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79 Cards in this Set
- Front
- Back
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Clonidine |
Mechanism -a2AR agonist -predominant activity at CNS (sympatholytic, reduce blood pressure) -reduced TPR -reduced CO Indications -HTN emergency -ADHD (slow/extended release used in children with stimulant-refractory ADHD) -Tourette's (no EPS!) |
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alpha-Methyldopa |
Mechanism -a2AR agonist -predominant activity at CNS (sympatholytic, reduce blood pressure) -reduced TPR -reduced CO Indications -gestational HTN Adverse -SLE-like syndrome |
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Tizanidine |
Mechanism -a2AR agonist -predominant activity at CNS Indications -muscle relaxant |
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Phentolamine |
Mechanism -reversible a1AR and a2AR antagonism -short acting -vasodilation -decrease PVR -decrease BP Indications -cocaine HTN -MAO-inhibitor plus tyramine (wine/cheese) HTN emergency -Pheochromocytoma (DURING surgery) Adverse -orthostatic hypotension and reflex tachycardia (due to a1AR blockade) |
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Phenoxybenzamine |
Mechanism -irreversible a1AR and a2AR antagonist -covalent, long-acting -may take DAYS to restore tissue responsiveness to alpha stimulation (new receptor synthesis) Indications -cocaine HTN -Pheochromocytoma (given BEFORE surgery) Adverse -orthostatic hypotension and reflex tachycardia (due to a1AR blockade) |
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"osins" Prazosin Terazosin Doxazosin Tamsulosin |
Mechanism -a1AR specific antagonist -vasodilation Indications -BPH (relax urethra & prostate smooth muscle) -HTN -Prazosin for PTSD nightmares Adverse -first dose orthostatic hypotension and reflex tachycardia |
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Mirtazapine |
Mechanism -antagonizes pre-synaptic a2AR leading to NE and 5HT release Indications -Atypical antidepressant |
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ABEAM Atenolol Betaxolol Esmolol Acebutolol Metoprolol |
Mechanism -b1AR antagonism -CARDIOSELECTIVE -reduce cardiac O2 demand -increase diastolic filling time (improve coronary flow) Indication -Acute Coronary Syndromes (reduce infarct size when started within 24 hrs, decrease mortality) -long term CHF therapy (decreased mortality) -reduce cardiac remodeling by CA -Esmolol IV for HTN emergency |
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Carvedilol |
Mechanism -non-selective bAR antagonist -a1AR antagonist Indications -reduce post-MI mortality -reduce CHF mortality |
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Labetalol |
Mechanism -mixed aAR and bAR antagonist -a1AR inhibition causes vasodilation -rapid onset of action Indications -gestational HTN -IV for HTN emergency -acute aortic dissection |
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Broad Beta Blocker Class (end with "lol") |
Mechanism -b1AR selective antagonism: A through M -b1/b2 non-selective antagonism: N through Z -antagonize SA and AV node b1AR to reduce HR -decrease cardiac contractility by antagonizing b1AR in myocardium -inhibit Renin production by b1AR blockade Indications -chronic stable angina (decrease contractility and HR, thereby decreasing myocardial O2 demand) -CHF (reduce cardiac remodeling by CA) -long-term HTN treatment, especially post-MI or in CHF -essential tremor -migraine prophylaxis -hypertrophic cardiomyopathy -anti-arrhythmic -IV Labetalol and Esmolol for HTN emergency Adverse -asthma/COPD exacerbation -impotence -can cause HEART BLOCK (b1AR antagonism at AV node) -BB toxicity treated with GLUCAGON |
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Propranalol |
Mechanism -non-selective bAR antagonists |
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Pindolol Acebutolol |
Mechanism -bAR antagonist with partial agonist activity Adverse -AVOID in CHF or post-MI |
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Quinidine Procainamide Disopyramide |
Class 1A Antiarrhythmics Mechanism -NCB -increase AP duration -increase ventricular effective refractory period -prolong QT Indications -atrial and ventricular arrhythmias -re-entrant and ectopic SVT and VT Adverse -Quinidine: CINCHONISM (HA, tinnitus) -Procainamide: reversible SLE -Disopyramide: HF -TCP -prolonged QT Torsade |
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Lidocaine Mexiletine (Phenytoin) |
Class 1B Antiarrhythmics Mechanism -NCB -decrease AP duration -preferentially affect ischemic/depolarized Purkinje and Ventricular tissue Indications -acute ventricular arrhythmia -Post-MI arrhythmia -Digitalis-induced arrhythmia Adverse -CNS stimulation/depression -Cardiovascular depression |
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Flecainide Propafenone |
Class 1C Antiarrhythmics Mechanism -NCB -significantly prolong effective refractory period in AV node and accessory bypass tracts -no effect on AP duration!! Indications -SVT (including AFib) -last resort in refractory VT Adverse -Proarrhythmic (contraindicated post-MI) |
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Metoprolol Propranolol Esmolol Atenolol Timolol Carvedilol |
Class II Antiarrhythmics Mechanism -BB -decrease SA and AV nodal activity by decreasing cAMP and Ca2+ currents -suppress abnormal pacemakers by decreasing slope of Phase IV depolarization Indications -SVT -ventricular rate control for AFib and AF -block peripheral T4-->T3 conversion Adverse -impotence -COPD/asthma exacerbation -bradycardia, AV block, HF -CNS (sedation) -MASKS symptoms of HYPOGLYCEMIA -unopposed a1AR antagonism (never given alone in PHEO or COCAINE tox!!!) -Metoprolol: dyslipidemia -Propranalol: exacerbate Prinzmetal angina vasospasm Treat BB overdose with GLUCAGON |
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Amiodarone Ibutilide Dofetilide Sotalol |
Class III Antiarrhythmics Mechanism -KCB -increase AP duration -increase effective refractory period -prolong QT -Amiodarone has class I, II, III, and IV effects Indications -AFib -AF -Amioadrone, sotalol: Ventricular tachycardia Adverse -CHECK PFT, LFT, TFT during amiodarone -Amio: pulmonary fibrosis, hepatotoxicity, hypo/hyperthyroidism, corneal deposits, neuro defects, constipation, bradycardia, heart block, HF -Sotalol: torsade, excessive beta blockade -Ibutilide: torsade |
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Verapamil Diltiazem |
Class IV Antiarrhythmics Mechanism -CCB -decrease conduction velocity -increase ERP -increase PR interval Indications -nodal arrhythmias (SVT) -rate control in AFib Adverse -constipation -flushing -edema -HF, AV block, SA node depression |
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Adenosine |
Mechanism -increase K+ flow out of cell -hyperpolarize cell -decrease intracellular Ca2+ -effects blunted by CAFFEINE and THEOPHYLLINE Indication -FIRST LINE for diagnosing/treating SVT -very short acting, must be pushed quickly Adverse -flushing -hypotension -chest pain, feeling of impending doom -bronchospasm |
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Digoxin |
Cardiac glycoside Mechanism -direct inhibition of Na+/K+ ATPase, elevating intracellular [Na+] -indirectly inhibits Na+/Ca2+ exchanger, elevating intracellular [Ca2+] -POSITIVE INOTROPE -stimulates vagus to REDUCE HR Indications -acute HF to increase contractility -AFib (decrease AV node conduction) Adverse -cholinergic: (N/V/D, blurry yellow vision), arrhythmia, AV block -hyperkalemia -must monitor levels in RENAL FAILURE, verapamil use, amiodarone use, quinidine use Antidote -normalize K+ slowly -cardiac pacer -anti-Dig Fab -Mg2+ |
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Lovastatin Pravastatin Simvastatin Atorvastatin Rosuvastatin |
Mechanism -HMG-CoA reductase inhibitor -inhibit conversion of HMG-CoA to mevalonate (cholesterol precursor) Lipid metabolism -SIGNIFICANT LDL decrease -HDL increase -triglyceride decrease Indications -lower cholesterol -decrease mortality in CAD patients Adverse -hepatotoxicity/increase LFT -MYOPATHY (with FIBRATES or NIACIN) |
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Cholestyramine Colstipol Colesevelam |
Mechanism -bile acid resin -prohibit bile acid reabsorption (cause GI cholesterol loss) Lipid metabolism -LDL decrease -slight HDL increase -slight triglyceride increase Adverse -GI upset -decreased absorption of other drugs and fat-soluble vitamins (ADEK) |
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Ezetimibe |
Mechanism -prevent cholesterol absorption at small intestine brush border Lipid metabolism -LDL decrease Adverse -diarrhea -rarely, LFT increase |
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Gemfibrozil Clofibrate Bezafibrate Fenofibrate |
Mechanism -upregulate lipoprotein lipase -increase triglyceride clearance -activate PPAR-a to induce HDL synthesis Lipid metabolism -decrease LDL -increase HDL -SIGNIFICANT TG decrease Adverse -MYOPATHY (especially with STATINS) -cholesterol gallstones |
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Niacin (B3) |
Mechanism -inhibits lipolysis by hormone sensitive lipase in adipose tissue -reduce hepatic VLDL synthesis Lipid metabolism -decrease LDL -increase HDL -decrease TG Adverse -red flushed face (decrease by NSAID or long-term use) -hyperglycemia -hyperuricemia |
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Drugs for Gestational HTN |
Hydralazine (increase cGMP, vasodilation) Labetalol (beta blocker) Methyldopa (a2AR antagonist, central sympatholytic) Nifedipine (dihydropyridine CCB) |
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Drugs for Essential HTN |
Thiazide diuretics ACE-I ARB Dihydropyridine CCB ("pines") |
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Drugs for HF HTN |
Diuretics ACE-I ARB Spironolactone/Eplerenone |
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Drugs for DB HTN |
ACE-I ARB CCB Thiazides BB |
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Drugs which can cause Torsade |
ABCDE anti-Arrhythmics (class IA, class III) anti-Biotics (macrolides) anti-"C"ychotics (haloperidol) anti-Depressants (TCA) anti-Emetics (ondansetron) TREAT WITH MAGNESIUM |
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G-Protein Pharmacology Gs = increase heart contractility, relax smooth muscle Gi = decrease heart contractility, constrict smooth muscle Gq = constrict smooth muscle |
QISS and QIQ till you're SIQ of SQS Q- a1AR (vasc, pupil dilator, intestine/bladder) I- a2AR (central sympatholytic) S- b1AR (heart) S- b2AR (vasc, bronch, uterine, ciliary) Q- M1 (CNS, enteric nervous system) I- M2 (heart) Q- M3 (exocrine, bladder, broncho, pupil) S- D1 (vasc) I- D2 (modulates CNS NT release) Q- H1 (increase mucus and vasc permeability) S- H2 (gastric acid secretion) Q- V1 (vasc smooth muscle contraction) S- V2 (increased H2O resorption by aquaporin) |
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Nicotinic ACh Receptors |
Ligand-gated Na+/K+ channels (depolarize) Anatomy -expressed on autonomic ganglia (Nn) -expressed at adrenal medulla (Nn) -expressed on skeletal muscle (Nm) |
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Muscarinic ACh Receptors |
GPCRs (act through 2nd messengers) M1 -coupled to Gq, activates IP3/DAG -CNS and enteric nervous system M2 -coupled to Gi, inhibits CA -decrease HR at SA node -decrease contractility at atria -decrease conduction velocity at AV node -NO PARASYMPATHETIC AT VENTRICLES M3 -coupled to Gq, activates IP3/DAG -gland secretion -bladder contraction -pupillary sphincter contraction (miosis) -ciliary muscle contraction (accommodation) -bronchoconstriction -NO mediated vasodilation in healthy vessels with BP drop, but vasoconstriction in atherosclerotic vessels |
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Bethanechol |
Muscarinic Agonist -resistant to AChE!! Action -increase secretion and motor activity of gut -stimulate detrussor muscle -relax bladder sphincter muscles Clinical Use -non-obstructive GI disorders -postoperative/neurogenic ileus -congenital megacolon -non-obstructive urinary retention (post-op, post-partum, neurogenic due to SC damage) Adverse -asthma, COPD, peptic ulcer exacerbation |
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Pilocarpine |
Muscarinic Agonist -resistant to AChE!! Action -increase salivary secretion -reduce IOP be inducing ciliary body contraction (outflow of aqueous humor) -lens accommodation -activation of pupillary sphincter causing miosis (pressure relief in acute glaucoma) Clinical Use -dry mouth (Sjogren, radiation) -open-angle glaucoma -acute angle-closure glaucoma Adverse -asthma, COPD, peptic ulcer exacerbation |
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Carbachol |
Muscarinic and Nicotinic Antagonist Action -pupillary sphincter activation causing miosis (pressure relief in acute angle-closure glaucoma) Adverse -asthma, COPD, peptic ulcer exacerbation |
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Methacholine |
Muscarinic Agonist Action -bronchial smooth muscle contraction (exacerbate asthma and COPD) Clinical Use -methacholine challenge instigates asthma |
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Varenicline |
Nicotinic Partial Agonist Clinical Use -smoking cessation |
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Acetylcholinesterase Inhibitors |
"stigmines" increase synaptic ACh Effects -myosis -bronchospasm -bladder and bowel activation AND -effect at NMJ jxn (treatment of MYASTHENIA GRAVIS) -reversal of neuromuscular blockade after anesthesia Naturally occurring Tertiary agents: -CNS penetration -physostigmine (competitive treatment of ATROPINE and Jimsonweed OD seen in gardners) Synthetic Quaternary agents: -No CNS penetration -edrophonium (5 minute activity, used for MG diagnosis) -pyridostigmine (FIRST LINE FOR MG) -neostigmine |
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Non-depolarizing neuromuscular blockade |
Agents -Rocuronium -Vecuronium -Cisatricurium -Pancuronium -tubocurare Mechanism -nAChR antagonist at NMJ endplate Used as muscle relaxants in surgery Can be reversed with AChE inhibitors -neostigmine |
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Depolarizing neuromuscular blockade |
Succinylcholine Mechanism -nAChR agonist -phase 1 is IRREVERSIBLE (potentiated by AChE inhibitors) |
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Organophosphate poisoning |
Parathion Malathion Echothiophate Irreversible cholinesterase inhibitors Main cause of acute cholinergic poisoning Found in pesticides Guy working in his garage Reverse peripheral effects with pralidoxime -regenerates cholinesterase -must be given early (before aging) Reverse central effects with atropine -muscarinic antagonist -no effect on nicotinic (NMJ) effects) |
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Donepezil Galantamine Rivastigmine |
Central cholinesterase inhibitors
treat ALZHEIMER |
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Edrophonium test for flaccid paralysis |
Short acting (5-15 minute) cholinesterase inhibitor Reversal of symptoms -likely MG -destruction of nAChR Worsening of symptoms -likely cholinergic storm |
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Symptoms of Cholinergic Poisoning |
DUMBBELSS -diarrhea -urination -miosis -bradycardia -bronchospasm -excitation of muscles and CNS -lacrimation -sweating -salivation |
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Anticholinergic Toxicity |
Hot as a hare (decreased sweating) Dry as a bone (urinary retention, dry mouth) Red as a beet Blind as a bat (mydriasis, cycloplegia) Mad as a hatter (M1) Rapid pulse acute angle-closure glaucoma in elderly Urinary retention in prostatic hypertrophy |
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Ipratropium Tiotropium |
M3 antagonist treatment of COPD and asthma |
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Atropine |
Reverses all cholinergic toxicity EXCEPT neuromuscular (need pralidoxime for that) |
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Benztropine |
Central M1 antagonist Treatment of Parkinson tremor Treatment of drug-induced Parkinsonism (EPS) No effect on Parkinson bradykinesia (treats the relative ACh excess which results from central Parkinson DA deficiency) |
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Oxybutynin Tolterodine |
M3R antagonist Treat incontinence (relax bladder and ureter smooth muscle) Relief of bladder spasm after urologic surgery |
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a1AR |
Gq coupled -IP3/DAG activation, increased Ca2+ Anatomy -arterial and venous beds (constriction) -increase systolic and diastolic BP, increase venous return -pupillary dilator muscle (mydriasis) -urethral sphincter and prostatic smooth muscle (urinary retention) |
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a2AR |
Gi coupled -decrease cAMP Anatomy -central sympatholytics -pancreatic islets (decrease insulin release) -adipocytes (decrease lipolysis and FA release) -ciliary body (decrease aqueous humor production) |
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b1AR |
Gs coupled -increase cAMP, Ca2+ influx Anatomy -SA node, AV node (increase HR) -cardiac myocytes (increase contractility) -juxtaglomerular cells (increase renin release) |
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b2AR |
Gs coupled -increase cAMP, PKA activation, inhibition of myosin LCK (smooth mm relaxation) Anatomy -bronchodilation -coronary and skeletal mm artery vasodilation -decrease SVR, decrease diastolic pressure -adipocytes (increase lipolysis and FA release) -pancreatic islets (increase insulin release, can cause hypokalemia by driving K+ intracellularly) -liver (gluconeogenesis) -ciliary body (increase aqueous humor production, increase IOP in glaucoma) |
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Phenylephrine |
Mechanism -a1AR agonist Clinical Use -hypotension (vasoconstrictor, increases systolic and diastolic BP) -rhinitis (decongests via nasal vasoconstriction) -mydriatic agent for optho MAP elevation may cause baroreceptor-mediated reflex bradycardia (not functional in autonomic dysfunction (as in diabetic neuropathy) where phenylephrine may cause a dramatic pressor response) |
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Norepinephrine |
Mechanism -a1AR and a2AR agonist -mild b1AR activity Clinical Use -increases systolic and diastolic BP -causes reflex bradycardia which overcomes b1 chonotropy, but NOT b1 increased contractility -hypovolemic and distributive shock |
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Generation of Catecholamines |
Tyrosine -->Tyrosine Hydroxylase (BH4) L-DOPA -->DOPA Decarboxylase (B6) Dopamine -->Dopamine b-hydroxylase (inside vesicle) NE |
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Metyrosine |
Mechanism -inhibits tyrosine hydroxylase -prevents conversion of tyrosine to L-DOPA Clinical Use -sympatholytic -antiHTN |
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Cocaine |
Mechanism -inhibition of NET and DAT -accumulation of NE and DA in the synapse Peripheral (NET inhibition) effects: -HTN -tachycardia -mydriasis -myocardial ischemia (coronary vasospasm) Central (DAT inhibition) effects: -arousal -addiction -seizures Adverse -NEVER GIVE BETA BLOCKERS (can cause unopposed a1AR stimulation and severe vasoconstriction/HTN) |
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Atomexitine |
Mechanism -selective NET inhibitor Clinical Use -ADHD |
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Reserpine |
Mechanism -inhibition of VMAT (recycles CA back into presynaptic vesicles) -deplete NT stores |
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Methylphenidate |
Mechanism -amphetamine (reversal of NET, non-vesicular release of CA/NE into synapse) Clinical Use -treatment of ADHD -appetite suppressant |
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Modafinil |
Increase CA in the synapse Clinical Use -Narcolepsy -appetite suppressant |
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Dopamine |
Mechanism D1: -coupled to Gs (cAMP, PKA activation, smooth muscle relaxation) -expressed on RENAL VASCULATURE -stimulated at LOW DOSES -increased GFR, increased RPF, increased Na+ excretion -increased RPF distinguishes DA from other CA D2R: -can cause psychosis b1AR: -activated at medium doses -cardiac activation a1AR: -activated at low doses -vasopressor |
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a1AR |
Gq Expression -vascular smooth muscle contraction -pupillary dilator muscle contraction (mydriasis) -intestinal and bladder SPHINCTER muscle contraction Agonist -Norepinephrine -Phenylephrine -Dopamine (at low doses) Antagonists -"osins" (selective) -phentolamine (reversible, non-selective) -phenoxybenzamine (irreversible, non-selective) -Carvedilol (also bAR antagonist) -Labetelol (also bAR antagonist) |
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a2AR |
Gi Expression -decrease sympathetic outflow -decrease insulin release -decrease lipolysis -increase platelet aggregation -decrease aqueous humor production Agonists -Clonidine -a-methyldopa -Tizanidine Antagonists -phentolamine (reversible, non-selective)) -phenoxybenzamine (irreversible, non-selective) -Mirtazepine (central, leads to NE & 5HT release) |
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b1AR |
Gs Expression -increase heart rate -increase myosite contractility -increase renin release -increase lipolysis Agonists -NE -Dopamine (at medium doses) -Isopreternol (nonselective bAR agonist) Antagonists -"olols" A-M (selective b1AR antagonism) -"olols" N-Z (non-selective bAR antagonism) |
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b2AR |
Gs Expression -vasodilation -bronchodilation -increase lipolysis -increase insulin release -decrease uterine tone (tocolysis) -ciliary muscle relaxation (anti-accommodation and decrease the loss of aqueous humor) -increase aqueous humor production Agonists -Isopreterenol (nonselective bAR agonist) -Terbutaline (b2AR selective agonist) |
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M1R |
Gq Expression -CNS -enteric nervous system |
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M2R |
Gi Expression -decrease heart rate -decrease contractility of atria |
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M3R |
Gq Expression -increase exocrine gland secretions (lacrimal, salivary, gastric) -gut peristalsis -bladder contraction -bronchoconstriction -pupillary sphincter muscle contraction (miosis) -ciliary muscle contraction (accommodation and increase the loss of aqueous humor) |
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D1R |
Gs Expression -renal vasodilation |
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D2R |
Gi Expression -modulate brain neurotransmitter release |
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H1R |
Gq Expression -increase nasal and bronchial mucus production -increase vascular permeability -contraction of bronchiole smooth muscle -pruritis, pain |
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H2R |
Gs Expression -increased gastric acid secretion |
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V1R |
Gq Expression -vasoconstriction |
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V2R |
Gs Expression -H2O/urea permability and reabsorption in CCD of kidneys |
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Peripheral Chemo/Baroreceptor Anatomy |
Carotid sinus -baroreceptor (fires with increased pressure) -afferent limb is GLOSSOPHARYNGEUS (CN9) -efferent signal by VAGUS (CN10) to SA node -compress neck = bradycardia Carotid body -chemoreceptor (fires with decreased O2 <60mmHg and <90%SAO2) -afferent limb is GLOSSOPHARYNGEUS (CN9) -efferent signal by VAGUS (CN10) to lungs -decrease O2 = increase ventilation Aortic Arch -baroreceptor (fires with increased pressure) -afferent limb is VAGUS (CN9) -efferent signal by VAGUS (CN9) to SA node -increase pressure = bradycardia |
