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a1 receptor (class q)
Vascular smooth muscle contraction, ↑pupillary dilation (mydriasis), intestinal and bladder sphincter contraction, ↓Renin, NO CYCLOPLEGIA, can cause sexual disfunction, ↑TPR, and ↑After-load
a2 receptor (class i)
↓sympathetic release ↓insulin release ↓lipolysis ↑platelet aggregation(epinephrine). ↓cAMP
b1 receptor (class s)
↑heart rate and contractility, ↑renin release, ↑cAMP, ↑lipolysis (+inotropic)
b2 receptor (class s)
vasodilation, bronchodilation, ↓uterine tone (tocolysis), DOES NOT USE NE. All blood vessels affected. ↑HR, ↑contractility, ↑lipolysis, ↑insulin release, ciliary muscle relaxation, ↑aqueous humor production, ↑gluconeogenesis
M1 receptor (class q)
CNS, gastric parietal cells (↑H+ production). Contraindicated for PUD.
M2 receptor (class i)
decreased heart rate and atrial contractility
M3 receptor (class q)
stimulates glandular secretions (lacrimal,sweat, gastric), ↑gut peristalsis, ↑pupillary sphincter muscle contraction (miosis), ciliary muscle contraction (accommodation), ↑bladder contraction. Contraindicated for COPD/Asthma patients.
D1(Dopamine) receptor (class s)
renal vascular smooth muscle relaxation via vasodilation. Typical drug “Fenoldopam” which ↑RBF, ↑GFR, ↑Na+ secretion
D2 receptor (class i)
↓sympathetic release, modulates transmitter release (especially in brain)
H1(Histamine) receptor (class q)
↑sinus and bronchial mucus production, ↑vascular permeability, bronchial constriction, itching(pruritus), and pain
H2 receptor (class s)
increased gastric acid secretion
V1(Vasopressin) (class q)
vascular smooth muscle contraction
V2 (class s)
↑H2O reabsorption in collecting tubules of kidneys. Found in kidneys
Muscarinic and Nicotinic receptors are located where?
They are located on the post-synaptic terminal located on the effector cells
The re-uptake of Choline into the pre-synaptic terminal is inhibited by what?
Vesamicol inhibits what process?
uptake of ACh into the synaptic vesiclec causing a release in the reduction of ACh.
Botulinum Toxin inhibits what process?
release of ACh from the vesicles
What receptor does the somatic motor neuron synapse with?
Neuromuscular junction using ACh with (Nm receptor) on skeletal muscle
Metyrosine inhibits what process?
Conversion of Tyrosine Hydroxylase to Dopa
what is MAO-A
MAO-A is the metabolic process for the Adrenergic nerve terminal. It also takes part in supplying the NE mobile pool and is converted into VMA in the urine. COMT is methylated and oxidized by MAO
Name 3 drugs that inhibit the reuptake of NE and are indirect general agonist (sympathomimetics)
Cocaine, TCA’s, and Amphetamines
Out of the 3 drugs that inhibit the reuptake of NE, which drug’s also releases stored catecholamines?
Amphetamine and Ephedrine
Where is Phenylalanine made?
The liver
Which drugs inhibit the the release of stored catecholamines?
Bretylium and guanethidine
AChE inhibitors act on what process?
AChE inhibitors prevent the uptake of AChE on the post-synaptic membrane
Reserpine’s effect on the Noradrenergic membrane is?
inhibits the uptake of dopamine into the storing vesicle
What is the process of Guanethidine?
Guanethidine prevents the release of (exocytosis) of NE
What are the Direct Cholinomimetic muscarinic agonist (paraysympathomimetics) drugs?
Bethanechol, Carbachol, Pilocarpine, and Methacholine
Muscarinic agonist. Longer acting than ACh (resistant to AChE). Treatment of ileum and urinary retention. Bowels and Bladder!
Muscarinic/nicotinic agonist. Applied to eye to causes contraction of ciliary muscle, relief of open-angle glaucoma. Also constricts pupil
Muscarinic agonist. Stimulates tears, sweat, and Saliva. Constricts pupil and ciliary muscle. Also used for acute glaucoma
Muscarinic Agonist. Causes bronchoconstruction when inhaled. Used for asthma challenge test.
What are the 6 Anticholinesterases (indirect cholinomimetics?)
Neostigmine, Pyridostigmine, Edriphonuim, Physostigmine, Echothiophate, and Donepezil
Quaternary amine. Treatment of of ileum, urinary retention, and MG. Post-op reversal of neuromuscular junction blockade (Nm)
Quaternary amine. Treatment of MG. Long acting
Very short acting (10-20 mins.) Diagnosis of MG via anti-AChR Ab test.
Tertiary amide (can enter CNS). Treatment of glaucoma. Antidote for atropine toxicity
Alzheimer disease. Increase of endogenous ACh
What are the negative effects of cholinomimetic agents?
exacerbation of COPD, asthma, and peptic ulcers
What are the cholinesterase inhibitor poisoning symptoms?
DUMBBELSS (Diarrhea, Urination, Miosis, Bronchoconstriction, Bradycardia, Excitation (skeletal muscle and CNS), Lacrimation, Salivation
What is the treatment for cholinesterase inhibitor poisoning?
Atropine (Muscarinic Antagonist), and Pralidoxime (2PAM) which regenerates Cholinesterase.
What are some muscarinic receptor anatagonist (anti-muscarinic)
Atropine, Antihistamines, tricyclic antidepressants, Antipsychotics, Quinidine, Amantadine, Meperidine, Ipratropium, Scopolamine, Benztropine, trihexyphenidyl, Tropicamide
How does a muscarinic receptor antagonist work?
Tertiary amine. Opposite effects of DUMBBELSS. decreased epithelial secretions, mydriasis, cycloplegia, hyperthermia, vasodilation, tachycardia, sedation, urinary retention, constipation
antispasmodic, antisecretory, management of AChE inhibitor OD, antidiarrheal, ophthalmology (long acting)
Ophthalmology (topical)
Asthma and COPD (no change in mucus viscosity)
treats motion sickness and causes sedation and short term memory block
Lipid-soluble. Used in parkinsonism and in acute extrapyramidal symptoms induced by antipsychotics
Hexamethonium (nicotinic antagonist)
Used to prevent vagal reflexes due to sympathetic stimulation. Can be used to prevent reflex bradycardia caused by increased bp due to increased norepinephrine. Excess hexamethonium can cause orthostatic hypotension, blurred vision, constipation.
Name 11 Direct Sympathomimetics
Epinephrine, Norepinephrine, Isoproterenol, Dopamine, Dobutamine, Ritodrine, Metaproterenol, Albuterol, Salmeterol, Terbutaline, and Phenylephrine
Function: a, B agonist. Clinical Usage: Treatment of anaphylaxis, open-angle glaucoma, asthma, hypotension. Prolongs the effect of local anesthesia. Adverse effects: Increased systolic blood pressure + decreased blood pressure=widened pulse pressure
Function: Mainly a-receptor agonist, but has some B-receptor activity. Clinical usage: Treatment of hypotension. Adverse effects: Splanchnic vasoconstriction and decreased renal perfusion, increased systolic, increased diastolic=little/no change in pulse pressure. Reflexive decrease in heart rate
B1B2 agonist. Treatment of AV conduction block. Decrease in diastolic BP (induces reflexive increase in heart rate)
D1=D2>B> a agonist. Inotropic and chronotropic. Treatment for shock, especially with heart failure
B1>B2 agonist. Inotropic. Treatment of heart failure. Used in cardiac stress test
B2 agonist. Reduces premature uterine contractions
metaproterenol & albuterol
selective B2 agonists (B2>B1). Treatment of asthma (acute)
selective B2 agonist (B2>B1). Long-acting treatment of asthma
selective B2 agonist (B2>B1). Treatment of asthma
Name 4 indirect sympathomimetics
Amphetamine, Ephedrine, Cocaine, Tyramine,
Indirect general agonist (sympathomimetic). Re-uptake inhibitor. Induces catecholamine release from terminals. Treatment for narcolepsy, obesity, and ADHD. a1 agonist which increases BP
Indirect general agonist. Induces catecholamine release. Treatment for nasal congestion, urinary incontinence, hypotension (HTN crisis). Penetrates CNS
Indirect general agonist. Inhibits reuptake of catecholamines. Vasoconstriction, local anesthetic. Never give B-Blockers if cocaine intoxication is suspected. Can lead to a1 activation causing extreme hypertension.
Similar mechanism to amphetamines, cleared by MAO (MAO inhibitors can cause hypertension, especially with tyramine-rich foods such as wine and cheese).
Name 2 sympathoplegics
a-methyldopa and clonidine
Agonist of central a2-adrenergic receptors which decreases sympathetic outflow
used to treat hypertension by decreasing sympathetic tone
What are the non-selective (a1 and a2) Alpha-blockers?
Phenoxybenzamine and phentolamine
What are phenoxybenzamine and phentolamine used for?
Treatment of pheochromocytoma. Also used to treat Raynaud’s syndrome
What are the a1-selective Alpha blockers? (ZOSIN)
Prazosin, Terazosin, and Doxazosin
Treatment of HTN, urinary retention (BPH).
Treatment of HTN, urinary retention (BPH). May cause orthostatic hypotension
Treatment of HTN, urinary retention (BPH). Usually taken at bedtime
Name the a2-selective Alpha blocker
Treatment of depression. Can cause sedation, increased serum cholesterol, and increased appetite
What are the non-selective (b1 and b2) Beta blockers? (olol)
Propranolol (migranes), Timolol (glaucoma), Nadolol
What are the b1 selective Beta blockers
Metoprolol, Atenolol, Betaxolol, Esmolol (very short acting)
What are the mixed a and b blockers Beta blockers?
Carvedilol and Labetalol
What are the partial b-agonist
Pindolol and acebutolol
Beta 2 receptor blocker: used for sedation, thyrotoxicosis, performance anxiety, and essential tremor. Inquired in plasma lipids
B2 receptor antagonist. Used to treat Glaucoma.
Beta2 blocker. Treats HTN and Angina
B2 blocker
Beta 1 blocker. Used to treat HTN and Angina for survival of heart attack. (extended release) Long acting.
Beta 1 blocker. Used to treat HTN and prevent Angina.
Beta 1 blocker. Used to treat open angle glaucoma, HTN, and Angina
Beta 1 blocker. Used to treat A. Fib and arrhythmia.
Beta blocker. Used to treat severe heart failure
Beta blocker. Used to treat HTN. Used for chronic treatment of high blood pressure during pregnancy.
partial beta-receptor (agonist) drug used as a local anesthetic. Moderate lipid solubility. Elimination half-life 3-4 hrs. Also used for HTN and angina.
Beta blocker. Used to treat HTN and irregular heart rate (arrhythmia)
Beta blockers that start with A-M
are B1 blockers
Beta blockers that start with N-Z
are B2 blockers
Beta-blocker treatment for HTN
decreased CO, decreased renin production (b1-blockade of JG cells). JG cells release Renin
Beta-blocker treatment for Angina
decreased HR, decreased isotropy, decreased myocardial O2 consumption
Beta-blocker treatment for MI
decreased mortality with use of metoprolol, carvedilol, and bisoprolol
Beta-blocker treatment for SVT
propanolol/esmolol to decrease AV conduction.
Heart failure (CHF)
slows progression of CHF (decreased cardiac demand)
Side effects of Beta-blockers include?
Exacerbation of asthma, impotence, bradycardia, AV blockade, sedation, Decreased glucagon secretion

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