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176 Cards in this Set
- Front
- Back
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what receptor does the eye use in sympathetics
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a1
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what muscle is affected by the sympathetics in the eye
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contraction of the dilator pupillae (radial muscle. receptor a1. this leads to pupil dilation (mydriasis)
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what is the sympathetic response of the heart
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up cardiac output. via B1. up heart rate and up force of contractility
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what is the sympathetic affect on bronchi
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relaxation of smooth muscle. lead sto broncho dilation via receptor B2
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what sympathetic receptor is on the bronchi
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B2
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what sympathetic receptor is on the heart
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B1
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what sympathetic receptor is on the uterus
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B2
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what sympathetic receptor is on the GIT
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B2 for relaxation of the git
A1 for the contraction of sphincters |
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what sympathetic receptors are found in the bladder
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B2-relaxation of the detrusor
A1-contraction of the trigone(which prevents retrograde ejaculation) |
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what sympathetic receptors are found in the genitourinary smooth muscle
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A1-does ejaculatioon and contracts the vas deferens
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what parasympathetic receptors are on the heart
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M2-slows sa node
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what cns control cener monitors temperature and osmolality
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hypothalamus
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what autonomic center monitors visual (pupil diameter, accomodation)
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the midbrain=edinger westphal nucleus
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what autonomic control center in the cns monitors cardiovascular parameters such as BP, HR, respiratoion, rate and depth
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medulla-NU tractus solitarisCVS
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is parasympatheitc nervous system anarobolic or catabolic
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it is anarobolic-it conserves and stores energy
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what are the 4 parasympathetic cranial nerves
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3, 7, 9, 10
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what is the only cns cranial nerve
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cranial nerve 2
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what type of receptors are on the effector target organ of parasypmatheitc NS
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muscarinic-M1-M3
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what type of receptor is on the postganglionic PS neuron
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N2 nicotinic
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what is released at the neuroeffector junction n parasymp cholinergic system
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ACH and also VIP
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what type of recewptor is on the skeletal muscle of the somatic nervous system
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N1 nicotinic (neuromuscular junctions)
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what type of receptors are on the target organ in sympathetic nervous system
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alpha and beta
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what is released in sympathetic NS at both ganglia
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ach at pre and NE at post
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what typ eof nerves are found at the presynaptic terminal of the adrenal medulla
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those nerves are pelvic splanchnic- there is no postganglionic essentially becasue the adrenal medulla functions as the postganglionic releasing epinephrine into the blood.
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what type of receptors are on the target organ in sympathetic nervous system
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alpha and beta
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what does the adrenal medulla release into the systemic blood system
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epinephrine
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what is another word for nicotinic nachr
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ionotropic
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what is released in sympathetic NS at both ganglia
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ach at pre and NE at post
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what type of tropic receptor are muscarinic machr
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metabotrpic and they are all g protein linked. metabotropic g proteins are slower than ionotrpic
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what typ eof nerves are found at the presynaptic terminal of the adrenal medulla
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those nerves are pelvic splanchnic- there is no postganglionic essentially becasue the adrenal medulla functions as the postganglionic releasing epinephrine into the blood.
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what does the adrenal medulla release into the systemic blood system
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epinephrine
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M2 are receptors for the ...?
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Heart
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what is another word for nicotinic nachr
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ionotropic
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M3 are receptors for the ...?
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smooth muscle and glands
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what type of tropic receptor are muscarinic machr
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metabotrpic and they are all g protein linked. metabotropic g proteins are slower than ionotrpic
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M2 are receptors for the ...?
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Heart
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what do M1 receptors do
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they are in the cns and they are on autonomic ganglia where they mediate slow excitatory response
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M3 are receptors for the ...?
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smooth muscle and glands
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what are the otehr things released via cotransmission at the autonomic ganglia
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neuroactive peptides such as enkephalin, Subs P, GnRH
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what do M1 receptors do
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they are in the cns and they are on autonomic ganglia where they mediate slow excitatory response
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what are the otehr things released via cotransmission at the autonomic ganglia
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neuroactive peptides such as enkephalin, Subs P, GnRH
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what g protein is associated with M1 and M3
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Gq-
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What does Gq do in muscarinic transmission
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it activates phospholipase C which enhances IP3 and DAG which leads to an increase in Ca++ and PKC
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what g protein is associated with muscarinic M2 transmission
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M2 is found in cardiac muscle and is the Gi protein
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what does the Gi protein do in muscarnic cardiac muscle
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it lowers adenylate cyclase which will lower camp which will lower CA++ conductance. this will lead to the inhibition of cardiac muscle excitability at he SA node and will lower the HR
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what is the parasympathetic response in the eye
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during PS the eye does contraction of the sphincter pupillae (circular muscle) as well as contraction of th eciliary muscle (so the lens becomes more convex)------this leads to pupil constriction called miosis and near vision accomadation. all this is done with the M3 receptor
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what receptor is on the eye for parasymp
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M3
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what happens to the salivary glands in paraympathetic activity and what receptor is on the salivary glands
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secretion will be enhanced and it will be the M3 receptor
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what happens to the bronchi during PSymp activity
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contraction of the smooth muscle via the M3 receptor
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what happens in pSymp activity to the heart and what receptor is affected
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in ps the HR drops and you have brachycardia. this is done via the M2 receptor
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what happens to the git during parasymp activity and what receptor is in the git for ps
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M3 receptor and you have contraction of git muscle but relaxation of sphincters
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what happens during pSymp activity in the urinary bladder
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the M3 receptor is stimulated and you have contraction of the detrusor muscle and relaxation of the sphincter
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what happens in parasympathetic activity in the sweat glands
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secretions go up so you have more sweating and more heat loss. all on M3 receptors
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what happens in endothelial cells of blood vessels in parasympathetic activity
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release of NO and vasodilation via M3 receptors
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what happens in parasympathetic activity to the external genitalia
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you get an erection due to vasodilation of blood vessels on M3 receptors
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how does an erection occur in the corpora cavernosum
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ach and No are released at the post ganglionic parasymp junction where the ach binds to M3. the M3 enhances DAG and IP3 which then enhabces iNOS. the iNOS combines with the NO (all of this is inthe endothelial cell. then the NO which gets enhanced by the iNOS goes into the vascular smooth muscle cell and enhances GTP to cGMP via guanalate cyclase. so you now have lots of cGMP which leads to relaxation and vasodilation
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what is sildinafil
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it is viagra-it blocks the phosphodiesterase activity which is when the cGMP gets broken down. so if it doesnt get broken down then you have prolonged relaxationa nd vasodilation.
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what things are released at the effector organ end of the sympathetic system
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neuropeptide Y, ATP, NE. these are released onto a1, a2, B1, B2, B3 receptors. there are also a2 receptors on the presynaptic terminal of the postganglionic sympathetic fiber
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what kind of transmitter i released from the postganglionic neuron of a sweat gland
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there is NO postganglionic neuron in a sweat gland. dont forget this you idiot
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what is the sympathetic response of the eye
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contraction of the dilator pupillae (radial muscle) this leads to mydriasis or pupil dilation (receptor a1)
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whjat sympathetic receptor is on the eye
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a1
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what sympathetic receptor is found on the heart
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B1
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what is the sympathetic repsonse in the heart
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up HR and velocity-up force of contraction so you have increased cardiac output. B1 receptor
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what happens to the bronchi in sympathetic activity
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relaxation of smooth muscle leading to bronchodilation. B2
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what sympathetic receptors are found in the bronchi
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B2
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what is the sympathetic response in the uterus
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relaxation of smooth muscle leading to uterine relaxation. B2
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what sympathetic recptor is on the uterus
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B2
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what receptors are found in the GIT for sympathetics
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B2 for motility and tone --------a1 for contraction of sphincters
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what receptor is found in the bladder for sympathetics
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B2 and a1-----B2 for the relaxation of the detrusor muscle and a1 for the contraction of the sphincters (trigone) the a1 contraction prevents retro grade ejaculation
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what receptors are found in the genitourinary smooth muscle for sympathetics
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a1-it contracts the vas deferens leading to ejaculation
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if you have a1 you do what to blood flow
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lower blood flow
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what happens to blood flow with B2 receptors in sympathetics
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increase blood flow
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what receptors are found inthe pancreas for sympathetics
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a2 and b2- these lead to lower insulin release which leads to enhanced glucose conc
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what receptors are found in the liver for sympathetics
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B2- ups glycogenolysis which leads to uped glucose
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what sympathetic receptors are found on skeletal muscle
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B2- increased glycogenolysis and uped glucose
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what sympathetic receptors are found on adipose tissue
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B2, B3--these lead to uped lipolysis which leads to uped free fatty acids in the blood
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wehat ion is increased with the binding to a1 receptors in sympathetics`
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calcium
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what are the efects of NE on adrenergic receptors (specifically on a1)
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Ne activates a1 to activate Gq to activate phospholipase C which leads to contraction through the ehnacement of DAG to PKC and also via another route of enhanced IP3 to enhanced Ca++- both end routes lead to smooth muscle contraction
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what happens specifically to smooth muscle in B2 activation
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B2 activation results in phshporylation of myosin light chain kinase and the RELAXATION of smooth muscle
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where do we find sympathetic B1 receptors
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Heart and kidney
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what g protein is associated with B1 and what is the action of it
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Ne on B1 activates Gs- the Gs enhances adenylate cyclase to make more camp from atp and that increases ca++ and PKC
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what action does B1 activation have on the kidney
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ups renin release
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what action does B1 activation have on the heart
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ups HR and force of contraxction
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what g protein is associated with a1
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Gq
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what g protein is associated with B2
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Gs
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what does B2 do.
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relaxation of smooth muscle
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how does B2 do smooth muscle relaxation
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two ways---first. B2 to Gs toincreased adenylate cyclase activity increasing camp from atp leading to increased ca++ adn PKA. at the same time Gs to opening of K+ channels. the second way is simialr to the first in that B2 to Gs to uped Camp to uped Ca++ to uped PKA to phosphorylation of MLC kinase which lowers the affinity of Ca++ to calmodulin which leads to muscle relaxation
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what is the action of B3 receptors
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in adipose tissue which operate via Gs proteins and leads to increased lipolysis and more energy availability
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what do a2 receptors do in the pncreas
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via Gi they decrease adenylate cyclase activity leding to decreased ca++ in the B cells of the islets . this leads to less insulin release and more glucose stores (this is all postsynaptic but remember that a2 is also found on the presynaptic terminal)
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what does a2 do on the presynaptic terminal
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the a2 receptor on the presynaptic functions to regulate the further release of NE into the synaptic cleft by negative feedback.
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what is the receptor on sweat glands for sympathetic cholinerfgic
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M3. remember there is no postganglionic neuron in a sweat gland- activation of M3 leads to uped sweating. a cholinergic antagonist would lower sweating
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in general what do a1 receptors do
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contraction-(bld vessels, vasoconstriction, ejaculation, radial of eye)
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in general what do a2 do
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two things- lead to th elowering of insulin release in the postsynaptic and leads to the negative feedback of NE from the presynaptic terminal
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what do B1 receptors do in general
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in the heart they in crease HR and contractility. inthe kidney thye lead to increased renin release
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what do B2 receptors do in general
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relaxation (example-bronchial smooth muscle dialtion, uterus relaxation, and liver glycogenolysis
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what aree the three functions of cholinergic transmission in the cns
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arousal and attention, cognitive function, memory retention---all via basal nucleus of meynert. these neurons are affected with dimentia. you can help fix dimentia with increased ach
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what two components make ach
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acetyl coa +choline via choline acetyltransferase
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what breaks down acetycholine
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acetylcholinesterase
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what is a snare
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in the nerve terminal when ca++ channels open to evoke th erelease of ACH the snares adn syntaxin help the vesicle fuse with the presynaptic membrane
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what happens if there is too much ach at the nmj
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muscle weakness and apralysis due to nodissociation and muscle flexion which does not release
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what are the two ways ach can lead to paralysis
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slow ach release from resynaptic terminal or delayed dissociation and degradatioon of ach in the nmj
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when a cholinesterase breaks down acetylcholine what two things are formed
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choline+acetate
ythe choline is recycled back into the presynaptic terminal |
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what is the action of botulinum toxin
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prevents the release of ach form the presynaptic terminal by preventing the fusion of the vesicle to the membrane- this leads to paralysis and muscle weakness
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what two diseases use botulinum toxin (clostridium botulinum) for cures
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dystonias(spasmodic torticollis)
inject (small amounts) into any spastic muscle |
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what are the two main types of anticholinesterases
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reversible and irreversible (organophosphates)
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what does an anticholinesterase do
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prevents the breakdown of ach in the nmj- this can lead to muscle weakness or the excess ach can mimiic parasympathetic affects
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what are the three main reversible anticholinesterases
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Edrophonium
physostigmine neostigmine |
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wehat is neostigmine
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reversible anitcholinestersase=not lipid soluble so it cannot cross the BBB
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what is Physostigmine
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highly lipid soluble reversible anticholinesterase- it can cross the blood brain barrier
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what is edrophonium
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reversibler anticholinesterase which is very very short acting
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what is myasthenia gravis
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autoimmune disorder where antibodies formed ower the number of nACHR rec on skeletal muscles whch lowers the ability of skeletal muscles to be activated.
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how do you treat myasthenia gravis
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get more ach in the nmj by using anticholinesterases ---especially Neostigmine. this can cross the bood brain barrier. you can initial test with fast acting edrophonium.
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what are the adverse affects of reversible anticholinesterases
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the increased ach can mimic parasympathetic activity and can lead to increased salivation, diarreah, and a slow heart rate (bradycrdia)
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how do you treat glaucoma
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give a reversible anticholinesterase to cause miosis which will increase the outflow of aqueous humor to lower the intraoccular pressure
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how do you relieve abdominal pain
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give a reversible anticholinesterase so that the M3 receptors in the GIT are activated and the smooth muscle is activated which ups th emotility of the gut
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what is atropine
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atropine is a competitive antagonist at the muscarininc receptors. if you give anticholinesterse then the ach can overcome the atropine and out compete the atropine
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what drug do you give to fix atropine poisoning
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physostigmine (crosses BBB)
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what is alzheimers
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deficiecy of cholinergic neurons in the cns
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what drug do you give to treat alzheimers
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Rivastigmine- it is a anticholinesterase which will lead to more ach in the cleft but it only is affective for 6 months
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what are the two main irreversible anitcholinesterases
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Parathione
DFP diisopropylflourophosphate |
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what happens to the ACHe molecules with irreversible anticholinesterases
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due to a covelant bond there must be new ACHe molecules synthesized- you can give the antidote of Pralidoxime as a cholinesterase reactivator
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what is Pralidoxime
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antidote to irreversible anticholinesterases to help restore some ACHe function
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what is the active ingredient in pesticides
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Parathion
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WHat does parathion do to the body
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it is an irreversible anticholinesterase which leads to paralysis of respiratory muscles unless you give atropine to block the muscarinic affects or if you give pralidoxime to reazctivate cholinesterase enzyme
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what are the two main ingrediaents of weapons of mass destruction of chemical warfare
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sarin
tabun both are irreversible anitcholinesterases which can be rversed with atropine or pralidoxime |
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what are two main drugs which are agonists at the cholinergic receptor
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succinylcholine (nicotinic agonist)
carbachol (muscarinic agonist) |
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what is muscarine
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amanita muscaria mushroom
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what does a succinylcholine do
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it is a depolarizing blocker-it activates the nachr receptor to excessivity so the ache takes longer to break down the ach which will eventully due to excessive stimulation lead to desensitisation of the nACHr which leads to muscle paralysis-
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what is the main use of succinyl choline
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used to paralyse muscles during surgery for tracheal intubation
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how do you achieve flacid paralysis
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give nicotinic antagonists- this makes the Nm receptors on skeletal muscle prevent ach binding- you can overcome it by simply giving ach
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what is d tubocurarine
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it is arrow poison which is more selective on neuromuscular nicotinic receptor than on ganglionic nicotininc receptor- so you can relax muscles during surgery but you must put patient on respirarator ---d tubo is a nicotinic antagonist
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can you overcoem the affects of succinylcholine with anticholinesterases
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NO
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can you overcome the affects of d tubocuraraine
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yes=with neostigmine
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when should you give muscarininc agonists
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to help with glaucoma/ restore git function after surgery/ treat xerostomia
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what drugs do you give to treat glaucoma
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Carbachol- it is a mitotic agent which is resistant to cholinesterase
PILOCARPINE-mitotic agent and increases saliva secretion |
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what is a parasympatholytic
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blocks the affects of the para system by binding to th emuscarininc receptors and prevent ach from exerting its affects
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what does atropine do
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it is a uscarinic receptor anatagonist which does pupil dilation/ tachycardia/ and lowers secretions. so it essentially does sympathetic type stuff
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when do you use atropine
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for eye exams as a mydriatic or to reverse slow heart rate/ or to lower salivation or to counteract mushroom muscarine poisoning
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what is the biosynthesis pathwya of catecholamines
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tyrosine to
DOPA to Dopamine to NorEpinephrine to epinephrine |
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where is norep turned to epineph
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adrenal medulla
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how is NE stored in vesicles
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VMAT=cesicular monoamine transporter (uptake 2)-----the vmat uses the H+ gradient generated by the H+/atpase to transport DA and recycled NE into vesicles
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what does the VMAT transport
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all monoamines=not very specific=NE, EPI, DA 5HT
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what controls for the majority the sympathetic outflow
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the limbic system and the hypothalamus
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what is MAO
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it is metabolism of NE which is found in the nerve terminals (an example is vanillyl mandelic acid)
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what is COMT and what does it do
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it is found in the liver and it metabolises NE which escapes fromt he synaptic cleft
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what are the three ways NE gets reuptaken
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Uptake 1 by NET
MAO in nerve terminal CVOMT in liver |
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what is the action of a1 in post synaptic transduction
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a1-Gq-up IP3 and DAG- p Ca++(from IP3) and up PKC (from DAG)--then the uped ca++ causes phosporylation of myosin and calmodulin acticvity which leads to contraction of smooth muscle
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what is the action of a2 in post synaptic transduction
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a2-Gi-lowered adenylte cyclase leading to lowered camp or...
openning of K+ channels for hyperpolarization or... closing of neuronal ca++ channels which lowers NE release |
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what is the action of B1 in post synaptic transduction
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B1-Gs-uped adenylate cyclase- uped camp-uped PK's=more phosphorylation of ca++channels
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what is the action of B2 in post synaptic transduction
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B2-to Gs to up adenylate cyclase to uped camp to uped PKA to phosphrylation of MLCKinase which leads to csmooth muscles relaxation and ...
at the same time Gs to opened K+ channles - to hyperpolarization- to smooth muscle relaxation |
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overall does NE casue more or less free energy and glucose
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more. it causes more energy to be available
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where is NE released from
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sympathetic nerve terminals
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where is epinephrine released
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into blood from adrenal medulla
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norepinephrine mainly affects which receptors
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a1 and B1
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epinephrine mainly affects whcih receptors at high an flow concentrations
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low conc= B1 B2
high conc=a1 |
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what does NE do to diastolic and systolic BP
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it raises both of them---give norep for circulatory collapse and shock
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what does EPI do to both diastolic and systolic BP
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epi raises systolic but lowers diastolic BP
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what happens when there is an inhibition of catecholamines storage in vesicles
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short term it mimics sympathomimetic becasue lots of NE gets out but long term your stores are depleted (sympatholytic effect)
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how do amphetamines affect catecholamines
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they are inhibitors of storage bydisplacing the catecholamines from the vesicles and also by inhibiting the MAO-they also block NET and DAT-----all of which lead to more NE in cleft also more Dopamine in cleft
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what are the uses of amphetamines
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narcolepsy=
ups alertness lowers fatigue lowers apetite gives you insomnia |
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what is pseudoephedrine
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over the counter lesser version of amphetamines-decongestant in cold medicines
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what is methylphenidate
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ritalin=structural analog to amphetamines-improves attention id ADHD patients
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how does cocaine affect the catecholamines
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it is an inhibitor of catecholamine reuptake-so it prolongs the action of the catecholamines in the cleft. it is a potent inhibitor of NET.
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imipramine
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tricyclic antidepressant (inhibitor of catecholamine reuptake)
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what do tricyclic antideptressants do
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they block serotonin (5HT) reuptake. they aslo block muscarininc alpha receptors and histmaine receptors
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what is the drug which inhibits the synthesis of Ach
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Hemicholinium
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what does hemicolineum do
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inhibits the synthesis of Ach by compteting with choline for transport into the cholinergic nerve terminal
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name a drug which inhibits the release of ach
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botulinum toxin "botox"
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what is botox's mode of action
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inhibits release of ach from cholinergic nerve terminals by preventing fusion of the synaptic vesicle with the preseynaptic nerve membrane- you can use these with spasms like spasmodic tortilcollis
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what are three main reversible anticholinesterases
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physostigmine/ neostigmine/ edrophonium- they act by bindng to the active site on the cholinesterase
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which reversible anticholinesterase can cross the blood brain barrier
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physostigmine
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what is myasthenia gravis
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autoimmune disease in which the body produces antibodies that attack the nicotinic skeletal muscle receptors which reduce there number
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what is the tensilon test
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when you suspect a patient with myasthenia grvis you have them do a fatiguing activity like steps and then give ephodrium and if it gets better you know they have MysGrav
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what does the alkalai light chain do in the myosin filament
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it is involved in myosin actin interaction
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what does the regulatory light chain in myosin do
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it is involved in the atpase activity to hydrolyze atp
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what do troponin T,I,C do
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t=binds troponin to tropomysoin
I=binds tropomy/troponin complex to the actin C=binds calcium |
