Flashcards in PHARM SHIT YOU NEED TO KNOW Deck (191)
What NT does the somatic nerv sys use? And what is the effector organ?
AcH; skeletal muscle (motor)
What are the NTs for sympathetic inn to the smooth muscles, cardiac cells, and gland cells? Include pre-/postganglionic.
preganglionic = Ach
postganglionic = NE
What are the NTs for sympathetic inn to the sweat glands? Include pre-/postganglionic.
preganglionic = Ach
postganglionic = Ach
What are the NTs for sympathetic inn to the adrenal gland's medulla ganglion? Include pre-/postganglionic.
preganglionic = Ach
postganglionic = cells of the medulla which secrete epi/NE
What are examples of neurohormones?
vasopressin (ADH) & oxytocin
What effect does NE have on the heart? On the brain? On the eyes? In the intestine?
heart - inc HR, force, BP
brain - inc signals (inc alertness)
eyes - dilates pupil
intestine - inc sphincter tone (contracts) & relaxes mm--can cause constipation
*recall that NE is released during postgang sympathetics (w/ the exception of sweat glands & adrenal medulla)
what types of fibers/nerves are cholinergic?
1. pregang fibers of both sympathetic & parasympathetic nerv sys
2. postgang PS fibers
3. post gang sympathetic n for sweat gland
4. pregang sympathetic fibers to adrenal gland
5. somatic nn
What are some excitatory NTs?
dopamine, NE, epi, glutamate, acetylcholine
What are some inhibitory NTs?
serotonin, glycine, GABA, anandamide (this last one could also have excitatory effects--not sure yet)
What is anandamide?
endogenous cpd similar to marijuana that has anti-anxiety effects and related to bliss or delight
What are the events occurring during an erection involving NO and NE?
NE is released in blood vessels all the time, but when NO is released during erection, its effect overpower the vasoconstriction caused by NE until ejaculation. Then the NE overpowers the NO lowering the blood flow.
What does NO do?
opposes the excitatory actions of blood vessels (vasodilation, inc blood flow); in smooth muscle it will cause hypotension
What molecule does NO activate during an erection?
activates soluble guanylate cyclase
what does guanylate cyclase do?
synthesizes cGMP from GTP
_____ is believed to be the main vasoactive nonadrenergic, noncholinergic neurotransmitter and chemical mediator of penile erection
Nitric oxide (NO)
Acting as a second messenger molecule, ____ regulates the activity of calcium channels as well as intracellular contractile proteins that affect the relaxation of corpus cavernosum smooth muscle
What is released from terminals of specific sensory neurons and associated w/ inflamm and pain?
- it coexists w/ excitatory NT glutamate in primary afferents that respond to painful stimul.
- may be involved in neurogenic inflamm
calcitonin gene related peptides function?
potent vasodilator and can function in the transmission of pain. When CGRP is derived from DRG when synthesized in the dorsal horn of the spinal cord, it may be linked to transmission of pain.
what types of fibers/nerves are adrenergic?
postgang fibers of sympathetic sys (except for those innervating sweat glands--cholinergic nn)
*also adrenal medulla are modified sympathetic neurons that release epi/NE
what types of fibers/nerves are nitrergic?
postgang fibers innervating sex organs, some postgang fibers in intestine & lower esophageal sphincter
What enzyme converts NE to epi?
PNMT = phenylethanolamine N-methyltransferase
Metyrosine is used to treat what disease?
pheochromocytoma (tumor of adrenal gland)--secrete high amts of catecholamines
what is the rate limiting step of NE synthesis?
tyrosine hydroxylase step; used in tx for pheochromacytoma (drug: Metyrosine)
Issues w/ DOPA decarboxylase results in...? What is the tx for this?
degeneration of neurons in brain that release DOPA; L-DOPA or carbidopa
What is carbidopa used for?
Tx for Parkinson's; used in adjunct w/ L-DOPA
*carbidopa does NOT cross the blood-brain barrier, so it works in the periphery (reduces metabolism of L-DOPA in periphery)
*L-DOPA is in the periphery, but is not blocked completely in the brain--so it is more available there, if we reduced its metabolism in the periphery.
What is the main goal of the tx for parkinson's?
inc production of dopamine!
- this is done by increasing levels of DOPA by using L-DOPA & carbidopa.
- reduce DOPA metabolism in the periphery (you want more of it in the brain!)
Disulfiram is used to treat what?
alcoholism; inhibits actylaldehyde dehydrogenase; disulfiram chelates w/ Cu in dopamine-B-hydroxylase (enzyme that converts dopamine to NE), inhibiting it!
- you will accumulate acetylaldehyde if you use this drug... so if you drink and take this drug, you may get hypertension!!
What is reserpine? Tx for?
- an inhibitor of DA & NE uptake into synaptic vesicles (blocks VMAT)
- inhibits NE production bc blocked entry of dopamine into the vesicle
- also no storage of NE (depletes NE from nn)
- tx for hypertension & psychosis; to reduce agitation in horses
- does NOT interfere w/ uptake from nerve memb--only the vesicles!!
What is reserpine's effect in the brain?
depletes dopamine, NE, serotonin
*when they began to use reserpine to treat hypertension & psychosis, pts began to show suicidal tendencies.