distribution:
Newral tissue esp. in riesue terminal all other tissues in cluding gut &
lives.
V. imp safcty drug fxn).
1. In lives, breakdown injuect indirectly acting amines in dictry & so,
abnoxious effect not occur common cold prep.
FXNX:
1. oxidative deamination of amines.
2. safety value fxn in neurons
3. Inactive endogentous & ingested amines (tyramine.)
Any inhdirctly acting amine, entee the nerve teemina immediately, breoken
down before it reaches pre-synaptic space.
TYPES & SELECTIVITY
TYPE-A
Pre-for substrate NA & 5HT
Systemtic inhibitor Clorgyline, Moclobamide.
TYPE-B
Prefer substance, Phenylethlamine
Benzlamine.
Dopamine.
Specefic in tibitors Selegiline
Rasagiline.

18. NON SP. SUBSTRATE OF BOTH ENZYMES:
Tyramine (cheese tomates, bananas
Lassi, curd, hot drinks, Red wine.)
NON- SELECTIVE INHIBITORS OF BOTH ENZYMES.
Pargyline (use3d for RX of HTN for long time)
Trylcypromine.
Imprniazide3.
Used for Rx of TB anjtidor but not effective.
MAO (MONOAMINE OXIDASE)
Moa
A) Inhibition of MAO
(Both A & B)
• Block by covalent binding
• Action lasts for 2-3 weeks.
• Moclobamide revesible & short acting
• Iranylcypromine Not irreversibly
• Most druigs non selective
• Blocking MAO A antidepressant eff.
b). DOWN REGULATION OF RECEPTORS.
Adaptive changes:
• delayed down reg of B-adr & 5th (like ICA)
X2 B %HT2 downregulation.
2 pools
* Intracytoplasmic pool.
Intravesicular pool.
B) Otrher enz.
C) Also inhibit: Other oxidases involves in oxidative deamination of
drugs & toxic subst responsible for drug interaction e.g tyrammine,
pathidine.
Actions of MAO
• I/N cytoplasmic conc of 5HT (Most)
NA DA (least)
I/C cytoplasmic pol (releasable) of amines.
Spon leaking, indirectly acting drugs.
• similar changes in peciphecy,

19. • Heart
• Lever
• Kidneys
• But not response of these organs, to peripheral nerve stimulation
Like TCA , Action is not immediate.
Normal Subjects:
• Motor activity In contrast
• Euphoria with TAC
• Excitement Drousiness
Sedation
Motor activity
Confusion
Depressed patients
• Effect on amines develop rapiely
• Improvement of symptoms
• Some CNS shin with phenalizin and in contrast to TAC as iot is CNS
depressant Tranylcypromine.
Therapentic uses of MAO
1) Moderate to serve depression
• Endogenrous
• Reactive
• A typical
2) If the pt is not responsive to TAC or
• Allegic to TAC or
• Associated symptoms: having anxity, Phobias &
hypochondnasis
3) Phobic States e.g. Hight Phobia
4) Hyupomrinia Hydrophobia
PHAEMACOKINETICS OF MAO.
Well absorbed orally
Effect appears in 2-3 weakss.
Metabolism liver
Excretion Kindneys.

20. A/E of MAO
1. Postural hypotensionb (pasgyline)
used to treat HTN not used now as drug interactions.
2. Excesive central stimulation
3. Tremors.
4. Exeitment.
Water retention:
1. Varsodilators—associated with salt & water retention.
2. Anti diabetic water rentation)
3. MAO water rentantion.
Insomina
Convulsion
3.Conuvlsion followed by depression.
4. Wt gain appetite (TCA also allse wt gain)
5. Atropine like effect (Same as TCA)
6. Racently hepato to xicity hydrazine decivatives.
7. Water retention. Edema.
8. Muscle tone & eflexes
TOXICITY OF MAO.- I
Agitfation Delerium, Nervouysnems,
Seizures (Same as TCA.)
Hyperthecnia, shock, coma
RX.
Supportive
Phenothiazines (Chlorpromazine), may be helpful X-block.
INTELACTIONS WITH FOODS & DRUGS:
D) food (Cheese RXN)
Sideef fect with N therapentic doses may be halmful or useful)
e.g anti cholinergic for Rx for bilacy colic, urine retention, constipation.
Toxic effect at higher doses.
Tyramine absocbed in GIT MAO in gut wall, cause its break down.. if
freaches circulation. Destroyed, if centre never terminal destroyed, so MAO
safety,.
*Sever hyectensive crsisi.

21. * Throbbin headache, hyperply rexia restlessness, cerlbrovas cular, accident,
sub acachroiod henorage.
Risk with moclob emdi- A
Rever sible short acting MAO-I
MAO-A selective.
Tyramine containing substdances.
Tomato.
Cused.
Banana.
Soft drink.
Beans (red)
Cheese.
DRUGS:
Interactions of MAO,
Indirectly acting syrup aruines e.g ephedrine, amphetamine,
phemylpropanolamine.
Their breakdown by MAO safety if not severce HTN.
TCA + MAO-I Excitement, HTN,
Hyperytrexia, convulsions.
Post synaptic effects ed potentiating effects so MAO+I pathdine
hyperpyrexia, restlessness,
Pathdine, cylic, responses. Pathidosis, cause dowsiness etc, but here it
causes stimulation.
Response to lerodopa HTN & excitement,
Dopamine breakdown by MAO, dopamine as MAO inhibit.
T ½ other drugs are oxidative deaminated.
MAO-I T SSR-I serotoin syrdeome.
Malignant hyperthermia.
SELECTIVE SECOTONIN RE-UPTAKE.
INHIBITORS (SSRI)
Fluoxetine (ufrex) (prozac)
Pacoxetine.
Fluvoxamine.

22. Sertraline (ffaverine)
Citalop ram.
ESC; talopram
Mixed Lofepramine
Trazodone Atomoxetine.
FLUOXETINE:
Chemistry:
A phemyl to ly/plprpy/amine
MAO.
Selectivly inhibit 5ht receptlake in CNS newons.
Little eff on NA/DA.
Min binding with muscalinic witrh TCA histaminic & adr receptor.
May ultimately eff final common path through NA (Hypothsis).
Dulling of depressive ideation rather than emphonic shinulation (Just like
TCA no producing any stimulatory effect on
CNS safety effect, as side effects as no anti
cholinergic, anti histaminc, adrenergic
blocking effect.
Intermueiom suotonergic narrator
signposting 5ht recap-vely coupled with
reuptake of NA reuptake is blocked.
Kinetics:
Well absorbed P/O
Peak Plasma corc 4-8 hrs
Extensive hepatic demethylation
Nor fluoxitive lactive)
Ilimination t floxctive (2-4 days)
Nor flouxetive (7-9 days)
So total also with age
Antipsychotic Metabolism
Ant diabetics disturbed
DOA (Action by fluoxitive as well as mentabolite non-flouxetive)
Plasma pr binding
Like TCA
Wo 20-45 L/Kg
Onest of action after 1-3 wks

23. Inactive metabolites exc in urine
Post synaptic eff:
Serotonin recap activity ( Adaptive Changes)
Time course depends on clinical improvement of pt symptoms.
Uses: flouxetine
1) Deprersion (Major)
2) Bulinia nberuosa & Obesity TAC further
3) Observise complulsive disorders. IST LINE DRUGS SSRI.
4) Seasonal affective disorders, esp those accompaniued by
CHO carving & wt gevin.
5) Prophylaxis of recussent depressive episopdes.
6) Chronic anxiety (persistant).
7) Prophylaxis for panic attacks preferable is benzodiazapenes.
8) Alcholoison.
9) Alcholishion.
10) Premenstrual dysphoric disorder
Opposite of enphoria.
A/E OF FZUOXETINE.
1. GIT.
Anorexia, nausea, vomiting, dyspepsia
Useful in bulimia nervosa dry mouth, diakhea.
2. NEWCOLOGCAL:
• Anxiety, rewousners, headache.
• Restlessness, Insomnia, Fatigue.
• TYremors, dizziness, convulsions.
• May ppt. mania or hypomania.
• May cause violent suicidal thought (but may be due to discase.
Suicidal thoughts more with pt with SSRI. Than TCA.
3. AUTONOMIC.
Anorexia, wt loss, sweating dry mouth.
4. Endocrine.
Libido.
5. Allergic.

24. Skin rashes, puctis, urtic caria (0.4%) rarcly fatal systemic vascultis
wings, kidneys, liver.
6. OTHERS:-
Nausea, vomiting, Central excitation, convulsion, death.
RX.
1. Induction of emesis
2. Gastric lavsage
3. Ieizures resporid to diazepam.
4. other symtommatic measures.
CI:
Kidney & lives diseas EPI lepsy doses of anti epititic has to.
Drug Interactions:
Flouxetine inhibit drug metabolizing enzymes & pleasma coric of
halopecidol.
TCA.
Warfarin.
Antagonism of Anti convulasants.
Combinatioin of SSRI with Li Tryptophan or MAO-I may efficacy, But CI
due to side effect.
SSR I + MAO-I stores of Monoamines + inhibilted uptake
Syuaptic conc, suptonin syndrome.
SECOTORIN SYDROME: LIFE THREATNING.
*Hyperthermia, muscle, rigidity, cyclones.
* restlessness,hypereflexiia rapid. Changes in mental status & vital signs
death.
*Worst life threatening RXN
* So no MAO-I 2 wks before & 5 wks after SSRI.