Pharmacology Drugs Flashcards

(39 cards)

1
Q

Agents that affect nerve A.P?

A
Tetrodoxin
Local anesthetics (lidocaine, bupivacaine, procaine)
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2
Q

Agents that affect Vesicular aCh release?

A

Botulinum Toxin

Tetanus Toxin

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3
Q

Agents that affect depolarization?

A

Curare Alkaloids

Succinylcholine

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4
Q

Agent that inhibits AcHe?

A

cholinesterase inhibitors

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5
Q

Which agent is a competitive non-depolarizing ANTAGONIST? how does it work ?

A

Curare Alkaloids: binds to the nACh receptors, competes with ACh, and decreases EPP (end plate potential)

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6
Q

Which agent binds acetylcholinesterase ?

A

cholinesterase inhibitor

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7
Q

Explain what happens with calcium if Dantrolene agent is used?

A

It blocks ryanodine receptors and inhibits further Ca 2+ release (calcium remains sequestered in SR)

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8
Q

What agent causes N/V/D after consuming canned food or veggies or fish?

A

Botulinum Toxin

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9
Q

Which agent would cause increase in muscle facisculations?

A

Succinylcholine

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10
Q

What agent would you administer to pt with hyperthermia?

A

Dantrolene

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11
Q

Which agent blocks Na+ channels and results in decreased A.P?

A

Tetrodoxin or local aenesthetics

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12
Q

which agent cleaves the SNARE complex involved in exocytosis?

A

botulinim toxin

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13
Q

What does tetanus toxin do?

A

blocks fusion of synaptic vesicles by targeting synaptobrevin (inhibitory neurotransmitters that relax contracted muscle can’t work) –> spastic paralysis

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14
Q

Which agent can be used to treat migraines?

A

Botulinim Toxin

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15
Q

Which agent results in flaccid paralysis of muscles ?

A

Curare Alkaloids (bc they inhibit ACh binding to nAChR)

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16
Q

Which receptor is for smooth muscle contraction

A

muscarinic receptors

17
Q

mAchRs are _________ receptors and nAChRs are ________receptors?

A

G- protein

Ligand gated ion channels

18
Q

What proteins are involved in FUSION and release of AcH

A

VAMPS and SNAPS respectively

19
Q

What agent is a depolarizing blocker agonist? How does it work?

A

It binds to nahRs and initially causes depolarization and then eventually leads to receptor blocking

20
Q

what does cholineacetyltransferase (ChAT) do? in what disease is there a decrease of ChAT?

A

combines acetyl coenzyme A with choline (choline enters cell through choline transporter)

alzheimers

21
Q

what transports ACh into vesicles for storage? What does it need in order to do this?

A

ACh vesicular transporter; ATP

22
Q

what do mAChr do in cardiac muscle?

A

decrease heart rate, conduction velocity, contraction,

23
Q

which channel is ionotropic? which is metabotropic?

A

nAChRs are ionotropic; mAChRs are metabotropic (use second messengers)

24
Q

what makes the nAChRs select for positive ions?

A

negatively charge amino acids in pore (aspartic and glutamic acid)

25
d-tubocurarine is an antagonist of what?
skeletal nAChR
26
pt presents with symmetric weakness, b/l cranial neuropathies, blurred vision, dry mouth, vomiting. what toxin did they probably ingest?
botulism toxin
27
pt presents with lockjaw, stiff neck, sweating, and tachycardia. what toxin did he ingest?
tetanus toxin
28
which agent that affects depolarization is used in anesthesia? how do you reverse their effects?
curare alkaloids bc they cause flaccid paralysis use AChE inhibitor so that you can increase ACh levels
29
how can succinylcholine cause flaccid paralysis? how is this agent clinically relevant?
stays in NMJ for too long, sometimes blocks NaChR used as induction agent for anesthesia/used for intubation
30
how do you reverse succinylcholine's paralysis effects?
time
31
agent that affects muscle contraction?
dantrolene (inhibits ryanodine receptors in SR and blocks release of Ca2+)
32
how are cholinesterases clinically helpful?
help Alzheimer's, Parkinson's, myasthenia gravis
33
how is dantrolene clinically helpful?
malignant hyperthermia, spasticity
34
common sx for myasthenia gravis?
ptosis (drooping) of eyelids and mouth
35
2 examples of nondepolarizing blockade drugs, 1 example of depolarizing blockade drug?
d-tubocurarine and curare alkaloids; succinylcholine
36
in malignant hyperthermia what mutation can occur due to taking succinylcholine?
mutation in ryanidine receptor --> sarcoplasmic reticulum can't sequester calicum --> continuous contractin --> heat
37
describe CO2 levels, pH levels, and O2 consumption levels when you have malignant hyperthermia?
increased CO2, decreased pH, increased O2 consumption
38
if malignant hyperthermia goes untreated, what can occur?
rhabdomyolysis (hypermetabolic state --> muscle damage --> muscle tissue breakdown --> dumping hemoglobin into blood stream --> kidney clogged (KIDNEY FAILURE)
39
what drug do you use to txt malignant hyperthermia and/or spasticity?
dantrolene bc it binds to RYR (inhibiting further Ca2+ release)