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100 Cards in this Set
- Front
- Back
What NT do ALL preganglionic nerve fibers release?
What Receptor type does this act on? |
Ach
acts on nicotinic receptors |
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Where do preganglionic PNS nerves come from?
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Cranial sacral, CN's and S3/S4
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How long are postganglionic PNS fibers?
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very short
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What NT do postganglionic PNS nerves use?
On what receptor type? |
Ach
on Muscarinic |
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Where do preganglionic SNS nerves come from?
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T1-L2
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Where are pregnaglionic SNS cell bodies located?
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lateral horn of the gray matter
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Where do most pre-ganglionic SNS fibers terminate?
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in the paravertebral chain ganaglions
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How does the paravertebral chain fire?
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in a coordinated discharge
(this gives you the chill up your spine effect!) |
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What NT do post ganglionic SNS nerves that innervated sweat glands release?
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Ach
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What NT do post ganglionic SNS nerves that innervate renal vasculature release?
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Dopamine
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What NT do MOST Post-ganglionic SNS nerves release
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NE (nore epi)
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What place do pre-ganglionic SNS fibers go to, that releases Epi?
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the adrenal medulla
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What three places, is ACh released, acting on Nicotinic receptors?
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Pre-ganglionics of both SNS/PNS
Nerves to the adrenal medulla (causes epi release) and Motor neurons (NMJ) |
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What two places is ACh released, acting on Muscarinic receptors
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post-ganglionic PNS
sweat glands (from SNS) |
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Where is NE release from? What two receptor types does it act on?
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this is released from post ganglionic SNS fibers.
acts on Alpha and Beta 1 (NOT 2) receptors |
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Where is Dopamine released from? acting on?
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SNS nerves, acts on renal vasculature smooth muscle
(note, Dopaminergic nerves MUST lack dopamine-B-hydroylase to prevent it begin converted into NE!) |
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What functions does the myenteric plexus control?
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this controls the muscle functions, contraction and relaxation
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what functions does the submucosal plexus control?
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this controls secretions, absorption, and blood flow
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What does Vagal input do to the enteric nerves? what NT?
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this uses ACh, and is excitatory.
causes stimulation of smooth muscle motion, AND secretions |
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What does sympathetic input to the enteric nerves do? What NT?
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this uses NE, and is inhibitory on GI motion
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What does PNS and SNS overall do to the GI tract?
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this is modulatory, GI activity can occur in the absence of these signals
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What is the major intrinsic transmitter in the GI system? what does it do?
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Serotonin (5-HT) is the major intrinsic transmitter. this si excitatory- increase GI motility and activity
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What does NO do to the GI tract?
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this is inhibitory
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What are the 3 major inhibitors of GI motility?
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NO
VIP ATP (on a P2Y) |
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What 3 things are released with ACh to excite the GI system?
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Substance P
Neurokinin A ATP (on P2X) |
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What does the compound Vesamicol do?
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this blocks TRANSPORT of ACh into Vesicles
(vesicle- may-clot-, clots block things) |
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What does botulinum toxin do
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this blocks the RELEASE of ACh (which messes with the snaps and snares)
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What drug blocks Choline reuptake (to be repacked into ACh by choline acetyltransferase)
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Hemicholinium
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What is the rate limiting step in NE synthesis?
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Tyrosine-> L-dopa (done by tyrosine hydroxylase)
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What drug blocks the tyrosine-> L dopa conversion?
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metyrosine
(this is just a methylated tryosine, and thus blocks the conversion! just like hemicholinium blocks choline transport- look for a random molecule stuck on the intended molecules name) |
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What regulates (increases) the expression of tyrosine hydroxylase (and this NE production)
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this is increased during increased SNS activity (SNS activity goes up, needs more NE, induces tyrosine hydroxylase)
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What slows down tyrosine hydroxylase activity?
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NE feed back through presynaptic alpha 2 receptors
(as all alpha 2 receptors are inhibitory) |
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Where are the catecholamines stored (DA, NE, Epi)? by what?
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these are store in vesicles by VMAT (vesciular monoamine transporter)
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What prevents VMAT's actions?
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reserpine
(causes all the catecholamines to Re surface, rather than be stored) |
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What terminates the actions of NE in a normal cleft?
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NET (NE transporter)
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What drugs block the reuptake of NE?
(both illicit and prescription) |
antidepressants and cocaine
|
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What do amphetamine, ephedrine, and tyramine do in a nerve terminal?
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these get taken up by NET, into vesicles by VMAT. pushing NE and DA out- where they are released by NON-Ca+ dependent process
(maybe this could be blocked by Reserpine?) |
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What must be intact for Amphetamine to work?
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the noradrenergic innervation (aka the presynaptic process)
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What two enzymes break down NE?
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Monoamine Oxidase
and Catechol-O-methyl Transferase |
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Where is MAO located?
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on the outer surface of mitochondria in the nerve terminal
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Where is COMT located?
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most places in the body (especially the liver)
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What metabolite does a urine test for NE and EPI look for?
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VMW
(NE/EPI are hormones you would have in your body when your all jacked up driving your BMW (or VMW) fast!) |
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What metabolite does a urine test for Dopamine look for?
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HVA
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Where are M1 receptors found?
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in the CNS, and exocrine glands
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What do M1 receptors do? mechanism?
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these are Gq, PLC-> IP3/DAG. increases calcium and depolarizes the cell
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Where are M3 receptors?
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these are found in exocrine glands, smooth muscle, and endothelium.
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What is the mechanism of M3 receptors?
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Gq, PLC-> IP3/DAG, increased Ca2+ and depolarizing.
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Where are M2 receptors found?
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Heart, some smooth muscle, and Presynaptically
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What is the mechanism of M2 receptors?
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these are Gi,- inhibit adenylyl cyclase, lower cAMP.
Opens K+ channels, and Hyperpolarizes cells |
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How does M2 receptor affect heart rate?
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this SLOWS heart rate, by hyperpolarizing the cells reducing thier NT release rate
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Where are N(n) receptors found?
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autonomic gangila and adrenal medulla
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Where are N(m) receptors found?
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in skeletal muscle
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What do ALL nicotinic receptors do?
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these ALL open Na+ channels and depolarize neurons or muscle cells.
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What is the mechanism of alpha 1 receptors?
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these are Gq (PLC, IP3, DAG)
depolarizes the cell Excititory |
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What is the mechanism of Alpha 2 receptors?
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Gi
this inhibits adenylyl cyclase, decreasing cAMP levels Inhibitory |
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What is the mechanism of Beta 1 receptors?
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These are Gs, they increase cAMP, and are excitiory
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Where are B1 receptors found?
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these are found are pre and post synaptic sites on the heart
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where are alpha 1 receptors found?
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these are found in smooth muscle
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where alpha 2 receptors found?
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these are found in presynaptics, platelets, lipocytes, and smooth muscle
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What is the mechanism of Beta 2 receptors?
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these are Gs, stimulated adenylyl cyclase
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Where are B2 receptors found?
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smooth muscle, bronchioles, heart
(may stimulate, OR relax depending on the tissue) |
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Where are B3 receptors found, mechanism?
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these are found on lipocytes.
Gs (like all B's) |
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Where are D1/D5 receptors located?
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these are in the brain and renal vascular bed
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Where are D2,D3,D4 receptors located?
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brain and other random tissues
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What is the mechanism of action of D1, D5 receptors?
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these stimulate adenylyl cyclase, increasing cAMP
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What is the mechanism of action of D2, D3, D4 receptors?
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these inhibit adenylyl cyclase
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What is the end result of increased intracellular cAMP?
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activates PKA, and thus intracelular enzymes
Ion channels Ca2+ and K+ and contractile proteins |
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What 3 receptor types are linked to Gq?
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M1, M3, and A1 (PLC)
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What 2 receptor types are linked to Gi?
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M2, A2 (inhibits adenylyl cyclase)
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What receptors are linked to Gs?
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all beta receptors (stimulate adenylyl cyclase)
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What two receptor types inhibit NE release from presynaptic terminals?
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Alpha 2a, and Alpha 2c
(these are auto receptors, as they prevent the release of the NT that binds them) |
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What receptor types increase NE release from presynaptic terminals?
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presynaptic B receptors
(these are auto receptors, as it promotes the release of the NT that binds it) |
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What do presynaptic M2 receptors on noradrenergic terminals do?
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these DECREASE NE release
(called a heteroreceptor- as it uses a different NT than the one it regulates) |
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What input do blood vessels primarily receive?
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SNS input
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What innervates sweat glands
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SNS releasing ACh
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Where are M2's located on the heart? What do they do?
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Located at the Atrium.
Decrease SA node HR Slows AV conduction (PNS) |
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What do M2/ M3 receptors do to the lungs?
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these cause Bronchoconstriction, especially in asthmatics
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What do B1/B2' receptors do in the heart?
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These increase Heart Rate,
Automaticity, and Contractility |
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What do B2 receptors do in the lung?
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these respond to circulating EPI
relax bronchioles (epi pen!) |
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What do B2 receptors do in skeletal muscle?
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these relax BV's here, increasing blood flow.
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What do B2's do in coronary arteries?
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these dilate coronary arteries
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What do Alpha 1's do to skin BV's?
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the SNS acts on Alpha 1's (Gq) to Constrict blood vessels in skin, and constrict veins.
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What do M3's do to salivary and lacrimal glands?
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these cause profuse secretion (PNS)
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What do M3 receptors do to the eye?
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(PNS)
MIosis, contraction of ciliary muscle- for near vision (and reduces intraocular pressure) |
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What type receptors incruease sweating?
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M1/M3 (SNS)
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What do Alpha 1's do to the eye?
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(SNS)- these constrict the radial muscle, DILATION of the pupils
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What do alpha receptors do in the nose?
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these cause vasoconstriction in nasal passes- reducing swelling, allowing decongestion
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What Parasympathetic receptor is in the bowel and bladder? 4 man actions in these regions?
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Contraction of GI
Secretion in GI Contract bladder- peeing promote erection M3 receptors for all |
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What SNS receptor promotes ejaculation?
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Alpha 1
|
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What SNS receptor promotes Renin release?
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B1
|
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What does the SNS do to the bowel and bladder?
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Relaxes GI tract, decreases secretions
Relaxes bladder/uterus Contractions sphincters in the bladder |
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What 3 metabolic effects are related to SNS stimulation?
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glycogenolysis
Lipolysis potassium uptake in skeletal muscle |
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What does a Fast infusion of NE do to BP? how?
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this is a vasopressor via Alpha 1's which constrict BV's.
Rapid NE also causes B1 to increase HR. This creates a Large BP increase |
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What does a Slow infusion of NE do to BP? how?
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This still constricts BV's via Alpha 1 receptors,
but there is compensation- with decrease SNS outflow, and increased PNS input. Results in Bradycardia... So increase BP, but not too much. |
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What causes Miosis? For what range of vision?
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Cholinergic input (PNS)
used for near vision |
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What agents are used to treat glaucoma? why?
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cholinergic (PNS) ones, these contract the ciliary muscles, increasing outflow and decreasing intraocular pressure.
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What is cycloplegia?
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this is ciliary muscle blocked by cholinergic antagonists (so no pupil constriction or near vision accommodation)
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What do alpha receptors do to the eye?
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these cause Mydriasis (pupil dilation)
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What class of drugs can lower interocular pressure by limiting aqueous humor production?
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beta blockers
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What do Beta receptors do the aqueous humor?
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these increase production of aqueous humor
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