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Pharmacology Flashcards

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1
Q

neostigmine

A

cholinergic agonist
quaternary acetylcholinesterase (does not cross BBB)
reverses anesthetic paralysis
SLUDGE

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2
Q

pyridostigmine

A

cholinergic agonist
long(est) acting acetylcholinesterase, quaternary (does not cross BBB)
preferred drug in myasthenia gravis
SLUDGE

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3
Q

physostigmine

A

cholinergic agonist
tertiary acetylcholinesterase (does cross BBB = CNS effects)
antidote for atropine
SLUDGE, convulsions, coma

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4
Q

pralidoxime

A

cholinergic ANTagonist
regenerates acetylcholinesterase
treats OD on cholinergic agonists
anti-SLUDGE

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5
Q

benzocaine

A

local anesthetic, ester
topical-only anesthetic
if internal use, serious methylglobinemia –> cyanosis

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6
Q

tetracaine

A

local anesthetic, ester

long-duration LA used for spinal anesthesia

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7
Q

mechanism of action of all local anesthetics

A

blocks Na+ channels on nociceptive receptors, especially small and unmyelinated neurons

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8
Q

adverse events of all local anesthetics if they are administered IV

A

v tach, v fib, other potential arrythmias, heart block, bradypenia, hypotension, convulsions, coma, possible death

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9
Q

lidocaine

A

local anesthetic, amide

most commonly used LA, intermediate duration, can be topical, injected subQ, spinal anesthesia

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10
Q

bupivicaine

A

local anesthetic, amide
long duration, used for epidurals
heart problems are especially severe if IV

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11
Q

atropine

A

anti-cholinergic muscarinic antagonist
blocks downstream muscarinic signalling (G-protein pathway)
has CNS effects, antidote to acetylcholinesterase inhibitors (anti-SLUDGE), treats bradycardia, bedwetting, pupil dilation
can cause tachycardia, hyperthermia, delirium, dizziness, anti-SLUDGE

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12
Q

scopolamine

A

anti-cholinergic muscarinic antagonist
blocks downstream muscarinic signalling (G-protein pathway)
long-acting and has CNS effects - prevents vomiting from motion sickness, surgery, etc.
sedation, confusion, anti-SLUDGE

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13
Q

glycopyrrolate

A

anti-cholinergic muscarinic antagonist
blocks downstream muscarinic signalling (G protein pathway)
similar to atropine, but in PNS only: anti-acetylcholinesterase, bradycardia, etc.
like atropine, tachycardia, anti-SLUDGE (no CNS side effects like delirium, dizziness, hyperthermia)

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14
Q

botox

A

anticholinergic
cleaves SNAREs that are needed for neurotransmitter vesicle fusion to pre-synaptic membrane, so ACh is not released
spasm, strabismus, dystonia, hyperhydrosis (execs sweating), tension/migraine headache, cosmetics
3-6 months duration

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15
Q

pilocarpine

A

cholinomimetic muscarinic agonist
direct muscarinic agonist = directly binds to muscarinic receptor and induces G protein signalling
ciliary contraction in glaucoma, tear and salivary gland production in Sjorjen’s syndrome
SLUDGE

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16
Q

tubocurarine

A

non-depolarizing NMJ blocker (curare)
nicotinic receptor competitive antagonist (binds active site) without depolarizing post-synaptic membrane
no longer used d/t many side effects, but is the parent compound for other curares

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17
Q

atracurarium

A

non-depolarizing NMJ blocker (curare)
as with other curares, nicotinic receptor competitive antagonist (blocks active site) without post-synaptic membrane depolarization
no CNS effects, intermediate-acting time
anesthetic paralysis and intubation
of currently used curares, most likely to cause side fx: widespread histamine, PNS neurotoxin (e.g. seizure)

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18
Q

rocurarium

A

non-depolarizing NMJ blocker (curare)
as with other curares, non-depolarizing nicotinic receptor competitive antagonist
no CNS effects, short-acting
anesthetic paralysis
similar side fx to other curares but less extreme d/t more quickly metabolized

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19
Q

succinylcholine

A

depolarizing NMJ blocker
step 1: ACh mimetic, causes widespread vasiculations
step 2: desensitization/receptor fatigue
step 3: broken down by plasma pseudocholinesterase
rapid onset (<1 min) and short duration (<10 min)
in genetically susceptible individuals (pseudocholinesterase mutations), effects can last for several hours

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20
Q

sugammedex

A

NMJ blockade reversal
releases/sequesters non-depolatorizing NMJ blocker from active site of nicotinic receptor, restoring normal signalling. sugammedex-curare complex then excreted renally.
reverses effects of non-depolarizing NMJ blockers
reasonably safe, fast-acting

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21
Q

aspirin

A

non-selective COX inhibitor, primarily COX1
IRREVERSABLE acetylation by acting as a steric block on COX.
anti platelet in addition to normal NSAID antiinflammatory antipyretic analgesic fx
Aspirin itself is rapidly excreted (within an hour) but effects last as long as it takes to make new COX/platelets
possible Reye’s syndrome in kids but this is being questioned now
Most GI effects of the NSAIDs because it is most partial to COX1; also, renal compromise and salycism

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22
Q

ibuprofen

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A

non-selective COX inhibitor, about 50:50 COX1:COX2
anti-inflammatory, anti pyretic, analgesic
t1/2 = 2-2.5 hour, reversible
competitive inhibition of arachidonic acid binding, which prevents arachadonic acid –> prostaglandin rxn. prostaglandins cause vasodilation, capillary permeability, platelet aggregation
AEs: GI bleeding, kidney compromise

23
Q

naproxen

Study These Flashcards
A

non-selective COX inhibitor, about 60:40 COX1:COX2

similar to ibuprofen, but slightly less selective and much longer t1/2 (12-16 h)

24
Q

indomethacin

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A

non-selective COX inhibitor, slightly less COX2 than naproxen
similar to ibuprofen, but less selective and intermediate t1/2 (4-6 h)
better for gout than other NSAIDs

25
celecoxib
COX2 inhibitor too bulky to fit in COX1 binding site = fewer side fx, stronger moderate-to-severe inflammatory pain e.g.. OA, RA, ankylosing spondylitis fewer GI fx, no platelet fx
26
acetaminophen
non-opioid analgesic; it's own class for mild pain and fever. no anti-inflammatory fx. Inhibits COX by different mechanism than NSAIDs but it's not completely known how liver toxicity at >3000 mg/day, no platelet fx, not contraindicated in asthma
27
diazepam
benzodiazepine (Valium), antispasmodic at CNS level GABA-A receptor allosteric agonist potentiates GABA effects: facilitates GABA binding to receptor (Cl- channel) --> hyerpolarization and post-synaptic neuron inhibition memory problems, agitation, hallucinations, mood changes, clumsiness, slurred speech ...
28
baclofen
antispasmodic/muscle relaxant at CNS level GABA-B receptor agonist directly activates GABA receptors leading to more K+ efflux, hyper polarization, and post-synaptic neuron inhibition dizziness, weakness, confusion, headache, drowsiness...
29
gabapentin
AED/anti-spasmodic/neuropathic pain/adjuvant at CNS level similar effects to GABA but doesn't actually have any effect on GABA receptors prevents neurotransmitter release by blocking pre-synaptic Ca++ channels no significant drug interactions, no liver metabolism (excreted directly into urine) drowsiness, dizziness, headache, uncontrollable shaking (seizure-like event), anxiety, loss of balance...
30
tizanidine
antispasmodic/muscle relaxant presynaptic alpha-2 adrenergic receptor agonist treats spasms, cramping, muscle tightness associated with MS, back pain, or spinal injuries dizziness, drowsiness, weakness, paresthesias...
31
dantrolene
anti-spasmodic/muscle relaxant, not strictly speaking an NMJ drug binds ryanidine receptor to prevent release of calcium from the sarcoplasmic reticulum
32
list opioid agonists from most potent to least
``` fentanyl (>80x morphine) hydromorphone heroin morphine ~ oxycodone (fewest off-target side fx) ~ methadone tramadol (1/10 morphine) tapentadol codeine ```
33
opioid agonists: PD, sfx
act on endogenous pre- and post-synaptic opioid receptors (mu, kappa, delta = MOP, KOP, DOP) to INHIBIT neuron transmission 3 possible mechanisms: - adenylate cyclase inhibition (cAMP) - reduced Ca++ influx at pre-synaptic (inhibits nt release) - increase K+ efflux post-synaptic (hyperpolarized) associated with range of opioid effects analgesia, euphoria (sometimes dysphoria), miosis (eye), respiratory depression, constipation, nausea, vomiting, cough suppression, hypogonadism long term d/t endocrine (GnRH, LH, FSH) inhibition, urinary retention, gallbladder spasm, histamine release, truncal rigidity, addiction, tolerance
34
buprenorphine
opioid partial mu receptor agonist (kappa receptor antagonist) ceiling effect to many pharmacologic effects including analgesia and euphoria high binding affinity to receptors, naloxone minimally effective less misuse potential, used in opioid use disorder
35
naloxone
competitive opioid receptor antagonist t1/2 = 1-2 hours (multiple injections or continuous infusions needed) poor oral bioavailability
36
naltrexone
competitive opioid receptor antagonist longer acting than naloxone t1/2 4 hours, also produces active metabolite with t1/2 = 12-16 hours good p.o. bioavailability can be used for OD or withdrawal maintenance in opioid use disorder
37
loperamide
opioid agonist used to treat diarrhea does not cross BBB, does cross gut but rapidly metabolized so very little in systemic circulation
38
diphenoxylate
opioid agonist | used to treat diarrhea - does not cross gut or BBB
39
dextromethorphan
opioid agonist and glutamate NMDA receptor antagonist used to treat cough several potential mechanisms - recent double blind studies show little to no effect a codeine analog no analgesic, gi, sedative fx OTC
40
codeine
opioid agonist used to treat cough via CNS effects - weak opioid with less addictive potential recent double-blind studies show little to no efficacy, older double-blind studies show good efficacy, reasons for discrepancy not know
41
AEDs for pain
topiramate, lamotrigine, carbamate all block Na+ channels topiramate also block Ca++ channels and inhibits glutamate release lamotrigine also blocks Ca++ channels and potentiates GABA effects (gabapentin also technically AED, Ca++ channel blocker)
42
amitriptyline
tricyclic antidepressant, adjuvant analgesic for neuropathic pain inhibits norepinephrine and serotonin reuptake (by NET and SERT) Na+ channel blocking inhibit ascending nociceptive activity "tricyclic" = 3 cyclic rings
43
duloxetine
SNRI, adjuvant analgesic for neuropathic pain (Cymbalta) inhibits norepinephrine and serotonin reuptake (by NET and SERT) Na+ channel blocking inhibit ascending nociceptive activity
44
ketamine
non-competitive NMDA receptor antagonist may potentiate GABA activation induces dopamine weak mu opioid receptor agonist persistent NMDA activation by glutamate --> hyperexitability is one mechanism of central pain @spinal cord
45
capsaicin
destroys nerve endings, differential effect on small and unmyelinated neurons such as nociceptive
46
hydrocortisone/cortisol
glucocorticoid
47
prednisone/prednisolone
``` glucocorticoid 4x cortisol short half life, low cost fewer mineralocorticoid (Na+/K+) effects ``` prednisone = prodrug to prednisolone prednisolone commonly prescribed in liver failure when prednisone can't be broken down
48
methylprednisolone
glucocorticoid 5x cortisol | commonly used for allergy and most autoimmune diseases
49
dexamethasone
glucocorticoid 25x cortisol t1/2 = 1-2 days drug of choice for most long-acting purposes, e.g. allergy and autoimmune diseases
50
morphine PK
no ceiling for analgesia (more drug = less pain), dose limited by side fx peak 30 min to 1 h after administration, t1/2 = 2-3.5h active metabolite as well as direct morphine effects limited oral bioavailability
51
methadone PK
t1/2 = 1-1.5 days, analgesic effect only 4-6 hours milder withdrawal symptoms hence utility in opioid use disorder excellent oral bioavailability 7-8x morphine also an NMDA antagonist so useful in neuropathic pain
52
NMDA is a receptor for...
glutamate. excitatory. ionotropic.
53
mechanism of action glucocorticoids
phospholipase A2 inhibitor. shuts down entire prostaglandin/COX/thromboxane/leukotriene pathway overall activates anti-inflammatory pathways and inhibits inflammatory pathways

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