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FA - Neurology > Neuro - Pharmacology (Neuromuscular blocking, Parkinson, Alzheimer, Huntington, & headache drugs) > Flashcards

Neuro - Pharmacology (Neuromuscular blocking, Parkinson, Alzheimer, Huntington, & headache drugs) Flashcards

Pg. 495-497 in First Aid 2014 Sections include: -Neuromuscular blocking drugs -Dantrolene -Parkinson disease drugs -L-dopa (levodopa)/carbidopa -Selegiline -Alzheimer drugs -Huntington drugs -Sumatriptan

1
Q

What are 2 uses for neuromuscular blocking drugs?

A

Used for muscle paralysis in surgery or mechanical ventilation.

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2
Q

For what receptor are neuromuscular blocking drugs selective?

A

Selective for motor (vs. autonomic) nicotinic receptor

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3
Q

What are the 2 types of neuromuscular blocking drugs?

A

(1) Depolarizing (2) Nondepolarizing

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4
Q

Give an example of a depolarizing neuromuscular blocking drug.

A

Succinylcholine

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5
Q

What is succinylcholine, and what action(s) does it have?

A

Succinylcholine - strong ACh receptor agonist (depolarizing neuromuscular blocking drug); Produces sustained depolarization and prevents muscle contraction

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6
Q

What are the phases in the reversal of neuromuscular blockade due to succinylcholine? Briefly describe each.

A

Phase I (prolonged depolarization); Phase II (repolarized but blocked; ACh receptors are available, but desensitized)

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7
Q

Does Phase I or Phase II reversal of blockade (due to succinylcholine) have an antidote? If so, what is it?

A

Phase I - no antidote; Phase II - antidote consists of cholinesterase inhibitors

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8
Q

What effect do cholinesterase inhibitors have on Phase I versus Phase II of reversal of (succinylcholine) blockade?

A

Phase I - No antidote. Block potentiated by cholinesterase inhibitors.; Phase II - antidote consists of cholinesterase inhibitors

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9
Q

What are 3 complications that may result from use of depolarizing neuromuscular blocking drugs?

A

Complications include (1) hypercalcemia, (2) hyperkalemia, and (3) malignant hyperthermia.

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10
Q

Name 6 nondepolarizing neuromuscular blocking drugs.

A

(1) Tubocurarine (2) Atracurium (3) Mivacurium (4) Pancuronium (5) Vecuronium (6) Rocuronium

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11
Q

What is the mechanism of nondepolarizing neuromuscular blocking drugs?

A

Competitive antagonists - compete with ACh for receptors

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12
Q

What class of drugs work in the reversal of blockade due to nondepolarizing neuromuscular blocking drugs? What are 2 examples of such drugs?

A

Cholinesterase inhibitors; Reversal of blockade - neostigimine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors

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13
Q

For what is neostigimine used in the context of neuromuscular blockade? What additional drug must be given with neostigime, and why?

A

Reversal of nondepolarizing neuromuscular blockade (as cholinesterase inhibitor); Must be given with atropine to prevent muscarinic effects such as bradycardia

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14
Q

What is the mechanism of dantrolene?

A

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

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15
Q

What are 2 clinical uses for dantrolene?

A

Used to treat (1) malignant hyperthermia and (2) neuroleptic malignant syndrome (a toxicity of antipsychotic drugs)

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16
Q

For which toxicity of antipsychotic drugs is dantrolene used?

A

Neuroleptic malignant syndrome

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17
Q

What causes Parkinsonism?

A

Parkinsonism is due to loss of dopaminergic neurons and excess cholinergic activity.

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18
Q

What are the 4 different strategies behind Parkinson disease drugs?

A

(1) Dopamine agonists (2) Increased dopamine (3) Prevent dopamine breakdown (4) Curb excess cholinergic activity

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19
Q

What are 3 examples of Dopamine agonists? Which type of Dopamine agonists are preferred for Parkinson disease?

A

(1) Bromocriptine (ergot) (2) Pramipexole (3) Ropinirole (non-ergot); Non-ergots are preferred

20
Q

What are 2 examples of Parkinson disease agents that work by increasing dopamine?

A

(1) Amantadine (may increase dopamine release) (2) L-dopa/carbidopa (converted to dopamine in CNS)

21
Q

By what mechanism can Amantadine be used for Parkinson disease? For what other conditions can it be used? What is a toxicity of Amantadine?

A

Amantadine (may increase dopamine release); also used as an antiviral against influenza A and rubella; Toxicity = ataxia

22
Q

What are 3 examples of Parkinson drugs that work by preventing dopamine breakdown?

A

(1) Selegiline (selective MAO type B inhibitor) (2) Entacapone (3) Tolcapone (COMT inhibitors - prevent L-dopa degradation –> increase dopamine availability)

23
Q

What is the ultimate effect of selegiline, and how does it accomplish this? For what disease is it used?

A

Prevent dopamine breakdown; Selegiline (selective MAO type B inhibitor): Parkinson disease

24
Q

What is the ultimate effect of entacapone, and how does it accomplish this? What other drug shares this effect and mechanism? For what disease are they both used?

A

Prevent dopamine breakdown; COMT inhibitors - prevent L-dopa degredaton –> increase dopamine availability; Tolcapone; Parkinson disease

25
Q

What type of drug is Benztropine? What is its ultimate effect? In what disease is it used?

A

Antimuscarinic; Curb excess cholinergic activity; Parkinson disease; Think: “Park your Mercedes BENZ”

26
Q

Again, what type of drug is Benztropine? What effects does it have in terms of alleviating Parkinson disease symptoms?

A

Antimuscarinic; Improves tremor and rigidity but has little effect on bradykinesia

27
Q

Name 5 drugs that can be used in Parkinson disease. In addition, what is used for essential or familial tremors?

A

(1) Bromocriptine (2) Amantadine (3) Levodopa (with carbidopa) (4) Selegiline (and COMT inhibitors) (5) Antimuscarinics; Think: “BALSA”; For essential or familial tremors, use a Beta-blocker (e.g., propranolol)

28
Q

What is the ultimate effect of L-dopa (levodopa)? How does it work, and how does it differ from dopamine?

A

Increase level of dopamine in brain; Unlike dopamine, L-dopa can cross blood-brain barrier and is converted by dopa decarboxylase in the CNS to dopamine

29
Q

What is carbidopa? What is its use in the treatment of Parkinson disease symptoms?

A

Carbidopa, a peripheral decarboxylase inhibitor, is given with L-dopa to increase the bioavailability of L-dopa in the brain and to limit peripheral side effects

30
Q

What is the clinical use of L-dopa (levodopa)/carbidopa?

A

Parkinson disease

31
Q

What is (more short-term) toxicity associated with L-dopa (levodopa)/carbidopa, and what causes it?

A

Arrhythmias from increased peripheral formation of catecholamines

32
Q

What is a long-term toxicity of L-dopa (levodopa)/carbidopa? What is this called? What occurs in between doses?

A

Long-term use can lead to dyskinesia following administration (“on-off” phenonmenon), akinesia between doses

33
Q

What is mechanism and effect of selegiline?

A

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

34
Q

What is the clinical use of selegiline? What is a toxicity to consider?

A

Adjunctive agent to L-dopa in treatment of Parkinson disease; May enhance adverse effects of L-dopa

35
Q

Name 4 Alzheimer drugs.

A

(1) Memantine (2) Donepezil (3) Galantamine (4) Rivastigmine

36
Q

What is the mechanism and effect of Memantine?

A

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

37
Q

What are 3 toxicities associated with Memantine?

A

(1) Dizziness (2) Confusion (3) Hallucinations

38
Q

What is the mechanism of donepezil? Name 2 other drugs that share this mechanism and can also be used for Alzheimer disease.

A

AChE inhibitors; Galantamine, Rivastigmine

39
Q

Name 3 AChE inhibitors that can be used for Alzheimer disease. What are 3 toxicities associated with them?

A

Donepezil, galantamine, rivastigmine; (1) Nausea (2) Dizziness (3) Insomnia

40
Q

What are 3 neurotransmitter changes in Huntington disease?

A

Decreased GABA and ACh, Increased dopamine

41
Q

Name 3 treatments for Huntington disease.

A

(1) Tetrabenazine and (2) Reserpine (3) Haloperidol

42
Q

What is the mechanism and effect of Tetrabenazine? Which other Huntington drug shares this mechanism and effect?

A

Inhibit vesicular monoamine transporter (VMAT); limit dopamine vesicle packaging and release; Reserpine

43
Q

What type of drug is Haloperidol, and for what condition is it used?

A

Dopamine receptor agonist; Huntington disease

44
Q

What is the mechanism of Sumatriptan, and what 3 effects does it have?

A

5-HT 1B/1D agonist. Inhibits trigeminal nerve activation; Prevents vasoactive peptide release; Induces vasoconstriction

45
Q

For what is Sumatriptan used clinically?

A

Acute migraine, cluster headache attacks; Think: “a SUMo wrestler TRIPs ANd falls on your HEAD”

46
Q

What are 2 toxicities associated with Sumatriptan? In what patient populations is Sumatriptan contraindicated?

A

Coronary vasospasm (contraindicated in patients with CAD or Prinzmetal angina), Mild tingling

47
Q

What is the half-life of sumatriptan?

A

< 2 hours

FA - Neurology (30 decks)

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