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*Pharm > Psych Meds > Flashcards

Psych Meds Flashcards

1
Q

What are anesthetic considerations w/ SSRIs?

A
  1. inhibit CP450 system (inc plasma levels of other drugs)
  2. inhibit platelet aggregation (inc risk of bleeding)
  3. serotonin syndrome (confusion, ataxia, fever, shivering, diaphoresis, muscle rigidity, hyperreflexia)
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2
Q

What is the MOA for SSRIs?

A

all block reuptake of serotonin

newer drugs also block NE and/or DOPA

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3
Q

What do SSRI’s treat?

A

mild-mod depression, OCD, PTSD, panic/social disorders

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4
Q

Which antidepressants are favorable and why?

A

SSRIs are safest

min effects on BP, CV, sz threshold

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5
Q

What do TCA’s treat?

A 
depression
chronic pain (inhibits overactive inflammatory response)
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6
Q

What other drugs are TCAs similar to?

A

LA’s and phenothiazines

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7
Q

What is the MOA of TCAs?

A

block reuptake of serotonin and/or NE presynaptically

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8
Q

Whats the diff b/n tertiary and secondary amines of TCAs?

A

tertiary - blocks serotonin/NE reuptake

secondar - blocks NE reuptake only

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9
Q

What is the e1/2t for TCAs?

A

long 10-80 hours

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10
Q

What drugs should be avoided w/ TCAs?

A

MAOIs can cause CNS tonxicity w/ TCAs

hyperthermia, seizure, coma

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11
Q

What effect does TCAs have on sympathomimetics ? How would you dose sympathomimetics w/ TCAs on board?

A
  • makes them unpredictable
  • indirect acting - exaggerated response d/t lots of NE
  • acute trx - more dramatic response d/t lots of NE
  • chronic tx - desensitized receptors
  • LOWER DOSES!!! or use potent direct acting
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12
Q

How do TCAs affect:

  1. inhaled anesthetics
  2. opioids
  3. barbituates
  4. anticholinergics
A
  1. may need higher MAC (d/t inc catecholamines)
  2. decrease opioid dose (d/t CNS affects?)
  3. decrease barbituate dose (CNS affects?)
  4. may have central anticholinergic syndrome (toxicity) treat w/ physostigmine
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13
Q

W/ TCAs is it better to use atropine or glycopyrrulate for trx? Why?

A

glyco because it does not cross BBB

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14
Q

What happens w/ overdose of TCAs?

A
  • fatal myocardial pression
  • or fatal ventricular dysrhythmias

Sx: agitation, excitement/delirium, seizures –> to coma, resp depression, dysrhythmias, sudden death, anticholinergic effects

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15
Q

How do you treat overdose for TCAs?

A

vent support

manage CNS/CV toxicity

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16
Q

How do you discontinue TCAs?

A

wean to prevent withdrawal

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17
Q

What are MAOs?

A

enzyme system in mitoch membrane that metabolizes monoamines = DOPA, Sero, Epi, NE

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18
Q

What is the MOA for MAO inhibitors?

A

drug forms complex w/ MAO enzyme resulting in inc NTs

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19
Q

Why are MAOI’s not often used?

A
  • s/e
  • lethal OD
  • difficult dosing
  • diet restrictions
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20
Q

What does MAO A enzyme degrade? MAO B?

A

A - sero/NE/Epi, (tyramines)

B - phenylethylamine, DOPA

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21
Q

Which psych meds have active metabolites?

A

TCAs (long e/12t = 10-80 hrss)

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22
Q

What is the most common s/e of MAOIs?

A

-ortho hypotension (especially in elderly!!!)

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23
Q

What type of diet do MAOIs need and why?

A
  • tyramine free diet

- tyramine + inhibited breakdown of monamines = massive catecholamines = HTN crisis, hyperpyrexia, CVA

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24
Q

What foods are part of the MAOI diet restriction?

A

-cheese, wine, liver, fava beans, avocado, cured meats

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25
Q

What drugs do MAOIs interact with?

A
  • cold/allergy
  • nasal decongestant
  • opioids
  • sympathomimetics
  • TCAs, SSRIs
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26
Q

What opioid cannot be used w/ MAOI? Why

A 
demerol!! causes:
excitatory respone (type I) - agitation, muscle rigidity, hyperpyrexia
depressive response (type II) - hypotension, resp depression, coma
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27
Q

Which sympathomimetic cannot be given w/ MAOIs?

A
  • ephedrine!!

- use direct acting only and dec dose by 1/3 and titrate

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28
Q

How do MAOIs affect MAC?

A

may need higher MAC w/ gases

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29
Q

What happens w/ OD of MAOIs?

A

excessive SNS discharge - tachycardia, hyperthermia, mydriasis, seizure –> coma
minimize SNS stimulation or hypotension during anesthetic care

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30
Q

What is the MOA of anxiolytics?

A

-enhance GABA

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31
Q

What are the pharm effects of anxiolytics?

A 
Sedation
Anxiolysis
Anterograde amnesia
Anticonvulsant
Muscle relaxant (spinal level)
32
Q

Name 2 types of anxiolytics

A
  • benzos for anxiety/insomnia

- buspirone (non-benzo) for anxiety d/o (not panic)

33
Q

What are the CNS effects of anxiolytics/benzos?

A
  • dec CBF, CMRO2

- does not dec ICP response to DVL

34
Q

What are vent effects of benzos?

A
  • dose dependent suppresion
  • hypoxemia/hypovent enhanced w/ opioids
  • CO2 response curves flattens, does not shift
35
Q

What are CV effects of benzos?

A

w/ induction dose, SVR dec –> BP dec

CO unchanged

36
Q

What is midazolam’s solubility/protein binding/distribution?

A

water soluble
90% protein bound
rapiddistribution = short DOA

37
Q

Compare potency b/n midaz and diaz

A

midaz is 3x potency of diaz

38
Q

What is the sedation dose for midazolam?

A

1-2.5 mg up to 5 mg

39
Q

What is the premed/ped dose for midaz?

A

0.5 mg/kg PO

40
Q

What is the induction dose for midaz?

A

0.1-0.2 mg/kg over 30-60 sec

41
Q

What is the solubility/protein/DOA for valium?

A

highly lipid/protein bound

prolonged DOA

42
Q

What do you need to be cautious w/ when administering IV/IM valium?

A
  • burns
  • highly viscous
  • ph 6.9
43
Q

What is the premed dose for valium PO/IV?

A

10-15 mg PO

0.2 mg/kg IV

44
Q

What affect does valium have on MAC?

A

it reduces MAC

45
Q

What is the anticonvulsant dose for valium?

A

0.1 mg/kg IV

46
Q

What is the MOA of phenothiazines and thioxanthenes? Effects?

A

block DOPA receptors in BASAL ganglia and limbic of forebrain

  • block DOPA = EPS
  • block in chemoreceptor trigger zone of medulla = antiemetic effect
47
Q

What kind of safety margine do phenothiazines and thioxanthenes have?

A

large, OD rarely fatl

d/t blocking forebrain

48
Q

What are s/e of phenothiazines and thioxanthenes?

A
  • EPS = tardive dyskinesia, acute dystonic reactions
  • CV - dec BP, direct cardiac depression, prolonged QT
  • sedation
  • dec seizure threshold
  • CNS level skel muscle relaxation
  • antiemetic (prevents opioid induced N/V!!!!)
  • neuroleptic malignant syndrome
49
Q

What is tardive dyskenisia and acute dystonic reactions?

A
  1. tardive dyskinesia - unctrolled movment
    - 20% of pts for therapy >1 yr, elderly/women more, permanent/no trx
  2. acute dystonic reactions - occurs w/in few weaks
    - muscle rigidity/cramping in neck, tongue, face, back, etc
    - resp distress from laryngeal dyskinesia (LARYNGOSPASM!!!) -trx w/ diphenhydramine 25 mg IV
50
Q

What is neuroleptic malignant syndrome?

A

develops 24-73 hours usually in men = hyperthermia, hypertonicity of muscles, instability of ANS, fluctuating LOC

51
Q

How do phenothiazines and thioxanthenes affect opioids?

A

-potentiation of opioids (sedation/vent depression/analgesia)

52
Q

What class is haldol and what drug does it more resemble?

A
  • class = butyrophenes

- but resembles phenothiazines structure and s/e

53
Q

What are CV effects of droperidol (butyrophenes)?

A
  • antidysrhythmic
  • large doses –> WPW syndrome/tachy dysrhythmias
  • prolonged QT
  • torsades
54
Q

What is the black box warning for droperidol (butyrophenes)?

A

-12 lead EKG prior to and continue for 2-3 hrs

55
Q

What is droperidol (butyrophenes) used for?

A
  • neurolept analgesia: combo w/ fentanyl (Innovar) - prolongs fentanyl
  • antiemetic: comparable w/ zofran, not for motion sicknes
56
Q

What is lithium for?

A

treat bipolar disorder

57
Q

What is the MOA for lithium?

A

competes w/ Na+/Ca/Mg –> affects membrane, H2O, NTs

58
Q

How is lithium distributed?

A

thruout total body water and excreted via kidneys

59
Q

How does lithium affect kidneys?

A
  • lithium and Na+ competitive in proximal tubules
  • causes polydipsia/polyuria (impaired concentration)
  • dec sensitivity to ADH
  • monitor RFTs Q6 mos
60
Q

How does lithium affect EKG?

A

flattened t wave or t wave inversion

61
Q

How do you trx severe toxicity of lithium?

A
  • emergency
  • HD
  • osmotic diuresis
  • IV bicarb
62
Q

Anesthetic considerations for lithium.

A

-pre op labs and EKG
-anesthesia requirement may be DECREASED
-NMB may be prolonged
(kidneys)

63
Q

What is the MOA for antiepileptics?

A
  • dec neuronal excitability
  • enhance inhibition of neurotransmission
  • by altering ion currents and enhancing GABA
64
Q

What do you monitor for antiepileptics?

A

-routine plasma concentration levels to guide dosing and compliance

65
Q

How do therapeutic ranges affect antiepileptics?

A
  • does not = efficacy

- titrate to effect

66
Q

What other lab testing do you monitor w/ use of antiepileptics?

A
  • LFTs, heme

- d/t lifethreatening bone marrow suppresion and hepatotoxicity

67
Q

What is the prototype for antiepileptics? Trx

A

phenytoin

trx partial/generalized seizures

68
Q

What is the MOA of phenytoin?

A

regulat neuronal excitability (spread)

by regulating Na+ and Ca+ transport across membranes

69
Q

What is the pH of phenytoin?

A

ph = 12

precipitates in solutions of <7.8 ph

70
Q

How do you infuse phenytoin?

A

-no faster than 50 mg/min

71
Q

Describe metabolism of phenytoin.

A

levels <10 mcg/ml = first order kinetics
more 10mcg/ml = zero order
-hepatic enzyme INDUCER!!!

72
Q

What are s/e of phenytoin?

A
  • CNS toxicity = nystagmus, ataxia, diplopia, vertigo, neuropathy
  • allergic rash - stevens johnson syndrome
73
Q

What is MOA of fosphenytoin?

A

blocks Na+ channels

74
Q

What is fosphenytoin used for?

A
  • status epilepticus

- neurosurgery to prevent seizures

75
Q

What is the dose for fosphenytoin?

A

10-20 mg/kg IV

76
Q

What is the MOA of phenobarbitol?

A

modulates post synpatic actions of GABA and glutamate

77
Q

What effect does phenobarbitol have on metabolism?

A

-CP450 INDUCER/ENHANCER

*Pharm (6 decks)

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