04 - Psychiatric and CNS Drugs Flashcards

0
Q

SSRI work by increasing the amount of _____ in the synapse

A

Serotonin

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1
Q

Most broadly prescribed class of antidepressants

A

SSRI

Also used for anxiety, OCD, social phobia, PTSD

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2
Q

Examples of SSRIs

A

Fluoxetine
Sertraline
Paroxetine
Escitalopram

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3
Q

Side effects of SSRIs

A
Insomnia
Agitation
Headache
Nausea
Diarrhea
Sexual dysfunction
Platelet dysfunction
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4
Q

SSRI inhibit which hepatic cytochrome? This increase levels of

A

P450 (esp fluoxetine)

Increases levels of TCA, some neuroleptics, and antiarrhythmics (metoprolol)

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5
Q

SSRIs can potentially cause ______ especially together with MAOIs, carbamazepine, or Linezolid (abx)

A

SEROTONIN SYNDROME

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6
Q

Is overdose on SSRIs lethal?

A

Not typically

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7
Q

Other commonly used antidepressants inhibit the reuptake of

A

Other neurotransmitters (dopamine, NE)

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8
Q

Venlafaxine and bupropion side effects

A

Venlafaxine - minimal anticholinergic effect, hypotension

Bupropion - less sexual dysfunction, hypotension; also smoking cessation

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9
Q

TCAs are highly effective but have poor

A

Side effect profiles

Anticholinergic (dry mouth, tachycardia, urinary retention, GI slowing)
Orthostatic hypotension, PR prolongation, cardiac depression
Sedation, lowered seizure threshold

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10
Q

Is overdose on TCAs lethal?

A

Yes, it has a narrow therapeutic index

Myocardial depression, ventricular dysrhythmias

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11
Q

Overdose on TCA can cause threat up to ____ days even after the comatose phase resolves

A

10

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12
Q

At low doses, TCAs are commonly used for

A

Chronic pain syndromes

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13
Q

TCAS work by blocking the reuptake of

A

NE (and sometimes serotonin)

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14
Q

TCAs have ____ protein binding. What drugs can affect the protein binding of TCAs?

A

Strong

Phenytoin
Aspirin

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15
Q

Examples of TCAs?

A

Amitriptyline
Nortriptyline
Imipramine
Clomiprimine

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16
Q

Drug interactions with TCAs are related to their ____ effects and _____ uptake-blocking actions

A

Anticholinergic

Catecholamine

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17
Q

With sympathomimetics, TCAs have exaggerated ____ response! especially with _____ agents. When is this not true?

A

Pressor
Indirect-acting agents

May have attenuated response with chronic TCA users

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18
Q

Increases likelihood of postoperative delirium when used with TCAs

A

Atropine

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19
Q

How do TCAs affect opioids and barbs?

A

Potentiates

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20
Q

MAO is an enzyme that metabolizes

A

Catecholamines (monoamines)

Dopamine, serotonin, NE, Epi

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21
Q

MAO subtype that metabolizes serotonin, NE, epi, and tryamine

A

MAO-A

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22
Q

MAO-A and ____ leads to the formation of ____ which is seen in pheochromocytoma

A

COMT

Vanillylmandelic acid

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23
Q

MAO subtype that metabolizes tyramine

A

MAO-B

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24
Q

T or F? Most MAOIs are reversible and nonselective inhibitors

A

FALSE, irreversible and nonselective

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25
Q

Examples of MAOIs

A

Phenelzine
Tranylcypromine
Isocarboxazid
Selegiline (Parkinson’s)

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26
Q

Rarely used due to side effects and complex dosing

A

MAOIs

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27
Q

Some side effects of MAOIs?

A
Orthostatic hypotension
Sexual dysfunction
Weight gain
Anticholinergic
Sedation
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28
Q

Do MAOIs cause dysrhythmias?

A

No

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29
Q

If you take MAOIs, you should avoid ____ in your diet because it can lead to ______ response (like pheo!!!)

A

Tyramine
Indirect sympathetic response

Avocados, cheese, liver, fava beans, chianti

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30
Q

MAO-B inhibitors (selegiline) require no dietary restriction except at

A

Very high doses

Because most tyramine is deaminated by MAO-A

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31
Q

Overdose of MAOIs is

A

Lethal

Tachy, hyperthermia, hypermetabolism (rigidity), seizures, coma

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32
Q

A suggested treatment for MAOI overdose

A

Dantrolene

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33
Q

Should MAOIs be stopped 2-3 weeks before anesthesia?

A

No data to support

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34
Q

Sympathomimetics should be used ____ in conjunction with MAOIs. Consider using _____ > ______

A

With caution

Direct > indirect

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35
Q

Avoid using ____ with MAOIs during local/regional anesthetics

A

Epinephrine

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36
Q

Can cause excitatory OR depressive reactions with MAOIs

A

Opioids, mostly with meperidine

37
Q

Lithium is the treatment of choice for ____ but requires measurement of

A

Bipolar disorder

Plasma concentrations

38
Q

Lithium is filtered by the kidneys and reabsorbed in the

A

Proximal tubule (competes with Na)

39
Q

Na depletion (dehydration, diuretics) can ____ lithium levels

A

INCREASE

40
Q

Side effects of lithium

A

Polydipsia
Polyurethane
Hypothyroidism

41
Q

Lithium causes a prolonged response to

A

Depolarizing and nondepolarizing NMB

42
Q

Avoid using _____ with lithium

A

Diuretics (loop, thiazide)

NSAIDs

43
Q

Lithium used with neuroleptic drugs increase risk of ____ side effects and

A

Extrapyramidal

NMS

44
Q

Lithium toxicity is exacerbated by

A

Dehydration
Na restriction
Diuretics
NSAIDs

45
Q

Sever lithium toxicity may require

A

Osmotic diuresis or dialysis

46
Q

Effects of lithium toxicity

A
Lethargy
Weakness
QRS widening
Heart block
Hypotension
Confusion
Seizures
47
Q

Used for treatment of schizophrenia or bipolar disorder

A

Antipsychotic drugs (neuroleptics)

48
Q

Examples of antipsychotic drugs

A
Chloropromazine (thorazine)
Clozapine (clozaril)
Haloperidol (haldol)
Risperidone (risperdal)
Droperidol
49
Q

Antipsychotic drugs work by blocking ____ receptors

A

Dopamine

50
Q

One side effect of all neuroleptics except _____ is _____, which are movement disorders

A

Clozapine

Extrapyramindal effects

51
Q

Tardive dyskinesia is the abnormal, _____ movement of

A

Involuntary
Face, neck, tongue

Caused by neuroleptics

52
Q

Acute dystonic reaction is acute muscle _____ in the face, neck, tongue and

A

Rigidity/clamping
Larynx

Caused by neuroleptics

53
Q

What is the treatment for acute dystonic reaction?

A

Diphenhydramine
Benztropine

These are anticholinergics

54
Q

Other extrapyramidal effects caused by neuroleptics?

A

Parkinsonism - rigidity, tremor, bradykinesia/akinesia

Akathesia - restlessness

55
Q

Neuroleptic malignant syndrome causes rigidity that may lead to _____ and renal failure (myonecrosis)

A

Ventilators requirement

56
Q

Symptoms of NMS?

A

Hyperthermia
Muscular hypertonicity
Autonomic instability
Mental status changes

57
Q

What is the incidence and mortality of NMS?

A

Incidence: 0.5-1%
Mortality: 20-30%

58
Q

Treatment for NMS?

A

Dantrolene (relax muscles)

Amantadine/bromocriptine (dopamine agonists)

59
Q

Nondepolarizing NMBs will cause _____ in NMS but not in MH

A

Flaccid paralysis

60
Q

Neuroleptics cause alpha blockade, which leads to these side effects?

A
Orthostatic hypotension
Prolonged QTc (->VTach)
61
Q

Neuroleptics block the inhibition of prolactin, causing

A

Galactorrhea

Gynecomastia

62
Q

Neuroleptics decrease corticotropin release, leading to

A

Decreased corticosteroids

63
Q

Weight gain and hyperglycemia are side effects of

A

Neuroleptics

64
Q

CNS effects of neuroleptics

A

Sedation, antiemetic, dysphoric response (droperidol)

65
Q

Which neuroleptic causes agranulocytosis?

A

Clozapine

66
Q

How do neuroleptics affect opioids?

A

Potentiate on

67
Q

Best drugs to stop a seizure QUICKLY

A

Barbs
Benzos
Propofol

68
Q

Which channel does phenytoin block?

A

Na

Also Ca and NMDA

69
Q

What percent of phenytoin is protein bound? Caution with

A

90%

Hypoalbuminemia

70
Q

Therapeutic serum level of phenytoin?

A

10-20 mcg/mL

71
Q

Phenytoin levels can be increased by

A

Amiodarone
Fluconazole
Isoniazid
Coumadin

72
Q

Phenytoin levels can be decreased by

A
Chronic alcohol
Antineoplastics
Phenobarbital
Diazepam
Calcium
73
Q

Phenytoin is metabolized by hepatic enzymes with ____ kinetics at high plasma levels

A

Zero order

74
Q

Side effects of phenytoin?

A

CNS - nystagmus, ataxia, NV
Gingival hyperplasia
Teratogen

75
Q

How can you avoid hypotension with phenytoin?

A

Slow infusion <50 mg/min

Can precipitate

76
Q

What can you infuse more quickly without hypotension than phenytoin?

A

Fosphentoin - prodrug

77
Q

Levetiracetam (keppra)

A

Unknown mechanism
No significant side effects, no hepatic metabolism, min protein binding
Decreased dosing in renal

78
Q

Gabapentin is most commonly used for

A

Chronic neuropathic pain, diabetic neuropathy

Requires multiple daily doses
No protein binding, no hepatic metabolism

79
Q

Medication used for Parkinson’s?

A

Levodopa

80
Q

Levodopa is a dopamine precursor that unlike dopamine can cross

A

Blood brain barrier

81
Q

What converts levodopa to dopamine?

A

Dopa carboxylase

82
Q

Levodopa is up usually given with ____ to prevent decarboxylation before crossing the BBB

A

Carbidopa

83
Q

Levodopa does not cause orthostatic hypotension

A

False

84
Q

Abrupt cessation of levodopa causes

A

Parkinsonian symptoms, NMS

Dr. Altose asks, “when was your last dose and what happens if you miss a dose?”

85
Q

You may need to give levodopa _____ via NG

A

Intraoperatively

86
Q

Can cause skeletal rigidity when used with levodopa

A

Haloperidol, droperidol

Due to dopamine antagonism
Usually avoid metoclopramide and promethazine

87
Q

How does levodopa act with anticholinergic drugs?

A

Synergistically

88
Q

Dopamine agonists at such ad bromocriptine and pergolide are used for

A

Parkinson’s disease

89
Q

Anticholinergic drugs (benzotropine) restore ______ balance with Parkinson’s. They help with _____ and salivation but very little with

A

Ach/dopamine

Tremor and salivation
Rigidity

90
Q

Amantadine may facilitate _____ release and delay ____? What is it used for?

A

Dopamine
Reuptake

Parkinson’s

91
Q

MAO-B inhibitor that can be used for Parkinson’s treatment?

A

Selegiline - not involved and NE metabolism