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Pharmacology N926 > Final Exam Drug MOA, indications, side effects, PK/PD > Flashcards

Final Exam Drug MOA, indications, side effects, PK/PD Flashcards

1
Q

agonist antagonist drugs

A 
pentazocine
butorphanol
nalbuphine
buprenorphine
nalorphine
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2
Q

Mu1 receptor effects

A 
analgesia
euphoria
miosis
bradycardia
urinary retention
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3
Q

Mu2 receptor effects

A

analgesia
respiratory depression
physical dependence
constipation

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4
Q

Kappa Receptor Effects

A 
analgesia
dysphoria, sedation
low abuse potential
miosis
diuresis
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5
Q

delta receptor effects

A 
analgesia
respiratory depression
physical dependence
constipation
urinary retention
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6
Q 
Morphine MOA
Onset
T1/2
Vd
metabolism
metabolite
SE
contraindications
A

agonist at opioid receptors at presynaptic and postsynaptic sites in CNS (brain and SC) that are normally activated by endogenous ligands. opioids mimic these ligands to modulate pain.
ex) enkephalins, endorphins, dynorphins. most effective against slow dull pain.
Onset 15-30min
elimination t1/2 1.5-3h
Vd large
poor lipid solubility
mostly ionized
conjugated by the liver
metabolite morphine 6 glucoronide
-histamine release, accumulation of metabolite in impaired renal function, respiratory depression.
contraindications: acute pancreatitis, cholecystectomy, renal patients, older population

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7
Q 
Meperidine MOA, uses
potency
Elimination t1/2
Vd
duration of action
metabolism
SE
contraindications
A

kappa and mu agonist
anti shivering postop
1/10 as potent as morphine
elimination t1/2 3-5h
duration of action 2-4h
large
first pass metabolism demethylization (normeperidine) and hydrolysis (meperidinic acid) (phase 1)
-normeperidine metabolite t1/2 15h (greater than 30h in renal failure)
structurally similar to atropine. increased HR, mydriasis, delirium, seizures. in high doses, negative inotropic effects or histamine release
-contraindications: renal patients, patients taking MAOI’s or fluoxetine r/t serotonin syndrome

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8
Q 
fentanyl
t1/2
context sensitive half time
Vd
metabolism
SE
A

elimination t1/2 3-6h
increases with infusions greater than 2h, or 260minutes
large Vd
lipid soluble
redistribution
first pass uptake in lungs
secondary peaks
metabolized by n dealkylation and hydroxylation (phase 1)
no active metabolites
-can see bradycardia, increased ICP, myoclonus

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9
Q 
alfentanil 
potency
t1/2
context sensitive t1/2
Vd
duration of action
metabolism
SE
contraindications
A

elimination half time 1.5h
least potent, fastest onset due to high fraction of un ionization
60 minutes
small
nonionized
short duration of action
metabolized by piperidine n dealkylation and amide n dealkylation (phase 1)
-hypotension, dystonia, less potent than fent
-contraindicated in parkinsons

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10
Q 
remifentanil
t1/2
metabolism
Vd
context sensitive half time
SE
A

t1/2 15-30min

  • hydrolysis by nonspecific plasma esterases, no active metabolites, ester linkage
  • small Vd
  • context sensitive half time 4 minutes
  • SE: can induce seizure like activity, decrease BP, hyperalgesia (give ketamine or mag)
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11
Q 
sufentanil
potency
t1/2
metabolism
metabolite
Vd
context sensitive half time
SE
contraindications
A 
t1/2 2.4-5h
-5-10x more potent than fentanyl
-Protein binding (alpha 1 glycoprotein)
Highly lipid soluble
Metabolized by N-dealkylation and O-demethylation (phase 1)
Some activity
Clearance sensitive to hepatic flow
-metabolite desmethyl sufentanil
-Vd large
-context sensitive t1/2 30min
-SE: more potent than fentanyl. may cause chest wall rigidity. first pass pulm uptake
contraindications: avoid in renal patients
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12
Q

butorphanol MOA, SE**

A

-Low affinity for Mu receptor – produces antagonism
Moderate affinity for Kappa receptor – analgesia and anti-shivering
-Dysphoria “doesn’t feel right”
Increase in catecholamine response (increased HR, CO, BP)
Limits effects of concomitant opioid agonists

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13
Q

nalbuphine MOA, SE

A

-Antagonist effect at Mu receptor
chemically related to naloxone
If given before opioid – diminish effects of morphine-like drugs
If given after opioid – can reverse depression of ventilation effects but maintain analgesia
-Catecholamine stimulation effects – beneficial for cardiac patients
Less dysphoria than pentazocine and butorphanol

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14
Q

edrophonium MOA, t1/2, SE, onset

A

build up Ach at NMJ, give with atropine.
t1/2 30min-2h
-SE: bronchoconstriction, salivation, lacrimation, bradycardia
-onset 30-60seconds

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15
Q

neostigmine MOA, half life, SE, onset

A

build up ach at NMJ. give with glycopyrrolate
t1/2: 1-2h
SE: increased bowel motility, urination, bradycardia
onset: 1 minute

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16
Q 
acetaminophen
MOA, uses
metabolism
metabolites
half life
consideration
A

antagonism of NMDA, substance P and NO pathways. activates serotonergic pathway.

  • analgesic and antipyretic
  • metabolized in liver
  • n acetyl p benzoquinoneimine=liver failure by depleting glutathione
  • t1/2 2-3h
  • IV form is expensive
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17
Q

ibpruphen
metabolism
half life

A

through oxidation

t1/2 2-2.5h

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18
Q 
ketorlac
Vd
metabolism
half life
considerations
A
  • weak acid, increased protein binding
  • low Vd
  • conjugated
  • 2.5-8.5h
  • most commonly used periop
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19
Q 
celecoxib
MOA
Vd
metabolism
absorption
t1/2
considerations
A
  • COX 2 inhibitor
  • weak acid, increased protein binding and decreased Vd
  • absorbed in GI rapidly
  • conjugated
  • t1/2 11-16h
  • less GI toxicity, increased CV risk, part of ERAS protocol
  • good choice for patients with allergic rhinitis/nasal polyps+ asthma who may experience anaphylactic shock with other NSAIDS.
20
Q 
succinylcholine
MOA
chemical makeup
metabolism
recovery
half life
contraindications
A
  • depolarizing NMB, stimulates cholinergic receptor at NMJ opening ion channel
  • 2 Ach molecules together
  • rapid hydrolysis by butyrylcholinesterase. has to drift into blood stream to be deactivated.
  • recovery 9-13min
  • t1/2 45 seconds
  • pedes patients <5years, hyperkalemia, MH history.
21
Q 
atracurium
MOA
metabolism
duration of action
SE
half life
A

benzylisoquinolinium, nondepolarizing

  • metabolism by hoffmann elimination, ester hydrolysis
  • intermediate acting
  • histamine release huge
  • half life 20 minutes
22
Q

cisatracurium
MOA
metabolism
half life

A

benzylisoquinolinium, nondepolarizing

  • spontaneous degradation via hofmann elimination, NO ester hydrolysis
  • half life under an hour
23
Q 
vecuronium
MOA
duration of action
onset
chemical difference
half life
A
  • steroidal acetyl ester thought to facilitate action with nAchR. non depolarizing
  • intermediate acting, onset 2-4m
  • no quaternizing methyl group
  • t1/2 80 minutes
24
Q 
rocuronium
MOA
duration of action
onset
half life
A

steroidal nondepolarizing

  • intermediate acting
  • onset 1.7min
  • half life 70min
  • least potent
25
``` pancuronium MOA duration of action onset SE half life contraindications ```
- steroidal non depolarizing - long acting - onset 2.9min - vagolytic properties - half life 130min - most potent - dont use with renal patients because 3-OH metabolite can prolong block
26
atropine indications side effects half life
- used in combination with edrophonium to prevent PSNS SE - several metabolites, crosses BBB, dry mouth, tachycardia, Gi upset, blurry vision - t1/2 2-3h
27
``` glycopyrrolate chemical makeup MOA indications half life ```
- quarternary ammonium, antisialagogue effect - used in combination with neostigmine to prevent PSNS SE, does NOT cross BBB - half life 2-3h
28
``` scopolamine MOA indications SE half life reversal contraindication ```
- decreases activity of RAS, muscarinic antagonist. blocks communication between vestibular nerves and vomit center - enhances effects of opioids/benzos, antisialagogue effect - sedation, mydriasis, cycloplegia, restlessness, hallucinations - half life 4.5h IV, 72h patch - reversal: physostigmine .01-.03mg/kg, q15-30m - contraindications: closed angle glaucoma. CROSSES BBB.
29
``` thiopental MOA distribution Vd metabolism metabolite SE half life ```
- potentiate GABA receptors (flood of chloride in to hyper polarize, inhibitory response) - terminated by rapid distribution - acid, binds with albumin however - large Vd - oxidized (phase 1) - metabolite is pentobarbital - SE: decrease ICP, CBF, CMRO2, MAP, CO. exacerbates porphyria - t1/2 9-11h
30
``` methohexital MOA uses Vd metabolism half life SE ```
- facilitates actions of GABA receptors - lowers seizure threshold - acid, large Vd - phase 1 - half life 4h - SE: do NOT give to porphyria patients
31
``` diazepam MOA absorption Vd metabolism metabolites SE half life ```
- facilitates actions of GABA - rapidly absorbed in GI - large Vd, bound to albumin - oxidative pathway, N demethylation - desmethyldiazepam, oxazepam - SE: minimal depressive effects on ventilation, minimal decrease in BP CO SVR - half life 40h or >
32
``` lorazepam MOA onset peak metabolism Vd t1/2 ```
``` facilitates GABA onset 1-2m peak 20-30min conjugated in liver Vd large t1/2 14h ```
33
``` midazolam MOA chemical property metabolism duration of action SE Vd t1/2 ```
- facilitates GABA - water soluble with imidazole ring - metabolism by oxidation, phase 1 - short duration of action - decreases CMRO2, CBF - Vd large - half life 1.9h
34
``` flumazenil MOA metabolism metabolites DOA Vd half life ```
selective benzodiazepine antagonist - metabolized by hepatic microsomal enzymes to inactive metabolites - DOA 30-60 - Vd small - t1/2 40-80min
35
``` propofol MOA metabolism SE metabolite Vd half life ```
- selective modulator of GABA - metabolized by CYP450 - neuro protectant, does decrease BP and cause respiratory depression - metabolite is 4 hydroxypropofol - Vd large - half life .5-1.5h
36
``` ketamine MOA metabolism metabolite SE Vd half life ```
- binds non competitively to phenylcyclidine site on NMDA receptors. antagonizes glutamate. weak action on GSBS - demethylation by CYP450 - metabolite norketamine - no respiratory depression. does cause dissociative state, increased CBF and CMRO2 and ICP - Vd large - half life 2-3h
37
``` etomidate MOA metabolism SE Vd half life ```
single isomer R+. selective modulator of GABA, allosteric drug. also acts on alpha 2 adrenergic receptors - metabolized by hydrolysis - CBF and CMRO2 decreased, myoclonus possible - large Vd - half life 2-5h
38
dexamethasone MOA, use
usually used for cerebral edema, attaches to cytoplasmic receptors to enhance or suppress changes in DNA transcription. produces anti inflammatory and immunosuppressive response. targets cells with 11 beta hydroxysteroid dehydrogenase.
39
``` oxytocin MOA indications contraindications SE ```
- stimulates uterine contraction, lowers threshold for depolarization by activation of calcium channels and increased prostaglandin production - indicated for induction of labor and to reduce and prevent uterine atony/decrease hemnorrhage - contraindications: do not bolus, and hypotension can be an issue - SE: vasodilation, SVR/BP decreases, tachycardia
40
``` hemabate MOA indications contraindications SE ```
- increases myometrial calcium levels and increases MLCK activity and contraction. prostaglandin - indicated for PPH, uterine atony, reduces need for hysterectomy. 80-90% effective for PPH refractory to oxytocin and ergot alkaloids - contraindicated for reactive airway diseases (use misoprostol instead).
41
``` methergine MOA indications contraindications SE ```
ergot alkaloid. -not clear MOA -indicated as 2nd line treatment for uterine atony. decreases postpartum blood loss and PPH -produces tetanic uterine contractions restricting their use during post delivery period -dont give IV: profound HTN, severe n/v, cerebral hemorrhage. dont give to HTN at baseline or cardiac patients SE: n/v, HTN
42
ondansetron MOA, consideration
5ht3 antagonist, inhibits central and peripheral stimulation of these receptors. works on CTZ of area postrema and NTS. -slow IVP r/t abdominal cramping, renal dosages considered.
43
metoclopramide MOA
centrally acting dopamine receptor antagonist in CTZ, peripherally acting as cholinomimetic in GI tract (facilitates Ach transmission at muscarinic receptors)
44
Promethazine MOA, SE, duration, contraindications
acts on D2 H1 and muscarinic receptors. SE: sedation, hypotension, EPS (r/t D2), 4-6h duration contraindicated in elderly r/t confusion
45
sugammadex
modified gamma cyclodextrin that encapsulates and deactivates NMDB's. only for steroidals (roc>vec>pancreatic) -also encapsulates progesterone

Pharmacology N926 (16 decks)

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