Psych/ECT exam 4 Flashcards

(57 cards)

1
Q

SSRI MOA

A

block re-uptake of serotonin at presynaptic memrbraines

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2
Q

Most common antidepressant

A

SSRI

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3
Q

SSRI anesthesia consideration

A

Discontinuation syndrome - continue SSRIs through peri-operative period

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4
Q

SSRI discontinuation syndrome s’sx

A

N/V
abdominal pain + diarrhea
Sleep disturbance
irritability and mood swings

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5
Q

TCA MOA

A
  1. inhibit synaptic reuptake of NE and serotonin
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6
Q

TCA anesthesia considerations - first 4-6 weeks of treatment

A
  1. Increased neurotransmitter availability = increased anesthesia requirements
  2. Increased catecholamines can cause exaggerated response to INDIRECT vasopressors (i.e. ephedrine) - use phenylephrine for hypotension
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7
Q

TCA anesthesia considerations all the time

A

Increase risk of anticholinergic syndrome (post - op delirium)

especially considering when using anticholinergics such as robinol

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8
Q

Serotonin syndrome: what is it, cause and main features

A

overstimulation of 5HT receptors

Common cause: 2 or more sertonergic drugs

main features: clonus, hyperreflexia, delerium

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9
Q

Serotonin syndrom treatemtn

A
  1. stop drug and supportive care
  2. cryohetadine
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10
Q

MAOI MOA

A

Inhibit metabolic breakdown of NE and serotonin (liver)

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11
Q

MAOI anesthesia considertaions

A
  1. Indirect hypertension
  2. May increase MAC
  3. avoid abrupt changes in SNS activity (i.e. not deep enough or too deep)
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12
Q

With MAOI, avoid

A
  1. merperidene (know triggering agent)
  2. Indirect - acting sympathomimetic (ephederine)
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13
Q

Pre-operative lithium levels should be

A

Less than 2mEq/L

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14
Q

Sodium and lithium

A

Sodium depletion reduces renal excretion of lithium

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15
Q

Lithium and neuromuscular blockade

A

Lithium prolongs NM blockade

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16
Q

Lithium and anesthesia

A

Lithium decreases anesthetic requirements

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17
Q

Anorexia anesthesia consideration

A

cardiomyopathy and hypokalemia

need EKG and maybe ECHO

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18
Q

Schizophrenia MAO

A

domaine dysfunction - treat with dopamine blockers

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19
Q

Antipsychotics act on

A

dopamine receptors

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20
Q

Neuroleptic Malignant syndrome differential diagnosis

A

shortly after neuroleptic medication

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21
Q

Main inhibitory neurotransmitter in the brain

A

GABA

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22
Q

Alcohol MOA

A

reduces excitatory neurotransmitters (asptarate, glutamate)

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23
Q

Aspatrate and glutamate act through

A

NMDA receptors (and non)

24
Q

How does alcohol affect brain function?

A

disrupts balance between inhibitory and excitatory neurotransmitters

25
Long term ETOH exposure compensation
Brain attempts to tilt balance back toward equilibrium = tolerance
26
ETOH withdrawal occurs from
excitation of neurotransmitter system from compensation
27
Acute ETOH risk
aspiration of gastric contents because laryngeal reflex is blunted
28
Acute intox ETOH anesthetic effeects
1. exaggerated responses to anesthetic agents 2. Decreased requirements 3. additive depressant effect
29
Long term ETOH mechanism
change in receptor level of protein composition of receptor -->decreased in GABA-A function -->decreased sensitivity to neurotransmission
30
Chronic ETOH electrolyte imblanace
Hypomagnesia
31
delirium tremens begins
2 -4 days after cessation of drinking
32
Delirium tremens is characterized by
tremor agitation fever tachycardia confusion delusions hallucinations
33
Anesthesia role in medically-assisted withdrawal
-high dose benzos to counteract sympathetic response -sympatholytics -control airway for safe sedation
34
VTA (what it stands for and association)
Ventral tegmental area associated with the reward pathway
35
VTA neurons contain ____ which is released____
dopamine, which is released in the nucleus accumbens pathway is activated by rewarding stimulus
36
Illicit drugs anesthetic considerations
all cause NE reuptake blockade =central and peripheral effects of increased endogenous NE
37
Smoked drugs and MAC
Acute - decrease MAC Chronic - increase MAC
38
Cocaine MOA
Blocks reuptake of endogenous catecholamines presynaptically = increase BP, HR, Temp
39
Cocaine use: caution with
beta blockade - can lead to unopposed alpha 1 mediated coronary and peripheral vasoconstriction/spasm
40
Cocaine HTN treatment:
alpha blockade (phentolamine) and NTG or vasodilator (nitropursside)
41
Cocaine EKG/cardiac risk
prolonged QT interval and torsades
42
Cocaine: avoid
1. ketamine 2. pancuronium potentiates CV toxicity of cocaine
43
Cocaine acute intoxication MAC
Increases MAC - they are revved up with lots of catecholamines so you need a lot more
44
Meth anesthesia considerations
similar to cocaine
45
Affinity of hemoglobin for CO is
200 x greater tahn oxygen so CO binds first
46
ECT anesthesia goals
1. provide neuromuscular blockade to prevent fractures and muscle injury 2. produce unconsciousness
47
ECT seizure lasts
minimum 25 seconds to ensure adequate antidepressant efficacy
48
ECT seizure parasympathetic CV response:
1. transient bradycardia 2. occasional asystole (hypotension, bradydysrthythmia)
49
ECT seizure sympathetic CV respsonse:
during clonic phase 1. prominent HTN 2. tachycardia
50
ECT seizure responses (7)
1. Increased CBF 2. Raised ICP 3. Cardia dysrhythmias 4. Myocardial ischemia, infarction 5. neurologic vascular events 6. increased IOP 7. Increased intragastric pressure
51
ECT side effect on memory
short term memory loss
52
Most common long term effect associated with ECT
memory impairment
53
ECT risks and SE (5)
1. myalgia 2. HA 3. Emergence agitation 4. staus epilepticus 5. sudden death
54
Absolute ECT contraindications (6)
1. pheochromocytoma 2. recent MI 4-6 weeks 3. Recent CVA (3 month) 4. recent intracranial surgery (3 mnths) 5. Intracranial mass lesion 6. Unstable cervical spine
55
ECT gold standard induction agent
Methohexital 0.5.- 1 mg/kg
56
Ketamine and ECT
Ketamine prolongs seizure duration (proconvulsant) but also has negative effects
57
Conditions that prolong seizure duration in ECT
Hyerventilation/hypocapnia