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ACE Review - Pharm Flashcards

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1
Q

Moa clopidogrel and ticlopidine

A

Inhibit adenosine diphosphate receptors.

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2
Q

Moa aspirin

A

Stops cox1 from changing arach to thromboxane.

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3
Q

Moa tirofibran and abciximab.

A

Irrev binder of g3p2 receptors.

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4
Q

Moa of Gabapentin.

A

L type calcium channels on the alpha 2 delta subunit.

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5
Q

Does Gabapentin work on GABA receptors?

A

no

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6
Q

common triggers for malig hypertherm

A

volatiles and succ

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7
Q

what gene mutation is prone to malignant hyperthem

A

ryr1 gene in chrom 19

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8
Q

malignant hyperthermia moa

A

irregular release of intracell calcium…intracell contraction, atp, depletion, acidosis, cell death

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9
Q

dose if dantrolene

A

2.5mg/kg

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10
Q

does nitrous oxide cause MH

A

no

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11
Q

does intravenous anesthestics cause MH

A

no

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12
Q

how to treat hyperkalemia in MH

A

bicarb, glucose/insulin, calcium chloride

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13
Q

is cacl or ca gluconate adding to hypercalemic state of MH

A

no, the hypercalcemic state occurs intracell, not extracell, main goal is to treat arrythmia

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14
Q

what is not a treatment drug for MH assoc arrythmia

A

calcium channel blockers because they work against dantrolene

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15
Q

goal urine output in MH

A

2cc/kg/min

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16
Q

goal temp of MH

A

36-38, not higher or lower

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17
Q

is 2.5mg/kg dantrolene enough

A

no sometimes titrated up to 10mg/kg

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18
Q

what kind of mm relaxant is roc

A

monoquaternary aminosteriod

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19
Q

what is likely to decrease when given atropine

A

decrease in bronchopulmonary tone

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20
Q

what happens to body temp when given atropine

A

it increases body temp because there is a decrease in sweat gland secretions

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21
Q

what happens to the urine when given atropine

A

decrease urine output because it prevents urethral relaxation

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22
Q

what happens to the gi tract when given atropine

A

constipation, decrease acid secretion, decrease LES tone

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23
Q

what happens to the eye with atropine

A

mydriasis and increased intraocular pressure

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24
Q

which muscarinic recepter does atropine work on

A

m3

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25
Q

if there is a decrease in cardiac output, the rate of change of FA/FI is less likely affected by what

A

the less soluable gas is minimally affected by a decrease in cardiac output

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26
Q

what is the value used to measure the solubility of a gas

A

bloodgas partition coefficient

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27
Q

what gases are more affected by a decrease or change in cardiac output

A

soluble gases

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28
Q

what are the solubility of the gases

A

iso 1.46 sevo 0.65 dess 0.46, nitro 0.42

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29
Q

what are the effects of IV anesthetics on cerebral blood flow

A

most decrease cbf…like propofol.

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30
Q

what is the one IV anesthetic that actually increases cbf

A

ketamine

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31
Q

what do gases do to your cerebral blood flow

A

increase

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32
Q

what kind of cancer does doxyrubicin help treat

A

leukemia and lymphoma; wilms tumor, osteogenic sarcoma, breast carcinoma

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33
Q

what is the most common pathology seen by using doxyrubicin

A

cardiomyopathy

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34
Q

what is the screening test of choice for doxyrubicin

A

echocardiogram

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35
Q

why cant you use an ekg for doxyrubicin

A

ekgs most likely will show non-specific changes…like sinus tach, st segment changes, low voltage qrs

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36
Q

if a pt is getting 400mg/m^2, what is the chance of having cardiomyopathy

A

0.14%

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37
Q

if a pt is getting 550mg/m^2 doxyrubicin, what is the chance of having cardiomyopathy

A

7%

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38
Q

what does the increase in dose to increase of chances of cardiomyopathy with doxyrubicin mean?

A

cardiomyopathy is dose dependant

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39
Q

when can late onset of doxyrubicin induced cardiomyopathy occur

A

4 years after completion of doxy treatment

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40
Q

how common is doxy cardiomyopathy of late onset

A

it happens in 65% of patients

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41
Q

how specific and sensitive is echo in detecting doxy assoc cardiomyopathy

A

81%specific, 64% sensitive

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42
Q

what is the echo followup timeline after completing doxy treatment

A

at 3 6 and 12 months after completion and q 2 years after that

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43
Q

should we use cxray to screen doxy assoc cardiomyopathy

A

no…it usually detects late signs…and pts benefit from early intervention rather than late intervention

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44
Q

what is propofol infusion syndrome

A

myocardial failure, dysrythmia pluse 2 of 3 other criteria

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45
Q

what is the other possible criteria of propofol infusion syndrom

A

metabolic acidosis, rhyabdomyolysis, hyperkalemia

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46
Q

what kind of EKG finding do you find in propofol infusion syndrome

A

brugada like ekg signs…st elevated in v1-v3 without actually having ischemia

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47
Q

why do you mainly see propofol infusion sydrom in critically ill pt

A

because they have a very high energy requirement

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48
Q

how does propofol infusion syndrome hurt critically ill pt

A

at doses 130mcg/kg/min or higher, it can inhibit mitochondrial energy production and prevent oxidation of fatty acids

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49
Q

what is precentage of death In peds poplulation with propofol infusion syndrome

A

71%

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50
Q

what is the percentage of death in adults with propofol infusion syndrome

A

31%

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51
Q

what is the difference of an infiltrated IV versus an extravasiated IV

A

extravasiated iv has vesicants

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52
Q

what are vesicants

A

those that causes blisters

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53
Q

what are examples of vesicants

A

pressors, drugs that has Ca and K, some abx, mannitol and chemo agents

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54
Q

how does mannitol cause blisters

A

because it is hyperosmolar…driving fluid into the extravasation

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55
Q

what is the treatment for mannitol blisters

A

pressors and pH neutralizing solutions

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56
Q

when is surgery needed for mannitol extravasation

A

when compartment syndrome is present

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57
Q

what is the cross reactivity of pcn to 3/4th gen cephalosporins

A

5-12%

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58
Q

what are the other drugs can you use if pcn allergy

A

vanco and clindamycin

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59
Q

is there data to support premedication to prevent anaphylactic reaction to meds?

A

no..

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60
Q

what factors affect placental tranfer in drugs

A

lipid soluble, unionized, small molec weight, low protien binding

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61
Q

what affects a drugs ionization

A

the drugs pka and the environment ph

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62
Q

why does neuromuscular blocking drugs not cross placenta

A

because it is highly ionized

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63
Q

why does isoflurane cross over placenta so fast

A

because it is highly lipid soluble and low molec weight

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64
Q

why does sufent cross the placenta so fast

A

because it is highly lipid soluble

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65
Q

what narcotic has a black box warning

A

methadone

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66
Q

what kind of black box risk is there for methadone

A

cardiac arrythmias

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67
Q

what are 2 things dangerous about methadone

A

it prolongs QTc, it has a huge variability in patients bioavailability

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68
Q

what other drug do you have to do serial EKGS for like methadone users

A

droperidol

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69
Q

where does methadone get broken down

A

liver

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70
Q

what p450 enzymes does methadone get broken down into

A

3A4, 2D6

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71
Q

what meds might increase methadone because they inhibit 3A4 P450?

A

grape fruit and fluoroquinone antibiotics

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72
Q

what meds might increase methadone because they inhibit p450 2d6

A

SSRI fluoxetine, paroxitine

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73
Q

why does methadone vary so much in patients.

A

at certain doses, methadone actually induces its own metabolism, bioavailability varies among pts as well

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74
Q

why does methadone not work so well in cancer patients.

A

methadone is highly protien bound. In cancer patients, they have a reactive protien Alpha1A that is increased and binds the drug…decreasing its availabilty

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75
Q

do inhaled steriods for asthma cause adrenal corticoid suppression

A

no

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76
Q

what electrolyte abnormality do you see in pt using short actiing beta 2 agonist

A

hypOkalemia and hypOmag

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77
Q

what caution do you need to have when using mucolytics with asthma patients

A

they can actually cause bronchospasm

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78
Q

what is the onset and duration of short acting beta 2 agonist drugs for asthma

A

onset 5 mins duration 4-5 hours

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79
Q

what is an example of a short acting beta 2 agonist asthma drug

A

albuterol

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80
Q

what is the onset and duration of long acting beta 2 agonist for asthma drugs

A

no immediate effect…duration 12 hours s/p inhaler use

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81
Q

what are some examples of long acting beta2 agonist asthma drugs

A

salmaterol

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82
Q

what is bad about long beta 2 agonist

A

black box warning showing an association of increased mortality 1/1125 pts studied

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83
Q

along with short acting betal 2 agonist, what other drugs are used to treat asthma

A

inhaled corticosteriods

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84
Q

does using short term beta 2 agonist along with long acting beta 2 agonist

A

no they do not affect eachother

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85
Q

if the beta2/steriods inhaler fails to work, what is the next step of meds

A

parentral steriods

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86
Q

when do you see the effect of parentral steriods

A

4-6 hours onset

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87
Q

when pt becomes intolerant to beta 2 steriods…what other drugs can be used

A

anticholinergic…like ipratroprium

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88
Q

when is ipratroprium most effective

A

it is more effective in COPD pts

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89
Q

what is albuterol plust ipratropium

A

that is combivent

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90
Q

what is a dangerous side effect of combivent

A

flu like symptoms that occur in 1/20 pts

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91
Q

when is a pt on oral/parentral steriods for asthma be considered andreal suppressed

A

at least 2 weeks usage w/in the last 6 months

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92
Q

what happen to electrolytes with chronic lasix

A

hypoKalemia hypoMag

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93
Q

what is increased in chronic lasix usage

A

bicarb

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94
Q

how is calcium affected with chronic lasix usage

A

it is not affected

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95
Q

what happens to bicarb in chronic lasix usage

A

it is increased 2ndry to contraction alkalosis and due to H and Cl secretion for Na preservation

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96
Q

is poor o2 sat a good indicator of cyanide toxicity

A

no, actually your pulse ox would actually read a normal sat

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97
Q

is measuring serum cyanid levels a good way to test for cyanide toxicity

A

toxicity is dependant on dose and rate of release of cyanide…cyanide levels are difficult to attain and thus not a good way to check for toxicity

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98
Q

is a brown color of blood a good way to check for cyanide toxicity

A

actually the blood will be bright red…think of other pathology like meth-hemoglobinemia…which will be brown

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99
Q

what drug has cyanide as a metabolite

A

nitroprusside

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100
Q

what happens to the mix venous blood of cyanide poisoning

A

it is elevated

101
Q

why dose cyanide cause a mix venous to have a higher amount of o2

A

because it displaces o2 from the hemoglobin

102
Q

if cyanide displaces o2 from hemoglobin, what else is elevated other than mix venous o2

A

partial pressure of o2 in blood

103
Q

what is the best and easiest way to check for toxicity by cyanide

A

check blood ph it will show metabolic acidosis

104
Q

what is a drug that can help with cyanide toxicity

A

thiosulfate, vitamin b12

105
Q

how dose thiosulfate work

A

it increases renal elimination of cyanide

106
Q

how does cyanide work to cause metabolic aciosis

A

it binds cytochrome oxidases and thus, prevents aerobic metabolism

107
Q

how does vitamin b12 prevent cyanide toxicitiy

A

it chelates cyanide

108
Q

what poison can be used to treat cyanide toxicity

A

methhemoglobin

109
Q

what is the byproduct if methemoglobin is used for cyanide toxicity

A

cyanmethhemoglobin

110
Q

what drugs can produce methemoglobin

A

amyl nitrite and sodium nitrite

111
Q

what is the risk of using thiosulfate for cyanide toxicity

A

thiosulfate has sulfar that pushes cyanide to metabolize into a renal excreted metabolite…thiocyanide…this in itself is toxic

112
Q

which patients should not use thiosulfate to treat cyanide toxicity

A

renal patients bc the thiocyanide that is produced cannot be excreted

113
Q

what are the symptoms of thiocyanide toxicity

A

tinnitus, visual changes, seizures

114
Q

xxxxxxxxxxxxxxxxxxxxxxxxxx

A

xxxxxxxxxxxxxxxxxxxxxxxxxx

115
Q

what ionotrop causes increase cardiac ouput and decrease pulm vascular resistanc

A

milrinone

116
Q

what is the tem for a drug able to increase ionotropy and decrease vascular resistance

A

inodilator

117
Q

what does milrinone do moa

A

it is a phosphodiesterase inhibitor

118
Q

what happens when you inhibit phosphodiesterase

A

it increases cAMP

119
Q

what does that increase increase in cyclic amp do to pulm vasculature

A

it dilates pulm vasculator

120
Q

what is the mechanism of action of epi

A

both beta and alpha direct activity

121
Q

what is baclofen

A

it is a GABA B Agonist

122
Q

what is baclofen used for

A

muscle spasticity

123
Q

when is baclofen intrathecally indicated

A

multiple sclerosis, ALS, cerebral palsy, spinal cord injury

124
Q

when is baclofen indicated for peripheral nerve problems

A

peripheral, trigeminal, and glossphypharyngeal neuropathy

125
Q

what is the side effect of baclophen

A

drowsy, weakness, hypotonia,

126
Q

what is amytriptyline

A

it is a tca for antidepressant

127
Q

what is amitriptyline moa

A

serotinine reuptake inhibitor

128
Q

what is fluoxetine

A

it is a ssri

129
Q

what is the danger of getting both tca and ssri tx

A

serotinine syndrome

130
Q

what is the danger of serotonine syndrome

A

qt prolongation…inhibition of the perkinje fibers

131
Q

how do you treat qt prolongation of serotonin syndrome

A

bicarb

132
Q

why do you treat prolongation of serotonine syndrome with bicarb

A

because bicarb helps secrete tca out faster

133
Q

can you diurese or hemodyalize pt to get rid of tca

A

no, it is not good as bicarb…bc tca is highly protien bound, its very difficult to excrete the drug these ways

134
Q

how does bicarb excrete tca fast

A

it makes tca the neutral form, so it is less protien bound

135
Q

When does anaphylaxis occur in anesthesia

A

It occurs a few minutes after induction of anesthesia

136
Q

What are 3 predictors that the anaphylactic reactions will be severe

A

It’s rapid onset. Bradycardia. The absence of rash before hemodynamic changes

137
Q

Whst are 2 labs that need to be drawn to confirm the diagnosis of anaphylaxis

A

Histamine and tryptase levels

138
Q

How many different grades of anaphylaxis are there.

A

There are 4 grades of anaphylaxis

139
Q

Grade 1 anaphylaxis

A

Presence of cutaneous mucous signs

140
Q

Grade 2 anaphylaxis

A

Multivisceral signs

141
Q

Grade 3 anaphylaxis

A

Life threatening multivisceral signs

142
Q

Grade 4 anaphylaxis

A

Cardiovascular collapse

143
Q

When should histamine be collected

A

Within 30 min for grade 1 and 2. Within 2hr for grade 3 and 4

144
Q

When. Should tryptase be ordered

A

Within 15-60 min for grade 1 and 2. Within 30min to2hr for grade 3 and 4

145
Q

What is the most common med in anesthesia that causes allergies

A

Muscle relaxants

146
Q

What is the first medication to give during severe anaphylaxis

A

Epinephrine. Cardiovascular stability is priority

147
Q

What is associated with poor outcomes of anaphylaxis.

A

Late or absence of epinephrine administration

148
Q

Should fluids be giving during anaphylactic reactions ?

A

Yes. 50% of intravascular volume could third space secondary to increase vascular permeability

149
Q

What happens if epi is not able to reverse anaphylaxis instability.

A

Use vasopressin

150
Q

If anaphylaxis is not severe, what medications can be used

A

Hydrocortisone and benadryl

151
Q

What two nmb causes histamine release

A

Mivacurium and atricurium

152
Q

What influences the amount of histamine release from mast. Cells by nmb

A

The dose and rate of admin

153
Q

What toxicity is amiodarone associated with

A

Pulmonary toxicity

154
Q

What other drug is associated with pulmonary toxicity

A

Bleomycin

155
Q

What percent of pt get pulmonary toxicity associated with amiodarone

A

6%

156
Q

What is the best predictor of pulmonary toxicity associated with amiodarone

A

Cumulative dose

157
Q

What is the mortality rate of pulmonary toxicity secondary to amiodarone

A

10%

158
Q

What is associated with patients who get ARDS related to amiodarone

A

High oxygen fio2 given intraoperatively

159
Q

Besides pulmonary complications what are other complications associated with amiodarone

A

Thyrotoxocosis

160
Q

What complication is associated with doxorubicin

A

Cardio toxicity

161
Q

high or low blood to gas partition coefficient will have a faster rate of induction

A

a lower blood to gas partition coefficient will have a faster rate of induction

162
Q

what drug can be used PO for chemo related nausea and vomitting

A

emend aka aprepitant

163
Q

how does emend work

A

it is an NK1 antagonist….antagonist of substance P

164
Q

what are the adverse effects of emend

A

none

165
Q

which is more effective, zofran or emend

A

emend, about 50 times more

166
Q

when should emend be given

A

1-3 hours before surgery

167
Q

can u use zofran even after giving emend

A

no interactions at all

168
Q

what are the 3 side effects of protatmine

A

histamine release, igE mediated allergic reaction, of anaphylactoid reaction

169
Q

what is ige mediated hypersensitivity

A

it is a type II hypersensitivity (aka previous exposure to protamine will cause allergic response after a second exposure

170
Q

what kind of pre-exposure will cause a type II hypersensitivity to protaine

A

pts getting NPH, protamine zinc insulin, fish allergy

171
Q

what kind of surgry predisposes pt to protamine type II hypersensitivity

A

vasectomy

172
Q

what is an anaphylactoid reaction

A

it is a type iii hypersensitivity…it is like an allergic reaction (igE mediated) but is actually complement and IgG mediated

173
Q

what is the risk associated with protamine anaphylactoid reaction

A

it causes massive pulmonary htn and possible right sided heart faiilure

174
Q

what is the dose of protamine to fully reverse heparin

A

0.6 to 1 mg protamine for every 100Units heparin used

175
Q

what is the most common side effect of protamine

A

hypotension

176
Q

does protamine affect platelets

A

yes, it may decrease the count…but this is transient and clinically insignificant

177
Q

what two herbal meds may cause irreversible platelet function

A

garlic and gensing

178
Q

what herbal medication is taken as a sedative

A

kava

179
Q

what happens if acute injestion of kava, what are the anesthestic requirements

A

decreased anesthestic requirements

180
Q

what happens if prolong use of kava…what happens to anesthestic requirements

A

increase anesthetic requirement

181
Q

what herbal medicine has been used for weight lost

A

ma huang aka ephedra

182
Q

wat are adverse effects of mahuang

A

stroke and cardiac attacks and tachycardia

183
Q

What is benzocaine toxicity

A

Methemoglobinemia

184
Q

What patients are prone to damage from methemoglobinemia

A

G6PD deficiency, M type hemoglobin, Methemoglobin reductase deficiency

185
Q

What age in pediatric patient does methemoglobinemia hurt

A

less than four months

186
Q

What is the saturation of oxygen methemoglobinemia

A

84%

187
Q

Treatment for methemoglobinemia

A

Methylene blue

188
Q

Treatment for Cyanide toxicity

A

Sodium thiosulfate

189
Q

What treatment for Cyanide toxicity next methemoglobin

A

amyl nitrite and sodium nitrate,…They make red blood cells form methemoglobin which displaces cyanide from cytochrome oxidase molecules

190
Q

What treatment for cyanide toxicity and that making vitamin B12

A

Hydroxocobalamin

191
Q

Herbal medicine. When should it be stopped before surgery.

A

If there is unknown data for the herbal medicine, stop it 2weeks before surgery

192
Q

Herbal medicine. What is ginger used for

A

Has been used for nausea.

193
Q

Herbal medicine. What problem can ginger cause.

A

It is antiplatele and can cause bleeding.

194
Q

Herbal medicine. What is kava

A

It is a pepper derivative that can be used for anxiety.

195
Q

Herbal medicine. How does kava affect anesthesia.

A

It potentiates benzos

196
Q

Herbal medicine. Does kava cause and change in bleeding.

A

No

197
Q

Herbal medicine. What is St. John’s wart.

A

It is believed to work like an snri for depression.

198
Q

Herbal medicine. Is St. John warts an MAOI

A

No.

199
Q

Herbal medicine. What effects does St. John’s wart have on the body.

A

It can inhibit some liver enzymes

200
Q

Herbal medicine. What anesthetic problem can happen when St. John warts inhibit liver function.

A

It can make drugs like alfentanil, benzos , and snri increase in the system

201
Q

Herbal medicine. What does St. John’s wart do to bleeding.

A

It can become an antagonist to warafin

202
Q

Herbal medicine. What is valerian.

A

It is a medicine believed to help with anxiety.

203
Q

Herbal medicine. When should valerian be stopped prior to surgery

A

It should not be stopped because it can cause withdrawl

204
Q

acetylcholinesterase inhibitors. where do they function

A

at the acetylchoinesterase enzyme

205
Q

acetylcholineasterase inhibitors. how does neostigmine work at the enzyme

A

it makes a covalent bond with the enyzme

206
Q

acetylcholinesterase inhibitors. how does edrophonium work at the enzyme site

A

it makes an ionic bond with the enzyme

207
Q

scopolamine patch. what is it used for

A

post op nausea and vomit

208
Q

scopolamine patch. when should it be started.

A

it should be started the night prior to surgery

209
Q

scopolamine patch. what is the most common side effect

A

dry mouth

210
Q

scopoloamine patch. what is the least likely side effect

A

agitation

211
Q

atricurium. how is it degraded

A

1/3 hoffman and 2/3 nonspecific plasma esterases

212
Q

atricurium. are nonspecific plasma esterases the same as plasma cholinesterases

A

nope

213
Q

cisatricurium. how is it degraded

A

by hoffman elimination

214
Q

gabapentin. how does it work

A

voltage gated calcium channel

215
Q

gabapentin. where on on the voltage gated calcium channel does it work.

A

the alpha 2 delta subunit

216
Q

gabapentin. what happens after it binds to the calcium channels

A

it decreases glutamate and excitation of nociceptive pathways.

217
Q

GABAa. what drugs work here

A

benzo, prop, flumazenil, etomidate

218
Q

voltage gated Na channels. what drugs work here

A

local anesthetics

219
Q

phase II block. what characteristics on a twitch monitor

A

twitchs with fade. fasiculations after post tetanic stimulation

220
Q

phase II block. who is more prone to get it, adults or children

A

adults

221
Q

atypical plasma cholinesterase. what is it aka

A

pseudocholinesterase, butyrylcholinesterase

222
Q

alcohol withdrawl syndrome. what is the mortality if withdrawl occurs

A

up to 35%

223
Q

alcohol withdrawl syndrom. in operative pt. what is the best treatment for these pt

A

pre-emptive treatment…identifying the pts at rist and pre-emptive treatment. decreases mortality risk from 35 down to 5%

224
Q

allergic reaction. what is the cross reactivity between pcn and cephalosporins

A

10 percent

225
Q

allergic reaction. if a pt has a pcn allergy, would they be more prone to get allergic reaction after admin of a 1st gen cephalosporin or later gen

A

1st generation beause they share a side chain of pcn

226
Q

allergic reaction. how specific is skin testing for allergy to pcn / cephalosporins

A

95-97% specific

227
Q

allergic reaction. how sensitive is skin testing for allergy to pcn/ cephalosporin

A

50% sensitive

228
Q

amidarone. how long is the half life

A

about 29 days

229
Q

amiodarone. how long after discontinuation do u see its effects

A

up to 45 days

230
Q

amiodarone. what endo side effect do u see

A

hyper hypo thyroxicosis can all be seen

231
Q

amiodarone. what is the most serious consequence of amiodarone use

A

irreversible pulmonary fibrosis

232
Q

Organophosphate. What kind of drug is it.

A

Anticholinesterase.

233
Q

Organophosphate. What symptoms do you see.

A

Ach overload. You get bradycardia. Excess gi diarrhea. All your glands secrete. Bronchoconstriction.

234
Q

Organophosphates. What do you see on EKG.

A

Qt prolonged because the heart conduction slowed down.

235
Q

Organophosphates. What is the treatment

A

Atropine.

236
Q

Organophosphates. How can you tell it is ortanophosphate on the exam.

A

Mitosis. Look at the eyes.

237
Q

Organophosphates. What is it the reciprocal of.

A

Atropine toxicity.

238
Q

toxicity treatment. what does methylene blue treat

A

methhemoglobinemia

239
Q

toxicity treatment. what does n-acetylcysteine treat

A

acetaminophen toxicity

240
Q

toxicity treatment. what does amyl nitrite treat

A

cyanide toxicity

241
Q

lithium. what is the effect on muscle blockade

A

it increases sensitivity to both depol and non depol mm blockers

242
Q

lithium. what electrolyte effects of li

A

hypOk and hyper Ca

243
Q

Lithium. what effects on barbs and benzos

A

increase effect

244
Q

remi. how does it help in neuro cases in pt w seizures

A

when ready to resect seizure focus, a high dose of remi can be given and it can decrease eeg at non seizure area and expose the seziure focus

245
Q

somatostatin. what med is this used for

A

carcinoid crisis

246
Q

dexemetomidine. what is its moa

A

alpha 2 blocker

247
Q

dexemetomidine. how does it work similarly to an snri

A

both snri and dex promote alpha 2 block in the spinal cord…which prevent ascending pathway of nociception

248
Q

dexemetomidine. what does it do to cpp

A

drecreases bc it decreases map

ACE (18 decks)

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