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Anesthesia: Basic > Pharm > Flashcards

Flashcards in Pharm Deck (61):
1

half life of benzos in order: alprazolam, diazepam, lorazepam, midazolam, temazepam

midazolam 1.5-2.5hrs (6x potent than diaz)
alprazolam 6-24hrs
temazepam 10hrs
lorazepam 11-22hrs (10x potent than diaz)
diazepam 40 - 100hrs

2

PRIS (propofol infusion syndrome) signs

- metabolic lactic acidosis
- rhabdomyolysis
- refractory bradycardia
- cardiac failure
- renal failure
- hyperkalemia
- hypertriglyceridemia
- hepatomegaly / fatty liver
- pancreatitis

4mg/kg/hr for > 48hrs

3

What does ED-95 mean?

The dose of NMB needed to reduce twitch height by 95%. The dose for tracheal intubation is typically 2x ED95.

4

Rank midazolam from greatest bioavailability to least

IV > SQ > IM > sublingual > intranasal > rectal > oral

5

What drugs are metabolized by CYP 3A4

acetaminophen
alfentanil
dexamethasone
fentanyl
lidocaine
methadone
midazolam
propofol (3A4, mostly 2B6)
sufentanyl

*note: midazolam inhibits 3A4, may slow down metabolism of other drugs

6

What drugs inhibit CYP3A4

grapefruit
antifungal drugs
protease inhibitors
mycin ABX
protease inhibitors
SSRI

7

What drugs increase activity of CYP3A4

rifampin
rifabutin
tamoxifen
glucocorticoids
carbamazepine
barbiturates
St. John's

8

what metabolizes codine to morphine?

CYP 2D6
morphine = active metabolite of codine
**inhibits 2D6 = SSRI, quinidine

9

If someone is on SSRI, what narcs do you want to avoid?

oxycodone (prodrug) --> oxymorphone
codine --> morphine
hydrocodone --> hydromorphone (more potent)
**SSRI inhibits CYP 2D6 --> responsible for converting to active metabolite morphine

*note: hydromorphine --> hydromorphone-3-glucuronide (no analgesic effects), accumulation causes neuro-excitation (agitation, restless, myoclonus)

10

what drugs are cleared by ester hydrolysis

esmolol
remifentanyl
succinylcholine (butylcholinesterase)

11

Kidney elimination of: pancuronoum, vec, roc

pancuronium 85%
vecuronium 20-30%
rocuronium 10-20%

12

neostigmine elimination

50% renal excretion
1/2 life increases from 77 --> 180min in renal failure

13

low dose vs high dose dopamine receptors?

low dose: 0.5-3mcg/kg/min --> activates D-1 --> vasodilate renal, mesenteric, coronary arteries

moderate: 3 - 10 mcg/kg/min --> stim a-1, stim b-1 --> NE release at nerve terminals

high> 10mcg/kg/min

14

What pH and temp conditions encourage hoffmann elimination?

- increased pH and increased temp --> faster hoffmann elimination

*note: intubating dose of cisatracurium (0.1-0.15 mg/kg),

15

cisatracurium: intubation dose, duration, half-life

intubating dose (0.1 - 0.15 mg/kg)
duration 30-60mins
half-life 25mins

16

contraindications to suggamadex (gamma-cyclodextrin) use?

pediatric pts
renal failure (>95% kidney excretion)
didn't use roc or vec
reversal of roc/vec in ICU pts
known hypersensitivity to suggamadex or components

*suggamadex is line-incompatible with zofran, ranitidine, verapamil

17

what eye drops can cause sux to last much longer?

echothiophate = anticholinesterase --> miosis
inhibits pseudocholinesterase
95% reduction in butylcholinesterase

18

what diuretics are potassium-sparing?

the K+ STAEs
Spironolactone
Triamterene
Amiloride
Eplerenone

19

nicardipine: type of drug, metabolism, preload/afterload effects, 1/2 life, elimination

CCB --> dilates coronary and peripheral arteries
(+) ionotropic effect --> increases HR
liver = prolonged in liver failure
1/2 life = 3-13mins
elimination = bile, feces

ARTERIOLAR vasodilation --> decreased afterload w/o affecting preload

20

How to deal with hypotension 2/2 ACEi/ARB

1st line = phenylephrine, ephedrine, glyco
2nd = norepinephrine, vasopressin (no data for)

**giving bolus 0.5-1U vasopressin is equivalent to giving 30min of 0.03U/min. Can decrease cardiac output, decrease gastric perfusion, lactic acidosis

21

What effects do acetylcholinesterase inhibitors have on succinylcholine?

AChI inhibit plasma butyrlcholinesterase --> prolonged SUX duration

22

Why does excessive dosing of AChI (neostigmine) cause weakness?

extra ACh --> pre-synaptic / post-synaptic desensitization/ inactivation of Na channels --> prevents depolarization

23

nitroprusside: MOA toxicity, preload/afterload effects

1) cyanide --> cytochrome c oxidase --> inhibits aerobic respiration --> metabolic gap lactic acidosis
2) cyanmethemoglobin --> can't carry oxygen
3) thiocyanate --> CNS toxicity

arterial and venous dilator --> decreases preload and afterload

24

what immunosuppressant drug prolong's NDNMB?

cyclosporine
also has nephrotoxic and neurotoxic effects
metabolized by CYP3A4 (if patient uses St. John's wort, increases metabolism --> subtherapeutic levels of drug --> organ rejection)

25

how do you calculate time constant for equilibrium of an anesthesia circuit

volume or capacity of circuit / FGF

26

S/E fospropofol?

paresthesias
onset ~4mins since has to be metabolized by endothelial and hepatic alk phosphatase to active drug

27

onset and duration of H2 blockers

cimetidine: onset 1 - 1.5hr, duration 3-4hrs
ranitidine: onset 1hr, duration 9-10hrs
famotidine: onset 1 hr, duration 10-12hrs

28

meperidine: use, MOA, metabolism, elimination, S/E

MOA: synthetic opiod, binds to mu and kappa receptor
use: pain, post-op shivering
metabolism: liver --> normeperidine (no analgesia, CNS excitatory effects)
1/2 life meperidine : 2.5 - 4hrs
1/2 life normeperidine: 15-30hrs
elimination: liver and kidney
S/E: normeperidine --> CNS excitatory / neurotoxic--> Sz. Don't use in pt's taking MOAi. Normeperidine inhibits serotonin reuptake --> serotonin syndrome

*be careful in pts with renal/liver failure as normeperidine accumulate
**Libby Zion died of phenylzine (MOAi) + meperidine

29

anaphylaxis vs anaphylactoid reaction?

anaphylactic: IgE/type 1 --> mast cell degranulation and histamine release. Need priming/sensatization event. Triggers = muscle relax, latex, ABX

anaphylactoid: direct stimulation of histamine release (mechanism does not involve IgE). Triggers = protamine, IV contrast, opiods, thiopental, d-tubocurarine

clinically indistinguishable

30

metoclopramine: use, MOA,

Rx: gastroparesis, nausea PPX

MOA: dopamine antagonist (chemoceptor triggers zone in CNS) and serotonin antagonist (anti-nausea), peripheral cholinergic agonist (increase gastric emptying, reduced gastric fluid, increased LES tone, opens pyloric sphincter).

S/E: don't use in parkinson pts, can cause extra-pyramidal effects (Rx: benadryl, benztropine)

31

What are methemoglobin-inducing drugs?

prilocaine
benzocaine
quinine
metoclopramide
sulfonamides
dapsone
chloral hydrate

32

What are EMLA contraindications?

- allergy to amides
- class 3 anti-arrhythmic: amiodarone, bretylium, satolol, dofetilide
- methymoglobinemia
- infants (<12mo) on methymoglobin-inducing agents

33

What over the counter herbs/supplements increase bleeding risk?

Gingko = PLT aggregation in vitro
Ginger = inhibit thromboxane synthase --> thromboxane --> PLT aggregation + vasoconstriction
Garlic = PLT aggregation
Vit E = PLT aggregation
Echinacea when on warfarin

34

What are the effects of different receptors of opiods: mu, kappa, delta

u1: analgesic
u2: respiratory, GI/constipation, dependence
u3: anti-inflammatory, unknown
kappa: analgesia, dysphoria
delta: resp, GI, dependence, GU

35

contraindication to using ACEi

aortic stenosis
bilateral/single renal artery stenosis
pregnancy (teratogen)
angioedema

36

list order of NMB prolongation with gas?

des > sevo > iso > halo > TIVA
DISH? but out of order so DSIH

37

Rank fluoride ion production in halogenated agents from most to least

methylflurane > sevo > enflurane > iso > des

MSEID

38

What can you determine from:
- solubility or blood:gas coefficient
- oil: gas coefficient
- why does NO2 have a faster onset than desflurane?

- less soluble, lower blood:gas --> faster FA/Fi ratio
- oil: gas --> potency. higher coefficient, higher potency, lower MAC (takes less % of drug to get the job done)
- desflurane has a lower blood:gas so you'd think it'd be a faster onset than NO2. The difference is NO2 is delivered in very high concentration

39

signs of nitroprusside toxicity

- elevated MVO2
- tachyphylaxis
- metabolic acidosis

40

What does pre-treatment of NDNB before SUX help with?

- fasiculations, increases in ICP, intragastric pressure

note: it will NOT prevent increased intra-ocular pressure. No not use sux with open eye injuries.

41

2-chloroprocaine: onset, half life, duration, elimination

- onset = 6-12 mins
- half-life = 45 seconds
- peak = 10-20 mins
- duration = 30-60 mins --> 60-90 w/ epi
- eliminated by plasma cholinesterases; prolonged with plasmacholinesterase deficiency

42

Which volatile agents are a/w lowest seizure potential?

desflurane
isoflurane

all agents decrease seizure potential though

43

What volatile agent increases cerebral perfusion the most?

halothane

44

Which volatile agent increases CMO2 brain?

NO2
don't use in neuro cases!

45

How does cirrhosis affect paralytic dosing?

- cirrhosis --> increased volume of distribution --> increase intubating dose of roc, vec,
- clearance depends on hepatic metabolism --> longer duration (roc, vec, pan)

- sux degradated by pseudocholinesterase. If cirrhosis, less production --> sux lasts longer (increases from 3min --> 9 min)

46

barbiturates: considerations

decreases cardiac output
myocardial suppression
venous pooling
decreased sympathetic output

respiratory depression
induces ALA synthase: pts w/ porphyria can have acute porphyria attack
- do not do intra-arterial injection --> crystalizes --> thrombosis/vasospasm

47

Etomidate: considerations

Adrenal suppression: 11-b-OH, 17-a-OH
- N/V (30%)
- thrombophlebitis / pain on injection

48

ketamine: considerations

- increases ICP, intra-ocular pressure --> do not use if cranial masses or open-globe

49

opiods: consideration

- DO NOT develop tolerance to miosis and constipation
- renal failure --> risk of toxicity w/ morphine and meperidine
- decreases cerebral blood flow
- N/V, biliary cholic, constipation
- better than gas at mediating stress response!

50

meperidine: considerations

- atropine-like structure --> vasolytic effects
- local anesthetic effects 2/2 Na channel interactions
- serotonin syndrome if pt on MOAi or SSRI
- can be fatal
- good for post-op shivering

51

methadone: MOA, 1/2 life, considerations

- mu agonist, NMDA antagonist
- lipid soluble, long 1/2 life (15-60hrs)
- large 1/2life variability 2/2 CYP differences

52

fentanyl vs. alfentanyl

compared to fentanyl, alfentanyl has...
- 4x faster onset
- 1/4 the duration
- 1/4 the potency (need 4x the dose of fentanyl)

53

ketamine: considerations

- factors that increase incidence of emergence delirium: age, female, personalities (excentric), on multiple meds
- airway reflexes remain intact (cough, gag)
- reverse emergence delirium with physiostigmine --> increases ACh in the brain. Theory that emergence delirium may represent an anticholinergic response in the brain
- S/E: nystagmus, pupil dilation, salivation, increases ICP

54

Which CV drugs can be given IM?

atropine
glyco
ephedrine
epinephrine
phenylephrine
hydralazine
vasopressin (minimal vasoactive effects)

55

ephedrine: considerations

alpha, beta agonist
indirectly releases NE
can give IM
be careful in someone taking MAOi's --> trigger release of accumulated catecholamines --> exaggerated response

56

Which ABX prolong NMB?

aminoglycosides
polymyxins
tetracyclins
linomycin
clindamyin

MOA: decreases prejunctional ACh release --> less ACh --> less AP
- depresses post-functional receptor sensitivity

57

list volatile anesthesics in order of potency

most potent
Halothane --> iso --> enflurane --> ether --> sevo --> des --> NO

HIEESD

58

What volatile anesthetic uptake Fi/Fa is most affected by change in cardiac output?

low cardiac output states readily allow uptake of blood-soluble anesthetic agents like iso
F
faster rate of increase if CO is lower for iso compared to des

59

What drugs are known to activate NMDA antagonist

ketamine
mag sulfate
nitrous oxide
opiods: methadone, tramadol

60

nesiritide: moa

recombinant form of human BNP
- vasodilation
- natriuresis
- diuresis

61

nitroglycerine: MOA, preload/afterload effects

direct acting vasodilator
cGMP production
venous dilation--> pooling --> decreased preload