Neuro 4 Flashcards

1
Q

When do anti-depressants increase the risk of suicide?

A

in patients < 25years

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2
Q

What is major depressive disorcer MDD?

A

unipolar debilitating depression

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3
Q

What is dysthmia?

A

less severe form of depression, can function but just not at your best

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4
Q

discontinuation syndrome of SSRI SNRI and TCA

A

dizziness and paresthesia for 1-2 days post DC for 1 week or more

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5
Q

discontinuation syndrome of MAOIs

A

delirium with psychoses, excitement, confusion

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6
Q

Anti depressant kinetics

A

inhibit CYP metabolism - beware of drug to drug interactions
highly protein bound - issue in anorexia/malnourished
absorption is rapid

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7
Q

4 types of antidepressants

A

MAOIs
amine reuptake inhibitors
serotonin receptor antagonists
atypical heterogenous drugs

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8
Q

Name a MAOI

A

tranylcypromine (parnate)

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9
Q

how to MAOIs work?

A

cause build up of endogenous catecholamines
also antihistamine antagonists
down regulation of adrenergic and serotonin receptors

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10
Q

when do we actually use MAOIs?

A

only for depression unresponsive to newer drugs

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11
Q

where are MAO-A receptors?

A

NE and dopamine neurons

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12
Q

where are MAO-B receptors?

A

serotonin and histamine neurons

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13
Q

SE of MAOIs?

A

orthostatic hypotensin
weight gain
sexual dysfunction (high incidence)
sedation vs insomnia / restlessness

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14
Q

why can’t you eat tyramines when taking MAOIs?

A

They cause endogenous catecholamine release which an lead to HTN crisis

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15
Q

What types of Amine reputake inhibitors are there?

A

tricyclic antidepressants
SNRIs
SSRIs

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16
Q

Mech of action of trazadone?

A

5HT2 antagonist

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17
Q

how do tricyclic antidepressants work?

A

non selective NE and serotonin reuptake inhibitors

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18
Q

TCA side effects?

A

sexual dysfunction
anticholinergic
excitatory symptoms

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19
Q

name a TCA

A

imipramine (tofranil)

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20
Q

name two SNRIs

A

reboxatine
venlafaxine (effexor)

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21
Q

SSRI pregancy class?

A

Class C

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22
Q

SSRI pregnancy class?

A

Class C

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23
Q

name a SSRI

A

fluoxetine (prozac)

24
Q

SSRI SE

A

sexual dysfunction
GI upset
HA, insomnia, hypersonmia

25
Q

name two atypical heterogenous antidepressants

A

mirtazapine ( remeron)
lithium

26
Q

how does mirtazapine (remeron) work?

A

presynaptic alpha 2 antagonist
increases NE and serotonin release
no sexual side effects
not really used, reserved for unresponsive MDD

27
Q

how does lithium work?

A

ill defined mechanism but does do glutamate reuptake

28
Q

how is lithium metabolised/excreted?

A

not metabolized, it is excreted entirely in urine

29
Q

AE of Lithium?

A

motor hyper activity
hypothyroidism
polyuria and polydypsia

30
Q

when is Lithium contraindicated?

A

sick sinus syndrome

31
Q

main toxicty of anti depressants?

A

can cause seizure and CV collapse

32
Q

What anti depressants cause CNS depression (sedation)?

A

TCAs

33
Q

what antidepressants toxicty can cause CNS stimulation?

A

SSRIs and MAOIs

34
Q

what antidepressants toxicty can cause HTN?

A

TCAs

35
Q

waht andidepressants toxicty won’t affect BP?

A

SSRIs

36
Q

what antidepressants toxicty has variable BP effects depending on diet?

A

MAOIs

37
Q

which antidepressants toxicty cause anti cholinergic effects?

A

MAOIs and TCAs

38
Q

which antideprssants toxicity have no ANS effects?

A

SSRIs

39
Q

Lithium’s toxic CNS effects?

A

hypothyroidism
weight gain
mental confusion
withdrawl

40
Q

Lithium’s toxic ANS effects?

A

nephrogenic diabetes insipidus (blocks ADH)

41
Q

the following are all seen in what condition?
tardive dyskinesia
tardive dystonia
tardive akathisia
rabbit syndrome
neuroleptic malignant syndrome

A

Parkinson’s disease

42
Q

autonomic dysfunction seen in Parkinson’s disease

A

sexual dysfunction
sphincters
choking
sweat abnormalities
sensory issues

43
Q

main issue in parkinsons disease?

A

lack of dopamine in the brain

44
Q

ways to treat parkinsons disease

A

D2 stimulation
symptom mgmt
levodopa/carbidopa
MOAI??
COMT inhibitor??

45
Q

how much of levodopa actually reaches brain?

A

1-3% the rest is metabolized to dopamine peripherally

46
Q

what does carbidopa do?

A

inhibits dopa decarboxylase inhibitor

47
Q

adding carbidopa decreases levodopa dose by how much?

A

75%

48
Q

AE of levodopa?

A

anorexia, N/V, cardiac arrhythmias, tardive dyskenesia

49
Q

how many pts on levodopa develop tardive dyskenesia?

A

80% who have been on it for >10 years

50
Q

when does benefit of levodopa decrease?

A

after 3-4 years

51
Q

name dopamine agonists for parkinsons treatment

A

pramipexole
ropinirole
rotigotine

52
Q

what do pramipexole and ropinirole have in common?

A

can be used for monotherapy in parkinsons
can be used in advanced disease
allows for decreased doses of levodopa

53
Q

Dreceptor for pramipexole?

A

D3

54
Q

receptor for ropinirole?

A

D2

55
Q

how is pramipexole excreted?

A

unchanged

56
Q

how is ropinirole excreted?

A

metabolized in the liver

57
Q

when would you DC any of the dopamine agonists in parkinsons?

A

cardiac arrhythmias