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Y2S1B2

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ANS drugs
Features
Autonomic Nervous System   Enteric (semiautonomous), Parasympathetic (CN III, VII, IX, X and S2-S4), Sympathetic (T1-12, L1-L5)  
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Cholinomimetic (cholinergic) Drug Breakdown: Direct Acting   Muscarinic (choline esters, alkaloids) and Nicotinic  
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Cholinomimetic (Cholinergic) Drug Breakdown: Indirect Acting   Edrophonium (short-acting), Carbamates (intermed-long acting), Organophosphates (very long-acting)  
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Adrenergic Agonists: Adrenoceptors   alpha1, alpha2, beta1, beta2  
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Adrenoceptors: alpha1   vasoconstriction, inc peripheral resistance, inc BP, inc closure of internal bladder sphincter, mydriasis  
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Adrenoceptors: alpha2   inhibition of NorEpi release, inhibition of insulin release  
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Adrenoceptors: beta1   tachycardia, inc lipolysis, inc myocardial contractility, inc release of renin  
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Adrenoceptors: beta2   vasodilation, slight dec peripheral resistance, bronchodilation, inc release of glucagon, relaxed uterine smooth muscle  
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ANS Direct-acting drugs   muscarine, carbachol, bethenachol, pilocarpine, nicotine, succinylcholine  
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ANS Indirect-acting drugs   echotiphate (irreversible), edrophonium, neostigmine, pyridostigmine, physostigmine, parathion, malathion, dichlorvos  
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Other ANS drugs   Acetylcholine, botulinum toxin, cocaine, dopamine, epinephrine, metanephrine, norepinephrine, saxitoxin, tetrodotoxin  
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Neurotransmitters: Parasympathetic NS   pre - ACH, post - ACH  
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Neurotransmitters: Sympathetic NS   pre - ACH, post - NE  
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Innervation of end organs:   some innervated by either PNS or SNS; some innervated by BOTH (PNS effect is usu opposite SNS);  
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Innervation of end organs: discharge pattern   PNS - "discrete" 1pre to 1 post; SNS - "diffuse" 1pre to many post  
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ANS Receptors: cholinergic   mucarinic, nicotinic  
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ANS Receptors: adrenergic   alpha, beta  
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Muscarinic Cholinergic Receptors: M1   CNS, ANS ganglia  
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Muscarinic Cholinergic Receptors: M2   heart  
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Muscarinic Cholinergic Receptors: M3   smooth muscle, glands  
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Muscarinic Cholinergic Receptors: M4 and M5   CNS  
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Nicotinic Cholinergic Receptors: Nn   CNS, ANS ganglia  
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Nicotinic Cholinergic Receptors: Nm   skeletal muscle  
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Neurotransmission   most NTs don't cross membranes; each binds to specific ptn receptors: Ion channels (change membrane pot/ion conc); Adenyl cyclase (inc ptn phosphorylation); DAG/IP3 (inc ptn phosph and intracellular Ca)  
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NT Release: Ca-dependent Exocytosis   AP --> depolarization --> enhanced Ca entry to nerve terminal; Ca enables fusion of storage granule ptns (synapsin/synaptobrevin) w/nerve terminal membrane followed by NT release  
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ACH Release - Quantal   Storage (one granule has <50K ACH molec); Release (ACH released from several hundred quanta)  
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Presynaptic Regulation of Transmitter Release: Autoreceptors   respond to NT released from its own nerve terminal; usu inhibits release of more NT  
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Presynaptic Regulation of Transmitter Release: Heteroreceptors   respond to NTs released from other nerve terminals or substances from nearby tissue or blood  
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Presynaptic Regulation of ACH Release: Dec ACH release from PNS - M2, M4 presynaptic receptors   stimulated by ACH released from PNS nerve terminals  
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Presynaptic Regulation of ACH Release: Dec ACH release from PNS - a2a, a2c presynaptic receptors   stimulated by NE released from SNS nerve terminals  
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Presynaptic Regulation of ACH Release: Inc ACH release from spinal nerves - Nn receptors   stimulated by ACH released from spinal nerves to skeletal muscle; prolongs NMJ fxn during prolonged high-frequency contraction of skeletal muscle  
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Stress Reaction: SNS in action - "Fight or Flight"   inc flow of oxygenated blood; inc skeletal muscle contractility; inc blood glucose; inc platelet aggregation; inc pupil diameter (mydriasis)  
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Stress Reaction: Increased flow of oxygenated blood - b2   dilate bronchi and vessels to skeletal muscle  
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Stress Reaction: Increased flow of oxygenated blood - b1   positive chronotropic (rate) and inotropic (force of contraction) cardiac effects  
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Stress Reaction: Increased flow of oxygenated blood - a1   constrict arteries to skin, GI, kidney and shunt blood to skeletal muscles; contracts spleen to inc RBCs in blood  
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Stress Reaction: Increase skeletal muscle contractility - b2   EPI increases rate and force of contraction  
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Stress Reaction: Increase/Maintain Blood Glucose - a1, b2   increase glycogenolysis  
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Stress Reaction: Increase/Maintain Blood Glucose - b2   increase glucagon secretion  
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Stress Reaction: Increase/Maintain Blood Glucose - a2   decrease insulin secretion  
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Stress Reaction: Platelet aggregation - a2   increases  
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Stress Reaction: eye - a1   contracts radial muscle of iris ==> mydriasis  
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Stress Reaction: eye - b2   relaxes ciliary muscle for far vision  
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Stress Reaction: sweat glands - a1   increase activity  
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Stress Reaction: sweat glands - M3   increases sympathetic cholinergic  
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Visual Accomodation - SNS   distant vision accomodation: relaxes ciliary body, tension on lens, flattens lens  
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Visual Accomodation - PNS   near vision accomodation; contract ciliary body, lessen tension on lens, thickens lens  
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Visual Accomodation - cycloplegia   loss of accomodation d/t antimuscarinic drugs (atropine)  
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Enteric Nervous System: myenteric and submucosal plexuses   contain interneurons w/transmitters ACH, NE, Substance P, enkephalins, vasoactive intestinal peptide (VIP); local reflexes maintain peristalsis/secretion; innervated by PNS, SNS and sensory nerves  
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Enteric Nervous System: ANS   modulates neural regulation  
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Enteric Nervous System: PNS   directly innervates smooth muscle and glands of gut  
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Enteric Nervous System: SNS   inhibits gut motility and secretions; synaps w/ PNS cells w/in intramural plexuses inhibits ACH release from PNS nerve terminals  
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Direct Acting: Muscarinic Agonists - Pilocarpine   Glaucoma  
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Direct Acting: Muscarinic Agonists - Carbachol   Glaucoma  
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Direct Acting: Muscarinic Agonists - Behanechol   postoperative ileus, megacolon, urinary retention  
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Indirect Acting: ACHE Inhibitors - Physostigmine   glaucoma  
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Indirect Acting: ACHE Inhibitors - Echothiophate   glaucoma  
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Indirect Acting: ACHE Inhibitors - Isoflurophate   glaucoma  
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Indirect Acting: ACHE Inhibitors - Decamerium   glaucoma, treats myasthenia gravis  
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Indirect Acting: ACHE Inhibitors - Edrophonium   diagnose myasthenia gravis; reverses NM blockade; supraventricular tachyarrhythmia  
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Indirect Acting: ACHE Inhibitors - Neostigmine   glaucoma, post-op ileus, megacolon, urinary retention, reverse NM blockade  
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Neurotransmission: Muscarinic Receptor Agonists   inc cGMP; inhibits cAMP activity; attenuate inc cAMP induced by EPI, NE; stimulates DAG and IP3 to inc phosphorylation and intracellular Ca  
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The Plan: Parasympathomimetic   Direct: Muscarinic receptor agonists; Indirect: Inhibits ACHI  
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The Plan: Parasympatholytic   Direct: Receptor antagonists; Indirect: Decrease ACH release  
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Parasympathomimetic Therapy Overview: Muscarinic Agonists   glaucoma, post-op ileus, congenital megacolon, urinary retention  
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Parasympathomimetic Therapy Overview: ACHE inhibitors   glaucoma, post-op ileus, congenital megacolon, urinary retention, diagnose/treat myasthenia gravis; reverse neuromuscular blockade; Alzheimer's disease  
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Parasympathetic Therapy Overview: Muscarinic Antagonists   antsecretory; examin retina/measure refraction; hypermotility of GI and urinary tract; urinary incontinence; IBS; COPD; Parkinson's Disease  
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Parasympathetic Therapy Overview: Ganglionic Blockers   hypertensive emergency  
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Parasympathomimetic Amines: adverse drug reactions (ADRs)   avoid IM or IV injections: hypotension (reflex tachycardia); miosis; hypersalivation/sweating; bronchoconstriction; GI discomfort; impaired cognition (pilocarpine)  
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Parasympathomimetic Amines: Contraindications   Asthma, CAD, bradycardia, peptic ulcer, GI/GU hypermotility or obstruction, COPD, HYPOtension  
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Parasympathomimetic Amines: Treatment of Glaucoma - Open Angle Primary   ocular angle is open; abnormal trabecular network impedes drainage of aqueous humor  
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Parasympathomimetic Amines: Treatment of Glaucoma - Open Angle Secondary   d/t inflammation, trauma, or ocular disease  
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Parasympathomimetic Amines: Treatment of Glaucoma - Mechanism and Caution   contract longitudinal ciliary muscle --> stretch/open trabecular network; Miosis --> iris moves away from ocular angle; Caution: Reduced accomodation  
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Parasympathomimetic Amines: Treatment of Glaucoma - Closed Angle   Medical emergency; lense position blocks access of aqueous humor to trabecular network; indication - short term prior to surgery; caution: Rx may inc IOP (miosis --> iris presses against lens and blocks anterior chamber)  
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Parasympathomimetic Amines: Pilocarpine, Pilocar, Pilopine HS Gel, Ocsert (time release); tertiary amine; lipophilic; pure muscarinic agonist   open-angle glaucoma - parasympathomimetic amine of choice; Xerostomia d/t radiation or Sjogren's syndrome (Cevimeline, Evoxac)  
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Parasympathomimetic Amines: Bethenechol (Urecholine)   relatively specific for M3 receptors of GI and GU; post-op urinary retention; GERD - inc LES pressure; Caution w/IM or IV injection --- circulatory collapse/cardiac arrest  
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Direct Acting Parasympathomimetic Amines: Muscarine alkaloids/Amanita muscaria ADRs   mushroom poisoning onset 15-30min; N&V, diarrhea; bronchial constriction; cutaneous vasodilation  
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Indirect Acting Parasymathomimetic Drugs: Reversible ACHE Inhibitors   broader use than muscarinic agonists; Reversible (Neostigmine, Prostigmin) and Irreversible (Organophosphates)  
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ACHE Inhibitor duration of action: Edrophonium   5-15 min  
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ACHE Inhibitor duration of action: Neostigmine   30min - 2hr  
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ACHE Inhibitor duration of action: Physostigmine   30min - 2hr  
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ACHE Inhibitor duration of action: Pyridostigmine   3 - 6hrs  
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ACHE Inhibitor duration of action: Ambenonium   4 - 8hrs  
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ACHE Inhibitor duration of action: Demacarium   4 - 6hrs  
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ACHE Inhibitor duration of action: Echothiophate   100hrs  
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Indirect Acting Parasympathomimetic Drugs: Reversible ACHE Inhibitors - Neostigmine (prostigmin)   urinary retention (contract bladder wall/relax internal sphincter); Parylitic Ileus; Open-angle glaucoma; Myasthenia gravis (skeletal muscle weakness d/t dec nicotinic receptors at NMJ; ACHE inhibitors inc ACH to stim available receptors  
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Parasympathomimetic "Irreversible" ACHE Inhibitors: organophosphates   phosphorylated ACHE enzyme is extremely stable; restoration of normal ACH fxn requires synthesis of new ACHE molecules (days); good absorption across body membranes ==> widespread distribution thru body and CNS  
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Indirect Acting Parasympathomimetic "Irreversible" ACHE Inhibitors: Echothiophate (phospholine)   open angle glaucoma (100hr duration)  
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Indirect Acting Parasympathomimetic "Irreversible" ACHE Inhibitors: Diazinon, Malathion, Malaoxon, Parathion   insecticides  
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Indirect Acting Parasympathomimetic "Irreversible" ACHE Inhibitors: Abuse   nerve gas (ricin, sarin, soman, tabun); symptoms occur w/in 6hrs w/50% inhibition; hypotension, miosis, bronchospasm, abdominal cramps, incontinence, arrhythmias, hypertension, respiratory paralysis, tremor, weakness, seizures, coma  
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Indirect Acting Parasympathomimetic "Irreversible" ACHE Inhibitors: Treatment of Nicotinic Effects - Pralidoxime (2-PAM, Protopam)   regenerates ACHE - breaks ACHE-organophosphate bond; IV q 5-30min; repeat in 30min PRN; Rapid injection --> laryngospasm, muscle rigididy, weakness  
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Indirect Acting Parasympathomimetic "Irreversible" ACHE Inhibitors: Aging   breaking one oxygen-phosphorous bond of inhibitor further strengthens phosphorous-enzyme bond  
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Indirect Acting Parasympathomimetic "Irreversible" ACHE Inhibitors: Treatment of Muscarini Effects - Atropine generic   blocks muscarinic receptors; IV q 5-15min to dry bronchial secretions; repeat or constant IV infusion; questionable efficacy to treat CNS toxicity  
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Indirect Acting Parasympathomimetic "Irreversible" ACHE Inhibitors: Treatment of Seizures   benzodiazepines  
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Parasympatholytic Muscarinic Receptor Antagonist: Atropine Indications - adjunct to general anesthesia   reduce bronchial secretion; prevent vagal reflex d/t organ manipulation  
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Parasympatholytic Muscarinic Receptor Antagonist: Atropine Indications - Myocardial Infarction   prevent reflex bradycardia; AV block  
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Parasympatholytic Muscarinic Receptor Antagonist: Atropine Indications - Mushroom poisoning   some mushrooms contain muscarininc alkaloids  
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Parasympatholytic Muscarinic Receptor Antagonist: Atropine Indications - Ophthalmic Examination   ciliary paralysis, mydriasis - facilitates examination of fundus  
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Parasympatholytic Muscarinic Receptor Antagonist: Tolerodyne (Detrol), Oxybutynin (Ditropan) Indications - Urinary incontinence   relax urinary bladder wall; contract internal sphincter  
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Antinicotinic Decreased ACH Release - Botulinum toxin (Botox)   decreases ACH release from spinal nerves into NMJ, temporary paralysis of skeletal muscle  
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Antinicotinic Decreased ACH Release: Botulinum toxin (Botox) Indications - Cosmetic   facial wrinkles (red facial mm contraction); hyperhydrosis, blepharospasm; skeletal muscle spasticity; multiple sclerosis (bladder and bowel symptoms)  
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Neuromuscular Junction Blockers Non-Depolarizing: Curare (d-tubocurarine) Indications - Adjunct to general anesthesia   Reversible competitive blockade of nicotinic receptors of neuromuscular junction --> flaccid paralysis  
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Neuromuscular Junction Blockers Non-Depolarizing: Similar Drugs - Mivacurium (Mivacron)   short acting; 10-20min  
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Neuromuscular Junction Blockers Non-Depolarizing: Similar Drugs - Vecuronium (Norcuron)   intermediate acting; 20-35min  
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Neuromuscular Junction Blockers Non-Depolarizing: Similar Drugs - Doxacurium (Nuromax)   long acting; >35min  
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Neuromuscular Junction Blockers Depolarizing: Succinylcholine (Anectine) Indications - Adjunct to general anesthesia   persistent opening of nicotinic receptor channel --> prolonged depolarization of motor endplate --> loss of electrical excitability; duration ~5-10min  
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Indirect Acting ACE Inhibitors: Ambenonium   treats myasthenia gravis  
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Indirect Acting ACE Inhibitors: Pyridostigmine   Reverses NM blockade  
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ACHE Inhibitors: Role in Alzheimers   40-90% dec in choline acetyltransferase in cortex/hippocampus b/f sx; correlation w/ dec ACH, mental status score & sx; Nerves passing thru plaques are damaged and have disrupted NTs; the axons project to cortex/hippocampus for memory/cognition  
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ACHE Inhibitors: Role in Alzheimers - IV physostigmine   significant improvement of visual recognition  
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ACHE Inhibitors: Role in Alzheimers - Butyl-cholinesterase   may have role in plaque development  
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Cholinergic role in Alzheimers - The Flaws   function of other NTs also decrease (seratonin, NE); cholinergic dysfunction may be a result not a cause of Alzheimers  
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ACHE Inhibitor Role in Alzheimers: Tacrine (Cognex) - additional MOA   blocks neuronal K channels prolonging APs to increase amount of ACH released  
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ACHE Inhibitor Role in Alzheimers: Tacrine (Cognex) - Indications   mild to moderate conditions; dose-related improvement of cognition and attention tasks; slow decline may occur  
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ACHE Inhibitor Role in Alzheimers: Tacrine (Cognex) - ADRs   rate limitins/decreased use; liver toxicity; N&V, loose stools, dizziness, HA; tolerance develops to peripehral cholinergic effects  
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ACHE Inhibitors Role in Alzheimers: Donepezil (Aricept)   selective for CNS ACHE; few effects on peripheral ACHE (less effect on GI pseudocholinesterase)!! Long half-life = once daily dosing; mild to moderate improvement of cognitive testing/caregiver impression scale; efficacy dec w/continued therapy  
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NMDA Antagonists Role in Alzheimers: Memanthine (Namenda)   dose-dependent blockade of glutamine receptors; efficacy reduces rate of clinical deterioration; ADRs - HA, dizziness (mild, reversible)  
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ACHE Inhibitor Role in Alzheimers: Rivastigmine (Exelon)   efficacy, ADRs similar to donepezil  
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ACHE Inhibitor Role in Alzheimers: Galantamine (Razadyne)   efficacy and ADRs similar to donepezil and rivastigmine  
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Adrenergic Receptor Typical Effects: alpha1   stimulates  
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Adrenergic Receptor Typical Effects: alpha2   inhibits  
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Adrenergic Receptor Typical Effects: beta1   stimulates (heart)  
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Adrenergic Receptor Typical Effects: beta2   inhibits (bronchi of lung; dilation)  
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Adrenergic Receptor Typical Effects: beta3   stimulates lipolysis in fat cells (beta1 and beta2 have minor role)  
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Sympathomimetic: Direct acting   receptor agonist  
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Sympathomimetic: Indirect acting   increases synaptic NE  
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Sypatholytic: Direct acting   receptor antagonist  
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Sympatholytic: Indirect acting   decrease synaptic NE  
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Adrenergic Agonists: Structure/Activity Relationship: Non-catechol Amines (phenylephrine and amphetamine)   remove OH at benzene ring position 4; Less a and b receptor affinity than EPI; Poor substrates for MAO and COMT (won't be catalyzed as fast; last longer than NE); Oral absorption, long duration of action; Penetrates BBB (lipid soluble)  
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Adrenergic Agonists: Structure/Activity Relationship: Catecholamines (EPI, NE, Isoproterenol)   Agonist of a and b receptors (both OH needed for max binding); Do NOT cross BBB; Metabolized by neuronal MAO and COMTof liver/GI; Not orally active; Short duration; Readily oxidized (light/pH sensitive)  
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Adrenergic Agonists: Structure/Activity Relationship: alpha Carbon Substitution   poor substrates for MAO; prolongs duration of action of catecholamines and non-catecholamines  
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Adrenergic Agonists: Structure/Activity Relationship: beta OH   required for storage in nerve terminal granules  
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Adrenergic Agonists: Structure/Activity Relationship: Amine Nitrogen Substitution   beta receptor affinity increases as group on amine nitrogen increases in size (EPI > NE)  
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Adrenergic Agonists: Examples of Non-catecholamines   Amphetamine, Ephedrine, Dobutamine, Methyphenidate, Albuterol, Phenylephrine  
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Synthesis of Catecholamines   Tyrosine --> DOPA --> Dopamine --> NE --> EPI (bulkier amines stimulate beta receptors)  
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Cocaine   blocks reuptake of NE into nerve terminal  
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Alpha 2 receptors stimulated on nerve terminal has:   negative feedback on NE release  
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Radial m. of eye: SNS effect, adrenergic receptor   contracts (mydriasis); alpha1  
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Circular m. of eye: PNS effect; cholinergic receptor   Contract (miosis); M3  
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Trabecular network of eye: SNS Effect; Adrenergic Receptor   Increases outflow of aqueous humor; alpha2  
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Trabecular Network of eye: PNS effect; Cholinergic Receptor   Increases outflow of aqueous humor; M3  
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Ciliary Process (epithelium) of Eye: SNS Effect, Adrenergic Receptor   Increased synthesis of aqueous humor; Beta2 OR Decreases synthesis of aqueous humor; alpha2  
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Lungs: SNS Effect, Adronergic Receptor   Dilates; beta2  
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Lungs: PNS Effect; Cholinergic Receptor   Contract; M3  
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Heart Rate: SNS Effect: Adrenergic Receptor   increases; beta1  
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Heart Rate: PNS Effect: Cholinergic Receptor   Decreases; M2  
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Heart Force: SNS Effect: Adrenergic Receptor   Increases; beta1  
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Heart Force: PNS Effect: Cholinergic Receptor   Decreases; M2  
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Blood Vessels: SNS Effect; Adrenergic Receptor   constrict; alpha1  
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Coronary Arteries: SNS Effect; Adrenergic Receptor   dilate; inc work of heart increases synthesis of adenosine (vasodilator)  
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Coronary Arteries: PNS Effect; Cholinergic Receptor   Dilate; M2  
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Blood Vessels in Skeletal Muscle: SNS Effect; Adrenergic Receptor   Dilate; beta2  
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Skeletal Muscle Contractility: SNS Effect; Adrenergic Receptor   increases; beta2  
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Spleen: SNS Effect: Adrenergic Receptor   contracts; alpha1  
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Platelet aggregation: SNS effect; adrenergic receptor   increases; alpha2  
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Apocrine sweat glands (stress): SNS effect; adrenergic receptor   increases; alpha1  
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Sweat gland temperature regulation: SNS effect; Adrenergic Receptor   increases; M3 sympathetic cholinergic  
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Liver Glycongenolysis: SNS Effect; Adrenergic Receptor   Increases; alpha1, beta2  
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Fat Cell Lipolysis: SNS Effect; Adrenergic Receptor   increases; beta3 (small role of b1/b2)  
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Pancreas Insulin secretion: SNS Effects; Adrenergic Receptor   Decreases; alpha2 OR Increases; beta2  
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Pancreas Glucagon Secretion: SNS Effects; Adrenergic Receptor   Increases; beta  
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GI tract wall: SNS Effect; Adrenergic Receptor   relaxes; alpha2, beta2  
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GI tract wall: PNS Effect; Cholinergic Receptor   contracts; M3  
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GI tract secretion: PNS Effect; Cholinergic Receptor   Increases; M3  
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Kidney Renin Secretion: SNS Effect; Adrenergic Receptor   increases; beta1  
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Nasal, salivary, gastric secretory glands: SNS Effect; Adrenergic Receptor   decrease; alpha1  
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Nasal, salivary, gastric secretory glands: PNS Effect; Cholinergic Receptor   Increases; M3  
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Bladder Wall: SNS Effect; Adrenergic Receptor   relaxes; beta3  
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Bladder wall: PNS effect; cholinergic receptor   contracts; m3  
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Bladder internal sphincter: SNS effect; adrenergic receptor   contracts; alpha1  
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Bladder internal sphincter: PNS effect; cholinergic receptor   relaxes; M3  
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Ureter: SNS effect; adrenergic receptor   contracts; alpha1  
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Ureter: PNS effect; cholinergic receptor   relaxes; M3  
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Prostate capsule: SNS Effect; adrenergic receptor   contracts; alpha1  
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Uterus (pregnant): SNS effect; adrenergic receptor   relaxes; beta2  
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Uterus (pregnant); PNS effect; Cholinergic receptor   variable; M3  
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Penile arteries: SNS effect; adrenergic receptor   contracts (detumescence); alpha1  
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Penile arteries: PNS effect; cholinergic receptor   relax (erection); M3  
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SNS Postganglionic Nerve Terminal: SNS Effect; Adrenergic Receptor   decrease NE release; alpha2  
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SNS postganglionic nerve terminal: PNS Effect; cholinergic receptor   decreses NE release; M3  
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alpha1 Receptor Effects   contract radial m. of iris (mydriasis); increases sweating (stress); constricts vasculature of skin (inc TPR/BP); contracts spleen/prostate capsule/penile aa/seminal vesicles/bladder&GI sphincters; dec nasal/salivary/gastric secretions  
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alpha2 Receptor Effects   inhibit NE release; inhibit insulin release; dec synthesis of aqueous humor; increase platelet aggregation  
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beta1 Receptor Effects   increase rate/force of myocardial contraction; increase renin secretion (inc blood vol); relaxes ciliary m.  
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beta2 Receptor Effects   inc synthesis of aqueous humor; dilate bronchi; relax GI wall/bladder wall/pregnant uterus; inc skeletal muslce & liver glycogenolysis; inc glucagon secretion; inc skeletal m contractility  
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Metabolic Effects of beta receptors: Glycogenolysis   skeletal muscle (b2); liver (b2, a1)  
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Metabolic Effects of b receptors: Lipolysis   fat cells: b3 (a1, b1, b2)  
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Epinephrine (adrenaline, epipen): non-selectice a/b agonist (a1, b1, b2)   vasoconstriction (skin), inc rate/contractility of heart, dilates bronchi;  
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Epinephrine (adrenalin, epipen): Cardiac Arrest   injected directly into heart for b1 effects  
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Epinephrine (adrenalin, epipen): Hypersensitivity/Anaphylaxis   antagonize vasodilation induced by histamine/leukotrienes (normalize permeability of venules); beta2 bronchodilation inhibits release of inflammatory mediators  
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Epinephrine (adrenalin, epipen): Adverse Drug Reactions   tachycardia, increased BP  
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Epinephrine (adrenalin, epipen): Topical Hemostasis   a1 vasoconstriction; also prolongs effect of local anesthetics  
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Norepinephrine (noradrenalin, levophed): a/b non-selective agonist (a1, b1)   vasoconstriction, positive cardiac chrono/inotropic effects (VERY little effect on b2 vasodilation)  
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Norepinephrine (noradrenalin, levophed): Indication   shock - counteracts hypotension  
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Norepinephrine (noradrenalin, levophed): Adverse Drug Reactions   bradycardia (dt baroreceptor vagal reflex); inceased BP  
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Phenylephrine (neo-synephrine)   a1-Selective Agonist  
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Phenylephrine (neo-synephrine): Nasal decongestant   constricts nasal vasculature, shrinks swollen membranes  
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Phenylephrine (neo-synephrine): hypotension   antagonizes hypotension associated w/anesthesia  
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Phenylephrine (neo-synephrine): Mydriasis   contracts radial m. of iris  
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Epinephrine   a1, a2, b1, b2: slight inc in HR; slight drop in peripheral resistance; systolic inc/diastolic dec slightly  
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Norepinephrine   a1, a2, b1; baroreceptor reflex; HR slows; great inc in peripheral resistance; systolic rises/diastolic inc slightly  
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Isoproterenol   b1, b2; HR rises; big drop in peripheral resistance b/c no alpha constriction; systolic slight inc/diastolic drops  
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Miosis drugs   contraction of circular muscle fibers in iris; stimulated and iris goes towards center of pupil  
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Mydriasis drugs   alpha1 are dilator fibers; pulls iris muscle back to get dilation of pupil  
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Oxymetazoline (afrin): a1 selective agonist   nasal decongestant, OTC  
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Metaraminol (aramine): a1 selective agonist   shock-induced hypotension; prescritpion  
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Clonidine (catapres): a2 selective agonist   stimulates a2 presynaptic receptors to dec NE release; used for withdrawal from dependece-producing drugs (nicotine and opiate withdrawal inc NE release)  
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Clonidine (catapres): Hypertension   stimulates a2 receptors of vasomotor ctr to decreases SNS discharge and increase PNS discharge; Decreases HR, CO, and TPR  
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Clonidine (catapres): Precautions During Therapy   orthostatic hypotension (stimulationof presynaptic a2 receptors decreases NE release causing vasodilation)  
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Clonidine (catapres): Precautions about Abrupt Cessation   hypertension (decreased stimulation of presynaptic a2 receptors increases NE release)...must wean pt off drug  
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Clonidine (catapres): Drug Interactions   tricyclic antidepressants (TCA) block a1 receptors ==> block anti-HT effects of clonidine  
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a-Methyl Dopa (aldomet): a2a-Selective Agonist   metabolized to a-methyl NE  
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a-Methyl Dopa (aldomet): Hypertension   dt clonidine-like CNS MOA; safe use in pregnancy  
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a-Methyl Dopa (aldomet): Adverse Drug Reactions   limit use; hepatotoxicity; hemolytic anemia  
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Dobutamine (dobutrex): b1-Selective Agonist MOA   (-) isomer (a1 agonist + weak b1 agonist) and (+) isomer (a1 antagonist + potent b1 agonist) ==> NET EFFECT  
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Dobutamine (dobutrex): Inotropic effect > Chronotropic effect   increases contractility and CO; lack of b2 effect (less vasodilation/less activation of baroreceptor reflex; LESS TACHYCARDIA)  
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Dobutamine (dobutrex): Caution   tolerance w/prolonged use  
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Dobutamine (dobutrex): Indications   cardigenic shock, refractory CHF, acute cardiac compensation (IV infusion; 2min onset), Myocardial Infarction  
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Albuterol (proventil): Asthma   bronchodilation, anti-inflammatory, inhibit release of inflammatory mediators from mast cells, increase mucus clearance by cilia  
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Albuterol (proventil): Caution (downregulation/desensitization)   agonist of b receptors; activates adenyl cyclase, inc cAMP, activates phosphokinase A, phosphorylates b receptor protein = Reduced Effect of Agonist!  
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b2 Selective Agonist Inhalers: Albuterol   Onset (5min); Duration (4-6hr); acute bronchospasm, prevents exercise-induced asthma  
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b2 Selective Agonist Inhalers: Bitolterol (tornalate)   Onset (2-4min); Duration (4-6hrs)  
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b2 Selective Agonist Inhalers: Salmeterol (severent)   Onset (10-20min); Duration (>12hrs); maintenance (mild to moderate asthma); nocturnal symptoms; w/inhaled corticosteroid reduces need to inc steroid dose  
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Albuterol (proventil): Adverse Drug Reactions   tremor, tachycardia (b2 = 25% of cardiac b); arrhythmias with high dose; death???  
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Ritodrine (yutopar): b2 selective agonist   Indication for arresting premature labor  
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Ritodrine (yutopar): Adverse Drug Reactions   cardiac stimulation, hypotension, neonatal hypoglycemia  
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Dopamine (intropin): dopamine agonist MOA   "renal dose" <2ug/kg/min; stimulates D2 presynaptic and D1 postsynaptic receptors; diates renal/mesenteric/coronary vessels  
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Dopamine (intropin): b1 agonist   medium dose (2-10ug/kg/min); positive inotropic effect  
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Dopamine (inotropin); a1 agonist   High dose (10ug/kg/min); vasoconstriction  
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Dopamine (intropin): indications   shock a/w low CO and compromised renal fxn; CHF; acute renal failure  
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Fenoldopam (corlopam): Dopamine D1 Agonist   dilates renal, mesenteric, and coronary aa; reaches steady state serum level in 20min; (also weak a2 agonist)  
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Fenoldopam (corlopam): Indication   short term (up to 48hrs) Rx for severe hypertension  
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Fenoldopam (corlopam): Adverse Drug Reactions   dose-related hypotension; tachycardia (risk of exacerbated CHF); headache, flushing  
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Amphetamine (Dexedrine, Dextrostat): Increases Transmitter Release - Peripheral Effects   Increases release and inhibits uptake of NE  
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Amphetamine (Dexedrine, Dextrostat): Increases Transmitter Release - CNS Effects   increases release and inhibits uptake of NE in limbic system (d-isomer > l-isomer) as well as DA and Seratonin possibly by stimulating inhibitory pathways leading to frontal cortex and limbic system)  
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Amphetamine (Dexedrine, Dextrostat): Indications   Narcolepsy (65-85% efficacy); ADHD (impulsivity, hyperactivity, inability to focus, hypofxn of frontal cortex/limbic system?)  
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Methampthetamine (Desoxyn, "speed"): Increase transmitter release   compared to amphetamine there is a greater CNS effect and less severe peripheral effect  
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Amphetamine (dexedrine) and Methamphetamine (Desoxyn "speed"): Adverse Drug Reactions   anorexia, paranoia, aggressive behavior, arrhythmias, subarachnoid hemorrhage, convulsions, vomiting/diarrhea, euphoria, hypertension, ischemic stroke, coma  
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Methamphetamine (Desoxyn, Speed): Long-term abuse   loss of DA uptake; gray matter structure abnormalities, impaired memory and verbal learning, motor slowing, phsycosis  
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Methamphetamine "speed": Treatment   HT(a-antagonist/Na nitroprusside); NH4Cl (acidify urine to enhance clearance); Anxiety (benzodiazepine); Phychosis (haloperidol may inc meth serum concentration)  
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MDMA "Ecstasy" (d- and dl-amphetamine, Adderall): Increases Transmitter Release MOA in CNS   Releases and inhibits reuptake of seratonin; (3, 4-methylendedioxymethamphetamine)  
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MDMA "Ecstasy" (d- and dl-amphetamine, Adderall): Adverse Drug Reactions   LSD-like; hallucinations, perceptual disorders  
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Cocaine "crack": Indications   local anesthetic blockade of neuronal Na+ binding sites to prevent depolarization  
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Cocaine "crack": Adverse Drug Reactions   CNS effects dt inhibition of NE, DA, and serotonin reuptake; Tachyphylaxis (25mg line - 9g)  
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d- and dl-amphetamine (Adderall): Adverse Drug Reactions   this drug is abused; sudden cardiac death in children (family Hx of SVT, near drowning, cardiac structure abnormalities, heat exhaustion, heart attack); FDA prohibits use in cardiac defect pts; suspended in Canada  
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Methylphenidate (Ritalin, Concerta): Increases Transmitter Release   mild amphetamine, less CNS stimulation, appetite suppression, tachycardia, phsychosis; 3-5hr duration, tolerance develops  
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Atomoxetine (strattera): Inhibits NE uptake   selective inhibitor of NE uptake, not CNS stimulant; slower onset; second line Rx for non-responders/intolerant to CNS stimulants  
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Atomoxetine (strattera): compared to amphetamine   not a CNS stimulant, less "hill and valley" effects; less efficacy?  
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Atomoxetine (strattera): Adverse Drug Reactions   usu results in discontinuation (nausea, sedation, irritability, temper tantrums)  
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Atomoxetine (strattera): Suicidal Ideation?   FDA public health advisory issued 9/05; call for mfg to issue patient medicaiton guide for parents  
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Pemoline (cylert): Increase Transmitter Release   efficacy similar to methylphenidate  
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Pemoline (cylert): Adverse Drug Reactions   **Severe Liver Toxicity; CNS problems similar to methylpenidate; less cardiovascular problems  
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Pseudophedrine (Sudafed): Inc NE release/a1b1 agonist   increases release of NE, weak agonist of a1 and b1 receptors  
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Pseudophedrine (Sudafed): Indications   nasal decongestant, urinary incontinence (a1 contracts internal sphincter)  
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Pseudophedrine (Sudafed): Warning   similar to methamphetamine; must by capsules behind pharmacy counter now so sales are logged to prevent misuse  
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Ephedrine (ephedra, ma-huong): Increase NE release/a1b1 agonist: Indications   nasal decongestant, appetite suppression  
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Ephedrine (ephedra, ma-huong): Adverse Drug Reactions   seizure, troke, MI; withdrawn from market by FDA  
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Monoamine Oxidase (MAO) Inhibitors   located in nerve terminals, liver, GI mucosa, platelets; regulates degradation of catecholamines and serotonin in CNS/periphery  
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Hepatic MAO   metabolizes circulating monoamines such as indirect-acting sympathomimetic amines (dietary tyramine (tyrosine?))  
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MAO Inhibitors: MAO-A   role in adrenergic nerve terminals (ANS, CNS); preferentially deaminates NE, EPI and serotonin, Inhibited by Clorgyline  
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MAO Inhibitors: MAO-B   found in serotonin and histaminergic nerve terminals; deaminates Phenethylamine; Inhibited by Selegiline (eldepryl)  
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MAO-A and MAO-B   metabolize tyramine and DA; Inhibited by Phenelzine (Nardil) and Tranylcypromine (Partate)  
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MAO Inhibition Onset   occurs w/in few days but onset of clinical efficacy is several weeks; down-regulation of adrenergic and/or serotonin receptors  
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MAO Inhibitors: Caution   Irreversible Inhibition: it takes several weeks to regenerate MAO; 2wk washout of MAOI prior to start of sympathomimetic Rx (ex: many OTC cold products); Risk of fatal intracranial bleeds!!  
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MAO Inhibitors: Indications   treatment of resistant depression (2nd or 3rd line Rx); MAOI-A is more effective than MAOI-B for treating major depression (clinical efficacy occurs w/80% inhibition to enhance availabe dopamine)  
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MAO Inhibitors: Parkinsons Disease   degeneration of DA neurons that project from S. nigra to basal ganglia and striatum; DA deficit corrected by Levodopa; efficacy "wears off" after several years; Adjunct to L-dopa to increase available DA  
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MAO Inhibitors: Other Indications   phobias, social anxiety (phenylzine 77% effic; seligiline 32% effic); Refractory migraine, Panic disorder? (poorly designed trials/adequate dose/duration?)  
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MAO Inhibitors: Adverse Drug Reactions   Hepatotoxicity (Pheylzine-Nardil >> Tranylcypromine-Parnate); Hyperprolactinema; postural hypotension (mc); anti-ACh; sexual dysfunction-dose related  
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MAO Inhibitors: Drug Interactions   Meperidine (demerol); Dextromethorphan, Tricyclic antidepressants, SSRIs, L-tryptophan (inc serotonin synth); Sumatriptan (CNS 5-HT agonist)  
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MAO Inhibitors: Serotonin Syndrome   HT, shivering, diaphoresis, muscle rigidity, fever, agitation, hallucinations  
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MAO Inhibitors: "Cheese Reaction"   dietary tyramine increases release of catecholamine and 5-HT causing a HYPERTENSIVE Crisis (10mg - HT, 25mg - HTCrisis)  
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Selegiline (eldepryl): MAO Inhibitor   selective inhibitor of MAO-B; less risk for "cheese rxn;" dietary tyramine is metabolized by MAO-A (less tyramine to release NE and 5-HT)  
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Selegiline (eldepryl): MOA   metabolized to L-amphetamine + L-methamphetamine; Neuroprotection; prevents peroxide formation a/w oxidative deamination of DA?  
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a-Methyltyrosine (desmer): Decreases NE synthesis   inhibits tyrosine dydroxylase (rate limiting); depletes catecholamines in SNS nerve terminals, adrenal medulla, and CNS  
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a-Methyltyrosine (desmer): Indications   pheochromocytoma (tumor of adrenal medulla that secretes excessive EPI and NE  
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a-Methyltyrosine (desmer): Adverse Drug Reactions   Nasal stuffiness, diarrhea, impotence, hallucinations, depression, Parkinsonism (no NE to constrict a1 in nasal mucosa); exaggerated cholinergics = diarrhea (adronergics slow it down but they're blocked); no dopamine = hypercholinergic = muscle rigidity  
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Reserpine (serpasil): decrease NE storage   irriversibly blocks CCA uptake into nerve terminal storage granules (several day duration)  
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Reserpine (serpasil): Indications   hypertension (outdated)  
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Guanethidine (ismelin): inhibit NE release   displaces NE from storage granules = gradual long-term depletion; Irreversible damage of nerve terminal = sympathectomy  
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Guanethidine (ismelin): Indication   severe HT (outdated) vasodilation increases venous capacity  
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Guanethidine (ismelin): Adverse Drug Reactions   similar to a-methyltyrosine and reserpine  
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Phenoxybenzamine (dibenzyline): non-selective irreversible a-receptor agonist   a1 = a2; 48hr turnover time  
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Phenoxybenzamine (dibenzyline): Indications   1. Pheochromocytoma (long-term for inoperable cases; 1-3wks pre-op to control BP; concomitant Rx w/a-methyltyrosine and/or b-blocker; 2. Autonomic hyperreflexia dt spinal cord transection  
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Phentolamine (regitine): Non-selective Reversible a-Receptor Agonist   a1 = a2; indicated for: 1. Raynaud's disease (arterial injection/infusion; improves finger blood flow/digital pulse vol/forearm flow; reduces vasospasm); 2. Pheochromocytoma; 3. Erectile Dysfxn (intracavernosal injection)  
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Phentolamine (regitine): Adverse Drug Reactions   IV: severe tachycardia/arrhythmias/myocardial ischemia; vasodilation activates baroreceptor reflex/inc SNS activity; blockade of a2 presyn receptors inc NE release; 2. PO: tachycardia, nasal congestion; 3. Inhibits ejaculation  
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Prazosin (minipress): Selective Reversible a-Receptor Antagonist   a1 >>>>a2; 1. Benign prostatic hypertrophy (blocks a1a receptors [70% of receptors] relaxes prostate capsule, intern sphincter of bladder/urethra); 2. Hypertension (not monotherapy; block arteriole/vein a1b to dec venous return, TPR, CO/BP)  
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Prazosin (minipress): MOA acute and long-terem   1. Acute: baroreceptor reflex inc HR + renin (Na/H2O retention); 2. Long-term: HR and renin return to normal; Lack of a2 blockade = no increased release of NE  
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Prazosin (minipress): Adverse Drug Reactions   1. "first dose effect" Orthostatic Hypotension (OH) dt blockade of 1b receptors; possible CNS effect to dec SNS outflow; 2. 50% incidence of concomitant diuretic Rx (a1b blockade, CNS effect?)  
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Prazosin (minipress): "First Dose Effect"   OH after first dose (90min onset) - 1% incidence at >2mg; low dose 1mg at HS; HS dose titration; May also occur during rapid dose increase (after first few days of Rx or resumption of Rx after few days w/o drug)  
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Terozasin (hytrin): Selective Reversible a-Receptor Antagonist   indicated for: Hypertension and Benign Prostatic Hypertrophy  
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Terozasin (hytrin): Adverse Drug Reactions   First dose effect; slow titration schedule (days 1-3 = 1mg HS; days 4-14 = 2mg HS; wks 2-6 = 5mg HS; wks 7+ = 10mg HS)  
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Tamsulosin (Flomax): Selective Reversible a-Receptor Antagonist   indicated for: Benign Prostatic Hypertrophy; selective block of a1a receptors (inhibits contraction of prostate vascular smooth muscle; less affinity for a1b receptors in arterioles/veins so less OH (less need for dose titration); not studied for HT  
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Tamsulosin (Flomax): Adverse Drug Reactions   Priapism (prolnged and painful erection)  
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Tamsulosin (flomax): Advantages   initial Rx at lowest maintenance dose; dose anytime during day, no dose titration (shorter ~2wk onset of peak effect); OK to add to selective anti-hypertensives (altenolol, furosemide, enalapril, nifedipine)  
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Alfuzosin (uroxotral): Selective Reversible a-Receptor Antagonists   a Tamsulosin "me too" drug  
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Doxazosin (cardura): Selective Reversible a-Receptor Antagonists   indicated for: BPH and HT (effective as MONOTHERAPHY or w/diuretics, b-blockers, Ca-channel blockers, angiotensin-converting enzyme (ACE) inhibitors); exhibits "First Dose Effect"  
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Pharmokinetics of Selective Reversible a-Receptor Antagonists: Prozasin   Serum half-life = 2-3hrs; 2-3 dose/day  
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Pharmokinetics of Selective Reversible a-Receptor Antagonists: Alfuzosin   Serum half-life = 3-5hrs; 1dose/day  
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Pharmokinetics of Selective Reversible a-Receptor Antagonists: Terazosin   Serum half-life = 9-12hrs; 1dose/day  
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Pharmokinetics of Selective Reversible a-Receptor Antagonists: Tamsulosin   Serum half-life = 9-15hrs; 1dose/day  
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Pharmokinetics of Selective Reversible a-Receptor Antagonists: Doxazosin   Serum half-life = 22hrs; 1dose/day  
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b-Receptor Antagonists (Blockers)   compounds vary receptor selectivity, local anesthetic action, lipid solubility, elimination half-life; Partial b-agonist action (intrinsic sympathomimetic activity (ISA); Acebutolol, Carteolol, Penbutolol, Pindolol; less drop of rest-HR/CO/periph flow)  
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b-Receptor Antagonists (blockers): Pharmokinetics   First-pass metabolism (Propranolol, metoprolol) pt/dose variability; Long half-life, Renal excretion (dose adjust); Shorter half-life (1/day usu effective)  
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Sympatholytic b-Receptor Antagonists: 1st Generation Non-Selective   Propranolol (Inderal)  
🗑
Sympatholytic b-Receptor Antagonists: 2nd Generation Selective b1-Cardioselective beta blockers   Acebutolol, Altenolol, Betaxolol, Bisoprolol, Esmolol, Metoprolol  
🗑
Sympatholytic b-Receptor Antagonists: 3rd Generation Non-selective b-blockade + a-blockade (vasodilation)   Carvedilol (coreg), Labetolol (normodyne)  
🗑
Acebutolol   b1-selective; partial agonist, local anesthetic  
🗑
Atenolol   b1-selective  
🗑
Betaxolol   b1-selective; slight anesthetic  
🗑
Bisoprolol   b1-selective  
🗑
Carteolol   not selective, partial agonist  
🗑
Carvedilol   non-selective (also causes a1 adrenoceptor blockade)  
🗑
Celiprolol   b1-selective; partial agonist effects at b2 receptors  
🗑
Esmolol   b1-selective;  
🗑
Labetalol   non-selective; partial agonist, local anesthetic (also causes a1 adenoceptor blockade)  
🗑
Metoprolol   b1-selective; local anesthetic  
🗑
Nadolol   non-selective  
🗑
Penbutolol   non-selective; partial agonist  
🗑
Pindolol   non-selective; partial agonist; local anesthetic  
🗑
Propranolol   non-selective; local anesthetic  
🗑
Sotalol   non-selective  
🗑
Timolol   non-selective  
🗑
b-Receptor Antagonists: b1-cardioselective   b1>b2: heart and kidney (vs. b2>b1: lungs/liver/pancreas/arterioles); less likely to provoke broncospasm/vasoconstriction; safer for asthmatics, COPD, peripheral vascular dx, diabetes; preferred in ischemic heart disease to prevent second MI  
🗑
b-Receptor Antagonists: Effects on Heart   At Rest: modest reduction of HR and force of contraction; Stress Rxn: attenuate typical positive inotropic and chronotropic effects  
🗑
b-Receptor Antagonists: Effects on Eye   reduce formation of aqueous humor  
🗑
b-Receptor Antagonists: Effects on Kidney   antagonize release of renin  
🗑
b-Receptor Antagonists: Member stabilizing ("Quinidine-like" Effect)   blocks Na channels of nerve, heart, skeletal muscle; dose-dependent  
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b-Receptor Antagonists: Effects on Serum Lipids   Non-selective (reduce HDL, increase LDL and TGs); b1-Selective (improve lipid profile of dyslipidemic pts)  
🗑
b-Receptor Antagonists: Adverse Drug Reactions   Reduce insulin secretion mostly in insulin-dependent diabetics (hyperglycemia, hampers recovery from hypoglycemia, masks warning signs of hypoglycemia/hyperthyroidism (tachycardia)); Exacerbates Hypoglycemia (inc SNS tone, unopposed a1 vasoconstriction)  
🗑
b-Receptor Antagonists: Adverse Drug Reactions   Hypotension, Cardiac Failure (usu high dose; a/w prior LV dysfxn, neg inotropics); Bradycardia, heart block, Exacerbate bronchospasm in asthma/COPD; Exacerbate Raynaud's disease; Erectile Dysfxn (dec flow to corpora); CNS (depression, fatigue, no libido)  
🗑
b-Receptor Antagonists: Warnings - Exercise   attenuates the following: cardiac stimulation, bronchodilation, glycogenolysis and lipolysis  
🗑
b-Receptor Antagonists: Warnings - Pheochromocytoma   may result in paradoxical hypertension  
🗑
b-Receptor Antagonists: Warnings - Diabetics   prevents tachycardia seen in hypoglycemia; reduced insulin response to hyperglycemia; may need to adjust antidiabetic Rx  
🗑
b-Receptor Antagonists: Warnings - Abrupt Cessation of Rx   For pts predisposed to myocardial ischemia (MI, arrhythmia, death, inc sensitivity of b-receptors to EPI and NE; failure to dec physical activity); Uncompromised pts (tachycardia, inc sweating, malaise); **Taper dose over 2wks  
🗑
b-Receptor Antagonists: Contraindications   Bronchial asthma (non-selective, lacking ISA); Cardiac Failure (use w/caution in pts w/well-compensated cardiac failure); Cardiogenic shock; Severe bradycardia; Severe prolonged hypotension  
🗑
b-Receptor Antagonists: Indications   Hypertension, Migraine, Anxiety, Hyperthyroidism, Myocardial Infarction, Angina, Heart failure  
🗑
b-Receptor Antagonists: MOAs to lower BP via Inhibition of Renin Release   Pts w/low renin respond; drugs w/little effect on plasma renin lowers BP (pindolol)  
🗑
b-Receptor Antagonists: MOAs to lower BP in CNS   CNS concentration of Propranolol > Atenolol (have similar anti-HT effects); drugs w/poor CNS penetration lower BP  
🗑
b-Receptor Antagonists: MOAs to lower BP and Cardiac Output Reduction   similar CO decrease in responders and non-responders  
🗑
b-Receptor Antagonists: MOAs to lower BP via inhibition of NE   Presynaptic Inhibition of NE Release (b-agonists inc release) - role is unclear  
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b-Receptor Antagonists: MOAs to lower BP   different cardioselectivity, intrinsic sympathomimetic activity (ISA), membrane stabilizing effects (similar antiHT effects)  
🗑
b-Receptor Antagonists: Most Logical MOA   long-term Rx reduces peripheral resistance (inc NO, a1 antagonist, block Ca-channels, b2 agonist, antioxidant, open K-channels; Combined effect of reduced CO and reduced peripheral resistance  
🗑
Labetolol (normodyne, trandate): b1, b2, a1 Receptor Antagonist   indicated for: Preclampsia HT (IV); HT of pregnancy (doesn't aggravate peripheral vascular disease as much as pure b-blockers); HT emergency (decreases peripheral vascular resistance w/no effect on HR or CO)  
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b-Receptor Antagonists: Migraine Prophylaxis   unknown MOA; most widely used (atenolol, metoprolol, nadolol, propranolol); drugs w/ISA are ineffective  
🗑
b-Receptor Antagonists: Alcohol Withdrawal and Social Anxiety   blocks peripheral SNS effects  
🗑
b-Receptor Antagonists: Anxiety   useful for pts w/palpitations or tremor; for non-responders to benzodiazepine (ex: Valium); Typical onset = 1wk (take ahead of time); Taper to avoid rebound anxiety  
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b-Receptor Antagonists: Hyperthyroidism   palpitations, anxiety, tremor, heat intolerance; inhibits conversion of T4 to T3; minor effect unrelated to b-blockade  
🗑
b-Receptor Antagonists: Role in Ischemic Heart Disease   dec HR and contractility, slight BP dec myocardial O2 demand; countered slightly by inc ventricular vol and ejection time; Net Effect: Reduced Myocardial O2 Demand; (a1 stimulation in presence of b-blockade may constrict coronary aa)  
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b-Receptor Antagonists: Role in Ischemic Heart Disease - b-blocker of choice   no evidence to ID a b-blocker; Cardioselectives may be preferred in pts w/COPD, asthma or intermittent claudication; Labetolol = possible less coronary artery constriction (useful in pts w/little LV reserve)  
🗑
b-Receptor Antagonists: MI   recuce ventricular arrhythmias, recurrent ischemia and re-infarction; reduced workload dt reduced HR, systolic BP, and myocardial contractility  
🗑
b-Receptor Antagonists: Acute MI   n = 16,000; Atenolol IV, oral; 15% reduction in vascular mortality OR n = 6,000; Metoprolol 13% reduction in mortality in 1 month  
🗑
b-Receptor Antagonists: Post MI   short term dose of various b-blockers after MI are more beneficial; n = 1,884 pts for 12-33 mo, Timolol 39% red mortality and 28% red re-infarct; OR n = 3,837 for 27 months Propranolol 26% red mortality;  
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b-Receptor Antagonists: Angina   reduces frequency and severity of exertional angina  
🗑
b-Receptor Antagonists: Angina Pectoris   neg inotropic/chronotropic effects; red myocardial O2 demand; inc diastolic coronary perfusion time; Atenolol (reduced hospitalization for angina, need for revascularlization, death); Chronic/stable w/preserved LV fxn (question red in mortality; MI Hx pt)  
🗑
b-Receptor Antagonists: Perioperative   CABG after MI; 1yr mortality red from 12 to 4%; Non-cardiac surgery in pts w/coronary risk factors; fewer perioperative CV events  
🗑
b-Receptor Antagonists: Heart Failure   Bisoprolol w/pts with LVEF 34% red in mortality; significantly fewer CV deaths  
🗑
b-Receptor Antagonists: Heart Failure   Metoprolol extended release in pts w/LV ejection fraction; red mortality, sudden death and death dt worsening CHF  
🗑
b1-Cardioselective Receptor Antagonists   dose-dependent (high dose also blocks b2); patient-specific  
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Esmolol (brevibloc injection): b1-Cardioselective Receptor Antagonist   10-20min duration; hemodynamics return to baseline in 30min; Indicated for: Supraventricular tachycardia, Arrhythmias a/w thyrotoxicosis; Intra-operative/Post-op tachycardia and/or hypertension; Myocardial Ischemia  
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Esmolol (brevibloc injection): Drug Interactions   Succinylcholine (prolong duration of NM blockade by 5-8min); Digoxin (inc digoxin serum level by 20%); Morphine (inc esmolol serum level by 45%)  
🗑
Pindolol (visken): Mixed b antagonist + partial b agonist   desirable in asthmatics who cannot tolerate other b-blockers; desirable in pts w/low resting HR  
🗑
Labetolol (normodyne, trandate): b1, b2, a1 Receptor Antagonist   dec BP w/o reflex tachycardia and w/o red in HR; BP is lowered more in standing than supine position; OH First Dose Effect can occur (usu w/in 2-4hrs of large initial dose or on change of dose)  
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Labetolol (normodyne, trandate): Indications   Oral (Hypertension); IV for hospitalized pts (severe HT dt risk of OH, pt must be supine during injection; must be able to tolerate upright posture b/f ambulating)  
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Carvedilol (coreg): mixed b + a1 antagonist   compared to other b-blockers: produces more hypotension and dizziness; possible greater anti-hypertensive effect  
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