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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
What drugs do MAOIs interact with?
- cold/allergy - nasal decongestant - opioids - sympathomimetics - TCAs, SSRIs
26
What opioid cannot be used w/ MAOI? Why
``` demerol!! causes: excitatory respone (type I) - agitation, muscle rigidity, hyperpyrexia depressive response (type II) - hypotension, resp depression, coma ```
27
Which sympathomimetic cannot be given w/ MAOIs?
- ephedrine!! | - use direct acting only and dec dose by 1/3 and titrate
28
How do MAOIs affect MAC?
may need higher MAC w/ gases
29
What happens w/ OD of MAOIs?
excessive SNS discharge - tachycardia, hyperthermia, mydriasis, seizure --> coma **minimize SNS stimulation or hypotension during anesthetic care**
30
What is the MOA of anxiolytics?
-enhance GABA
31
What are the pharm effects of anxiolytics?
``` Sedation Anxiolysis Anterograde amnesia Anticonvulsant Muscle relaxant (spinal level) ```
32
Name 2 types of anxiolytics
- benzos for anxiety/insomnia | - buspirone (non-benzo) for anxiety d/o (not panic)
33
What are the CNS effects of anxiolytics/benzos?
- dec CBF, CMRO2 | - does not dec ICP response to DVL
34
What are vent effects of benzos?
- dose dependent suppresion - hypoxemia/hypovent enhanced w/ opioids - CO2 response curves flattens, does not shift
35
What are CV effects of benzos?
w/ induction dose, SVR dec --> BP dec | CO unchanged
36
What is midazolam's solubility/protein binding/distribution?
water soluble 90% protein bound rapiddistribution = short DOA
37
Compare potency b/n midaz and diaz
midaz is 3x potency of diaz
38
What is the sedation dose for midazolam?
1-2.5 mg up to 5 mg
39
What is the premed/ped dose for midaz?
0.5 mg/kg PO
40
What is the induction dose for midaz?
0.1-0.2 mg/kg over 30-60 sec
41
What is the solubility/protein/DOA for valium?
highly lipid/protein bound | prolonged DOA
42
What do you need to be cautious w/ when administering IV/IM valium?
- burns - highly viscous - ph 6.9
43
What is the premed dose for valium PO/IV?
10-15 mg PO | 0.2 mg/kg IV
44
What affect does valium have on MAC?
it reduces MAC
45
What is the anticonvulsant dose for valium?
0.1 mg/kg IV
46
What is the MOA of phenothiazines and thioxanthenes? Effects?
block DOPA receptors in BASAL ganglia and limbic of forebrain - block DOPA = EPS - block in chemoreceptor trigger zone of medulla = antiemetic effect
47
What kind of safety margine do phenothiazines and thioxanthenes have?
large, OD rarely fatl | d/t blocking forebrain
48
What are s/e of phenothiazines and thioxanthenes?
- 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
What is tardive dyskenisia and acute dystonic reactions?
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
What is neuroleptic malignant syndrome?
develops 24-73 hours usually in men = hyperthermia, hypertonicity of muscles, instability of ANS, fluctuating LOC
51
How do phenothiazines and thioxanthenes affect opioids?
-potentiation of opioids (sedation/vent depression/analgesia)
52
What class is haldol and what drug does it more resemble?
- class = butyrophenes | - but resembles phenothiazines structure and s/e
53
What are CV effects of droperidol (butyrophenes)?
- antidysrhythmic - large doses --> WPW syndrome/tachy dysrhythmias - prolonged QT - torsades
54
What is the black box warning for droperidol (butyrophenes)?
-12 lead EKG prior to and continue for 2-3 hrs
55
What is droperidol (butyrophenes) used for?
- neurolept analgesia: combo w/ fentanyl (Innovar) - prolongs fentanyl - antiemetic: comparable w/ zofran, not for motion sicknes
56
What is lithium for?
treat bipolar disorder
57
What is the MOA for lithium?
competes w/ Na+/Ca/Mg --> affects membrane, H2O, NTs
58
How is lithium distributed?
thruout total body water and excreted via kidneys
59
How does lithium affect kidneys?
- lithium and Na+ competitive in proximal tubules - causes polydipsia/polyuria (impaired concentration) - dec sensitivity to ADH - monitor RFTs Q6 mos
60
How does lithium affect EKG?
flattened t wave or t wave inversion
61
How do you trx severe toxicity of lithium?
- emergency - HD - osmotic diuresis - IV bicarb
62
Anesthetic considerations for lithium.
-pre op labs and EKG -anesthesia requirement may be DECREASED -NMB may be prolonged (**kidneys**)
63
What is the MOA for antiepileptics?
- dec neuronal excitability - enhance inhibition of neurotransmission - by altering ion currents and enhancing GABA
64
What do you monitor for antiepileptics?
-routine plasma concentration levels to guide dosing and compliance
65
How do therapeutic ranges affect antiepileptics?
- does not = efficacy | - titrate to effect
66
What other lab testing do you monitor w/ use of antiepileptics?
- LFTs, heme | - d/t lifethreatening bone marrow suppresion and hepatotoxicity
67
What is the prototype for antiepileptics? Trx
phenytoin | trx partial/generalized seizures
68
What is the MOA of phenytoin?
regulat neuronal excitability (spread) | by regulating Na+ and Ca+ transport across membranes
69
What is the pH of phenytoin?
ph = 12 | precipitates in solutions of <7.8 ph
70
How do you infuse phenytoin?
-no faster than 50 mg/min
71
Describe metabolism of phenytoin.
levels <10 mcg/ml = first order kinetics more 10mcg/ml = zero order -hepatic enzyme INDUCER!!!
72
What are s/e of phenytoin?
- CNS toxicity = nystagmus, ataxia, diplopia, vertigo, neuropathy - allergic rash - stevens johnson syndrome
73
What is MOA of fosphenytoin?
blocks Na+ channels
74
What is fosphenytoin used for?
- status epilepticus | - neurosurgery to prevent seizures
75
What is the dose for fosphenytoin?
10-20 mg/kg IV
76
What is the MOA of phenobarbitol?
modulates post synpatic actions of GABA and glutamate
77
What effect does phenobarbitol have on metabolism?
-CP450 INDUCER/ENHANCER

*Pharm (6 decks)

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