Lec 11 Autonomic Nts

Front 1

Different btwn pre-GN and GN fibers

Back 1

Pre-GN are myelinated and post-GN are not

Front 2

SNS and PS difference

Back 2

Other than function, SNS preGN to GN cell ratio is 1:20 with extensive overlap, while PS is 1:1

Front 3

Botuline does what

Back 3

inhibits vesicle fusion and hence no release of ACh

Front 4

What inhibits Choline uptake

Back 4

hemicholinium

Front 5

Mechanism of alpha 1

Back 5

via Gq

Front 6

Mech of alpha 2

Back 6

Gi

Front 7

Mech of beta 1, beta 2 and D 1

Back 7

Gs via increase AC and cAMP

Front 8

What blocks uptake of Dopamine into vesicle inorder to make NE

Back 8

resurpine

Front 9

What causes lipolysis in the fat cells

Back 9

SNS through beta 1 receptor

Front 10

vasodilation

Back 10

beta 2 and D1

Front 11

glycogenalysis receptors

Back 11

alpha 1 and beta 2, beta being dominant one (in liver and muscle)

Front 12

Epi action on vessels

Back 12

low dose: beta 2 are more sensitive than alpha one, so causes vasodilation
High Dose: alpha 1 predominates, causing vasoconstriction

Front 13

NE action's on which receptors?

Back 13

alpha 1 and 2, and beta 1. Not much on beta 2

Front 14

Isoproterenol action's on which receptors?

Back 14

beta 1 and beta 2 with little effect on alpha receptors... resulting in low BP

Front 15

How is Isoproterenol different than EPI?

Back 15

less hyperglycemia compared to EPI

Front 16

Dopamine effect's on what receptor?

Back 16

Low Dose: D1 in kidney, Beta 1 in heart
High Dose: stimulate alpha receptors

Overall: high HR, High MCF, High CO

Front 17

Dobutamine effect's which receptors?

Back 17

Beta 1 only resulting in higher MCF and HR

Less stimulation of HR than ISOP... so less arrhythmias than EPI, ISOP and DA

Overall: little effect on BP... just increase in contractility (better in a sick heart).

Front 18

compare EPI and NE

Back 18

EPI activates all receptors, resulting in overall decrease in TPR, with increase in Systolic and decrease in diastolic pressure.

NE causes overall increase in TPR as no beta 2 receptors are activated. both syst. and diastolic go up.

Front 19

Dopamine receptor dose effect

Back 19

going from low dose to high; D > beta > alpha.

Front 20

Bulky structure of a sympathomimetic amines does what?

Back 20

makes it more beta agonistic

Front 21

removal of OH group from catechol does what?

Back 21

makes it more CNS penetrative

Front 22

What's the significant of catechol group as far as breaking it down?

Back 22

these are needed so that the OH group can be methylated by COMT. So, ephedrine, phenylephrine, amphetamine etc are not broken down by COMT givig them increase half life and greater action.

Front 23

Amphetamine action?

Back 23

release NE from nerve terminal by displacing it

direct effect on alpha and beta just like NE action.

CNS effects:

Front 24

Ephedrine and pseudoephedrine action

Back 24

release NE from nerve terminal

directly stimulate beta 2 receptors. less CNS action than amphetamine

Front 25

What are the agents that displace stored catecholamines?

Back 25

amphetamine and ephedrine and pseudoephedrine

Front 26

agents that inhibit uptake of released catecholamine?

Back 26

cocain, tricyclic antidepressants (imipramine), antiobesity drugs (sibutramine).

Front 27

cocaine action?

Back 27

local anestheic, prevents uptake of NE by inhibiting the NE transporter... has CNS activity

Front 28

MAO inhibitors action?

Back 28

includes phenelzine... treat depression. can result in increased Tyramine due to lack of its breakdown leading to palpitations, headache and hypertensive crisis

Front 29

all about phenylephrine

Back 29

alpha 1, alpha 2 agonist (1 > 2)

Front 30

albuterol

Back 30

beta 2 agonist, cause less cardiac stimulation

Front 31

fenoldopam

Back 31

D1 agonist, lows BP, IV admin. for short term severe hypertension.

DA itself on the other hand increase BP b/c of its effects on beta and alpha receptors as well.

Front 32

What are irreversible alpha receptor blockers? function?

Back 32

phenoxybenzamine: decrease TPR and BP, reflex increase in HR and CO.

binds alpha receptors covalently.

Sharp drop in MBP in hypovolumic inviduals.

Front 33

non selective reversible alpha blocker?

Back 33

phentolamine: blocks a1 and a2... decreased TPR, and reflex cardiac stimulation.

Front 34

alpha 1 selective blocker?

Back 34

Prazosin: most widely used class of antagonists

less reflex tachycardia and greater antihypertensive efficacy.

Front 35

Therapeutic uses of alpha receptor antagonists?

Back 35

hypertension, pheochromocytoma, BPH, erectile dysfunction

Front 36

Side effects of alpha antagonists?

Back 36

postural hypotensions, nasal stuffiness, reflex cardiac stimulation, impaired ejaculation.

Front 37

How is HR increased in non-selective alpha antagonists?

Back 37

When alpha 2 is blocked, more NE is released, causing increased HR.

Front 38

beta 1 selective blocker?

Back 38

atenolol with just blocking b1, you aren't causing bronchoconstriction... good for people with asthma!

large dose of selective blockers become non-selective.

Front 39

beta blocker with partial agonist activity?

Back 39

pindolol is b1 and b2 clocker with ISA. Causes less slowing of HR at rest than those without ISA.

Front 40

non selective beta blocker?

Back 40

propranolol

Front 41

What are the effects of propranolol?

Back 41

Cardiac: decrease HR, MCF, CO, conduction vel., O2 demand, automaticity

Vascular: increased TPR, causing decrease renin [in hypertensive pts, a net effect of delayed drop in BP]

Front 42

What are the metabolic effects of propranolol?

Back 42

increased VLDL and decrease HDL

slows recovery of glc levels after insulin admin. in diabetics.

Front 43

What are the bronchioles effects of propranolol?

Back 43

bronchoconstriction

Front 44

indications for beta blockers?

Back 44

hypertension, ischemic heart dz (angina, post MI), arrhythmias, CHF, open angle glaucoma, prophylaxis for migraine headaches, termor (performance anxiety)

Front 45

contraindications for beta blockers

Back 45

bronchoconstriction, bradycardia, av block, cardiac arrest and failure,

Sudden withdrawal may cause angina, MI, elevated BP

excercebation of insulin-induced hypoglycemia, and maksing reflex tachcardia,

increased VLDL, decrease performance, sedation, depression

Front 46

what are some mixed antagonists?

Back 46

labetalol, carvedilol

Front 47

labetalol actions?

Back 47

sel. alpha 1 and non-selective beta blocker (1:3 ratio oral, 1:7 following IV)

Front 48

What are some uses of labetalol

Back 48

so alpha 1 and beta 1, 2 blocker

hypertension, pheochroocytoma induced HTN, angina pectoris

Front 49

What are some adrenergic neuron blockers?

Back 49

guanethidine: takes the NE transporter into the nerve end, preventing release of NE. No effect on adr. medulla, or BBB crossing
bretylium