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Boards: Basic > Pharm > Flashcards

Pharm Flashcards

1
Q

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

A

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

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2
Q

PRIS (propofol infusion syndrome) signs

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

4mg/kg/hr for > 48hrs

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3
Q

What does ED-95 mean?

A

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

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4
Q

Rank midazolam from greatest bioavailability to least

A

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

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5
Q

What drugs are metabolized by CYP 3A4

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

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

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6
Q

What drugs inhibit CYP3A4

A 
grapefruit
antifungal drugs
protease inhibitors
mycin ABX
protease inhibitors
SSRI
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7
Q

What drugs increase activity of CYP3A4

A 
rifampin
rifabutin
tamoxifen
glucocorticoids
carbamazepine
barbiturates
St. John's
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8
Q

what metabolizes codine to morphine?

A

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

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9
Q

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

A

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)

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10
Q

what drugs are cleared by ester hydrolysis

A

esmolol
remifentanyl
succinylcholine (butylcholinesterase)

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11
Q

Kidney elimination of: pancuronoum, vec, roc

A

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

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12
Q

neostigmine elimination

A

50% renal excretion

1/2 life increases from 77 –> 180min in renal failure

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13
Q

low dose vs high dose dopamine receptors?

A

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

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14
Q

What pH and temp conditions encourage hoffmann elimination?

A
  • increased pH and increased temp –> faster hoffmann elimination
  • note: intubating dose of cisatracurium (0.1-0.15 mg/kg),
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15
Q

cisatracurium: intubation dose, duration, half-life

A

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

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16
Q

contraindications to suggamadex (gamma-cyclodextrin) use?

A 
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

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17
Q

what eye drops can cause sux to last much longer?

A

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

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18
Q

what diuretics are potassium-sparing?

A 
the K+ STAEs 
Spironolactone
Triamterene
Amiloride 
Eplerenone
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19
Q

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

A 
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

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20
Q

How to deal with hypotension 2/2 ACEi/ARB

A

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

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21
Q

What effects do acetylcholinesterase inhibitors have on succinylcholine?

A

AChI inhibit plasma butyrlcholinesterase –> prolonged SUX duration

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22
Q

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

A

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

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23
Q

nitroprusside: MOA toxicity, preload/afterload effects

A

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

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24
Q

what immunosuppressant drug prolong’s NDNMB?

A

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)

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25
Q

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

A

volume or capacity of circuit / FGF

26
Q

S/E fospropofol?

A

paresthesias

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

27
Q

onset and duration of H2 blockers

A

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

28
Q

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

A

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
Q

anaphylaxis vs anaphylactoid reaction?

A

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
Q

metoclopramine: use, MOA,

A

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
Q

What are methemoglobin-inducing drugs?

A 
prilocaine
benzocaine
quinine
metoclopramide
sulfonamides
dapsone
chloral hydrate
32
Q

What are EMLA contraindications?

A
  • allergy to amides
  • class 3 anti-arrhythmic: amiodarone, bretylium, satolol, dofetilide
  • methymoglobinemia
  • infants (<12mo) on methymoglobin-inducing agents
33
Q

What over the counter herbs/supplements increase bleeding risk?

A 
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
Q

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

A

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

35
Q

contraindication to using ACEi

A

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

36
Q

list order of NMB prolongation with gas?

A

des > sevo > iso > halo > TIVA

DISH? but out of order so DSIH

37
Q

Rank fluoride ion production in halogenated agents from most to least

A

methylflurane > sevo > enflurane > iso > des

MSEID

38
Q

What can you determine from:

  • solubility or blood:gas coefficient
  • oil: gas coefficient
  • why does NO2 have a faster onset than desflurane?
A
  • 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
Q

signs of nitroprusside toxicity

A
  • elevated MVO2
  • tachyphylaxis
  • metabolic acidosis
40
Q

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

A
  • fasiculations, increases in ICP, intragastric pressure

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

41
Q

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

A
  • 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
Q

Which volatile agents are a/w lowest seizure potential?

A

desflurane
isoflurane

all agents decrease seizure potential though

43
Q

What volatile agent increases cerebral perfusion the most?

A

halothane

44
Q

Which volatile agent increases CMO2 brain?

A

NO2

don’t use in neuro cases!

45
Q

How does cirrhosis affect paralytic dosing?

A
  • 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
Q

barbiturates: considerations

A

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
Q

Etomidate: considerations

A

Adrenal suppression: 11-b-OH, 17-a-OH

  • N/V (30%)
  • thrombophlebitis / pain on injection
48
Q

ketamine: considerations

A
  • increases ICP, intra-ocular pressure –> do not use if cranial masses or open-globe
49
Q

opiods: consideration

A
  • 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
Q

meperidine: considerations

A
  • 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
Q

methadone: MOA, 1/2 life, considerations

A
  • mu agonist, NMDA antagonist
  • lipid soluble, long 1/2 life (15-60hrs)
  • large 1/2life variability 2/2 CYP differences
52
Q

fentanyl vs. alfentanyl

A

compared to fentanyl, alfentanyl has…

  • 4x faster onset
  • 1/4 the duration
  • 1/4 the potency (need 4x the dose of fentanyl)
53
Q

ketamine: considerations

A
  • 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
Q

Which CV drugs can be given IM?

A 
atropine
glyco
ephedrine
epinephrine 
phenylephrine
hydralazine 
vasopressin (minimal vasoactive effects)
55
Q

ephedrine: considerations

A

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

56
Q

Which ABX prolong NMB?

A 
aminoglycosides
polymyxins
tetracyclins
linomycin
clindamyin

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

57
Q

list volatile anesthesics in order of potency

A

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

HIEESD

58
Q

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

A

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
Q

What drugs are known to activate NMDA antagonist

A

ketamine
mag sulfate
nitrous oxide
opiods: methadone, tramadol

60
Q

nesiritide: moa

A

recombinant form of human BNP

  • vasodilation
  • natriuresis
  • diuresis
61
Q

nitroglycerine: MOA, preload/afterload effects

A

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

Boards: Basic (9 decks)

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