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Pharm 1 > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

what is the BEST drug for cerebral protection (CRMO2 and CBF decreased)

A

pentothal

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2
Q

what is the best drug for cardiomyopathy

A

etomidate

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3
Q

patients with _____ catecholamines should NOT be given ___________ (septic, critically ill patients)

A

LOW

ketamine

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4
Q

drugs which do NOT cause apnea have a HIGHER risk for laryngospasm risk (2)

A

etomidate

methohexital

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5
Q

which is the ONLY drug which can be used solely for TIVA (due to amnestic, analgesic properties)

A

ketamine

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6
Q

what 2 things should you pretreat with ketamine

A

robinul (for secretions)
versed (for dissociation)

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7
Q

true or false
all drugs are lipid soluble in the body

A

true
(water soluble outside)

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8
Q

which 2 drugs do NOT depress CV or respiratory

A

ketamine
etomidate

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9
Q

if you have an elderly patient, give an _________dose

Example range: 150-300mg, give the elderly ____mg

A

100mg

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10
Q

elderly patients have _________ circulation times and take __________ to go to sleep

A

longer time

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11
Q

methohexital vs. pentothal
methohexital is:
__________ lipid soluble
__________ half-life
__________ recovery

A

LESS lipid soluble

shorter half life

faster recovery

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12
Q

etomidate ___________ seizure threshold

A

lowers it (MORE likely to have seizures)

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13
Q

propofol ____________ seizure threshold

A

raises it (LESS likely to have seizures)

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14
Q

which drugs should NOT be used for acute polyphoria (2)

A

barbiturates
etomidate

“BarbEE”

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15
Q

Emesis (greatest to least)

A

Etomidate > ketamine > pentothal/methohexital > propofol

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16
Q

Hemodynamics: Cardiac (most safe to least safe)

A

Etomidate > methohexital > pentothal > ketamine > propofol

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17
Q

CSHT (shortest to longest)

A

Etomidate > propofol > ketamine > sufentanil > versed > methohexital > pentothal

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18
Q

barbiturates, which drug is MOST potent

A

methohexital

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19
Q

which drug should be used for LMA

A

propofol (decreased risk of laryngospasm)

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20
Q

Greater % drug BOUND = _________ diffusion

A

slower diffusion

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21
Q

Greater % drug UNboud = _________ diffusion

A

faster diffusion

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22
Q

which drug causes euphoria

A

propofol

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23
Q

which drug is best for asthma patients (B2 agonist)

A

ketamine

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24
Q

which drugs CAUSE pain on injection (3)

A

propofol
etomidate
methohexital (maybe)

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25
Q

which drugs cause increased excitatory/myoclonic activity (2)

A

methohexital (hiccups)
etomidate

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26
Q

which drug causes hiccups

A

methohexital

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27
Q

which drugs cause resp depression (2)
LESS likely for laryngospasm

avoid these drugs with COPD

A

propofol
barbiturates

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28
Q

which drug is good for minimizing emergence delirium

A

precedex

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29
Q

how long is propofol good for

A

6 hours

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30
Q

true or false
pentothal is UNSTABLE once reconstituted

A

true

(6 days at room temp; 2 weeks fridge)

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31
Q

which drug is bacteriostatic

A

pentothal (due to high pH)

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32
Q

which drug is NOT approved for general anesthesia by itself

A

precedex

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33
Q

which drug can be used with propofol during a TIVA so that a patient does NOT become apneic

A

precedex

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34
Q

MOA:
HYPERpolarization (cell becomes more negative) with efflux of K out of the cell

DECREASED norepi release due to presynaptic receptors (results in vasodilation)

INHIBITION of adenylyl cyclase, results in decreased cAMP, results in decreased calcium

A

precedex

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35
Q

ketafol

A

maintains BP
maintains spontaneous ventilation
reduces vomiting
increases sedation to reduce hallucinations
reduces risk of seizures

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36
Q

advantages of TIVA (4 main ones)

A

no PONV
malignant hyperthermia patients
bronchs (cannot be a closed system)
good for transport

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37
Q

what is the best indicator of patient awareness for TIVA

A

movement

(make sure you have at least one twitch on TOF)

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38
Q

CSHT propofol: <3 hours

A

10 minutes

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39
Q

CSHT propofol: >3 hours

A

25 minutes

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40
Q

CSHT propofol: >8 hours

A

40 minutes

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41
Q

CSHT remifentanil

A

always 4 minutes

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42
Q

which 2 anti-emetic drugs do you NOT redose

A

decadron

scopolamine

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43
Q

what is the only opioid that you titrate

A

remifentanil

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44
Q

what are the receptors that affect the vomiting center (6)

A

Histamine/H1
Serotonin 5HT3
Dopamine
Ach/muscarinic
Neurokinin 1
GABA
Substance P

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45
Q

what receptor (1) affects the vagal and enteric system

A

serotonin 5HT3

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46
Q

what receptors affect the vestibular system (motion sickness)

A

Ach/muscarinic

Histamine/H1

“HACH” sounds like “ahhhh”

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47
Q

what receptors affect the CTZ

A

serotonin 5 HT3

opioid receptors

dopamine

“SOD”

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48
Q

termination of effect

A

redistribution to muscle cells

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49
Q

what does the increase in BP for ketamine come from

A

increase in catecholamines

(that is why its not good to use if you have low catecholamines)

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50
Q

inhalation/volatile anesthetic
machine check is done
with a TIVA, remember safety processes

A
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51
Q

when reducing a drug during TIVA,

if NO response, reduce by ____%

A

reduce 20%

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52
Q

when reducing a drug during TIVA,

if there IS a response, ________ and increase by _____

A

bolus

increase by half

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53
Q

which patient population is contraindicated with dopamine blockers

A

parkinson’s

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54
Q

which drug causes adrenocortical suppression

avoid with __________ patients

A

etomidate

addison’s disease
very sick patients

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55
Q

which patient population is contraindicated for reglan

A

intestinal obstruction

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56
Q

what is the biggest negative with antihistamines

A

sedation

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57
Q

what is the best thing about 5HT3 blockers

A

minimal side effects
because only targeting one receptor

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58
Q

how long does scopalamine last

A

72 hours

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59
Q

what are the non-specific NSAIDS

A

COX 1

o Ketorolac
o Ibuprofen
o Naproxen
o Aspirin

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60
Q

what are the selective NSAIDS

A

COX 2

Celebrex

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61
Q

what are the side effects of COX 1 (non-selective) (3)

A

Decreased platelet aggregation
Decreased renal function
Increased GI toxicity risk

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62
Q

what is the negative side effect with COX 2 (selective)

A

increased CV risk

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63
Q

what are the benefits with COX 2 (selective) (3)

A

o Decreased pain, inflammation, fever
o Decreased GI toxicity
o No platelet effects

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64
Q

what patients are CONTRAindicated for NSAIDS (5)

A

nasal polyps
elderly
hypovolemia
CKD renal issues
history of gastric ulcers

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65
Q

what is major contraindication for aspirin

A

nasal polyps

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66
Q

what is the dose for IM ketamine

A

4-8 mg/kg

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67
Q

aspirin is eliminated after the life of the ____________
other NSAIDS are eliminated after the life of the _______

A

aspirin=life of platelet (7 days)
IRreversible!

other NSAIDS= life of drug

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68
Q

what is the protamine dose based on

A

heparin that is in CIRCULATION
(otherwise, overdose would be given)

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69
Q

Target-Controlled Infusion Systems (TCIs)
based on the pharmaco___________ model
for _________ patients

A

pharmacokinetic model

healthy patients, so be careful

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70
Q

initiation phase= ___________ pathway

A

initiation = EXtrinsic

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71
Q

amplification phase = __________ pathway

A

amplification = INtrinsic

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72
Q

propagation phase = __________ pathway

A

propagation = common

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73
Q

INITIATION:
vessel damage, leads to tissue factor ____, which binds to _____, which leads to _____, which leads to ___________

A

initiation phase

tissue factor= III
binds to VII
which leads to Xa
which leads to thrombin (which leads to amplification)

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74
Q

Vessel damage, leads to tissue factor (III), which binds to VII, which leads to Xa, which leads to thrombin

A

initiation

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75
Q

AMPLIFICATION:
____________ activates amplification of: ____________, ___, and ____

A

thrombin activates: platelets, V, XI

think: “platelets loveeee 5 and 11”

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76
Q

Thrombin activates amplification of: platelets, V, XI

A

amplification

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77
Q

COMMON:
____, ___, _________: activates ___

thrombin activates: platelets, ___, _____, this leads to ______-____ complex

______-____ complex switches reaction to “____se pathway” (which is 50x more efficient at Xa generation)

Increased ____ leads to large amounts of increased _________

A

VIII, IX, calcium: activates X

thrombin activates: platelets, V, VIII, this leads to VIIIa-IXa complex

VIIIa-IXa complex becomes Xase pathway

Increased Xa leads to large amounts of increased THROMBIN

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78
Q

VIII, IX, calcium leads to activation of X

Thrombin leads to activation of platelets, V, VIII leads to VIIIa-IXa complex

VIIIa-IXa complex switches reaction to “Xase pathway”

Increased Xa leads to large amounts of increased thrombin

A

common

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79
Q

IV induction agents

Enhancing/increases/agonizes the ______ inhibition properties
Inhibiting/stops/antagonize the _______ excitatory synapses

A

agonizes GABA

antagonizes NMDA

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80
Q

redistribution is the _______ phase

A

alpha

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81
Q

pentothal %

A

2.5%

25 mg/ml

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82
Q

the more drug bound, the __________ the diffusion

A

slower

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83
Q

Increases the DURATION of GABA
and
Directly MIMICS GABA at its receptor
and
activates glutamate, adenosine, nAch receptors

A

barbiturates

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84
Q

directly mimicking GABA at its receptor causes __________ channels to open

A

chloride

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85
Q

which drug (1) causes histamine release
(BOTH anaphylaxis and anaphylactoid)

A

pentothal

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86
Q

barbiturates, NORMOvolemic:

__________ decrease in BP
__________ in HR

A

MINIMAL decrease in BP (peripheral vasodilation)

increase in HR (reflexively)

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87
Q

barbiturates, HYPOvolemic or beta blockade:
__________ decrease in BP
___ _________ in HR

A

DRASTIC LARGE decrease in BP

no change in HR

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88
Q

true or false:
for PENTOTHAL, slowing the rate of administration (giving incrementally)
does NOT improve the decrease in BP or increase in HR
instead, it ultimately causes a larger dose

A

true

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89
Q

Decreased Vt
and
Decreased RR

(2) drugs

A

barbiturates (pentothal)
and
propofol

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90
Q

barbiturates shift the CO2 response curve to the ______

A

right
allows for a greater amount of CO2 to build up before the body decides to breathe

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91
Q

cerebral vaso___________: decreases CMRO2 and CBF

A

vasoconstriction

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92
Q

when does pentothal provide cerebral protection

A

INCOMPLETE cerebral ischemia (CBP, hypotension, circulatory arrest)

NOT cardiac arrest

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93
Q

which drugs cause tolerance (2)

A

ketamine, pentothal

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94
Q

which drug (1) causes hangover

A

pentothal

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95
Q

which drug requires a hard flush, due to precipitate

A

pentothal

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96
Q

for 1/2 lives, multiply by ____x to get TOTAL

A

multiply by 4

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97
Q

methohexital %

A

1%
10 mg/ml

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98
Q

what are CONTRAindications for methohexital (2)

A

retrobulbar block (due to hiccups)
acute intermittent porphyria

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99
Q

unique, carboxylated imidazole-containing compound

Water-soluble: acidic pH
Lipid-soluble: physiologic pH

A

etomidate

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100
Q

etomidate %

A

.2%
2 mg/ml

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101
Q

Mimics inhibitory effects of GABA, thereby causing increasing AFFINITY for GABA
depresses reticular activating system (RAS)

A

etomidate

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102
Q

disinhibition of subcortical structures that normally suppress extrapyramidal motor activity

A

excitatory activity

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103
Q

true or false:
etomidate decreases CMRO2, CBF

A

true

EVERY drug EXCEPT ketamine

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104
Q

Decreased Vt
and
increased RR

A

etomidate

think, “fast and shallow breathing when youre sick”

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105
Q

Inhibition of conversion of ____________ to cortisol
Decreases ________ and _____________ levels for 4-48 hours after dose

A

cholesterol to cortisol

cortisol and aldosterone

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106
Q

metabolism by plasma esterases, extremely fast (5x faster than pentothal)

A

etomidate

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107
Q

caution with seizure patients

A

etomidate

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108
Q

alpha2 adrenergic agonist (8x more selective than clonidine)

A

precedex

109
Q

true or false
precedex has a LONGER duration than propofol

A

true

110
Q

true or false
precedex only works in the spinal cord and pontine locus ceruleus

A

true

111
Q

precedex given as a fast, bolus can cause

A

vasoCONSTRICTION (hypertension!)
and
bradycardia

112
Q

what are risk factors to greater hypotension (5)

A

hypovolemic
elderly
diabetic
high sympathetic tone (stress, sick, septic)
LV dysfunction

113
Q

what is a CONTRAindication for precedex

A

heart block (due to decrease in HR)

114
Q

cyclodextrin

sedative/hypnotic

A

propofol

115
Q

propofol provides “some” analgesia (pain relief) for ___________, _______ pain

A

neuropathic, chronic pain

116
Q

metabisulfite
(propofol)

A

generic brand

117
Q

disodium edetate + NaOH
(propofol)

A

diprivan

118
Q

increased pain; not approved
(propofol)

A

ampofol
think, “i have an amp of pain”

119
Q

decreased pain but increased genital burning; not approved
(propofol)

A

aquavan
think, “aqua water in peeing”

120
Q

propofol %

A

1%
10 mg/ml

121
Q

GABAA receptor AGONIST: leads to inhibition of GABAA and hyperpolarization of cell membranes

A

propofol

122
Q

Uptake: lungs and liver (cytochrome P450)

In lungs, most of drug goes back into circulation after 1st pass

A

propofol

123
Q

Decreased HR, SVR, CO, BP

A

propofol

124
Q

Increased incidence with oculocardiac reflex (eye surgery)
“5 and dime”

A

propofol related bradycardia

treat with robinul after 2nd occurence

125
Q

metoclopramide

A

reglan

gastric motility

126
Q

glycopyrrolate

A

robinul

reduces secretions

127
Q

propofol causes broncho_____________

A

bronchoconstriction
(still okay to use with asthma)

128
Q

true or false
resp depression IS dose-dependent for propofol

A

true

129
Q

HPV is maintained

DOWNward shift of hypoxic response curve

A

propofol

130
Q

Propofol with no anti-emetic = _________ with anti-emetic

A

volatile

131
Q

anti-pruritic
anti-convulsant
anti-oxidant
anti-emetic

A

propofol

132
Q

unused propofol should be discarded within ___ hours

A

6 hours

133
Q

decreased IOP

A

propofol

134
Q

true or false:
PROPOFOL
autoregulation and PaCO2 is NOT affected

A

true

135
Q

Helps support SSEPs and MEPs (evoke potentials)
Seizure-like, but NOT seizure myoclonic movements

A

propofol

136
Q

benign GREEN urine

A

phenol

137
Q

benign CLOUDY urine

A

uric

138
Q

> 75 mcg/kg/min for >24 hours in the ICU

initially tachycardia, then bradycardia

causes metabolic/lactic acidosis

A

propofol infusion syndrome

139
Q

true or false:
PROPOFOL and KETAMINE inhibit platelet aggregation

A

true

140
Q

Antagonist, non-competitively binds to NMDA receptors to block it

Inhibits glutamate (excitatory transmitter)
S + R isomers: R is better for less side effects

interacts with ALL opioid receptors
-Anti-muscarinic
-Anti-nicotinic: analgesia
-Na+ channels: local anesthetic

A

ketamine

141
Q

anti-muscarinic

A

parasympathetic nervous system; visceral organs

leads to bronchodilation and sympathomimetic activity

142
Q

anti-nicotinic

A

NMJ

analgesia

143
Q

what are risk factors for emergence delirium (4)

A

> 15 years old
female
high dose
personality disorders

144
Q

ketamine “cocktail”

A

midazolam + glycopyrrolate (robinul)

145
Q

which drug has an active metabolite that contributes to prolonged analgesia

A

ketamine

146
Q

what are CONTRAindications for ketamine (8)

A

CAD*
Pulmonary HTN (due to increased myocardial O2 demands)
LOW catecholamines* (critically ill patients should be given etomidate)

Neuraxial techniques
Tachycardia
Psychologic reactions
Neurosurgery (increased ICP due to cerebral vasodilation)
Eye procedures (nystagmus)

147
Q

which is the best drug for OB, congenital heart issues, asthma

A

ketamine

148
Q

hyperalgesia + increased shivering

A

remifentanil

149
Q

which drug should you NEVER bolus

A

remifentanil

150
Q

NSAIDS
________ Vd
________ protein bound

A

SMALL Vd
HIGHLY protein bound (slow diffusion)

151
Q

which patients will have a LARGER effect of drugs that are HIGHLY protein bound

A

hypoalbumin (malnourished, elderly)

152
Q

best NSAIDS drug to use for decreasing CV risk

A

Naproxen

153
Q

what are CONTRAindications for NSAIDS (4)

A

HYPOvolemia (increases renal toxicity risk)
nasal polyps
allergic rhinitis
asthma

154
Q

true or false
NO antidote for NSAIDS or ASA

A

true

treat with:
Hydration
Alkalinize urine
Charcoal
Hemodialysis

155
Q

symptoms of toxicity from NSAIDS

A

N/V
Abdominal pain
CNS depression
Metabolic acidosis
Renal failure
Agitation
Hyperventilation
Coma

156
Q

A-OK

A

Atropine: 1 mg (vagolysis)

Ondansetron: 8 mg (block serotonin receptors, vagolysis)

Ketorolac: 30 mg (block thromboxane production; blocks platelet aggregation)

157
Q

what is acetaminophen metabolite

A

NAPQI
depletes antioxidant glutathione, directly damages liver cells

158
Q

why is aspirin “separated” from other NSAIDS
(2 reasons)

A

it has CV and cerebrovascular benefits

it IRREVERSIBLY inactivates COX1

159
Q

aspirin irreversibly inactivates ______: leading to inhibited platelet ______________

wait at least ___ days

A

inactivates COX1
inhibits platelet aggregation

7 days

160
Q

what NSAID is metabolized by liver + plasma esterases

A

aspirin

161
Q

ERAS

_____________ of NPO
combo of _____________ + _________ + ____________

A

elimination of NPO (instead, carb loading)

acetaminophen + NSAID + gabapentin

162
Q

ERAS is opioid __________

A

sparing

163
Q

TIVA _________________ functional vital capacity + catecholamines

A

decreases FVC, reduces catecholamines

this leads to increased costs :(

164
Q

should TIVA be given as an infusion or a bolus

A

an infusion!
to minimize side effects

165
Q

extrinsic + instrinsic pathways

based on “in _______”

A

in vitro

dated

166
Q

heparin (unfractionated)

1 unit = ___ ml, prevents blood from clotting for___ hour after combining with __________

A

1 unit = 1 ml
prevents blood from clotting for 1 HOUR after combining with CALCIUM

167
Q

MOA

Binds to antithrombin, this leads to enhanced binding with thrombin

A

heparin (unfractionated)

168
Q

Platelet count <100,000 or 50% drop

Heparin-dependent antibodies trigger platelet aggregation, leading to thrombocytopenia

Treatment: heparin alternative (direct thrombin inhibitors, Xa inhibitor)

A

Heparin-Induced Thrombocytopenia (HIT)

169
Q

MOA
alkalotic, combines with acidic heparin; acid/base reaction

A

protamine

170
Q

how much protamine is needed per 100 units

A

1 mg per 100 units

171
Q

what are risks with protamine (2)

A

heparin rebound (2-3 hours after)
due to FAST protamine clearance

anaphylaxis

172
Q

LMWH __________ affected by temp, renal and hepatic disease, protein binding, patient variability

A

heavily affected

173
Q

LMWH drug

A

lovenox (enoxaparin)

174
Q

true or false
NO reversal for LMWH + NOACs

A

true

175
Q

what type of monitoring for warfarin

A

INR (2-3) adjusts for non-standardization between commercial preparation
PT

176
Q

which anticoagulant requires frequent lab monitoring

A

warfarin

177
Q

reversal for WARFARIN (3)

A

Vitamin K
PCCs
FFP

178
Q

Newer Oral Anticoagulants (NOACs)
direct ____________ inhibitors
direct _____ inhibitors

A

thrombin + Xa inhibitors

179
Q

eliquis + xarelto

A

Xa inhibitors (NOACs)

180
Q

pradaxa + angiomax

A

thrombin inhibitors (NOACs)

181
Q

advantages of NOACs (3)

A

o No need for routine lab monitoring*
o Rapid onset
o Therapeutic range within hours

182
Q

monitoring for NOACs (2)

A

aPTT
TT (thrombin time)

183
Q

NOACs
LOW risk of blood loss

A

d/c 1 day before, resume 1 day after

184
Q

NOACs
HIGH risk of blood loss

A

d/c 5 days before

185
Q

NOACs
ELECTIVE procedures

A

Consider patient specific risks/benefits*

186
Q

NOACs
ER procedures

A

delay as long as possible

187
Q

Life-threatening hemorrhage: use ______ or recombinant _____

A

PCCs or VIIa

188
Q

MOA
Antagonist that binds to P2Y receptor, this inhibits platelet activation + aggregation

A

thienopyridines (platelet inhibitors)

think “thienoPYridines”

189
Q

thienopyridines drugs (2)

A

plavix (clopidogrel)
brilanta (ticagrelor)

190
Q

MOA
Increases cyclic AMP, this leads to decreased platelet function

A

dipyridamole (platelet inhibitors)

191
Q

MOA
Binds to platelets, this inhibits function

A

dextran (platelet inhibitors)

192
Q

MOA
Bind and inhibit fibrinogen receptor, this leads to decreased platelet aggregation

A

Platelet Glycoprotein IIb/IIIa Antagonists (platelet inhibitors)

193
Q

MOA
ACTIVATES plasminogen into plasmin, this INCREASES clot breakdown

A

thrombolytics

194
Q

example of thrombolytic

A

tPA

195
Q

true or false
use PCI (percutaneous cath lab) if available, instead of tPA (thrombolytic)

A

true

196
Q

risks with thrombolytics/tPA (2)

A

intracranial hemorrhage
angioedema (ACE inhibitors)

197
Q

MOA
BLOCKS conversion of plasminogen to plasmin, this leads to DECREASED clot breakdown/lysis

A

antifibrinolytics

198
Q

true or false
antifibrinolytics are NOT procoagulants*

A

true

199
Q

______________ are the opposite of thrombolytics (tPA)

A

antifibrinolytics (TXA)

200
Q

Reduces risk of death due to bleeding, regardless of the cause

Decreased blood loss, decreased blood products, no risk of thrombi

A

antifibrinolytics (TXA)

201
Q

3 types of antifibrinolytics

A

TXA
aminocaproic acid (amicar)
aprotinin

202
Q

CONTRAindications to antifibrinolytics (4)

A

o Hypersensitivity to antifibrinolytics
o Thrombus history
o Color vision deficit
o Renal impairment

203
Q

must give antifibrinolytic (TXA) ____ hours post-injury

A

<3 hours

204
Q

MOA
Analog of vasopressin, stimulates endothelial von Willebrand factor

A

Desmopressin (DDAVP)

205
Q

MOA
Binding site for IIb/IIIa receptors on platelets

Helps to create platelet aggregation (clotting)

Substrate of thrombin, XIIIa, plasmin

A

fibrinogen

206
Q

low fibrinogen (low clotting) should be treated with (2)

A

more fibrinogen
or
cryoprecipitate

207
Q

recombinant proteins (5)

A

o Fibrinogen
o PCCs
o VIII
o IX
o XIII

208
Q

MOA
VIIa + tissue factor, leads to increased thrombin, which leads to hemostasis (clot formation)

A

Recombinant Factor VIIa (NovoSeven)

209
Q

Very expensive (average dose $7000)

A

Recombinant Factor VIIa (NovoSeven)

210
Q

Factors II, VII, IX*, X

Similar to FFPs, but is faster + less volume for the patient

A

Prothrombin Complex Concentrates (PCCs)

211
Q

Good for urgent reversal (within hours)

(warfarin, hemophilia B)

A

PCCs

212
Q
  • Tests that are becoming more prevalent
  • Help to pinpoint the issue with a patient
  • Provides better treatment
A

TEG and ROTEM (Thromboelastography)

213
Q

Used on the surgical field for pro-coagulation
o Fibrin sealants (thrombin + fibrinogen)
o Topical thrombin
o Surgicel

A

Topical Hemostatics

214
Q

electrolyte imbalance that can occur with antiemetics (4)

A

Alkalosis
Hypochloremia
Hyponatremia
Hypokalemia

215
Q

PONV
HIGH/Positive risk factors

A

o POST-op opioids (AFTER surgery)
o General anesthesia
o Volatile anesthetics, nitrous oxide
o Female
o History of PONV/motion sickness
o Non-smoker
o Younger age (<50)
o Surgery (ENT, strabismus, abdominal, gyn, thoracic)

216
Q

PONV
MILD/Conflicting risk factors

A

o Menstrual cycle
o ASA physical status
o Muscle relaxant antagonists
o Level of anesthetist’s experience

217
Q

NOT/Disproven risk factors

A

o BMI
o Anxiety
o NG tube
o O2
o Peri-op fasting
o Migraine

218
Q

N/V
make sure patient is _________volemic

A

NORMOvolemic

219
Q

N/V
If prophylaxis FAILS

A

DONT give the same drug as before, use a DIFFERENT drug class

220
Q

N/V
If prophylaxis worked, then 6 hours later patient has PONV:

A

Give SAME drug

221
Q

o Low Risk: ____ drugs
o Moderate Risk: ____ drugs
o High Risk: ____________ approach

A

o Low Risk: 0-1 drugs
o Moderate Risk: 1-2 drugs
o High Risk: multimodal approach

222
Q

PDNV

Females are worse until day ___, then it equalizes

A

day 4

223
Q

POV

occurs in _____________

A

pediatrics
2x as likely to vomit as adults

224
Q

what is the greatest risk factor for POV

A

TYPE of surgical procedure

225
Q

highest risk procedures for POV for peds (4)

A

hernia repair
tonsillectomy
strabismus
genital repair

226
Q

age of greatest risk for POV

A

age 3-13

227
Q

vomiting center is located in the BRAINSTEM in the __________ medullary ____________ formation

A

lateral medullary reticular formation

228
Q

Floor of the 4th ventricle
(Outside BBB)

A

Chemoreceptor Trigger Zone (CTZ)

229
Q

Motion sickness

A

vestibular system

230
Q

Gag and retch response

A

Irritation of the Pharynx (vagus nerve)

231
Q

Mucousa of the GI tract

Stomach stretch

A

Vagal and Enteric Afferents

232
Q

Stress and anticipatory vomiting

A

CNS

233
Q

CTZ: which receptors

A

Dopamine
Serotonin 5HT3
Opioid receptors

234
Q

vestibular system: which receptors (2)*

A

Muscarinic (Ach)
Histamine (H1)

235
Q

Vagal and Enteric Afferents: which receptor*

A

Serotonin 5HT3
(then stimulates CTZ)

236
Q

what are the 7 receptors that contribute to vomiting center*

A

o Ach/muscarinic
o Histamine/H1
o Serotonin 5HT3
o Dopamine
o Substance P
o GABA
o Neurokinin 1

237
Q

Decreasing DOPAMINE input at the chemoreceptor trigger zone as well as anxiety

Decreases ADENOSINE reuptake leading to decreased synthesis, release, and postsynaptic action of dopamine at the CTZ

A

benzodiazepines

238
Q

Anticholinergic (Ach/muscarinic) + H1 blocker

A

antihistamines

239
Q

Anxiety
Anticipatory vomiting

A

benzodiazepines

240
Q

Motion sickness
Blocks oculoemetic reflex, this blockage leads to no vomiting

A

antihistamines

241
Q

Benadryl
Dramamine
Bonine
Phenothiazines

A

antihistamines

242
Q

Inhibition of DOPAMINE (dopamine antagonist) and
inhibition of Ach (muscarinic) receptors

A

phenothiazines (antihistamine)
phenergan, compazine

243
Q

what are the 2 phenothiazines (antihistamine)

A

phenergan, compazine

244
Q

Anticholinergic (Ach/muscarinic) + antihistamine + 5HT3 blocker

Blocks transmission to the medulla of impulses from overstimulation of vestibular apparatus (motion sickness)

Crosses BBB (lipid soluble)

A

scopalamine

245
Q

Motion sickness
sedation

A

scopalamine

246
Q

Dopamine blockade (alpha blockade)

Causes vasodilation due to peripheral alpha blockade (leading to decrease in BP)

A

Butyrophenones (Droperidol, Inapsine)

247
Q

side effects of Butyrophenones (Droperidol, Inapsine) (4)

A

Dissociative state, extremely sedating
“LOCKED IN”

Prolonged QT interval (torsades with very high dose); black box warning

Extrapyramidal effects

Hypotension

248
Q

MOA
Dopamine blockage in CTZ

Cholinergic stimulus to GI tract (increased gastric and small intestine motility)

A

Metoclopramide (Reglan)

249
Q

MOA
Endogenous vasoactive substance and neurotransmitter (causes emesis and pain), cerebral stimulant

Stored in the enterochromaffin cells of the GI tract

A

Serotonin 5HT3

250
Q

MOA
BLOCKS peripheral receptors on the intestinal vagal afferents (GI tract)

BLOCKS central receptors in the vomiting center + CTZ (vagal stimulation)

A

Serotonin 5HT3 Receptor Antagonists

251
Q

Vomiting/emesis only*
NO EFFECT on nausea
NO EFFECT on motion sickness
NO EFFECT on any other receptors (dopamine, histamine, adrenergic, muscarinic)

A

Serotonin 5HT3 Receptor Antagonists

252
Q

N/V
Give at the END of the case

A

zofran (5 HT3 blockers)

253
Q

MOA
Possibly inhibits prostaglandin synthesis centrally and endorphin release (?)

A

corticosteroids (decadron)

254
Q

Give right after induction

A

decadron (corticosteroids)

255
Q

MOA
Substance P: natural ligand in the neurokinin receptor in the vagus nerve

Affects CTZ

A

aprepitant (NK1 blocker)

256
Q

N/V

interacts with:
Coumadin
Calcium channel blockers
Anticoagulants
Seldane
Hismanal

A

aprepitant

257
Q

o OB patients with hypotension and N/V
o Give at the end of C-section

A

ephedrine

258
Q

Pulmonary disease/OSA: avoid ___________ drugs

A

antihistamines/sedation drugs

259
Q

large Vd=_________ distribution=_____ protein binding

A

large Vd, widely distributed, low protein binding
(large + low)

260
Q

decreases MAC >90%

A

precedex

261
Q

ketamine __________ peripheral reuptake of catecholamines

A

INHIBITS peripheral reuptake of catecholamines

262
Q

ketamine is a direct myocardial _____________

A

direct myocardial DEPRESSANT

263
Q

THERAPEUTIC aPTT range

A

45-90 seconds

264
Q

THERAPEUTIC ACT range

A

350-400

265
Q

heparin:
IV onset ________
SQ onset ________

A

IV: immediate
SQ: 1-2 hours

266
Q

warfarin:
elimination 1/2 _____- _____ hours
peaks _____- _____ hours
therapeutic ________ days

A

elimination: 24-36 hours
peaks: 36-72 hours
therapeutic: 5 days

267
Q

normal fibrinogen levels

A

200-400 mg/dL

(pregnancy is HIGHer)

268
Q

which anti-emetics have dopamine and should be used with caution with parkinsons?

A

reglan
butyrophenones (droperidol, inapsine)
phenothiazines (compazine, phenergen)

“PBR, elderly like PButteR”

Pharm 1 (9 decks)

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