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Flashcards in local anesthetics, NMJ drugs, etc Deck (22):

structure of local anesthetics

end in "caine." may be esters or amides. amides have 2 "i"s in their name.


How do local anesthetics work? What about tertiary amines?

they preferentially block Na channels by binding to specific receptors on the inner portion of the channel. since they preferentially bind active Na channels, they work best with rapidly firing neurons. tertiary amines penetrate membrane in their uncharged for, then bind toion channels


What drugs are usually combined with local anesthetics and why?

vasoconstrictors, like epinpherine. these decrease bleeding, and also increase the local concentration of the local anesthetic


What is the order of sensation loss when using local anesthetics?

Pain, temperature, touch, then pressure
because they prefer small to large. within that preference, they prefer myelinated to unmyelinated.


What are the uses and selectivities of neuromuscular blockade drugs?

used for paralysis in surgery. they preferentially affect the nicotininc (not muscarinic) receptors)


What are some toxicities of local anesthetics?

CNS excitiation, CV toxicitiy, HTN, hypotension, arrhythmias (esp with cocaine)


MOA of succinylcholine?

strong ACh receptor agonist that produces sustained depolarization and prevents muscle contraction.


Reversal of blockade for succinylcholine and potential complications

during the prolonged depol, there is no antidote, and the block will be made more potent by chiolesterase inhibitors.
during the time when the the cells have repolarized but are blocked, the ACh receptors are available but desensitized. In this case, give cholinesterase inhibitors.
complications: hypercalcemia, hyperkalemia, malignant hyperthermia


How does tubocurarine work?

competitive antagonist of the nicotinic receptor that competes with ACh for receptors.


Reversal of tubocurarine

neostigmine (musch be given with atropine to prevent muscarininc effects like bradycardia), or other cholinesterase inhibitors


How does dantrolene work?

prevents the release of Ca2+ from the sarcoplasmic reticulum in skeletal muscle


Strategy for parkinsons disease

dopamine agonists (bromocriptine), increase dopamine (amantadine/L-dopa with carbidopa), prevent dopamine breakdown (selegiline), and curb excess cholinergic activity )antimuscarinics)


How do you treat essential/familial tremor

beta blocker


What should I know about amantadine: uses, MOA, toxicity

it may increase DA release, so it is used in PD. it is also used as an anti-viral against influenza A and rubella. it can cause ataxia


What should I know benzotropine?

it is antimuscarininc and improves tremor and rigidity in PD but doesn't have an effect on bradykinesia


Why is L-dopa given with carbidopa?

it is a peripheral decarboxylase inhibitor that increases the the bioavailability of L-dopa in the brain and limits peripheral side effects.


Side effects of L-dopa?

arrhythmias from peripheral formation of catecholamines. may lead to dyskinesia after administration and akinesia btw doses (on-off phenomenon)


MOA of selegiline?

selectively inhibits MAO-B, which preferentially metabolizes dopamine. However, it may increase the adverse effects of L-dopa


Classes of alzheimer drugs

memantine: NMDA receptor antagonist that helps prevent excitotoxicity.
donepezile (rivastigmine, galantamine): AChE inhibitors.


What are the neurotransmitter changes in huntington's disease?

Decreased GABA, decreased ACh, increased dopamine


Treatments for huntingon disease

reserpine (and tetrabenzine): inhibit vesicular monoamine transporter, which limits DA packaging and release (these pts have too much DA)
haloperidol: DA receptor antagonist


Sumatriptan: MOA, contraindications

5-HT agonist that inhibits trigeminal nerve activation and induces vasoconstriction. it is contraindicated in coronary vasospasm like Prinzmetal or CAD

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