Flashcards in ANS drugs Deck (74)
Where parts of spinal cord do symp and parasymp originate?
Parasymp--->cranial sacral part
All ANS start with ___ neurotransmitter and the synapse at ___ receptor?
Where do you find Nm receptor?
What are the 2 exceptions for symp that do not use epi or norepi?
Sweat gland (ACh)
Adrenal medulla--->recieve ACh--->produce epi
D1 receptor stimulation at the kidney causes?
TPR or CO has a greater influence on BP?
Which 3 receptors control constriction or dilation of the blood vessels?
M3--->vasodilate via NO
What if you give alpha 1 agonist with M antagonist?
Increase BP without reflex bradycardia
What if you give beta 2 agonist and a beta 1 antagonist?
Decrease BP without reflex tachycardia
What kind of drug block both reflex tachy and bradycardia?
What are the 2 receptor that cause brady or tachycardia?
What are parasymp/symp affect on the eye?
Parasymp--->ciliary muscle (M)--->accommodate to near sight
Symp--->radial muscle (alpha 1)---->mydriasis
How do you cause cycloplegia (paralysis of accommodation)?
How is ACh produced?
Choline uptake--->choline + acetyl CoA---(choline acetyl transferase)--->ACh
Which drug block the uptake of choline?
AChE inhibitor can only work on ___ organs?
Where are M1/2/3 located?
M stimulation at LES cause constriction or relaxation?
Which M3 receptor is not innervated in your body?
M3 on blood vessel that does vasodilation through NO
Anti M would produce what kind of affect for M3 on blood vessel?
It would inhibit M3 on blood vessel but it would do nothing to the blood vessel since M3 is not innervated (thus no agonist to compete with)
M agonist and AChE inhibitor usually produce the same affect except for one place?
M3 on blood vessel--->AChE inhibitor has no effect there
What organs are only innervated by symp?
Sweat gland/blood vessels
AChE inhibitor activate both symp and parasymp, but why does it look like it's mainly parasymp?
Parasymp is the dominate force
What are the 4 M agonist drugs?
Which AChE inhibitor can cross the BBB?
Physostigmine (3rd ammine)
Neuromuscular blockade and myasthenia gravis have what in common?
They both work on Nm receptor
What's the rationale behind treating Alzheimer's with AChE inhibitor?
Alzheimer's--->lost of cholinergic nerve in Meynert's nucleus
Emesis is mediated by which M receptor?
Why is organophosphate fatal?
Permanent depolarization of diaphragm--->inhibiting breathing
Why do we need to be careful on using antimuscarinic on elderly pt?
Precipitate elderly pt for glaucoma
What are some other group of drugs that are antimuscarinic?
1st generation antihistamine/TCA/low potency typical antipsychotic/quinidine/amantadine (antiparkingson)/meperidine (opioid)
List some antimuscarinic drugs
"trop" and "scop"
What is Oxybutynin used for?
If a pt who is on pyridostigmine for myathenia gravis also takes atropine for side effect, would it interfere with pyridostigmine?
No--->Myathenia gravis has antibodies against Nm receptor--->atropine is M antagonist so it does not affect Nm
How is norepi produced?
Last step takes place in storage vesicle
What are the rate limiting step for ACh and norepi production?
Uptake of choline/tyrosine hydroxylase
How is norepi being taken out of the synaptic cleft once released?
COMT degrade norepi/norepi reuptake
What does MAO-A do?
It degrades norepi when norepi is reuptaken into the presynaptic neuron
What are the mechanism of amphetamine/TCA/cocaine
Amphetamine--->promote releasing of NE
TCA/cocaine--->prevent reuptake of NE
What do AMPT/clonidine/alpha methyldopa/reserpine/guanethidine do?
They all decrease NE release
AMPT--->tyrosine hydroxylase inhibitor
Clonidine/alpha methyldopa--->alpha 2 agonist
Reserpine--->destroy storage vesicle
Guanethidine--->replace NE in the vesicle (release wrong things)
Where do alpha 1 receptor found in your body?
Radial muscle of the eye/blood vessels/bladder (stimulate--->contract--->urinary retention)/kidney (decrease renin release)
Where do alpha 2 receptor found in your body and what happens if you stimulate them?
Presynaptic nerve terminal/platelets (aggregation)/pancreas (decrease insulin secretion)
Stimulate what receptor cause increase renin release?
What are the effect of increase cAMP on skeletal and smooth muscle?
What is special about beta 2 receptors and where are they found?
They are mostly not innervated (thus activated by epi)
Blood vessel (vasodilate)/uterus (relax)/branchioles (dilation)/skeletal muscle (contract)
What would happen to skeletal muscle if you take too much beta 2 agonist for asthma?
Muscle tremor (skeletal muscle has beta 2)
What are the metabolic affects of beta 2 receptor?
If stimulated--->increase glycogenolysis--->increase blood glucose
increase insulin secretion
What happens when you stimulate D1 receptor?
Increase renal perfusion--->increase GFR and Na secretion
What is dose dependent character of dopamine?
Low dose stimulate D1--->medium dose beta 1--->high dose alpha 1
What is fenoldopam used for?
D1 agonist for severe HTN
Between beta and alpha receptor, which one would be activated first in terms of doses?
Beta (low)--->alpha (high)
Which drug is a alpha 1 agonist? what does it used for?
Nasal decongestant/eye exam (dilate pupil)
Stimulation of what receptor increase pulse pressure?
Beta 1 (decrease diastolic pressure)
What are the nonselective beta agonist/beta 1 agonist/beta 2 agonist?
Beta 2: bronchodilator
Terbutaline--->also used to relax uterus during labor (prevent preterm labor)
What receptors do NE work on? what is its affect on the heart?
Alpha 1/alpha 2/beta 1 only (Beta 2 is not innervated)
Increase HR but then decrease (due to reflex bradycardia responding to increase BP caused by alpha 1)
What receptors do epi work on?
What are the affect of low and high dose epi?
Low dose--->same as isoproterenol (only beta1/2)
High dose--->same as norepi (mainly alpha1/beta1)
How to distinguish between norepi and high dose epi?
Give alpha 1 blocker
Norepi--->BP goes back to normal
Epi--->BP goes below normal because of beta 2 affect
Which one (epi or norepi) is used for anaphylaxis shock?
What does tyramine (cheese and wine) do?
Degraded by MAO-A
If taken MAOi--->tyramine increase NE release like amphetamine--->HTN crisis
What do MAO-A/B metabolize and where are they found?
MAO-A--->metabolize NE/5-HT/tyramine (found Anywhere)
Indirect adreoceptor agnoist (e.g. amphetamine/cocaine) can only work on what kind of tissue?
Why is reflex tachycardia worse with nonselective alpha blocker?
Blocking alpha 2 as well--->block an inhibitor--->increase NE activity--->worsen reflex tachycardia
What are the 2 non selective alpha blockers and which one is the competitive and which one is the noncompetitive inhibitor? and what are they used for?
Phenoxybenzamine--->noncompetitive (longer name)
They are used for pheochromocytoma
What are the alpha 1 blockers and what do they do?
"zosin" --->HTN and BPH
Tamsulosin--->alpha 1a receptor blocker--->BPH only
What is the alpha 2 blocker?
What are some affects of beta 2 blockade?
Bronchospasm/decrease aqueous humor production/decrease glucose/increase LDLs and TGs (prevent breakdown)
How to distinguish beta 1 or non selective beta blockers?
start with A-M--->beta 1 blocker only
What are 2 beta blockers that are also partial agonists?
Acebutolol and pindolol/they do not increase LDL and TG
What should we be cautious about pt who is on chronic beta blocker?
Don't abruptly stop the beta blocker
What can you give with beta blocker overdose?
Glucagon (increase cAMP to oppose beta blocker)
What are selective and nonselective beta blocker most commonly used for?
Nonselective--->glaucoma/migraine prevention/thryotoxicosis/performance anxiety/essential tremor
What is special about carvedilol and labetalol?
Nonselective beta blocker and alpha 1 blocker
Treat HTN and CHF