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104 Cards in this Set
- Front
- Back
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What is the major function of a1 receptors?
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increase vascular smooth muscle contraction, increase pupillary dilator muscle contraction (mydriasis), increase intestinal and bladder sphincter muscle contraction
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What is the major function of a2 receptors?
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decreased sympathetic outflow, decrease insulin release
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What is the major function of B1 receptors?
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increase heart rate and contractility, renin release and lipolysis
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What is the major function of B2 receptors?
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vasodilation, bronchodilitation, increase heart rate and contractility, increase insulin release and lipolysis, decrease uterine tone
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What is the major function of M1 receptors?
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parasympathetic
CNS, enteric nervous system |
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What is the major function of M2 receptors?
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decrease hear rate and contractility of atria
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What is the major function of M3 receptors?
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increase exocrine gland secretion (sweat and gastric acid), increase gut peristalsis, increase bladder contraction, bronchoconstriction, increase pupillary sphincter muscle contraction (miosis), ciliary muscle contraction (accomidation)
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What is the major function of D1 receptors?
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relaxes renal vascular smooth muscle
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What is the major function of D2 receptors?
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modulates transmitter release, especially in the brain
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What is the major function of H1 receptor?
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increase nasal and bronchial mucus production, contraction of bronchioles, pruritis, and pain
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What is the major function of H2 receptors?
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increased gastric acid secretion
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What is the major function of V1 receptors?
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increase vascular smooth muscle contraction
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What is the major function of V2 receptors?
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increase H20 permeability and reabsorption in the collecting tubules of the kidney (V2 is found in the 2 kidneys)
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What receptors work through Gq?
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HAVe 1 M&M
H1, a1, V1, M1, M3 Gq activates phospholipase C (converts lipids into PIP2) creates IP3 and DAG IP3 causes increase Ca2+ DAG makes protein kinase C and arachidonic acid |
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What receptors work through Gi?
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MAD 2's
M2, a2, D2 Gi inhibit adenylyl cyclase - decreased cAMP - decreased kinase A |
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What receptors work through Gs?
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Have DBV (DVD) 2,1,2,1,2
B1,B2, D1, H2, V2 Gs stimulates adenylyl cyclase - converts ATP into cAMP - increases protein kinase A levels |
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What type of receptors are preganglionic?
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Nicotinic - ligand gated Na+/K+ channel (Na+ rushes in)
all work via Ach located preganglionic and for somatic control of skeletal msucle |
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What receptors are Ach?
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nicotinic and muscarinic
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For the parasympathetic nervous system what receptor is post ganglionic?
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muscarinic - works via Ach - G protein coupled receptors work through 5 subtypes (M1-M5)
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Where do muscarinic receptors work in the sympathetic nervous system?
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postganglionic for sweat glands
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For the symphathetic nervous system what acts preganglionic? What works post ganglionic?
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Preganglionic - nicotinic receptors - ligand gated Na+/K+
Postganglionic - adernergic recetprs (NE) a, b - for cardiac and smooth muscle, gland cells, nerve terminals for renal vascular smooth muscle D1 works |
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Nicotinic receptors
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Ach receptors - ligand gated Na+/K+ channels - Na+ rushes in causes depolarization
Nn found in autonomic ganglia and Nm found in neuromuscular junction |
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Where is Nn found?
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nicotinic receptors found in autonomic ganglia
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Where is Nm found?
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nicotinic receptors found in the neuromuscular junction
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Muscarinic receptors
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Ach receptors - act postganglionic for parasympathetic and post ganglionic for sweat glands of sympathetic - G protein coupled receptors - work through secondary messengers; 5 subtypes M1-M5
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What receptors work on the adrenal medulla?
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nicotinic receptors (via Ach) signal the adrenal medulla to release NE and Epi
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What receptors work for the sympathetic nervous system post ganglionic?
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adernergic - work via NE (a and b receptors)
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What are the 3 tissues that the parasympathetic nervous system sends its input to?
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cardiac, smooth muscle, and glandular tissue
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How do things work at the neuromuscular junction for cholinergics?
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Na+/Choline symporter - brings in choline and Na+ fro the neuromuscular junction - acetyl-CoA + choline get packaged into vesicles by choline acetyltransferase - get released into neuromuscular junction with help of Ca2+ - the Ach can work on muscarinic or nicotinic receptors on
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What does hemicolinium do?
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blocks the symporter of Na+/Choline - can't get choline into the axon - so Ach can't be released
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What does vesamicol do?
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It inhibits Ach from going into vesicles in the presynapic axon - ultimately results in Ach not being able to be released
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What does Botulinum do?
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inhibits the vesicle with Ach in the presynaptic axon - from binding at the end and release the Ach into the neuromuscular junction (ultimately inhibits the release of Ach)
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What does acethlcholinesterase do?
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breaks down Ach into choline and acetate - the choline gets reabsorbed into the presynaptic axon via Na+/choline symporter (inhibited by hemicolinium)
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How do things work in a noradrenergic axon?
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tyrosine gets brought into presynaptic axon - via a transporter - gets converted into DOPA - dopamine - NE (get packaged into vesicles) and released into the neuromuscular junction where it acts on adernergic receptors (a or B)
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What does metyrosine do?
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inhibits the formation of DOPA from tyrosine
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What does reserpine do?
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inhibits NE from getting into vesicles so it can be released into the neuromuscular junction
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What does Guanethidine do?
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inhibits the vesicle with NE from releasing it into the neuromuscular junction
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What do amphetamines do?
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stimulate release of NE into the neuromuscular junction
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What do cocaine, TCAs and amphetamines do?
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inhibit reuptake of NE
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What is release of NE from a sympathetic nerve ending modulated by?
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Itself - the NE inhibits the release of more NE
Antiotensin II stimulates the release of more NE M2 receptors inhibit the release of more NE |
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What are cholinomimetic agents? What are the 2 big classes?
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Direct agonists: bethanechol, carbachol, pilocarpine, methacholine
Indirect agonists: Neostigmine, pyridostigmine, edrophonium, physostigmine, echothiophate |
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Bethanechol
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cholinomimetic - direct agonist
used for post operative and nuerogenic ileus and urinary retention MOA: activates bowel and bladder smooth muscle; resistance to acetylcholinesterase |
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Carbachol
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cholinomimetic - direct agonist
use: galucoma, pupillary constriction, release of intraocular pressure |
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Pilocarpine
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choliomimetic - direct agonist
use: potent stimulator for sweat and tears - used for glaucoma MOA: contraction of cilliary muscle of eye (open angle glaucoma), pupillary sphincter (narrow angle); resistance to acetylcholinesterase 'PILE on the sweat and tears" |
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What drug can be used for open and closed angle glaucoma?
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Pilocarpine - choliomimetic - direct agonist
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Methacholine
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choliomimetic - direct agonist
use: challenge test for diagnosis of asthma MOA - stimulates muscarinic receptors in airway when inhaled - causing bronchoconstriction |
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What are the indirect choliomimetic agents?
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Neostigmine, Pyridostigmine, edrophonium, physostigmine, echothiophate
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Neostigmine
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use: postoperative and neurogenic ileus and urinary retention, myasthenia gravis, reversal of neuromuscular junction blockade (post operative)
MOA - increase endogenous Ach; no CNS presentation 'NEO CNS = NO CNS penetration' |
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Pyridostigmine
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use: myasthenia gravis (long acting); does not penetrate CNS
MOA: increase endogenous Ach; increase strength |
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Edrophonium
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use: diagnosis of myasthenia gravis (very short acting)
MOA: increase endogenous Ach |
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What drug is used to diagnose myasthenia gravis?
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Edrophonium - increases endogenous Ach - should take away symptoms
indirect cholinomimetic |
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Physostigmine
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glaucoma (crosses blood-brain barrier - CNS) and atropine overdose
MOA: increase endogenous Ach |
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Echothiophate
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use: gluacoma
MOA: increases endogenous Ach indirect agonist cholinomimetic |
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diarrhea, urination, miosis, bronchospasm, bradycardia, excitation of skeletal muscle and CNS, lacrimation, salivation and sweating. What is going on? What should you give the person?
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DUMBBELSS
cholinesterase inhibitor poisoning - too much Ach!!! antidote: atropine (muscarinic antagonist) plus pralidoximine (chemical antagonist used to regenerate active choliesterase |
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What should atropine and pralidoxime be given for?
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acetylcholinesterase inhibitor poisoning - too much Ach
Atropine is a muscarinic antagonist Pralidoximine is a chemical antagonist that regenerates active cholinesterase |
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What does parathion and other organophosphates cause?
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cholinesterase inhibitor poisoning - too much Ach
*irreversible inhibitor DUMBBELSS |
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What are muscarinic antagonists?
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atropine, homatropine, tropicaminde, benztropine, scopolamine, ipratropium, oxybutynin, glycopyrrolate, methscopolamine, propantheline`
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Atropine use and application.
Similar drugs |
eye
use: produce mydriasis and cycloplegia (loss of cilliary eye muscle loose ability to accomidate) similar drugs: homatropine, tropicamide |
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Benztropine
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muscarinic antagonist
affects: CNS use: parkinson's disease "PARK my BENZ' |
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Scopolamine
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muscarinic antagonist
effects CNS use: motion sickness |
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Ipratropium
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muscarinic antagonist
effects: respiratory system use: asthma, COPD 'I pray I can breathe' |
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Oxybutynin, glycopyrrolate
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muscarinic antagonist
effects: genitourinary system use: reduce urgency in mild cystitis and reduce bladder spasms |
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Methscopolaine, propantheline, pirenzepine
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muscarinic antagonist
effects: gastrointestinal system use: peptic ulcer treatment |
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Atropine
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muscarinic antagonist
eye: increases pupil dilation, cycloplegia airway: decreases secretions stomach: decreases acid secretion (inhibiting ECL cells and inhibiting direct stimulation of parietal cells) gut: decreases motility bladder - decreases urgency in cystitis *blocks DUMBBELSS |
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What are the toxicity's of atropine?
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increased body temp, rapid pulse, dry mouth, dry flushed skin, cycloplegia, constipation, disorientation
- can cause acute angle-closure glaucoma in elderly, urinary retention in men with prostate hyperplasia, and hyperthermia in infants "Hot as a hare, dry as a bone, red as a beet, blind as a bat, mad as a hatter" |
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Hemamethonium
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nicotinic antagonist
use: ganglionic blocker. used in experimental models to prevent vagal reflex responses to changes in blood pressure ex. prevents reflex bradycardia caused by NE toxicity: orthostatic hypotension, blurred vision, constipation, sexual dysfunction |
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Epinephrine
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a1,a2,b1,b2 agonist
use: anaphylaxis, gluacoma (open angle only!), asthma, hypotension |
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NE
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a1,a2,b1 agonist (a>B)
use: hypotension (but decrease renal perfusion) |
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Isoproternol
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B1, B2 agonist
use: AV block (rare) |
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Dopamine
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D1=D2>b>a
inotropic and chronotropic |
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Dopamine
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D1=D2>b>a inotropic and chronotropic
use: shock (increase renal perfusion), heart failure |
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Dobutamine
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B1>B2 inotropic but not chronotropic
use: shock, heart failure, cardiac stress testing |
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phenylephrine
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a1>a2
use: pupillary dilatation, vasoconstriction, nasal decongestion |
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Metaproterenol, albuerol, salmeterol, terbutaline
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B2 agonist
MAST use: metaproterenol and albuterol for acute asthma salmeterol for long term treatment of asthma terbutaline - to reduce premature uterine contractions` |
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ritodrine
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b2 agonist
use: reduces premature uterine contractions |
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Amphetamine
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indirect sympathetic agonist - releases stored catecholamines
use: narcolepsy, obesity, ADD |
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Ephedrine
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indirect general agonist for sympathetics, releases stored catecholamines
use: nasal decongestion, urinary incontience, hypotension |
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Cocaine
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indirect general agonist for sympathetics, inhibits reuptake
use: causes vasoconstriction and local anesthesia |
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NE affect on heart rate and blood pressure
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NE (a>b)
B1 increases systolic BP a1 increases diastolic BP mean increase in BP decrease in heart rate (reflex bradycardia) |
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Epi affect on heart rate and blood pressure
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nonselective
B1 increases systolic BP B2 decreases diastolic BP average NO change in BP increase in heart rate (B1) |
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Isoproterenol affect on blood pressure and heart rate
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(B>a)
B1 decreases systolic BP (slight) B2 decreases diastolic BP average - decrease in BP B1 increases heart rate |
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clonidine, a-methyldopa
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a2 agonist, decrease central adrenergic outflow
use: hypertension, especially with renal disease (no decrease in blood flow to the kidneys) |
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Phenoxybenzamine and phentolamine
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non-selective alpha blocker
phenoxybenzamine (irreversible) and phentolamine (reversible) use: pheochromocytoma (use phenoxybenzamine before removing tumor, since high levels of released catecholamines will not be able to over come blockage toxicity: orthostatic hyoptension, reflex tachycardia |
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praxosin, terazosin, doxazosin
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a1 antagonist
use: hypertension, urinary rentention in BPH toxicity: 1st dose orthostatic hypotension, dizziness, headache |
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Mirtazapine
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a2 antagonist
use: depression toxicity: sedation, increase serum cholesterol, increased appetite |
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What happens to blood pressure when you give phenylephrine? What then happens if you give an alpha blocker?
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it increases (it is a a1 agonist)
after you give an alpha blocker - the blood pressure returns to normal (what it was before the phenylephrine was given) - b/c the alpha is blocked |
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What happens to blood pressure when you give epi? What happens when you then give an a antagonist?
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when you give epi - the blood pressure increases
when you give an a blocker - the blood pressure decreases - from B2 response |
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B blockers - applications
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acebutolol, betaxolol, esmolol, atenolol, metoprolol, propranolol, timolol, pindolol, labetalol
use: hypertension - decrease CO, decrease renin secretion (due to B-receptor blockade on JGA cells) angina: decrease heart rate and contracility, resulting in decrease O2 consumption MI: B-blockers decrease mortality SVT: propranolol and esmolol - decrease AV conduction veolocity (class II antiarrhythmic) CHF: slows progression of chronic failure glucoma: timolol - decreased secretion of aqueous humor |
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what has been shown to decrease mortality after an MI? Giving what drug?
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beta blockers
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toxicities of b-blockers?
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impotence, exacerbation of asthma, cardiovascular adverse effects (bradycardia, AV block, CHF), CNS adverse effects (sedation, sleep alterations); use with caution in diabetics
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What are the beta blockers that are OK for asthmatics?
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B1 only blockers
A BEAM acebutolol (partial agonist too), betaxolol, esmolol, atenolol, metoprolol |
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clonidine, a-methyldopa
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a2 agonist, decrease central adrenergic outflow
use: hypertension, especially with renal disease (no decrease in blood flow to the kidneys) |
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Phenoxybenzamine and phentolamine
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non-selective alpha blocker
phenoxybenzamine (irreversible) and phentolamine (reversible) use: pheochromocytoma (use phenoxybenzamine before removing tumor, since high levels of released catecholamines will not be able to over come blockage toxicity: orthostatic hyoptension, reflex tachycardia |
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praxosin, terazosin, doxazosin
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a1 antagonist
use: hypertension, urinary rentention in BPH toxicity: 1st dose orthostatic hypotension, dizziness, headache |
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Mirtazapine
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a2 antagonist
use: depression toxicity: sedation, increase serum cholesterol, increased appetite |
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What happens to blood pressure when you give phenylephrine? What then happens if you give an alpha blocker?
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it increases (it is a a1 agonist)
after you give an alpha blocker - the blood pressure returns to normal (what it was before the phenylephrine was given) - b/c the alpha is blocked |
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What happens to blood pressure when you give epi? What happens when you then give an a antagonist?
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when you give epi - the blood pressure increases
when you give an a blocker - the blood pressure decreases - from B2 response |
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B blockers - applications
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acebutolol, betaxolol, esmolol, atenolol, metoprolol, propranolol, timolol, pindolol, labetalol
use: hypertension - decrease CO, decrease renin secretion (due to B-receptor blockade on JGA cells) angina: decrease heart rate and contracility, resulting in decrease O2 consumption MI: B-blockers decrease mortality SVT: propranolol and esmolol - decrease AV conduction veolocity (class II antiarrhythmic) CHF: slows progression of chronic failure glucoma: timolol - decreased secretion of aqueous humor |
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what has been shown to decrease mortality after an MI? Giving what drug?
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beta blockers
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toxicities of b-blockers?
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impotence, exacerbation of asthma, cardiovascular adverse effects (bradycardia, AV block, CHF), CNS adverse effects (sedation, sleep alterations); use with caution in diabetics
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What are the beta blockers that are OK for asthmatics?
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B1 only blockers
A BEAM acebutolol (partial agonist too), betaxolol, esmolol, atenolol, metoprolol |
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What are nonselective beta antagonists?
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propranolol, timolol, nadolol, pindolol, labetalol - don't give to asthmatics
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What are the nonselective a and b antagonists?
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carvedilol, labetalol
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what beta blockers are partial B-agonists too?
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acebutolol, pindolol
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