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52 Cards in this Set
- Front
- Back
Bethanechol
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Direct muscarinic agonist
used Post-Op for neurogenic ileus and urinary retenion |
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Carbachol
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Direct muscarinic agonist
Glaucoma, pupillary contraction, and release of intraocular pressure |
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Pilocarpine
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Direct muscarinic agonist
Potent stimulator of tears, sweat, and saliva. Used in treatment of Sjogren's syndrome. |
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Methacholine
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Direct muscarinic agonist
Potent bronchoconstrictor, used in challenge test for asthma |
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Neostigmine
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Indirect muscarinic agonist (anticholinesterase)
4* amine -> ionized..cannot enter CNS. Used for treatment of myesthenia gravis, neurgenic ileus, and urinary retention. |
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Pyridostigmine
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Indirect muscarinic agonist (anticholinesterase)
Myestehania gravis (long acting); does not penetrate CNS; 4* amine which means it is ionized, cannot enter CNS. |
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Edrophonium
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Indirect muscarinic agonist (anticholinesterase)
Used for diagnosis of myestehnia gravis...can also be used to differentiate between myesthenia gravis or cholinergic crisis |
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What is a cholinergic chrisis?
What is the main conern? |
A cholinergic crisis is when the ACh receptor no longer responds to ACh...this occurs when anticholinesterases are used. The problem is that you can't give an agonist (receptors won't respond!). An antagonist would give the same problem, which is flaccid paralysis.
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What is the main difference in indirect agonists vs. direct agonists for muscarinic receptors?
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Direct receptors do not need a neurotransmitter to ellicit it's effects. Indirect receptors act on neurotransmitters.
Direct agonists can act on the endothelium muscaranic receptor, which has no nerve connections. Indirect agonists have no affect. Endothelium receptor causes release of NO, which causes vasodilation. |
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Physostigmine
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Indirect muscarinic agonist (anticholinesterase)
Tertiary amine (3*)...this means it is unionized and has good entry into CNS. It is primarily used for glaucoma and atropine overdose |
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Echothiphate
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Organophosphate- Indirect muscarinic agonist (anticholinesterase)
used primarily in glaucoma |
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Donepezil
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Indirect muscarinic agonist (anticholinesterase)
Crosses into CNS - used for alzheimers (can lead to respiratory failure becuase of patient population and muscarinic side effects) |
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Tacrine
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Indirect muscarinic agonist (anticholinesterase)
Crosses into CNS - used for alzheimers (can lead to respiratory failure becuase of patient population and muscarinic side effects |
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Organophosphates
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Indirect muscarinic agonist -anticholinesterase
Very lipid soluble and irreversibly phosphorylates choinesterase; main affect is flaccid paralysis. Tx - is Pam-2 (pralidoxime), but must be given within 6 hours. PAM-2 works by removing an R-group, which is bound to the phosphate inhibiting cholinesterase. Some nerve gases hydrolize the R group within 2 minutes. Once R group is removed, phosphorylation is irreversible. Chronic organophosphate exposure can lead to demylelination, which can lead to motor and sensory losses. |
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What are the three main effects you should think about when thinking about muscarinic agonists?
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Heart - decrease rate via M2
Secretions - increased via M1/M3 Smooth muscle contractions - increased via M1/M3 (also can cause vasodilation if direct acting agonist, via NO release) |
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Atropine
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Muscarinic antagonist...atropine effects increase with doses
1. Decreases secretions 2. Pupil dilation (mydriasis) and cycloplegia 3. Hyperthermia = all secretions decreased, so increase core temp. Can't sweat, so get vasodilation as cooling response...red face. 4. Tachycardia - AV nodal block (risk for arrythmia) - block at M2 receptor. 5. Sedation - block of ACh receptors in CNS causs Alzheimers like effects - memory losses/dementia 6. GI/GU - constipation, urinary retention. |
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Benztropine
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Muscarinic antagonist
Used mainly in Parkinson's treatment. A decrease in dopaimine leads to an increase of ACh...an increase of ACh leads to tremor and rigitidy. |
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Trihexyphenydyl
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Muscarinic antagonist
Used mainly in Parkinson's treatment. A decrease in dopaimine leads to an increase of ACh...an increase of ACh leads to tremor and rigitidy. |
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Scopolamine
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Muscarinic antagonist
penetrates CNS and goes to 8th nerve, blocks ACh receptors and is useful for treatment of motion sickness. |
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Pirenzepine
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Muscarinic antagonist
Mostly GI effects - used in peptic ulcer treatment |
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Propantheline
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Muscarinic antagonist
Mostly GI affects, used for peptic ulcer treatment |
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Hexamethonium
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Nictonic antagonist - blocks ANS at level of ganglia.
Prevents reflex responses to blood pressure changes |
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Mecamyline
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Nictonic antagonist - blocks ANS at level of ganglia.
Prevents reflex responses to blood pressure changes |
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Other classes of anti-muscuranic drugs
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1. Antihistamines (decrease secretions)
2. TCA's - go to CNS - can cause three C's = coma, convulsions, and cardiotoxicity (arrythmias) 3. Quinidine - anti-arythmatic, but can cause anti-artythmias. 4. Meperidine - opiate w/ potential anti-muscarinic affects. |
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Isoproterenol
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Direct agonist of B1 and B2 receptors equally.
Used for bronchospasms, heart shock, and bradyarythmias. |
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Phenylephrine
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a1 direct agonist - fast vasoconstriction - used mainy for nasal sprays and eye drops, but not well used due to danger of hypertensive crisis
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Albuterol
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Selective B2 agonist - used for asthma
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Methoaxamine
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a1 agonist - increases BP - used to illicit reflex bradychardia
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Dobutamine
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B1 selective agonist …use this in congestive heart failure. In chronic heart failure, the receptors wouldn’t really work well anymore. Lack of beta 2 will minimize vasodilation and hypotension. Use as a positive inotropic agent.
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Salmeterol
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selective B2 agonist, asthma
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Metaproterenol
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Selective B2 agonist, asthma
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Salmeterol
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Selective B2 agonist, asthma
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Terbutaline
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selective B2 agonist, asthma
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Ritodrine
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B2 agonist - reduces premature utrine contractions
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Amphetamine
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Indirect general sympathetic agonist - releases catelcholamines from pool inside cell. NEVER USE WITH MAO inhibitor.
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Cocaine
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Indirect general sympathetic agonist - releases catelcholamines from pool inside cell. NEVER USE WITH MAO inhibitor.
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Ephedrine
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Indirect general sympathetic agonist - releases catelcholamines from pool inside cell. NEVER USE WITH MAO inhibitor.
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Clonidine
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Centrally acting alpha 2 agonist...might get transient hypertension a tfirst, but after a few days will decrease hypotension
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a-methyl-dopa
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Centrally acting alpha 2 agonist...might get transient hypertension a tfirst, but after a few days will decrease hypotension
Treatment of choice for pregnant women |
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Epinephrine - low dose, medium dose, and high dose
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low dose epinephrine will bind to B1 and B2 receptors, so get an increase in HR (increase in systolic pressure) with a decrease in TPR (decrease in systolic) - this leads to a decrease in pulse pressure
Medium dose - starts to bind alpha 1 receptors, so get increase in TPR, but B2 will still be active, so no change in BP...however you will still have increased heart rate due to the strong B1 response, so increase in HR with no change in BP! High Dose - will bind to alpha 1, which will lead to an increase in BP....you will still have B1 activity, but B2 activity will be completely masked by A1 activity...dangerous increase in HR and BP. |
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Norepinephrine
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vasoconstriction leads to an increased in BP….also get a B1 stimulation of tachycardia….eventually you’ll get a reflux bradychardia (refluxes predominate!). This is not due to drug, baroreceptor reflex.
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Dopamine
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– at high doses, it can bind to other receptors….at lowest dowest it will bind to lowest receptors…great effect on coronary/renal….at medium doses, binds B1….this is beneficial in situations like shock…increase perfusion and increase heart rate. What about high levels of dopamine – A1 receptor – not good! This would increase ischemic potential. What if you block A1…you would go from hypertension to hypotension (just like epinephrine!), but by D1
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Phentolamine
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Comptitive inhibitor of alpha receptors..nonselective
Nonselective blockers – very opposing effects….alpha 1 blockade would drop blood pressure immediately, but it would raise up again due to alpha 2 blockade |
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Phenoxybenzamine
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non-selective alpha blocker
non-competitive inhibitor Phenoxybenzamine can’t be displaced from receptors, so getting an increased blood pressure wouldn’t be an issue here. What if you get an excessive response though? Nothing you can do, so it is dangerous….only used in hypertensive crisis. |
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Prazosin, terazosin, doxazosin
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Alpha 1 selective blocker - used for urinary retention in BPH...why? Relaxes sphincters!
Can also be used for hypertension...good co-morbid affect. |
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Mirtazapine
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A-2 selective blocker - used for depression
Toxicity? Sedation, increased serum cholesterol, and increased appetitie. |
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yohimbine
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selective alpha 2 blocker...used for sexual dysfunction.
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Who should Beta Blockers be avoided in? Why?
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Diabetics, due to their effects on insulin and glycogen release.
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Which type of Beta Blockers are selective for B1?
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Any Beta Blockers whose name starts with A-M
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What are the 2 Partial B agonists?
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Acebutolol (B1), pindolol
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Non selective alpha and B antagonists?
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Carvedilol, labetalol...used in CHF.
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What is an open angle glaucoma and what drug would you use to treat it?
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Open angle glaucoma is where there is no physical obstruction; the defect is at the canals of Schlemm, therefore primary treatment would be to reduce aquous humor.
Alpha agonist would decrease aqueous humor synthesis due to vasoconstriction (epinephrine or brimonidine) A B-blocker would decrase aqueous humor secretion (Timolol, betaxolol, carteolol) A closted angle glaucoma is when the iris is blocking the angle of outflow...you would want to constrict the iris in order to increase outflow...Pilocarpine would be the main treatment. Could also use echothiophate. |