Neurology Pharmacology Flashcards

1
Q

What is the use of neuromuscular blocking drugs?

A

Used for muscle paralysis in surgery or mechanical ventilation

Selective for motor nicotinic receptor

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2
Q

What are the two classes of NMB drugs?

A

Depolarizing and Nondepolarizing

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3
Q

What is the mechanism of dantrolene?

A

Prevents the release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle

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4
Q

Clinical use of dantrolene

A

Used in the treatment of malignant hyperthermia, a rare but life-threatening side effect of inhalation anesthetics and succinylcholine

Also used to treat neuroleptic malignant syndrome

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5
Q

What 5 majore drugs are used to treat Parkinson’s?

A

BALSA

Bromocriptine

Amantadine

Levodopa (with carbidopa)

Selegiline (and COMT inhibitors)

Antimuscarinics

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6
Q

What is the strategy of bromocriptine in treating Parkinson’s?

A

Dopamine agonist

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7
Q

What is hte strategy of amantadine in treating Parkinson’s?

A

Increase dopamine

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8
Q

What is the toxicity of amantadine?

A

Tremor

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9
Q

Whatis the strategy of L-dop/carbidopa in treating Parkinson’s?

A

Increase dopamine

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10
Q

What is the strategy of selegiline in treating Parkinson’s?

A

Prevent dopamine breakdown

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11
Q

What enzyme does selegiline inhibit to prevent dopamine breakdown?

A

Selective MAO type B inhibitor

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12
Q

What is the strategy of entacapone and tolcapone in treating Parkinson’s?

A

Prevent dopamine breakdown

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13
Q

What enzyme does entacapone and tolcapone inhibit to prevent dopamine breakdown?

A

COMT

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14
Q

What specific antimuscarinic is used to treat Parkinson’s?

A

Benztropine

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15
Q

What is the strategy of benztropine in treating Parkinson’s?

A

Curb excess cholinergic activity

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16
Q

Why is L-dopa used rather than dopamine to increase level of dopamine in brain?

A

Unlike dopamine, L-dopa can cross the BBB and is converted by dopa carboxylate in the CNS to dopamine

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17
Q

Why is carbidopa used along with L-dopa?

A

It is a peripheral decarboxylase inhibitor to increase the bioavailability of L-dopa in the brain and to limit peripheral side effects

18
Q

Toxicity of L-dopa

A

Arrhythmias from increased peripheral formation fo catecholamines

Long-term use can lead to dyskinesia following administration, akinesia between doses

19
Q

Mechanism of selegiline

A

Selectively inhibits MAO-B which preferentially metabolizes dopamine over NE and 5-HT, thereby increasing the availability of dopamine

20
Q

Clinical use of selegiline

A

Adjunctive agent to L-dopa in treatment of Parkinson’s

21
Q

Toxicity of selegiline

A

May enhance adverse effects of L-dopa

22
Q

Clinical use of memantine

A

Alzheimer’s

23
Q

Mechanism of memantine

A

NMDA receptor antagonist; helps prevent excitotoxicity (mediated by Ca2+)

24
Q

Toxicity of memantine

A

Dizziness

Confusion

Hallucinations

25
Clinical use of donepezil
Alzheimer's
26
Clinical use of galantamine
Alzheimer's
27
Clinical use of rivastigmine
Alzheimer's
28
Mechanism of donepezil, galantamine and rivastigmine?
AchE inhibitor
29
Toxicity of donepezil, galantamine and rivastigmine
Nausea Dizziness Insomnia
30
What neurotransmitter changes occur in Huntington's?
Decreased GABA Decreased Ach Increased dopamine
31
Clinical use of tetrabenazine
Huntington's
32
Mechanism of tetrabenazine
Inhibit VMAT to limit dopamine vesicle packaging and release
33
Clinical use of reserpine
Huntington's
34
Mechanism of reserpine
Inhibit VMAT to limite dopamine vesicle packaging and release
35
Clinical use of haloperidol
Huntington's
36
Mechanism of haloperidol
Dopamine receptor antagonist
37
Mechanism Sumatriptan
5-HT1B/1D agonist Inhibits trigeminal nerve activation Prevents vasoactive peptide release Induces vasoconstriction Half-life \< 2 hours
38
Clinical use of sumatriptan
Acute migraine, cluster headache attacks
39
Toxicity of sumatriptan
Coronary vasospasm Mild tingling
40
Contraindication of sumatriptan
Contraindicated in patients with CAD or Prinzmetal's angine (due to coronary vasospasm side effect)