Brainscape's Knowledge GenomeTM

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


See full index

Pharm 1 > final > Flashcards

final Flashcards

1
Q

enzyme that rapidly hydrolyzes Ach (<15 milliseconds) into acetic acid and choline

prevents the sustained depolarization of muscles!!

A

Acetylcholinesterase (AchE):

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

Burns, muscular dystrophy, stroke, immobilization, paralysis, Guillian-Barre

Channels remain open 4x longer, major issue with hyperkalemia!

A

extra junctional receptors

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

If you apply electrical activity directly to muscle, it will _____________ regardless of NMB (false positive)

A

retract

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

what lead goes directly to the nerve

A

BLACK

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

adductor pollicis brevis (thumb)

A

ulnar nerve

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

PLANTAR flexion of big TOE

A

Posterior tibial nerve

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

DORSIflexion of foot
(this is preferred for lower extremity)

A

Lateral popliteal/peroneal nerve

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

Facial nerve=orbicularis oculi or frontalis

reflects onset of ____________

A

laryngeal muscle relaxation

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

if using facial nerve, it is possible to _______dose the relaxant, _________estimate recovery, ______estimate blockade

A

it recovers first!
so you will overdose relaxant
overestimate the patient being recovered
and
understimate the blockade

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

If looking for onset of NMB use:

A

orbicularis oculi or frontalis

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

onset of NMB

A

small rapidly moving muscles, then
trunk, abd, then
diaphragm

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

recovery of NMB

A

diaphragm, then
small rapidly moving muscles, then
trunk, abd

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

what recovers first in NMB

A

diaphragm

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

what is the issue with single twitch

A

there is no control

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

Ideal for maintenance phase and helps decide whether you need to re-dose

A

TOF

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

true or false
4 twitches back are NOT an indication of recovery

A

true

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

2/4 means: ____ block

A

90% block

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

3/4 means: ____ block

A

80% block

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

4/4 means: ____ block

A

70-75% block still!!!

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

is headlift an indication of recovery?

A

NO (50-60%)

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

Easier to detect fade than TOF, still not great

A

double burst

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

Best indication of recovery for NMB

A

tetanus (tetanic stimulation)

painful

WAIT at least 10 minutes between! To avoid false info (due to increased Ach)

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

Post-tetanic twitches of ____ coincides with 1st twitch of TOF

A

10 PTT=1st twitch TOF

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

Post-tetanic twitch of 1 means ___ minutes (intermediate) or ____ minutes (long acting) until TOF has its 1st twitch

A

8 min=intermed
30 min=long acting

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

what is the indication of recovery

A

sustained tetanus with no fade

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

Always assess baseline twitches after _____, and before NMB; there is potential issue with ____ and atypical plasma cholinesterase and you need to know the source of what is wrong

A

Sch

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

Guidelines for Reversal:
no twitches

A

do not attempt (can PROLONG it)

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

Guidelines for Reversal:
1 twitch

A

30 minutes

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

Guidelines for Reversal:
2-3 twitches

A

4-12 minutes

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

Guidelines for Reversal:
4 twitches

A

2 minutes (edrophonium)
5 minutes (neostigmine)

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

Binds to the alpha subunits of the postsynaptic nicotinic receptor and mimics Ach; causes the muscle cell membrane to depolarize

A

Sch (depolarizers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

side effects of Sch

A

bradycardia, tachycardia
increased BP
increased SVR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

indications for Sch

A

difficult airway***
RSI
full stomach/aspiration risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Blockade is ENHANCED/accentuated by anticholinesterase

A

phase I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q
  • Fasciculations; rapid recovery, short duration of action
  • Decreased single twitch
  • Lack of fade of tetanus
  • Minimal fade of train-of-four
  • No post-tetanic twitch
A

phase I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q
  • Fade of tetanus
  • Fade in train-of-four
  • Posttetanic twitch
  • Prolonged duration in 50%
  • Blockade is REVERSIBLE/attenuated by anticholinesterase!
A

phase II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

which phase do you NOT use reversal

A

phase I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Metabolizes Sch
By the time it gets to the receptor, there is very little left

A

plasma/pseudo cholinesterase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Dibucaine 80

A

homozygous normal
5-10 minutes until recovery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Dibucaine 40-60

A

heterozygous atypical
30 minutes until recovery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Dibucaine 20

A

homozygous atypical
>3 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

which drug do you dose for TOTAL body weight for obese patients

A

Sch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Anticholinesterase Drugs
(leading to PROLONGED Sch)

A
  • Insecticides
  • Myasthenia gravis medications
  • Glaucoma medications
  • Chemo drugs
  • Alzheimer’s medications (not clinically significant)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Inhibitors of Plasma Cholinesterase
(leading to PROLONGED Sch)

A

reglan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Hyperkalemia (increase ___ to __ in labs)

A

.5 to 1

(Do NOT use Sch after 24 hours with burns)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Bad side effects of Sch

A

histamine
hyperkalemia
brady and tachy
increased IOP, ICP, IGP
myalgia
myoglob/rhabdo
MH
masseter spasm
skelatal muscle contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

If you give the nondepolarizing DEFASCICULATING dose, then you need to ___________ the Sch dose*

A

INCREASE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what is NOT prevented with defasciculating dose for Sch

A

hyperkalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Competes with Ach to bind with the alpha subunits on the postjunctional AchR to prevent the ion channel from opening and preventing the muscle cell membrane from depolarizing

A

Nondepolarizing NMBs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

________curonium:

A

steroidal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

________curium:

A

Benzylisoquinoline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what are NMBs reversed by

A

ANTIcholinesterase

Anticholinesterases metabolize acetylcholinesterase, leading to increased Ach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Less potent the drug=the _________ the number of the ED95=the more rapid the onset

A

less potent=higher number=more rapid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

fastest to slowest onset for NMBs

A

(SCh) > Rocuronium > Atracurium, Vecuronium, Mivacurium > Nimbex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

potency NMBs

A

Roc/Sch 0.3

Atracurium 0.2 

Vec/cisat 0.05 

Pancuronium 0.07 

Mivacurium 0.08
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

To facilitate MORE RAPID intubation, a small dose (1/10th the intubating dose) of the same NMB is given prior to the induction

A

priming dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

3 NMBs that cause histamine

A

atracurium
mivacurium
curare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

NMB plasma cholinesterase elimination

A

mivacurium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

NMB

Inhibiting histamine-N-methyl-transferase
(Like histamine)

A

vecuronium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Independent of organ function

Good for infusions

Indicated for pulm issues, organ dysfunction

hoffmann mainly

A

nimbex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Laudanosine*: metabolite that is a CNS stimulant (seizures in animals)

prolonged elim in renal failure

independent of organ function

A

atracurium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Anaphylactoid
(Like histamine)

good for RSI

NOT indicated for difficult airway

A

roc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

NMB can cause release of norepi

A

pancuronium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Block is LESS dense; patient will recover FASTER; must give BIGGER dose to have similar effect

A

resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

phenytoin would lead to increase in __________ to NMBs (leading to ___________ duration)

A

increased RESISTANCE
shorter duration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

what are the drugs for NMBs that cause increase in RESISTANCE

A

phenytoin
CHRONIC corticosteroids
aminophylline/theophylline
LARGE lasix

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

chronic hyperkalemia

A

nondepolarizers=more resistant
depolarizers=sensitive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

true or false

denser block= potentiated

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

volatile anesthetics = _________ anticholinesterases

A

RETARD

this leads to decrease in Ach, leading to more sensitivity to nondepolarizers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

which type of abx cause increased sensitivity to NMBs

A

aminoglycosides

gentamicin, neomycin, streptomycin, kanamycin, amikacin, tobramycin

NOT erythromycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

if giving Sch first, give a _________ dose of NMB

A

SMALLER DOSE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

elderly have ________ onset to drugs

A

slower onset

ALWAYS give smaller dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

reversals for NMBs

A

ANTIcholinesterases

edrophonium
neostigmine
pyridostigmine
physostigmine (ONLY lipid soluble/tertiary amine, cross BBB)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

which drugs are irreversible anticholinesterases

A

o Insecticides (dog dipper)
o Echothiophate (eye drops)
o Nerve gases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Once acetylcholinesterase is maximally inhibited, giving more anticholinesterase will ____ reverse a block

A

NOT reverse it

you will just have to WAIT for block to end
(IF GIVING Sch AFTER LARYNGOSPASM and nondepolarizer, BLOCK WILL BE PROLONGED)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

what is reversal of NMBs affected by

A

o Antibiotics
o Hypothermia
o Respiratory acidosis (PaCO2>50 mm Hg)
o Metabolic acidosis
o Hypokalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

true or false
anticholinesterases are the OPPOSITE of anticholinergics

A

true

anticholinergics treat anticholinesterases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Anticholinesterase Overdose*

A

TOO much Ach! (think of PNS symptoms)

NMJ: weakness ranging to paralysis

Miosis (constriction)
inability to focus vision
copious salivation
bronchoconstriction
bradycardia
abdominal cramps
loss of control of bowel and bladder

Confusion
ataxia
seizures
coma
respiratory depression

TREATMENT: atropine or pralidoxime

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

what are the anticholinergics

A

robinul (secretions + HR)
atropine (HR + CNS)
scopolamine (N/V/CNS + secretions)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Central Anticholinergic Syndrome

A

too much SNS

restlessness, hallucinations, somnolence, unconsciousness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

what type of NMBs does suggamedex work on

A

steroidal group

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

drug of choice for difficult airway

A

Sch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

which drugs inhibit plasma cholinesterase

A

neostigmine
cyclophosphamide
reglan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

true or false
do NOT use Sch for long cases

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

longest to shortest CSHT

A

FASR

fentanyl
alfentanil
sufentanil
remifentanil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

what is CSHT

A

distribution, metabolism, duration, infusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

the DRUGs affect on the body

A

pharmacodynamics

(ED95, MOA, sensitivity/resistance, etc)

88
Q

½ time between drug concentration in the blood and site of effect; accounts for the delay in effect

A

effect site equilibration

89
Q

Vd is __________ related to protein binding

A

inverse

90
Q

plasma level decreases to the point that drug diffuses away from site of effect and to peripheral groups or to elimination phase

A

redistribution

91
Q

besides NMB,
can occur with gentamycin, quinidine, tricyclic antidepressants, naloxone, local anesthetics

A

channel blockade

92
Q

treatment for central anticholinergic syndrome

A

physostigmine

93
Q

sugga is incompatble with what drugs

A

verapamil, ondansetron, ranitidine

94
Q

Neostigmine- paired with _______

Edrophonium- paired with \_\_\_\_\_\_\_\_\_\_\_
A

Neostigmine- paired with glyco

Edrophonium- paired with atropine
95
Q

Potency (most potent > least potent)

A

Sufentanil > Fentanyl > Alfentanil > Morphine > Tramadol > Demerol

96
Q

Lipid Solubility (most lipid > least lipid)

A

Sufentanil > Fentanyl > Alfentanil > Demerol > Morphine

97
Q

potency

A

Meperidine 1/10 as potent

Fentanyl 100 times more potent 

Sufentanil is 10 times more potent than fent  

Alfentanil 1/5 as potent as fent 

Remi 5 times more potent than fent
98
Q

o Closure of voltage-gated Ca2+ channels on PREsynaptic nerve terminals to cause a reduction of the release of neurotransmitters

o Opening of K+ channels to hyperpolarize the cell (conductance), thus causing inhibition of the POSTsynaptic neurons

A

opioids

99
Q

Alpha blockade causing direct aortic dilation

A

sufentanil + alfentanil

100
Q

treatment for sphincter of oddi

A

glucagon

101
Q

moderate increase in ICP due to vasodilation when without hypercarbia

A

fentanyl

102
Q

More intense, but LESS respiratory depression; can extubate sooner than fentanyl

A

sufentanil

103
Q

good alternative to morphine if in renal failure

A

dilaudid

104
Q

most reliable indication of respiratory depression is

A

decreased LOC

105
Q

what is NOT dose dependent for neuraxials

A

urinary retention

106
Q

glycine
Anxiolytic = ____________ (think STEM-SPINAL)

A

brainstem=anxiolytic

107
Q

glycine
muscle relaxant= ____________(think STEM-SPINAL)

A

spinal cord

108
Q

GABA
Anticonvulsant= _______________
(think C-C)

A

Anticonvulsant= brain motor circuits

109
Q

GABA
Sedation = __________ (think C-C)

A

cortex=sedation

110
Q

bind to benzodiazepine receptors (part of the GABA receptor), which ENHANCE the AFFINITY of binding of GABA to its receptor , opening of chloride channel, hyperpolarization of the neuron, inhibition of the neuron to excitation

A

benzos

111
Q

Apnea with larger doses and exaggerated in patients with COPD

A

versed

112
Q

Metabolite that prolongs sedative effect

best benzo hemodynamics

A

diazepam

113
Q

most potent
Lasts up to 6 hours- vented patients

A

lorezepam

114
Q

best to least for amnesia

A

lorezapam

115
Q

CNS stimulant; stimulates hypoxic drive via the activation of chemoreceptors in the carotid bodies (PaO2 is 38 mmHg)

A

doxapram

116
Q

doxapram does what to the lungs

A

increases Vt, with some RR increase

117
Q

most lethal to least lethal dose

A

morphine, fentanyl, alfentanil, sufentanil, then remi

118
Q

which drug causes weak alpha blockade

A

sufentanil

119
Q

SA node depression, slowed conduction through AV node

A

bradycardia in opioids

120
Q

decreased respiratory rate,
increased Vt

A

opioids

121
Q

accentuated vent depression

A

Older age >60 years
Occurrence of natural sleep/sleep disorders
Male
Opioid naivety
Chronic heart failure
Intra-articular morphine

122
Q

renarcotization (increase in resp depression)

A

1) Mobilization of opioids from other compartments (e.g., muscles, fat group)xcg rincreased blood flow, increased movement, warming
2) Reduction in stimulation post-extubation

123
Q

opioids cause cerebral vaso_______________ for NORMAL paco2

A

vasoconstriction (good thing)

cerebral vasodilation for HYPERcarbic patients

124
Q

MOA: direct stimulation of chemoreceptor trigger zone in floor of the fourth ventricle

A

opioids N/V

125
Q

Low lipid solubility of morphine

A

slow onset and prolonged duration

126
Q

o First-pass effect

A

Fentanyl and sufentanil

127
Q

termination of action for opioids

A

Small/single opioid doses: redistribution

Large/massive/repeated opioid doses: Metabolism

128
Q

opioid by plasma esterases

A

remi

129
Q

byproduct that is a CNS stimulant that can cause seizures with renal failure

A

normeperidine

do NOT give with renal failure

130
Q

An active metabolite that is toxic for renal failure patients, leads to prolonged duration

A

M6G

131
Q

When used with propofol for TIVA (total intravenous anesthesia), propofol inhibits degradation of alfentanil and sufentanil by ___-___%!

A

50-60%

132
Q

neuraxials ONSET

A

Morphine: ONSET 6-12 hrs until respiratory effects!

Sufentanil: 6 minutes

133
Q

MOA: interacting with opioid receptors in the trigeminal nucleus

A

pruritus

134
Q

treatment for pruritus

A

gabapentin

135
Q

neuraxial side effect NOT related to dose size

A

urinary retention

136
Q

Similar in chemical structure to atropine (antimuscarinic/anticholinergic)

Causes tachycardia! And increased bronchodilation

A

demerol

137
Q

More intense analgesia, LESS respiratory depression, extubated sooner!

A

sufentanil

138
Q

Single, brief stimulus
 Laryngoscopy
 Retrobulbar block (cataract)

A

alfentanil

139
Q

Opioid-Induced-Hyperalgesia
+
neuro assessments

A

remi

140
Q

o Great for patients with renal failure
o Similar metabolism to morphine

A

dilaudid

141
Q

rarely dysphoria

A

stadol

142
Q

antagonist agonist good for CV

A

nubain

143
Q

not good for CV patients

A

talwin and stadol

144
Q

narcan does not work

A

buprenex

145
Q

good for hyperalgesia

A

suboxone

146
Q

Hypovolemic patients (trauma, extreme dehydration): exaggerated MAJOR decrease in SVR and BP

A

versed

147
Q

 Decrease in Vt (tidal volume)!

A

benzos

148
Q

 Only slightly less potent than diazepam
 Drowsiness returns after 6 hours

A

o Dezmethyldiazepam

149
Q

o Competes with benzos and displaces them for the benzodiazepine receptor site on the GABA receptor

A

flumazenil

150
Q

o Displaces the opioid from the receptor, binds to receptor, inactivates it

A

narcan

151
Q

 Acute pulmonary edema
 Sympathetic stimulation due to rapid return of pain
 Tachycardia
 V fib
 HTN
 N/V
 Return of airway reflexes (could lead to laryngospasm)

A

narcan

o Critically ill
o CAD, CHF, cardiac surgery
o Lung dx
o Opioid dependence

152
Q

o Cerebrovascular disease
o Acute head injury
o CAD, HTN
o Asthma (reactive airways)
* Caution!

A

doxapram

153
Q

o Primary mechanism for redistribution/termination is redistribution from VRG to lean muscle group

A

iv anesthetics

154
Q

ideal IV anesthetic is ________soluble

A

water soluble

155
Q

pH of 10.5 (alkaline); bacteriostasis
 If mixed with acidic things (opioids, catecholamines, NMBs), will form precipitate

A

pentothal

156
Q

the more drug bound, the _________ the diffusion

A

slower

157
Q

MOA
Increases the DURATION of GABA
Directly MIMICS GABA at its receptor
Activates: glutamate, adenosine, nACh receptors

A

barbiturates

158
Q

normovolemic barbiturates

A

Minimal decrease in BP

Reflexively increase in HR (due to carotid sinus baroreceptor)

 Slowing the rate of administration (giving incrementally) does NOT change the decrease in BP or increase in HR

159
Q

 Decreased Vt and decreased RR

A

barbiturates

160
Q

Cerebral protection= gold standard*
* Only for incomplete cerebral ischemia: cardiopulmonary bypass, hypotension, circulatory arrest

A

pentothal

161
Q

which barb is an anticonvulsant

A

pentothal

(causes histamine)

162
Q

 Increased excitatory activity,

A

methohexital + etomidate

163
Q

o Increases AFFINITY for GABA
o Mimics inhibitory effects of GABA
 Depresses reticular activating system

A

etomidate

164
Q

 Decreased Vt; increased RR

A

etomidate

165
Q

 Adrenocortical suppression

A

etom

166
Q

o Plasma esterases

A

etom

167
Q

which drug for cardiac patients

A

etom

168
Q

o Alpha2 adrenergic agonist (8x more selective than clonidine)

A

precedex

169
Q

reduces emergence delirium
Titratable
o Easily arousable
o Antisialagogue (reduces secretions)
o Longer duration than propofol
o Decreased PONV

A

precedex

170
Q

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  decreased cAMP  decreased calcium

A

precedex

171
Q

Precedex given fast and bolus

A

HTN!!!
bradycardia

172
Q

o “Some” analgesia (pain relief) for neuropathic, chronic pain only

A

propofol

173
Q

GABA receptor agonist: leads to inhibition of GABA and hyperpolarization of cell membranes

A

propofol

174
Q

 Decreased HR, SVR, BP, CO
bronchoCONSTRICTION
 Extreme issues with hypovolemia, LV dysfunction, elderly (lead to exaggerated BP decline)

A

propofol

175
Q

best anti emetic

A

propofol

176
Q

 Decreased CMRO2, CBF, ICP, IOP

 Helps support SSEPs and MEPs (evoke potentials)

A

propofol

177
Q
  • > 75 mcg/kg/min for >24 hours in the ICU
  • Initially tachycardia, then BRADYcardia (lethal in peds)
  • Metabolic/lactic ACIDOSIS
A

Propofol Infusion Syndrome

178
Q

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

Inhibits glutamate (excitatory transmitter)

Interacts with all opioid receptors (mu, kappa, delta)
 Anti-muscarinic (leads to bronchodilation, sympathomimetic)
 Anti-nicotinic: analgesia
 Na+ channels: local anesthetic

A

Ketamine

179
Q

Lots of thick secretions (pretreat with antisialagogue: glycopyrrolate)

Emergence delirium occurs (midazolam)

A

ketamine

180
Q

DO NOT GIVE WITH

CAD* + pulmonary HTN

LOW catecholamines (critically ill)

A

ketamine

181
Q

causes bronchodilation (good for asthma)

A

ketamine

182
Q

Cardiac (most safe to least safe)

A

Etomidate > methohexital > pentothal > ketamine > propofol

183
Q

Emesis (greatest emesis to least)

A

Etomidate > ketamine > pentothal/methohexital > propofol

184
Q

Lipid Solubility (most lipid to least lipid)

A
  • Pentothal > methohexital
185
Q

Potency (greatest to least)

A
  • Methohexital > pentothal
186
Q

COX-1; Non-Selectives (1 & 2)
NSAIDS

A

decreased platelet aggregation
o Decreased renal function
o Increased GI toxicity risk

187
Q

NSAIDS

A

SMALL Vd
HIGH protein bound
malnourished, elderly will have GREATER effect

188
Q

Allergic reaction with nasal polyps

 Bronchoconstriction, rhinitis, urticaria, aseptic meningitis
 Reye’s syndrome (peds)

A

nsaids

189
Q

_______volemia (increases renal toxicity risk)

A

HYPO

190
Q

delayed bone healing
do NOT use with hypovolemia
do not use with ulcerative patients

A

toradol

191
Q

IRREVERSIBLY inactivates COX-1: leading to prolonged/inhibited platelet aggregation*

A

aspirin
(at least 7 days before using neuraxial)

192
Q

true or false
o Give TIVA as an infusion rather than bolus

A

true

193
Q

when is the largest thrombin produced

A

propagation phase (common pathway)

194
Q

MOA
o Binds to antithrombin  leads to enhanced binding with thrombin

A

heparin

195
Q

Dosed based on circulating heparin (often over-dosed)

clearance is fast

anaphylaxis

A

protamine

196
Q

Newer Oral Anticoagulants (NOACs)
and
Low Molecular Weight Heparin (LMWH)

A

no reversal

197
Q

Vitamin K ____ days for reversal

A

2-3 days

198
Q

elective procedures

A

Consider patient specific risks/benefits

199
Q

effects of aspirin are around for the life of the __________*; other NSAIDS effects are for the life of the drug

A

platelet

200
Q

Activates plasminogen into plasmin  increased clot breakdown

A

thrombolytics
(tPA)

201
Q

NOT a “procoagulant”
o Reduces risk of death due to bleeding, regardless of the cause*

 Blocks conversion of plasminogen to plasmin  decreased clot breakdown/lysis
 Decreased blood loss, decreased blood products, no risk of thrombi

A

antifibrinolytics
(TXA), amicar, aprotinin

202
Q

o Must give < 3 hours post-injury

A

antifibrinolytics

203
Q

indications

o Hemophilia
o Life-threatening hemorrhage
o CV surgery

very expensive

A

novoseven

204
Q

high risk for N/V

A

o Post-op opioids
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, laparoscopic)

205
Q

o If prophylaxis fails: don’t give the same drug as before, use a different drug class*

 If prophylaxis worked, then 6 hours later patient has PONV: give same drug

A
206
Q

peds are ____x as likely to vomit as adults

A

2x
(age 3-13)

207
Q

Dopamine
Serotonin 5HT3
Opioid receptors

A

Chemoreceptor Trigger Zone (CTZ)

208
Q

Muscarinic (Ach)
Histamine (H1)

A

vestibular system

209
Q

Irritation of the Pharynx (vagus nerve)

A

Gag and retch response

210
Q

Vagal and Enteric Afferents

Mucousa of the GI tract
Stomach stretch*

A

Serotonin 5HT3

211
Q

o GABA
o Acetylcholine = muscarinic
o Histamine = H1
o Serotonin 5HT3
o Dopamine
o Substance P
o Neurokinin 1

A

receptors

212
Q

MOA
 Anticholinergic (Ach/muscarinic) + antihistamine effect

A

antihistamines

213
Q

contraindicated with parkinsons

A

PBR

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

214
Q

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

A

scopolamine

215
Q

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

A

butyrophenones (droperidol)

216
Q

serontonin 5HT3 only has affect on

A

vomiting ONLY

217
Q

increases CRMO2 and ICP

A

ketamine

Pharm 1 (9 decks)

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