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Pharmacology > Anti Depressants > Flashcards

Anti Depressants Flashcards

1
Q

Anti depressants potentiate directly or indirectly —- or —-in the brain
Initial effect of drugs: directly responsible for antidepressant effects?
After 2-4 weeks?

A

Norepi
Serotonin
Inhibiting reuptake
Presynaptic inhibitory receptors decrease
This leads to the therapeutic response

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2
Q

SSRIs:
1-
2-
3-
4-
5-
6-

A

Citalopram cipram
Escitalopram cipralex
Fluvoxamine floxyferal
Paroxetine seroxat
Sertaline zoloft
Fluoxetine prozac

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3
Q

Action os SSRIs:
Both citalopram and fluoxetine are —— which respective —– are more potent

A

Specifically inhibit serotonin reuptake
(300-3000 fold greater sleectivity for serotonin as compared to Ne)
Little ability to block dopamine
Little blocking activity at muscarinic alpha adrenergic histamine H1 receptors
Racemic mixture (S more potent yaane escitalopram(s) more potent than citalopram)

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4
Q

Antidepressants take at least—– to produce improvement on mood and max benefit require——

A

2 weeks
12 weeks

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5
Q

Therapeutic indications for SSRI:

A

Depression
OCD (the only approved is fluvoxamine)
Panic disorder
GAD
Social anxiety disorder
Severe anxiety disorders

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6
Q

T or F
SSRIs are not well absorbed after oral administration
Well distributed
Plasma half lives between 20-30 hr
Food have little effect on all SSRIs
Peak levels are seen aprox 2 to 8 hrs on av

A

False
True ((15-30 L/kg))
False 16-36 hrs
False sertaline food increases its absorption
True

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7
Q

Metabolism of SSRIs
Inhibitors of cyp:

A

Cyp450 depedent glucuronide or sulfate conjugation
Fluvoxamine inhibits A2 c19 3A3/4
Fluoxetine and fluvoxamine c9
Paroxetine fluoxetine and less actively sertaline 2D6
Dosage adjusted with hepatic inpairment

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8
Q

Fluoxetine differs from other members by:

A

Much longer half life (50 hr)
S norfluoxetine is potent
(Half life 10 days)

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9
Q

Adverse effects of SSRIs

A

Headache
Sweating
GI
Weakness fatgue diarrhea
Sexual dysfunction
Changes in weight
Sleep disturbances
Suicidal thinking

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10
Q

Overdoses of SSRIs

A

Do not usually cause cardiac arrythmias
All the antidepresants may lower the seizures threshold
Serotonin syndrome(hyperthermia, tachycardia muscle rigidity sweating and myoclonus) when used with MAO or highly serotonin drug

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11
Q

Discontinuation of SSRIs
—— has the lowest risk of causing discontinuation problems

A

Headache
Agitation irritability
Nervousness
Change in sleep pattern
Floxetine

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12
Q

SNRIs
1-
2-

A

Duloxetine
Venlafaxine (effexor ER)

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13
Q

Actions and inducations

A

Effective when SSRIs are ineffective
Relief neuropathic pain like TCA

Major depressive state
GAD
Social anxiety disorder

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14
Q

Venlafaxine
Inhibitor of?
Minimal inhibitor of —-
Substrate of
Side effects
High doses?

A

Serotonin
At medium to high doses inhibits nor
Mild inhibitor of dopamine
Cyp450
Cyp2D6
Nausea, headache sexual dysfuntion dizzness insomnia constipation
High BP and heart rate

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15
Q

Duloxetine (cymbalta)
Contraidications
Indications
Side effects

A

Hepatic insuff
GAD
Diabetic neuropathic pain
Diarrhea sexual dys nausea
Possible ; incr in BP and HR

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16
Q

Atypical ADs

A

Bupropion (wellbutrin or zyban la)
Mirtazapine (remeron)
Nefazodone (serzone)
Trazodone (desyrel)

17
Q

Atypical ADs are more efficient than TCA and SSRIs

A

False
Different side effects

18
Q

Bupropion
Mode of action
Actions
Half life
Side effects

A

Weak dopamine and norepinephrine reuptake inhibitors
Decrease craving and withdrawal sx of nicotine it antagonise nicotinic receptor function
Short
Low incidence of sexual dys and wight gain
Increased risk of epileptic seizures at high doses

19
Q

Mirtazapin
Mode of action
Side effects

A

Ser and nor because it block alpha 2 presynaptic and 5HT2 receptors
Sedative because of antihistaminic effect (for patients having sleep difficulties)
Hematological side effects

20
Q

T or F
Murtazapin cause anti muscarinic side effects of TCA but doent interfere with sexual functioning

A

False
Don’t do both

21
Q

TCAs
Mode of action
Choice of drug depends on

A

Block NE and ser reuptake inhibitos
Tolerance to SE preexisting medical condition duration
If doesnt respond to one TcA may respond to another
Valuable for patients who doesnt respond to SSRIs

22
Q

T or F
At therapeutic doses they block dopamine transporters
Maprotyline and desipramine are selective inhibitors of NE reuptake

A

False
True

23
Q

Which receptors TCA blocks

A

Alpha adrenergic histaminic and muscarinic (cause of many side effects)
Amoxapine also blocks D2 receptors

24
Q

Actions of TcA;
Onset:

A

Elevate mood inprove metnal aletrness increase ohysical activity
2 weeks or longer
Necessitates slow withrawal to minimuze discontinuation syndrome and cholinergic rebound effects

25
Q

TCA effective in tx of :

A

Moderate to severe major depression
Chronic pain syndrome (neuropathic)
Enuresis in children (older than 6h

26
Q

Which drug us used to control bed wetting by causing contraction of internal sphincter

A

Imipramine (tofranil)
Used cautiosly because of induction of arrythmias

27
Q

Phamacokinetics

A

Well absorbed after oral adm
Lipophilic
Widely distributed
Variable 1/2 4-17 hrs for imipramine
Metabolized by liver microsomal enz
Excreted as in active metabolites in kid

28
Q

Adverse effects
1-
2
3-

A

Blockage of muscarinic receptors(blurred vis, xerostomia, urinary retention, constipation and glaucoma)
Blockage of alpha adrenergi(orthostatic hypotention dizziness and reflex tschy)
Block H1 eeceptors (sedation weight gain sexual dys lower than SSRIs)

29
Q

Cardiovascular adverse effects

A

On slide

30
Q

Precautions of TCA

A

Like all antidepressants used with caution in known bipolar patients because they may switch to manic episode

31
Q

T or F
TCAs have narrow therapeutic index
May exacerbate medical conditions such as epilepsy and arrythmias
We can associate with MAO

A

True (5-6 fold the max may be lethal of imipramine)
True
False never (risk of hyper)

32
Q

MAO inhibitors
Mode of action
Presence
Anti depressant action

A

Form stable complexes with MAO causing itreversible inactivation
In brain gut and liver (oxidative deamination of toxic substances like tyramine)
Delayed several weeks (altho its fully inhibited after several days)

33
Q

Therapeutic uses of MAO inhibitors

A

Depressed patients unresponsive to TCA
Low psychomotr activity
Phobic states

34
Q

Names of MaO inhibitors

A

Phenelzine (Nardil)
Tranylcypromine (parnate)
Sleegeline (eldepryl or deprenyl)

35
Q

Pharmacokinetics

A

Well absorbed after oral
Effects require 2-4 weeks
Enzyme regeneration varies but requires several weeks after termination

36
Q

T or F
We need minimum 1 week after MAO inhibitors termination to start another med

A

False
Minimum 2 weeks

37
Q

Adverse effects
Drug food interaction
Drug drug interaction

A

Drug food interaction (unable to degrade tyramine which inturn leads to release of large amounts of stored catecholamines from nerves causing head ache tachycardia hypertension cardiac arrythmias nausea)
With SSRIs cause serotonin syndrome both drugs require washout periods at least 2 weeks before other type is given
Exxxceotionnnnn: fluoxetine should beeee discontineud 6 weeks at least before AO is initiated

38
Q

Tx of mania
Lithium:
Mode of action
Mode of adm
Excretion
Toxic
Therapeutic index
Adverse

A

Mood stabilizer
Unknown (may be decrease norepinephrine release and increase serotonin)
Orally
Ion Secreted by kidney
can be toxic
Extreeemly lowwww
Headache,dry mouth polydipsia polyuria polyphagia GI (nausea vomittin) ataxia and tremors
Give lithium with food

39
Q

Names of
1-Antiepileptic drugs as mood stabilizers
2-Agents that improve manic sx
3-Management of mania
4-Bipolar depression

A

1-Carbamazepine, valproic acid and lamotrigine
2-Chlorpromazine and haloperidol
3-Risoeridone olanzapine aripiprazole and quetiapine
4-quetiapine and olanzapine+fluoxetine

Pharmacology (16 decks)

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