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

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

Flashcards in Neuro - Pharmacology (Neuromuscular blocking, Parkinson, Alzheimer, Huntington, & headache drugs) Deck (47):

What are 2 uses for neuromuscular blocking drugs?

Used for muscle paralysis in surgery or mechanical ventilation.


For what receptor are neuromuscular blocking drugs selective?

Selective for motor (vs. autonomic) nicotinic receptor


What are the 2 types of neuromuscular blocking drugs?

(1) Depolarizing (2) Nondepolarizing


Give an example of a depolarizing neuromuscular blocking drug.



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

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


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

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


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

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


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

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


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

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


Name 6 nondepolarizing neuromuscular blocking drugs.

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


What is the mechanism of nondepolarizing neuromuscular blocking drugs?

Competitive antagonists - compete with ACh for receptors


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

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


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

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


What is the mechanism of dantrolene?

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


What are 2 clinical uses for dantrolene?

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


For which toxicity of antipsychotic drugs is dantrolene used?

Neuroleptic malignant syndrome


What causes Parkinsonism?

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


What are the 4 different strategies behind Parkinson disease drugs?

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


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

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


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

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


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

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


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

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


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

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


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?

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


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

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


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

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


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

(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)


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

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


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

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


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

Parkinson disease


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

Arrhythmias from increased peripheral formation of catecholamines


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

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


What is mechanism and effect of selegiline?

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


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

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


Name 4 Alzheimer drugs.

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


What is the mechanism and effect of Memantine?

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


What are 3 toxicities associated with Memantine?

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


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

AChE inhibitors; Galantamine, Rivastigmine


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

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


What are 3 neurotransmitter changes in Huntington disease?

Decreased GABA and ACh, Increased dopamine


Name 3 treatments for Huntington disease.

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


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

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


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

Dopamine receptor agonist; Huntington disease


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

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


For what is Sumatriptan used clinically?

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


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

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


What is the half-life of sumatriptan?

< 2 hours

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