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Mech: muscarinic AND nicotinic stimulation S: Rarely used (ophthalmic) |
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Bethanechol (choline ester) |
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M: some GI/ urinary bladder selectivity (some M3 Selectivity S: promotes voiding by contraction of the detrusor and relaxation of the trigone and sphincter. Used to treat urinary retention when obstruction is absent |
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M: stimulates muscarinic receptors S: not used clinically and found in some mushrooms |
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M: muscarinic stimulation S: topical ophthalmic use to induce pupil constriction and decrease intraocular pressure during glaucoma |
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M: Acetylcholinesterase inhibitors S:counter anticholinergic toxicity IS NOT A QUATERNARY COMPOUND AND CROSSES THE BLOOD BRAIN BARRIER!!! |
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M: Acetylcholinesterase Inhibitor S: stimulate visceral smooth muscle |
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M: competitively inhibits the binding and stimulation of muscarinic receptors by ACh and other muscarinic agonists S: ENTERS CNS primary concerns: tachyarrhythmia, prolonged GI stasis, urine retention. Used during anesthesia to decrease salivary and airway secretions. Increased salivation possible |
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M:cholinergic antagonist S: similar effects as atropine. low dose: slight sedation high dose: excitement |
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M: Cholinergic antagonist S: Similar to atropine but NO CNS EFFECT used during general anesthesia to decrease salivary and airway secretions and to PREVENT BRADYCARDIA |
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M: Cholinergic antagonist S: used in the eye to produce mydriasis (dilation) and cycloplegia (cant focus) for ophthalmic exam shorter duration of action than atropine |
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M: Cholinergic antagonist S: Decrease bronchoconstriction and airway secretions NO ENTRY INTO CNS Promote bronchodilation |
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M: Cholinergic antagonists S: promote urine retention |
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M: Competitive NMJ blocker S: long duration,(2-3hr) renal elimination (increased half-life w/ renal dz) |
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M: Competitive NMJ blocker S: intermediate duration (.5-1 hr) spontaneous degradation (temp and pH dependent- reduced with hypothermia and acidosis, leading to incrased half life and duration of action) and hydrolysis HALF LIFE NOT INCREASED W/ RENAL DZ |
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M: Competitive NMJ blocker S: Short duration (15 min) rapid hydrolysis - half life not increased with renal dz promotes histamine release |
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M: Depolarizing NMJ blocker (non-competitive NMJ blocker) S: cause prolonged motor end plate depolarization by stimulation of NMJ nicotinic receptors rapid onset (1min) Ultra short acting (5min) histamine release hyperkalemia |
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M: adrenergic agonist S:Potent A and B agonists B1: increased cardiac output A1: vasoconstriction B2: increase skeletal muscle blood flow low dose: decrease BP via B2 dominance High dose: Increase BP via A1 dominance B2 powerful bronchodilator |
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M:adrenergic agonist S: major NT released by post ganglionic sympathetic nerves B1 EPI = NE B2: EPI >>>>> NE B3: EPI>NE intense vasoconstriction and increase in BP WILL NOT ACT ON B2 (NO LUNG EFFECT) |
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M: Adrenergic Agonist S: (low dose) stimulates vascular D1 receptors= vasodilation and increases renal blood flow and sodium excretion stimulates Cardiac B1 receptors- positive inotropic effect = Increase CO
(Higher Dose) stimulate vascular A1 receptors Vasoconstriction and decrease renal blood flow
USe low dose IV infusion for CHF with compromised renal function |
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M: Non- Selective B adrenergic agonist S: increased cardiac contractility (B1) with minimal changes in HR MINIMAL CHANGE IN BP |
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M: Selective B2 adrenergic agonist S: B2 agonist= Bronchodilator |
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M: Selective B2 adrenergic agonist S: used for allergic bronchitis, recurrent airway obstruction (heaves) |
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M: Selective A1 adrenergic agonist S: A1= vasoconstrictor. Decongestant, vasopressor |
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M: Selective A2 adrenergic agonist S: A2 agonist= CNS Depression Widley used as adjunct for sedation, anesthesia, and analgesia in veterinary med. High Safety profile which Allows for a lower dose of other anesthetic/analgesic agents with lower safety profiles |
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M: Non selective A antagonists. blocks irreversibly A1 and A2 receptors S: reduces urethral sphincter tone |
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M: Non-selective A antagonists. reversibly blocks A1 and A2 receptors S: increases urethral tone |
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M: Selective A1 adrenergic antagonists S: relax ARTERIAL AND VENOUS smooth muscle = vasodilation |
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M: Selective A2 adrenergic antagonists S: used to reverse sedative and analgesic effects of medetomidine. rapid reversal of sedation (min) with minimal risk for relapse into sedation Increases sympathetic activity |
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M: Nonselective B adrenergic antagonist with equal affinity for B1 and B2 receptors S: antiarrhythic action from decreased sympathetic stimulation. decreases HR, reduce Cardiac O2 demand |
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M: nonselective B adrenergic antagonist S: ocular use to decrease aqueous humor production during glaucoma |
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M: Selective B1 adrenergic antagonists S: Decreases heart rate and cardiac contractility - excessive sympathetic stimulation is proarrythmogenic, decrease cardiac arrhythmias |
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M: Class 1A: moderate conduction slowing S: prolongs the refractory period. Use: supraventricular tachycardia |
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M: Class 1B little conduction slowing. binds to inactivated sodium channels and keeps them in the inactivated state. S: Shortens refractory period. Use: ventricular tachycardia |
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M: Class 1 C: PROFOUND decrease in conduction vel. S: Use only in life threatening arrhythmias HUGE Tachycardia or fibrillation |
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M: Class 3: action potential prolonging Predominatly block K channels, thereby prolonging the action potential which increases the refractory period. S: do not affect the Na channels |
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M:Class 4: calcium channel blockers primary effect is to slow AV nodal conduction Use: decrease ventricular response to atrial fibrillation |
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Blocks AV nodal conduction |
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M:PDE3 Inhibitor- increase PKA activity-leads to increased calcium channel activity - increased ca- increased contraction S: increases calcium influx S: |
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M:Cardiac glycoside. Inhibition of the NA/K ATPase-increases intracellular sodium Na/Ca exchanger- activity is regulated Solely by the concentration of sodium and ca. Increased Sodium in the cell will decrease calcium efflux through the exchanger S: Decreases calcium efflux LOTS of other effects. Na/K ATPase is found in all cells |
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M: Enhance the contractile process directly. Increases calcium binding to troponin C. Enhances myocardial contraction. S: This effect requires only a small increase in energy (O2). Not associated with arrhythmias |
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M: ACE inhibitor. Prevents conversion of Ang 1 to Ang 2 |
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M: angiotensin receptor antagonist of AT1 receptors. Blocks pro-hypertensive effects of Ang 2 |
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M: Calcium channel antagoinist by decreasing channel activity S: usually temporary and it decreased total peripheral resistance |
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M: G THANG! NO-GC-cGMP-PKG S:Effect is VENOUS dilation |
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M: G thang!! NO-GC-cGMP-PKG S:Arterial AND venous dilation Light sensitive. sunlight produces cyanide. Should be slightly brownish. |
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M:Phosphodiesterase Type 5. Inhibition results in increased levels of cGMP which lead to increased PKG activity which leads to decreased Ca S: USeful for managing pulmonary hypertension throught vasodilation |
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M:Osmotic Diuretic. Amount filtered exceeds tubular transport. S:Used to treat or prevent oliguric renal failure, cerebral edema, acute glaucoma |
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M: Carbonic ANhydrase Inhibitor Increase loss of Bicarb and tendency to increase urine pH S:Weak diuretic effect. Used to treat metabolic alkalosis, glaucoma, altitude sickness |
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M:Loop Diuretic. Inhibit NaCl reabsorption in the thich ascending limb of the LOH. MOST EFFECTIVE DIURETIC S:May cause hypokalemia. May increase urinary loss of Ca. Used to treat oliguric renal failure, CHF, acute pulmonary hypertension |
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M: THiazide Diuretic. Block the Na/Cl channel. S: Not as effective as loop diuretics. Used to treat nephrogenic diabetes insipidus, udder edema in cattle, Ca containing uroliths |
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K Sparing Diuretics M: blocks aldosterone induces expression of multiple genes S: In vet med. most often used in combo with a loop diuretic |
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K Sparing Diuretic M: epithelial sodium channel blocker S: used in combo with loop diuretics |
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