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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
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

Boards: Basic (9 decks)

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