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
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