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MSK Final > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

membrane channel that transports choline into the cell

A

choline transporter

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2
Q

what is the enzyme that combines acetyl coenzyme a and choline to form ACh?

A

choline acetyltransferase (ChAT)

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3
Q

patients with alzheimer’s disease have reduced what?

A

cerebral production of ChAT

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4
Q

ATP dependent transporter that immediately shuttle ACh into storage vesicles after ACh synthesis

A

ACh vesicular transporter

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5
Q

When do voltage-gated Ca2+ channels open?

A

upon depolarization

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6
Q

What does Ca2+ promote?

A

vesicle membrane fusion

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7
Q

vesicular and plasma membrane proteins that initiate vesicle-plasma membrane fusion and release of ACh

A

VAMP and SNAPs

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8
Q

what is the enzyme that cleaves ACh into choline and acetate?

A

acetylcholinesterase (AChE)

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9
Q

What happens to choline after the cleavage of ACh?

A

choline is recycled back into the motorneuron via the choline transporter

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10
Q

LGICs select ions based on what?

A

the charge of the amino acids lining the pore of the channel

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11
Q

What is the charge of the amino acids lining the nicotinic cholinergic channel?

A

negative

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12
Q

what amino acids are lining the nicotinic cholinergic channel?

A

aspartic acid and glutamic acid

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13
Q

What are the agonists for the nAChRs?

A

nicotine, ACh, succinylcholine

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14
Q

What is combined to make ACh?

A

Choline and acetyl coenzyme a

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15
Q

What are two agents that affect the nerve action potential?

A

tetrodotoxin and local anesthetics

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16
Q

what are three examples of local anesthetics

A

lidocaine, bupivacaine, procaine

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17
Q

what is tetrodotoxin commonly referred to as?

A

Puffer fish poison

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18
Q

What is the MOA of tetrodotoxin?

A

it inhibits voltage-gated Na+ channels, which will then inhibit axonal conduction

19
Q

What is the MOA of local anesthetics?

A

it inhibits voltage-gated Na+ channels, which inhibits axonal conduction

20
Q

What are local anesthetics clinically used for?

A

utilized for pain control during a variety of clinical procedures

21
Q

What are two agents that affect vesicular ACh release?

A

botulinum toxin and tetanus toxin

22
Q

What is botulism caused by?

A

Clostridium botulinum

23
Q

Where is clostridium botulinum most commonly found?

A

vegetables, fruit, seafood, soil and marine sediment

24
Q

What is the MOA of botulinum toxin?

A

it cleaves components of the core SNARE complex involved in exocytosis, preventing the release of ACh

25
Q

How is botulism classically described?

A

acute onset of bilateral cranial neuropathies associated with symmetric descending weakness/ flaccid paralysis

26
Q

food-borne botulism symptoms often include what?

A

nausea, vomiting, diarrhea, abdominal pain and dry mouth

27
Q

What are the clinical uses of botulinum toxin?

A

temporary improvement in the appearance of lines/wrinkles of the face and prevention of chronic migraine headache

28
Q

What is tetanus toxin characterized by?

A

muscle spasms

29
Q

What causes tetanus?

A

clostridium tetani

30
Q

where is clostridium tetani found?

A

in the soil

31
Q

How does tetanus toxin block fusion of synaptic vesicles?

A

by targeting synaptobrevin

32
Q

after binding to the presynaptic membrane of the NMJ, tetanus toxin is internalized and transported where?

A

retroaxonally to the spinal cord

33
Q

Spastic paralysis is caused by tetanus toxin’s actions on what?

A

the spinal inhibitory interneurons, blocking release of inhibitory neurotransmitters that normally serve to relax contracted muscle

34
Q

how does generalized tetanus typically present

A

spastic paralysis with symptoms that include trismus (lock jaw), autonomic overactivity (restlessness, sweating, tachycardia), stiff neck, board-like rigid abdomen

35
Q

What is an antagonist that affects depolarization?

A

curare alkaloids

36
Q

what is the prototype of curare alkaloids?

A

d-tubocurarine

37
Q

How are curare alkaloids (d-tubocurarine) used clinically?

A

used during anesthesia to relax skeletal muscle

38
Q

How is paralysis after use of curare alkaloids (d-tubocurarine) reversed?

A

by increasing ACh in the NMJ by using an AChE inhibitor

39
Q

How is succinylcholine used clinically?

A

used as an induction agent for anesthesia

40
Q

How is paralysis caused from succinylcholine reversed?

41
Q

Curare alkaloids can be described as what kind of blocker?

A

a non-depolarizing blocker

42
Q

succinylcholine can be described as what kind of blocker?

A

a depolarizing blocker

43
Q

How are AChE inhibitors used clinically?

A

with dementia, myasthenia gravis, nerve gas, and organophosphate pesticide exposure, and reversal of neuromuscular blockade during anesthesia

MSK Final (16 decks)

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