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Psychiatry > Antidepressants and Mood Stabilizers > Flashcards

Antidepressants and Mood Stabilizers Flashcards

1
Q

What are the TCAs?

A

Amitriptyline
Imipramine
Nortriptyline

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2
Q

What are the MOA of the TCAs?

A

SNRIs: Decrease Serotonin and NE retake into presynaptic terminals, increasing neurotransmitter action and changing receptor profiles. Also blocks muscarinic Ach, serotonin, and histamine receptors, which leads to ADE.

+Serotonin, NE
-Ach, serotonin, and histamine

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3
Q

What are the AEs of the TCAs? how?

A 
Orthostatic hypotension: a blocker
Anti-SLUDGEBBB: mAch blocker
Glaucoma: mAch blocker
Sedation: a and histamine blocker
Weight gain
Sexual disturbance
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4
Q

What are the acute and chronic effect of TCAs?

A

Acute: drowsy, decreased cognition
Chronic: normal cognition, not drowsy

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5
Q

What is CI with TCAs?

A

Drugs: clonidine, alcohol
Disease: glaucoma

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6
Q

What are the atypical antidepressants?

A 
Not TCAs: 
Amoxamine
Maprotiline
Trazodone
Nefazadone
Mirtizapine
Buproprion
Venlafaxine
Duloxetine
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7
Q

What is the MOA/AE of amoxamine?

A

MOA: inhibts NE>5HT/DAT
AE: Blocks DOPA–>Extrapyrimidal: dopa antagonism

Use: depression in psychotic patients

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8
Q

What is the MOA/AE of maprotiline?

A

MOA: Serotonin/NE reuptake inhibitor (SNRI)
AE: seizure risk

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9
Q

What is the MOA/AE of Trazodone and nefazodone?

A

Use: Anxiety + insomnia

MOA: mild SSRI, SARI: but mainly a 5HT1a agonist/5HT2a blocker (weird…)
AE: CYP’s
Neftazone: hepatotoxic

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10
Q

What is the MOA/AE of mirtazepine?

A

MOA: presynaptic a2 antagonist leads to increased Serotonin/NE release
antagonizes 5HT2 receptors
AE: blocks sertonin, sedation (blocks histamine), WEIGHT GAIN (less GI and sex disturbance than SSRIs)

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11
Q

What is the MOA/AE of Buproprion?

A

Use: smoking cessation, slow release
MOA: weak dopa/serotonin/NE blocker
*METABOLITES–>SNRI
AE: restlessness, anxiety, SEIZURES

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12
Q

What is the MOA /AE of venlafaxine?

A

MOA: SSRI with NO antihistamine/Ach
AE: LOW ADs! small hypertension

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13
Q

What is the MOA/AE of duloxetine?

A

SNRI

AD: Cyps

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14
Q

What is the MOA of the SSRIs?

A

MOA: increase JUST serotonin effects
AE: sexual dysfunction, GI, teratogen, serotonin syndrome
*Low OD rate due to high TI

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15
Q

What is the MOA/AE of the MAOis?

A

MOA: IRREVERSIBLY inhibiti MAO-a and b via OXIDATIVE metabolism
AE: Tyramine reaction, less sleep, orthostatic hypotension, weight gain, sexual dysfunction

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16
Q

What are the targets of MAO A and B?

A

A: NE, serotonin, TYRAMINE

B: Dopamine

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17
Q

What patient profile leads to short effectiveness of MAOis?

A

Fast Acetylators

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18
Q

What is the acute and chronic patient effects in MAOis?

A

Acute: arousal and EUPOHORIA

Chronic: just arousal, no euphoria (2-6 weeks)

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19
Q

What are the SSRIs?

A 
Citalopram
Fluoxetine
Paroxetine
Sertraline
FLuvoxamine
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20
Q

What are the MOAis?

A

Trancypromine

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21
Q

What are the mood stabilizers?

A

Lithium
Valproate
Carbamazapine
Lamotrigine

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22
Q

What is the MOA/AE of Lithium?

A

MOA: IP3 signal inhibitor

AE: Diuretics/NSAIEDs-->renal toxic
Hits all high flow organs:
Brain: tremor, ataxia, sedation
Glands: edema, THYROID decrease
Kidney: nephrogenic diabetes insipidus
Teratogen: Ebstein anomaly
Skin: acne and psoriasis
Heart: swinging between tachycardia and bradycardia
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23
Q

What is the MOA/AE of Valproate?

A

MOA: Na/Ca blocker, Increase GABA and K conductance

AE: Inhibits UGT–>increases its own concentration
CI: Phenytoin displacement from proteins
Heartburn
Liver toxicity

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24
Q

What is the MOA/AE of Carbamazapine?

A 
MOA: Inhibit voltage gated Na channels
AE: induces Cyps--> DECREASES its own concentration, generates 10,11 epoxide metabolite
Decreases OCP efficacy=RED FLAG
Diplopia
Ataxia
Stevens Johnson syndrome
APLASTIC ANEMIA
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25
Q

What are the Benzodiazapines?

A 
Alprazolam
CHlordiazepoxide
Clonazepam
Clorazepate
Diazepam
Lorazepam
Oxazepam
Prazepam
26
Q

What is the MOA/AE of BZDs?

A

MOA: Allosteric GABA ^potency
*binds at unique site from flumazenil

AE: Sedation, Teratogen, Depenence, Tolerance

27
Q

Anxiety Rx?

A

Alprazolam, lorazepam, clonazepam

28
Q

Panic attack Rx?

A

Alprazolam

29
Q

BZD with TCA activity?

A

Alprazolam

30
Q

ONLY BZD with muscle relaxation?

A

Diazepam: “muscles Die with diazepam”

31
Q

Alcohol withdrawal Rx?

A

Chlordiazepoxide
Diazepam
Lorazepam with hepatic disease

32
Q

What is the MOA/AE of Buspirone?

A

MOA: Decrease Serotonin
Increase NE/Dopa
*slow onset

AE: same as BZDs???

33
Q

What is the MOA/AE of Propranolol?

A

MOA: Beta blocker for stage fright

*does not act in area of brain involving emotion, just autonomics

34
Q

What is the biogenic amine theory of depression?

A

Depression is due to DECREASES in NE and Serotonin

35
Q

What are the evidences for the biogenic amine theory of depression?

A
  1. our drugs work

2. Reserpine blocks monoamine storage and causes depression

36
Q

Locus ceruleus=

A

NE

37
Q

Raphe nucleus=

A

serotonin

38
Q

Why is response to antidepressants delayed?

A
  1. It takes a few weeks to reset cellular machinery: receptors and signals have to be synthesized
  2. stress hormones (cortisol) takes time to be regulated
39
Q

What is the recent evidence about cytokines?

A

They have a antidepressant effect (CI for NSAIDs?)

40
Q

What classes are included in atypical antidepressants?

A

SNRIs
NRIs
etc…

41
Q

What is the BLACK BOX warning for ALL antidepressants?

A

SUICIDAL THOUGHTS!!!!

42
Q

What are antidepressants substrates for in the BBB?

A

P-glycoprotein/ABCB1 transporter: MDR-1 testing shows that mutation in MDR-1 will decrease effectiveness of drugs because the receptor pumps them out of the brain

43
Q

What drugs are MDR-1/P-gp substrates?

A

Citalopram
Venlafaxine
Paroxetine
Amitriptyline

44
Q

What drugs are NOT MDR-1/P-gp substrates?

A

Mirtizapine

FLuoxetine

45
Q

Bed wetting Rx?

A

Imipramine

46
Q

TCA effects?

A

+: 5HT, NE

-: mAch, 5HT, Histamine

47
Q

Do TCAs have euphoria?

A

NO euphoria, MAOis have euphoria

48
Q

How are 3* amines metabolized to 2* amines?

A

Demethylation

49
Q

Imipramine–>

A

Desipramine

50
Q

Amitriptyline–>

A

Nortriptyline

51
Q

What is the tricyclic ring of TCAs metabolized by?

A

CYPs–>conjugation

52
Q

What other drugs are CI with TCAs?

A

Alcohol: potentiate
ANY other enruo drug, really
Clonidine

53
Q

What antidepressant probably has the least side effects?

A

Venlafaxine

54
Q

What is first line depression therapy?

A

SSRIs: citalopram/fluozetine/paroxetine/sertraline/fluvoxamine

55
Q

When is MAOi therapy indicated?

A

In patients unresponsive to other treatments and not suitable for electroconvulsive therapy.

56
Q

What else are MAOis used in?

A

Panic disorder
Agoraphobia
(ironic, because these drugs have scary side effects)

57
Q

Cold remedies, diet aids, stimulants with MAOis–>

A

Hypertensive reaction

58
Q

Meperidine, dextromethorphan with MAOis–>

A

FEVER, delerium , seizures, death

59
Q

Tyramine and SSRIs with MAOis–>

A

Serotonin syndrome

60
Q

What are the advantages to anticonvulsants for mania over lithium?

A

You can increase the dose faster, get a quicker response, and better TI. BUT, there is less experience and we are not sure that they work well in severe disease.

61
Q

What types of bipolar indicate lithium/anticonvulsant use?

A

Mild: anticonvulsant
Severe: Lithium

62
Q

What drug indicates liver monitoring?

A

Valproate

Psychiatry (7 decks)

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