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Pharmocology-Autonomics1.5/SANS/PANSoverview

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Question
Answer
SANS v PANS energy   SANS: not essential for life PANS:anabolic, esential for life  
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SANS v PANS dominant?   PANS dominant at rest  
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PANS efferent fiber origin?   craniosacral (CN 3,7, 9, 10) and sacral segs (2-4)  
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preganglionic PANS fibers?   long  
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postgang PANS fibers?   short  
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preganglionic fibers?   SANS: paravertebral ganglia on either side of SC PANS: ganglion cells distributed in networks or near organs  
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postganglionic fibers?   SANS: paravertebral ganglia on sides of SC to tissue innervated PANS: located on effector organs  
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PANS activity?   discrete and localized discharge  
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PANS princple neurotransmitter?   Ach  
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what systems lack duel innervation?   blood vessels  
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what neurotransmitter stimulates the nicotinic receptor at the adrenal medulla to release catacholamines?   Ach  
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what neurotransmiters do the adrenal medulla release?   NE (15%) and EPI (80%)  
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what drugs block NA channel?   local anasthetics, tetrodotoxin (puffer fish poison) and saxitoxin (shellfish poison)  
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what drugs increase permiability of Na channel to cause persistant depolarization?   batrachotoxin (s. american frog), and scorpion toxins  
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where does Ach work?   preganglionic PANS and SANS to nicotinic receptors. PANS postganglionic to muscarinic effector organ and few SANS effector cells. All somatic fibers use Ach.  
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hemicholinium and triethylcholine?   inhibit Ach synthesisby competing for choline uptake into presynaptic terminal  
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botulinum toxin?   block Ach release  
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black widow spider venom?   promote Ach release  
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Atropine?   blocks Ach activity at postsynaptic muscarinic receptors  
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Physostigmine?   inhibit enzymatic metabolism (Ache inhibitor)  
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where do catacholamines work?   NE work in SANS postganglionic to adrenergic receptors. EPI released from the adrenal medulla. DA is a CNS neurotransmitter.  
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catacholamine synthesis?   tyrosine to DOPA by tyrosine hydroxylase (RLS). DOPA to dopamine by aromatic aminoacid decarboxylase, then into storage granule. dopamine to NE by dopamine beta hydroxylase (nonspecific). NE to EPI by phenyl-N-methyltransferase in the AM cytoplasm.  
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what is catacholamine Uptake-1?   localized to presynaptic adrenergic terminal back into storage.  
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catacholamine uptake-2?   localized to non-neuronal tissues  
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enzymatic degredation of catacholamines?   MAO A and B ain the cytoplasm of the neuron. COMT for NT released from the adrenals that escapes the uptake-1 process. metabolites (MHPG, VMA, NMN)  
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destruction of Ach?   AchE to choline and acetate. Choline taken up by presynaptic terminal to reuse. Ach diffuses away. Butyrylcholinesterase can also hydrolyze Ach.  
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what is DA?   precursor of NE. NT in the CNS basal ganglia  
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what is 5HT?   CNS NT. regulate smoth muscle in cardiovascular and GI systems, platlet function  
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5HT synthesis?   tryptophan to 5-hydroxytryptophan by tryptophan hydroxylase. then to 5HT by dopa decarboxylase  
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how is 5HT metabolized?   MAO A and aldehyde dehydrogenase  
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alpha methyldopa, alpha methyltyrosine?   compete with enzymes to make false NT to inhibit storage of active NT.  
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reserpine, guanethidine?   inhibit, deplete storage of NE and DA.  
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guanethidine, bretylium?   reuptake-1, cause transient release of catecholamin followed by long lasting decrease in adrenergic activity.  
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clonidine?   acts at presynaptic adrenergic receptor to decrease NE release  
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imipramine, cocaine?   block uptake-1, reuptake of NE and DA  
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