Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Apex > Unit 4 Pharmacology: Intravenous Anesthetics > Flashcards

Unit 4 Pharmacology: Intravenous Anesthetics Flashcards

1
Q

Chemical name of propofol

A

2,6-diisopropylphenol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

MOA of propofol

A

GABA-A agonist, chloride conductance and neuronal hyperpolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

clearance of propofol

A

liver (CYP450) and extra hepatic metabolism. clearance exceeds liver blood flow. extra hepatic clearance occurs in the lungs (mostly)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

CV effects of propofol

A

decreased BP (d/t decreased SNS tone, vasodilation, myocardial depression)
decreased SVR
decreased venous tone-> decreased preload
decreased myocardial contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

respiratory effects of propofol

A

shifts CO2 response curve down and to the right (less sensitive to CO2). respiratory depression/apnea
inhibits hypoxic ventilatory drive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

CNS effects of propofol

A

decreased CMRO2
decreased CBF, ICP, IOP
no analgesia
anticonvulsant properties
myoclonus may occur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

risk factors of PRIS

A

propofol dose >4mg/kg/hr
infusion >48h
sepsis
continuous catecholamine infusion
high dose steroids
significant cerebral injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

clinical presentation of PRIS

A

acute refractory bradycardia and at least one of the following:
metabolic acidosis (base deficit >10mmol/L
rhabdomyolysis
enlarged or fatty liver
renal failure
HLD
lipemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how to minimize or eliminate pain of propofol on injection

A

giving an opioid, giving lidocaine, injecting into a larger or more proximal vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how is fospropofol metabolized

A

via the enzyme alkaline phosphatase to propofol.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

chemical name of fospropofol

A

phosphono-O-methyl-2,6 diisopropylphenol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

onset and DOA of fospropofol as compared to propofol

A

slower onset and longer DOA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

initial dose and repeat bolus of fospropofol

A

initial dose 6.5mg/kg
repeat bolus 1.6mg/kg not more than 4 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

chemical name of ketamine

A

2-(o cholphenyl)-2(methylamino) cyclohexanone hydrochloride

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

MOA of ketamine

A

NMDA antagonist (antagonizes glutamate).
secondary receptor targets: opioid, MAO, serotonin, NE, muscarinic, Na+ channels.
dissociates the thalamus (sensory) from the limbic system (awareness)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

DOA of ketamine

A

10-20 minutes (may require 60-90 minutes to return to full orientation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

clearance of ketamine

A

liver (P450 enzymes).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

active metabolite of ketamine

A

norketamine. 1/3-1/5 the potency of ketamine. renal excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

CV effects of ketamine

A

increase in SNS tone, CO, HR, SVR, PVR (caution if severe RV failure). will act as a cardiac depressant in someone with catecholamine depletion (sepsis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

respiratory effects of ketamine

A

bronchodilator, intact airway reflexes, maintains respiratory drive, does not significantly shift CO2 response curve, increase in PO and pulmonary secretions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

CNS effects of ketamine

A

increase in CMRO2, CBF, ICP, EEG activity. nystagmus, emergence delirium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

risk factors of ketamine induced emergence delirium

A

age >15 years, female gender, ketamine dose >2mg/kg, hx personality DO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

describe analgesic effects of ketamine

A

relieves somatic pain better than visceral pain
blocks central sensitization and wind up in dorsal horn of spinal cord
prevents opioid induced hyperalgesia (ex after remi infusion)
analgesic properties make it good for burn patients or pre existing chronic pain patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

ketamine and etomidate should be avoided in patients with a hx of

A

acute intermittent porphyria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

when compared to other induction agents, which drug undergoes the smallest amount of plasma protein binding?

A

ketamine (12%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

chemical name of etomidate

A

R-1-methyl-1-(a-methylbenzyl) imidazole-5-carboxylate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

DOA of etomidate

A

5-15 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

clearance of etomidate

A

CYP450 and plasma esterases. rapid awakening due to redistribution (not metabolism)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

MOA of etomidate

A

GABA-A agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

CV effects of etomidate

A

hemodynamic stability (minimal change in HR, SV, CO)
SVR decreased, which accounts for small reduction in BP
does not block SNS response to laryngoscopy. opioid or esmolol would help

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

respiratory effects of etomidate

A

mild resp depression (less than propofol or barbiturates)

32
Q

CNS effects of etomidate

A

decreased CMRO2, CBF, ICP.
CPP remains stable

33
Q

does etomidate provide analgesia

A

no

34
Q

etomidate decreases cortisol and aldosterone synthesis via inhibition of

A

11 beta hydroxylase (located in the adrenal medulla)

35
Q

relationship between etomidate and seizures

A

if the patient has a hx of seizures then it decreases the seizure threshold. if they do not have a hx of seizures then it has no effect.

36
Q

chemical make up of thiobarbiturates

A

sulfur molecule in the second position ex) thiopental, thiamylal

37
Q

chemical make up of oxybarbiturates

A

theres an oxygen molecule in the second position ex)methohexital, pentobarbital

38
Q

chemical name of thiopental

A

5-ethyl-5-(1-methylbutyl)-2-thiobarbituric acid

39
Q

is there pain on IV administration of thiopental

A

no

40
Q

MOA of thiopental

A

GABA-A agonist. depresses reticular activating system in the brainstem. low/normal dose increases affinity of gaba for its binding site while high dose directly stimulates the GABA-A receptor

41
Q

thiopental dose for adult and children

A

adult 2.5-5mg/kg
children 5-6mg/kg

42
Q

OOA thiopental

A

30-60 seconds

43
Q

DOA of thiopental

A

5-10 minutes

44
Q

clearance of thiopental

A

CYP450

45
Q

active metabolite after high dose of thiopental

A

pentobarbital

46
Q

CV effects of thiopental

A

HoTN is primarily the result of ventilation and decreased preload. myocardial depression is secondary cause.
causes non immunogenic histamine response.
baroreceptor reflex is preserved

47
Q

respiratory effects of thiopental

A

respiratory depression (shifts CO2 response curve to the right)
histamine release can cause bronchoconstriction (caution with asthma)

48
Q

CNS effects of thiopental

A

decrease in CMRO2, CBF, ICP, EEG activity.

49
Q

does thiopental have neuroprotection for focal or global ischemia

A

yes for focal ischemia (ex carotid endarterectomy), no for global ischemia

50
Q

what is acute intermittent porphyria caused by

A

defect in heme synthesis that promotes accumulation of heme precursors

51
Q

s/sx of acute intermittent porphyria

A

severe abdominal pain, n/v
anxiety, confusion, seizures, psychosis, coma, skeletal muscle weakness

52
Q

anesthetic management of acute intermittent porphyria

A

liberal hydration, glucose supplementation, heme arginate, prevention of Hothermia.

53
Q

gold standard for electroconvulsive therapy and dose

A

methohexital (induction dose 1-1.5mg/kg)

54
Q

dexmedetomidine class

A

imidazole

55
Q

dexmedetomidine MOA

A

alpha 2 agonist, decreases cAMP and inhibits the locus coeruleus in the pons (sedation)

56
Q

dose of dexmedetomidine (loading, maintenance)

A

1mcg/kg over 10 min
maintenance infusion .4-.7mcg/kg/h

57
Q

onset and DOA of dexmedetomidine

A

with loading dose: 10-20 min
after infusion is stopped: 10-30 min

58
Q

clearance of dexmedetomidine

A

liver (p450)

59
Q

describe the dexmedetomidine modulated alpha 2 negative feedback loop

A

acts on pre synaptic alpha 2 receptors which produces a negative feedback loop by decreasing NE release from pre synaptic nerve terminal. reduces SNS tone and produces sedation

60
Q

CNS effects of dexmedetomiding (CBF, CMRO2, ICP)

A

decreases CBF but no change in CMRO2 and ICP

61
Q

describe the MOA of dexmedetomidine as it relates to analgesia

A

alpha 2 stimulation in the dorsal horn of the spinal cord (decreases substance p and glutamate release)

62
Q

how can you administer precedex to a kid without an IV

A

nasal or buccal (3-4mcg/kg 1 hour before surgery)

63
Q

formulation of midazolam (and what happens in bottle versus body)

A

imidazole ring. in the vial (low pH), ring is open and hydrophilic. when it enters the body, ring closes and it becomes more lipophilic so it can cross the BBB more easily

64
Q

MOA of midazolam

A

gaba a agonist. increases frequency of channel opening- neuronal hyper polarization.

65
Q

dose of midazolam for sedation, induction, PO in kids

A

iv sedation: .01-.1mg/kg
iv induction .1-.4mg/kg
PO sedation .5-1mg/kg

66
Q

OOA and DOA of midazolam

A

IV 30-60 seconds
IV DOA 20-60 min

67
Q

active metabolite of midazolam

A

1 hydroxymidazolam (.5x potency of midazolam)

68
Q

CV effects of midazolam

A

decreases BP and SVR

69
Q

respiratory effects of midazolam

A

induction dose cases respiratory depression

70
Q

CNS effects of midazolam

A

induction dose (not sedation dose) decreases CMRO2 and CBF.
anterograde amnesia
anticonvulsant
anxiolysis
spinally mediated skeletal muscle relaxation (antispasmodic)
no analgesia

71
Q

why does diazepam take forever to metabolize

A

undergoes enterohepatic recirculation

72
Q

half life of diazepam

A

43 hours

73
Q

onset of lorazepam

A

slow

74
Q

greatest to least potency of diazepam, midazolam, lorazepam

A

lorazepam>midazolam>diazepam

75
Q

describe a time when remimazolam would be a good option

A

indicated for induction and maintenance for adults undergoing procedural sedation lasting 30 minutes or less

76
Q

flumazenil initial dose

A

.2 (titrated in increments until desired response is achieved)

77
Q

flumazenil DOA

A

30-60 min (for this reason, repeat dosing is necessary)

Apex (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions