N45-46 Flashcards

1
Q

Acetylcholine at motor end plate

A

Nicotinic coupled to Na channels for depolarization of the muscle cell and contraction

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2
Q

Acetylcholinesterase

A

hydrolyzes the ACh

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3
Q

GABA

A

inhibitory effects in CNS

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4
Q

Valium

A

enhances GABA effects for muscle relaxation

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5
Q

Dopamine

A

activation of DIRECT pathway, death of nigrostriatal neurons causes parkinsonism

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6
Q

Glycine

A

inhibitory (spinal reflexes)

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7
Q

Strychince and tetanus toxin

A

block glycine receptors and cause tetanic contractions

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8
Q

Aspartate and glutamate

A

excitatory

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9
Q

Antiepileptic drug (felbamate)

A

blcks NMDA (glutamate) receptors

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10
Q

Tubocurarine/Pavulon

A

competitive non-depolarizing nicotinic blockade

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11
Q

Succinylcholine

A

depolarizing blockade (initial depolarization followed by a blockade)

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12
Q

Neuromuscular blockades

A

cause paralysis by blocking neuromuscular junctions but still conscious

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13
Q

Acetylcholinesterase inhibitor

A

prevents hydrolysis of acetylcholine

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14
Q

Myasthenia Gravis

A

decreased number of cholinergic receptors, ACH inhibitors raise ACh in synaptic clefts

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15
Q

Insecticides

A

ACh inhibitors, ACh cannot unbind nicotinic receptor

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16
Q

Valium and benzo

A

enhances GABA in CNS for relaxation, does this by enhancing GABAs ability to open associated Cl channel for relaxation effect

17
Q

Benzo treats

A

acute muscle spasms

18
Q

Baclofen

A

GABA agonists that inhibits excitatory neurons

19
Q

Valium

A

treats spastic muscles, enhances GABA

20
Q

Baclofen

A

muscles spasms from UMN lesion, ALS, spinal cord injury (GABA agonist)

21
Q

Baclofen side effects

A

CNS depression

22
Q

Dantrolene

A

direct acting muscle relaxant, inhibits Ca release in SR (malignant hyperthermia, neuroleptic malignant syndrome)

23
Q

Convulsive stimulants

A

strychnine, tetanus toxin

24
Q

Strychnine

A

recurrent inhibition by renshaw cells via glycine inhibition, strychnine is a glycine antagonist –>tetanic seizures

25
Q

Tetanus toxin

A

inhibits release of glycine from renshaw cells

26
Q

Treatment for Parkinsons

A

death of dopaminergic neurons, resulting in increased ACh, treatment involves increased dopamine or reducing ACh

27
Q

Causes for Parkinsons

A

MPTP compound –> MPP+ toxin accumulates in substantia nigra

28
Q

I-DOPA

A

Dopamine precursor to raise dopamine levels

29
Q

Eldepryl

A

inhibits metabolism of dopamine by MAO-B

30
Q

Entacapone (Comtan)

A

inhibits COMTand slows metabolism of dopamine in cleft

31
Q

Bromocryptine (Parlodel)

A

stimulates dopamine receptors

32
Q

Amantadine (Symmetrel)

A

stimulates release of dopamine

33
Q

Benztropine (cogentin)

A

muscarinic antagonist