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Psychiatry > atypical antidepressants > Flashcards

atypical antidepressants Flashcards

1
Q

analogy of the antipsychotic drug loxapine

retains some DA receptor antagonism –> risk of extrapyramindal motor side effecs

may be used for depression in psychotic patients

mixed inhibitions: NET>SERT~SAT

A

amoxamine

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2
Q

selective inhibitor of NE reuptake. increased risk of seizures

A

maprotiline

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3
Q

moderate inihition of serotoni reuptake but primarily acts as a 5-HT2a antagonist and 5-Ht1a partial agonist (SARI).

useful in tx of depression characterized by anxiety and sleep disturbances. short t1/2(2-9 hr). inhibits CYP3A4. N

A

trazodone

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4
Q

why was a nefazodone, a drug similar to trazodone discontinued?

A

hepatotoxicity

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5
Q

a potent 5-HT1a partial agonist and SSRI (approved 1.21.2011)

A

vilazodone

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6
Q

analog of mianserin

enchances the release of serotonin and NE by antagonizing presynaptic alpha-2ARs. antagonizes 5-HT2 receptors.

potent antihisatiminic—>sedating. increased weight gain. Less GI and sexual disturbances than SSRIs. (tetracyclinc AD)

A

mirtazepine

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7
Q

weak blocker of DAT, SERT, and NET

active metabolit is an NE reuptake blcoker

causes agitation, anxiety, resltessness. _risk of seizure _

admin as dividied doses or slow release formulation (medium t 1/2)

also used as aid in smoking cesssation (ZYBAN)

A

buproprion

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8
Q

inhibits serotonin and NE reuptake (SNRI)

devoid of antishitaminergic, anticholinergic, and anti-adrenergic properties –>Does not have TCA like ADE

short t 1/2 (4-10hr)

produces a small: _sustained HTN, sweating, dizziness, nausea, anxiety _

A

venlafaxine

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9
Q

SNRI (serotonin and norepi reuptake) most potent one available (~100x more potent than VEnlafaxine) ~50% bioavailability, highly bound to plasma proteins (~95%) metabolized to CYP2D6 and CYP1A2.

t 1/2 ~12hr

A

duloxetine

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10
Q

recently approved (9/30/2012) “serotonin modulator and stimulator.”

Potent blocker of SERT and high efficacy partial agonist at 5-HT1a receptors. Partial agonist (5-HT-1b) and antagonist at 5-HT1d, 3a, and 7 receptors.

weak block of NET and B1-AR

A

vortioxetine

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11
Q

Flashbacks - fluoxetine

Paralyze - paroxetine

Senior - sertraline

Citizens - citalopram

are all ______?

A

SSRIs

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12
Q

what are the 5 SSRIs in our block?

FLashbacks

PAaralyze

SEnior

CItiziens?

A

Fluoxetine

Paroxetine

Sertaline

CItalopram

Fluvoxamine

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13
Q

first-line therapy in pts diagnosed with major depression.

also used to TX panic, OCD, social anxiety disordrer, ADHD, and some eating disorders

A

SSRIs

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14
Q

what are the three general behavior/clinical effects of SSRIs?

ASA

A

anxiety

stimulation

agitation (they go away after chronic admin (2-6 weeks)

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15
Q

what are the three ADE’s of SSRIs?

NLSC

A

Nausea

Low libido

Sexual dysfuncition

decreased CArdio and anti-cholinergic effect

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16
Q

which SSRI has increased risk of birth defects?

A

Paroxetine

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17
Q

which drugs are C/I when taking SSRIs? why?

A

MAOIs b/c lead to serotonin syndrome

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18
Q

describes wha:

onset within 24 hours of OD or concurrent MAOI.

due largerly to overstimuation of 5-HT1A receptors in central grey (midbrain) and medulla

A

serotonin syndrome

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19
Q

what is a syndrome characterzied by by:

hypepyrexia+hyperreflexia

tremor +shivering

myoclonus+agitation

seizures+confusion

delirium+cardiovascular collapse+coma

A

seretonin syndrome

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20
Q

what are the three monoamine oxidase inhibitors?

TIP?

A

T - tranylcypromine

isocarbazid

phenelzine

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21
Q

typically only used in pts who unrespeonsive to tx w/other antidepressants and for whom ECT is not suitable

also used for panic disorder, agoraphobia

A

Monoamine oxidase inhibitors

T-tranylcypromine
I-isocarboxazid

P-phenelzine

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22
Q

moa of MAOIs?

A

block oxidative metabolism of monoamines by i_rreversible . inhibition of MAO-A and MAO-B in nerve terminals. _

MAO-A metabolizes primarily NE, 5-HT and tyramine

MAO-B - mostly DA selective

23
Q

central effects of MAOIs? ASE

A

CNS stimulation

Agitation

possibly euphoria

chronic (2-6 wks): imporvemnts of most or all symptoms, CNS activation remains

24
Q

ADE of MOAIs. SOWS

A

remember as hypotension from fat, sex, and sleep disturbance.

S- sleep disturbance (increase arousal)

O - orthostatic hypotnesion

W- weight gain

S- sex dysfunction

25
Q

how are MAOIs inactivated?

A

acetylation

26
Q

which drugs have an interaction w/foods that contain high amts of tyramine?

A

MAOIs (cheese)

27
Q

what does MAO-A metabolize (3)?

A

NE, 5-HT, and tyramine

28
Q

what does MAO-B metabolize?

A

dopamine selective

29
Q

what are the general behavior side effects for MAOIs?

SAE

A

s-sedation

A - agitation

E- possible euphoria

30
Q

pharmacokinetics of MAOIs

where are they generally absored from?

is daily dosing required?

how are they inactivated?

A

Generally well absorbed from GI

daily dosing required in spite of irreversible enzyme inhibition!!

inactivated by acetylation

31
Q

b/c block of MAO irreversible, how long to drug effects persist?

A

drug effects persist 1-3 weeks

32
Q

drug interactions of MAOIs

Food + 3 class of drugs

A
  1. foods containing high amts of tyramine (cheese)
  2. sympathomimetic drugs( cold remedies, diet aids, and stimulants) –> acute hypertensive reaction
  3. sympathomimetic drugs(cold remedies, diet aids, stimulants) –>acute hypertensive reaction
  4. meperidine, dextromethorpham –> hyperpyrexia, delirium, convulsions, coma, death
  5. SSRIs.
33
Q

what are three mood stabilizers? VLC

A

lithium

valproate

carbamazepine

34
Q

what are lithium, valproate, and carbamazepine indicated for?

A

maintenance of manic depression

35
Q

what is acute mania typically treated with?

A

antipsychotics and benzodiazepines

36
Q

what is the MOA of lithium?

A

Mechanism of action: poorly understood.
Most favored hypothesis implicates Li inhibition of inositol phosphate signaling. Also inhibits neurotransmitter-stimulated adenylyl cyclase activity.
Effective in ~60 % of patients

37
Q

what are the pharmakokinetic of lithium?

how quickly is it absorbed?

A

Pharmacokinetics: Rapid (30 min- 2hr peak) and complete absorbtion (6-8 hrs). Distributes to total body water, some concentration in bone. Cleared in the urine, t 1⁄2 ~20 hrs. No metbolism.

38
Q

what are the ADE of litihum?

Neuro

glandular

renal

cardiac

other

A
  • *Adverse effects: *VERY NARROW therapeutic window. (target ~0.5-1.0 mEq/L) Toxic effects observed at > 1.5 mEq/L.**
    a) Neurologic/psychiatric: tremor, ataxia, hyperactivity, aphasia, sedation, fatigue
    b) Glandular: edema, mild hypothyroidism
    c) Renal: polydipsia, polyuria (nephrogenic diabetes insipidus),

d) Cardiac: bradycardia-tachycardia (“sick sinus”)
e) other: acne, folliculitis, and exacerbates psoriasis

39
Q

two drug classes that lithium interacts with

A

Drug interactions: Sensitive to diuretics and antiinflammatory drugs (NSAIDs)

40
Q

what are the two anti-convulsants frequently used in the management of bipolar disorder?

A

The anticonvulsants valproate and carbamazepine are now frequently used in the management of bipolar disorder.

They may be used alone or in combination w/Li or w/ other antipsychotics. Appear effective in either phase of manic depression (particularly valproate).

41
Q

what are the advantagesand disadvantages of anti-psychotics?

A

Advantages compared to Li: ↑dose faster, quicker response, better TI

Disadvantages compared to Li: less experience, efficacy questionable in severe disease

42
Q

what is the first line drug for bipolar disorder?

A

*Lithium is first line for bipolar disorder, however milder forms may be treated with anticonvulsants.

43
Q 
Valproic Acid
 Valproic acid (or Na Valproate) (DEPAKENE): is fully ionized at normal physiological pH and therefore valproate is assumed to be the active form.
44
Q

indication for valproate

A

Indications: Used as monotherapy or in combination with Li or antipsychotics.

45
Q

which drug?

Note: Effective in the treatment of absence, myoclonic, partial and tonic- clonic seizures. A drug of choice when absence seizures are also accompanied with tonic-clonic seizures.

A

valproic acid

46
Q

what is the MOA of valproate?

A

Mechanism of action: Inhibits voltage-gated Na channels by stabilizing the inactivated state of the channel. Block of channel activity is use-dependent. Also blocks Ca channels (T-type) to a lesser extent. Valproate also can stimulate GABA synthesis and inhibit GABA degradation. At high doses may increase resting K conductances.

47
Q

what are the drug interactions of valproate?

A

Drug Interactions: Valproate inhibits its own metabolism and the metabolism of other drugs. Valproate also displaces phenytoin from plasma proteins.

48
Q

toxicity of valproate (4)

A

Toxicity: Nausea,

abdominal pain,

heartburn are common.

Sedation may be
a problem. Hepatotoxicity can be common.Careful monitoring of liver function
is recommended.

49
Q

indications of carbamazepine

A

Indications: Used as monotherapy or in combination with Li or anti-psychotics.

50
Q

describes which drugs

Note: Drug of choice for partial seizures, also may be used for generalized tonic-
clonic seizures. Also effective for trigeminal neuralgia.

A

carbamazepine

51
Q

which drug described?

Pharmacokinetics: Absorption is from GI tract (100%), rate varies with patient. Time to peak 6-8 hr. Poor solubility. Bound (~ 70%) to plasma proteins (albumin).

Distributes slowly.

No displacement of other drugs which bind plasma proteins.

A

carbamazepine

52
Q

carbamazepine is metabolized by CYP3a4 to an active metabolit to which metabolite?

A

Metabolized primarily by CYP3A4 to an active metabolite (10,11-epoxide). Varies with patients. t1⁄2 36 hr after initial dose then may decrease to 20 hr. Cleared slowly.

53
Q

drug interactions for carbamazepine

what does it induce?

A

Drug interactions: Carbamazepine is a broad spectrum inducer of CYP2C and 3A families, in addition to induction of UGTs. Thus enhancing the metabolism of many drugs
Note: affects the metabolism of oral contraceptives.

54
Q

toxicity of carbamazepine

A

Diplopia (double vision) and ataxia are common.

Mild GI upset, unsteadiness.

At high doses drowsiness. Rash common idiosyncratic reaction. Some occurences of aplastic anemia.

Psychiatry (11 decks)

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