Autonomic Pharmacology Flashcards
⍺1 Receptors
Gq, Stimulatory
Increase IP3, DAG, Ca2+
Vasoconstriction
Mydriasis (pupil dilation)
Contraction, urinary retention
Glycogenolysis (increase blood glucose
⍺2 Receptors
Gi, inhibitory
Decrease in cAMP and adenylyl cyclase, causing inhibition of NE release
Decreased insulin secretion
β1 Receptors
Gs, increased adenylyl cyclase and cAMP
HEART– increased HR, contractility, AV node conduction
Increased lipolysis
Increased renin release from kidney juxtaglomerular cells, causing increased BP
β2 Receptors
Gs, increased adenylyl cyclase and cAMP
Bronchodilation
Vasodilation of vascular smooth muscle and arteries of skeletal muscle
Decreased GI motility, Inhibition of labor
Glycogenolysis, gluconeogensis (increase blood glucose)
β3 Receptor
Gs, increased adenylyl cyclase and cAMP
Increased lipolysis
Inhibition of urination
Phenylephrine
⍺1 agonist
decrease nasal congestion by vasoconstriction
raises blood pressure for hypotension during surgery
Modafinil
⍺1 agonist
treats narcolepsy
Clonidine and Dexmedetomidine
⍺2 agonists
stimulation of alpha2 leads to decreased SNS activity
treats hypertension
- transient increase in BP followed by sustained hypotension
- produce sedation and analgesia
Brimonidine
Alpha2 agonist
Treats glaucoma
Dobutamine
Beta1 agonist
Stimulation of beta1 in the heart– increased cardiac rate and cardiac output
Treats cardiac decompensation after cardiac surgery of CHF
Short Acting Beta Agonists (SABAs)
Beta2 agonists
Albuterol, Isoproterenol
- relive acute asthma by bronchodilation
Long Acting Beta Agonists (LABAs)
Beta2 agonists
Salmeterol, Formoterol, Indacaterol
- prolonged bronchodilation, prevents asthma attacks
Mirabegron
Beta3 agonist
Relieves overactive bladder (decreases urination)
Cocaine, Amphetamine, Tyramine
Inhibit reuptake of norepinephrine and dopamine
Stimulate alpha1 and beta1 receptors – increase SNS activity
Mixed Action Agonists
Direct binding and release of stored NE
long mechanism of action because they are poor substrates for COMT and MAO
Ephedrine, metaraminol
Ephedrine
Alpha1 and beta2 agonist
Vasoconstriction and bronchodilation
Decreased urination (because adrenergic agonists are fight or flight)
Metaraminol
Alpha1 direct, Indirect
Elevates blood pressure
Treats hypotension produced by drugs or pheochromocytoma
Dopamine
Nonselective Direct Acting Adrenergic Agonist (can act on both alpha and beta receptors)
dilation of renal and mesenteric veins
increased salt excretion
increased water excretion
treats CARDIOGENIC SHOCK
Alpha 1 Blockade (general effect)
Smooth muscle relaxation
Causes REFLEX TACHYCARDIA
Alpha 2 Blockade (general effect)
Norepinephrine release
T/F: Alpha Blockers affect the sympathetic stimulation of the heart
FALSE
Alpha blockers do NOT affect the sympathetic stimulation of the heart
Phentolamine
Nonselective Alpha Blocker
Reverses anesthesia in dentistry
treats erectile dysfunction
diagnose pheochromocytoma
Phenoxybenzamine
Nonselective Alpha Blocker
Treats pheochromocytoma
Alpha1 Blockers
End in “-osin”
Treat peripheral vascular disease (Raynaud’s, Buerger’s)
Prazosin, doxazosin, terazosin (tx hypertension)
Tamsulosin, alfuzosin, silodosin (tx benign prostatic hypertrophy and the painful urination/urinary retention)
Prazosin, Doxazosin, Terazosin
Alpha1 blockers (end in “-osin”)
treat hypertension
Tamsulosin, Alfuzosin, Silodosin
alpha1 blockers (end in “-osin”)
treat benign-prostatic hypertrophy and the painful urination/urinary retention associated
Beta Blockers (generalities)
Competitive inhibitors of beta-adrenergic receptors
End in “-lol”
Block the effect of catecholamines–> decrease sympathetic effects (mainly on heart)
Beta1 Block (generalities)
decreased heart rate
delayed conduction through AV node
Reduced contractility
Beta2 Block (generalities)
Bronchoconstriction
DO NOT USE ON ASTHMA AND COPD PATIENTS!!
ALL beta blockers are contraindicated for _______
Insulin dependent DIABETICS
Hypoglycemia usually causes tachycardia and lets the patient know they should eat something. Beta blockers will block the tachycardia, so the issue may go undetected.
Nonselective Beta Blockers (β1, β2)
propanolol, timolol, nadolol
Propranolol
Nonselective beta blocker
migraine prophylaxis (has high lipid solubility, so it can penetrate the CNS)
Timolol
nonselective beta blocker
decreases intraocular pressure, treats glaucoma
Beta1 Blockers
CARDIOSELECTIVE
metoprolol, atenolol, nebivolol
DO NOT USE ON PATIENT WITH AV HEART BLOCK
You can only block β___ in asthmatic patients
You can only block BETA1 in asthmatic patients
Beta1 is cardioselective and will not affect the lungs. If we blocked beta2, there would be increased bronchodilation, which would cause even more breathing trouble in an asthmatic/COPD patient
Metoprolol
Beta1 blocker (cardioselective)
Tx hypertension, angina
may lower risk of death after a heart attack
Atenolol
Beta1 blocker (cardioselective)
tx hypertension associated with ventricular ectopics in hyperthyroidism
Nebivolol
Beta1 blocker (cardioselective)
releases NO causing vasodilation
Carvedilol and Labetalol
Block β1, β2, ⍺1
Block increases of HR and BP
Decreases BP WITHOUT REFLEX TACHYCARDIA
Able to reduce both systolic and diastolic BP. You decrease both peripheral resistance and cardiac output.. it acts on both the vessels and the heart itself, so it decreases both systolic and diastolic.
Muscarinic Agonists (Parasympathomimetics)
increase PARASYMPATHETIC and sympathetic to SWEAT GLANDS
NO EFFECT ON BLOOD VESSELS
THERE ARE NO MUSCARINIC RECEPTORS ON SKELETAL MUSCLES
NEVER GIVE SYNTHETIC CHOLINE ESTERS VIA IV
Muscarinic Antagonists (Parasympatholytics)
increase SYMPATHETIC, decrease sweat glands
Acetylcholine
Muscarinic agonist
used to test for miosis (pupil constriction) after cataract surgery
Metacholine
Muscarinic agonist
used to diagnose asthma
Carbachol
Muscarinic agonist
Tx open angle glaucoma and emergency closed angle glaucoma– produce mitosis
Bethanechol
Muscarinic agonist
treat urinary retention and help increase GI tone
Cevimeline
Muscarinic agonist
tx of xerostomia associated with Sjogren’s Syndrome
Pilocarpine
Muscarinic agonist
Topically for glaucoma and orally for xerostomia
Atropine
Muscarinic antagonist
ANTIDOTE FOR MUSCARINIC TOXICITY OF CHOLINERGIC DRUGS
Pupil dilation
Blocks M3 in GI tract– reduction of motility
Decreased gastric acid secretion
Blocks M2 on heart– causes tachycardia (Atropine can help overcome bradycardia)
Blocks muscarinic receptors on salivary, sweat, and lacrimal glands
Scopolamine
Muscarinic antagonist
prevent motion sickness and post operative nausea
Ipratropium
Muscarinic antagonist
brochodilation and reduced mucous secretion
Benztropine, Trihexyphenidyl
Muscarinic antagonist
treats Parkinson-like disorders
Tropicamide
Muscarinic antagonist
Produces short acting mydriasis (pupil dilation) for better eye examination
Solifenacin
Muscarinic antagonist
treats overactive bladder
Glycopyrrolate
Muscarinic antagonist
Treats peptic ulcers in adults
Can treat chronic drooling from neurologic disorders
Nicotine
Ganglionic Blocker
stimulates and later depresses cholinergic function
Increased release of neurotransmitters (dopamine, serotonin, norepinephrine)
Increased GI motility and tone
Increased BP and HR (high doses can cause BP to fall)
Blood vessel constriction
Hexamethonium
Ganglionic blocker
Blocks nicotinic receptors
Trimethanphan
Ganglionic blocker
used for hypertensive urgencies and emergencies
blocks nicotinic receptors at both sympathetic and parasympathetic ganglia
Neuromuscular Blocking Agents (NMBAs)
Can be Non-depolarizing agents or Depolarizing Agents
Acts on acetylcholine receptors (different ways based on depolarizing vs. non-depolarizing)
Non-Depolarizing NMBAs
Bind the acetylcholine receptors at the neuromuscular junction so that it cannot depolarize– this inhibits muscle contraction
Cisatracurium
Pancuronium
Rocuronium and Vecuronium
Atracurium
Depolarizing NMBAs
mimics acetylcholine– much more resistant to acetylcholinesterase, so there is persistent depolarization
Succinylcholine
Succinylcholine
Depolarizing NMBA
binds nicotinic receptor that opens sodium channel– causes depolarization
Usually administered via IV, rapid onset of action
May cause HYPERKALEMIA due to continued flow of potassium into the extracellular fluid
