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77 Cards in this Set
- Front
- Back
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alpha 1 has what 3 main effects?
what G protein does it use |
vascular smooth muscle contraction (cause reflex bradycardia), dilate pupil, sphincter contraction
Gq mechanism (think Gq for contraction- which requires Ca2+ - like M3 is also Gq which contracts bronchioles) |
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Which receptor causes bronchodilation?
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B2
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which receptor causes pupillary sphincter contraction and ciliary muscle contraction (accomodation)
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M3 (Gq) along with gland secretions, gut peristalsis, bronchocontriction
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digoxin toxicity (4)
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1. cholinergic*: nausea, vomiting, diarrhea
2. vision: blurry yellow vision 3. arrhythmias*: increased PR, decreased QT, T wave inversion 4. hyperkalemia |
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what three things make digoxin toxicity worse?
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1. renal failure (low excretion)
2. hypokalemia (increases potency because digoxin binds to K+ binding site on Na/K ATPase) 3. quinidine: decreases digoxin clearance |
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how do nitrogylcerin, nitroprusside, and hydralazine differ
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nitrogylcerin = decreases preload (venodilator)
nitroprusside = decreases preload and afterload (veno/vasodilator) hydralazine = decreases afterload (vasodilator) |
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what is the effect on Vmax, Km, potency, and efficacy with competitive/non-competitive inhibitors?
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competitive: increase Km (decrease affinity), no effect on Vmax, decrease potency
non-comp = decreased Vmax, no effect on Km, decreased efficacy *efficacy = maximal effect a drug can produce *potency = amount of drug needed for a given effect |
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relate hydrophilicity/hydrophobicity to volume of distribution
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volume of distribution = amount of drug in body / amount of drug in plasma
hydrophilic (also large, charged drugs) = low Vd because lots of drug in plasma hydrophobic (also small, uncharged drugs) = high Vd because more drug in tussue |
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what is the formula for drug clearance?
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CL = rate of elimination of drug / plasma drug conc.
*this makes sense because higher drug conc. would take longer to clear, thus have a decreased rate of CL |
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what is the formula for half life
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t1/2 = 0.7 x Vd / CL
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what is the formula for loading dose
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loading dose = (Pc x Vd) / F
*bioavailability (F)= 1 when give IV |
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what is the formula for maintenance dose
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maintanence dose = (target conc x clearance) / bioavailability
= Cp x CL / F |
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3 drugs with zero order elimination
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zero-order = constant elimination regardless of target conc.
phenytoin, ethanol, aspirin |
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what type of drugs are eliminated through kidney, which are better for liver
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kidney --> urine (most drugs, esp. hydrophilic, low volume of distribution)
liver --> poop (esp. lipophilic and drugs that have high volume of distribution) |
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what is the difference between phase I and phase II metabolism
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phase I: reduction, oxidation, hydrolysis - CYP enzymes - usually yields slightly polar, water-soluble metabolites (usually still active)
phase II: (acetylation, glucoronidation, sulfation) usually yields very polar, inactive metabolites (renally excreted) *Old people first lose phase I metabolism |
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define bioavailability
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bioavailability: the amount of active drug that survives first-pass metabolism. something that must be considered with oral drugs which undergo hepatic metabolism.
can increase the bioavailability of drugs by using alternative routes of entry: sublingual (nitroglycerin), rectally, IV IV has a 100% bioavailability = 1 |
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safer drugs have high or low therapeutic index
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HIGH therapeutic index
TI = median lethal dose/median effective dose |
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what is the unique quality of sweat glands (eccrine/apocrine glands) in terms of its autonomic stimulation?
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sweat glands are sympathetic but use ACh on the effector using the muscarinic receptor.
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adrenal medulla is innervated by that nerve?
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sympathetic ACh drops on adrenal medulla's nicotinic receptor
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what G-protein linked receptor is responsible for uterine tone
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Beta 2 (tertbutaline- helps to decrease uterine contractions)
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What is the class and major function of the M1, M2, M3 receptors?
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M1 - Gq - CNS, enteric nervous system
M2 - Gi - decrease heart rate and contractility of atria M3 - Gq - Glands - sweat, gastric acid GI: gut peristalsis, bladder contraction Pulm: bronchoconstricton Eye: miosis, accomodation |
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What is the class and major function of the D1, D2?
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D1 - Gs - relaxes renal vascular smooth muscle
D2 - Gi - CNS dopamine *think of Gs as relaxing vessels - beta2 is a Gs that relaxes muscle vasculature and bronchioles |
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What is the class and major function of the H1, H2?
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H1 - Gq - nasal, bronchial mucus production, contraction of bronchioles, pruritus, pain
H2 - Gs - increase gastric acid secretion |
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What is the class and major function of the V1, V2?
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V1 - Gq - vasoconstriction
V2 - Gs - H20 permeability in collecting ducts |
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Nicotinic ACh receptors are what type of receptors
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ligand gated Na/K channels found in autonomic ganglia or neuromuscular jxns
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Rx for neurogenic ileus and mechanism
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bethanechol treats neurogenic/postoperative ileus/urinary retention by a direct agonist (probably M3, Gq)
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Direct cholinomimetic that treats glaucoma
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Cabachol (CARbon copy acetylcholine)
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contracting ciliary muscle for the eye is more helpful for what type of glaucoma?
constricting pupil is more helpful for what type of glaucoma? |
contracting ciliary muscle for the eye is more helpful for open angle (anterior eye, outflow block)
constricting pupil is more helpful for narrow angle (posterior eye, iris and lens stuck together) |
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Non-CNS penetrating acetylcholinestase inhibitor
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neostigmine (Not-in-yo-CNS-stigmine)
rx for postoperative/neurogenic ileus, reversal of neuromuscular junction blockade |
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long acting treatment of myasthenia gravis
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pyrdiostigmine
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short acting diagnosis of myasthenia gravis
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edrophonium
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2 acetylcholinestase inhibitors that treats glaucoma
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physostigmine, echothiophate
*physostigmine also treats atropine overdose |
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antidote for cholinesterase inhibitor poisoning (organophosphates- insecticides)
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atropine + pralidoxime (regenerates active AchE)
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muscarinic agonist used for parkinson's disease
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benztropine - curbs excess cholinergic activity and improves tremor and rigidity
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scopolamine
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muscarinic agonist that treats motion sickness
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ipratropium
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muscarinic antagonist that prevents bronchoconstriction and treats asthma, COPD
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2 muscarinic antagonists that reduce urgency in mild cystitis and for those with bladder spasms
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oxybutinin, glycopyrrolate
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methscopolamine, pirenzepine, propantheline
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muscarinic antagonists that treat peptic ulcers
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try to name 7 symptoms of atropine toxicity:
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hot as a hare (increased body temp from decreased sweating)
dry as a bone (dry mouth, dry skin) red as a beet (flushed skin) blind as a bat (cycloplegia- paralysis of ciliary muscle/no accomodation) mad as a hatter (disorientation/psychosis) |
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what are 3 uses of atropine
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1. acute angle closure glaucoma in elderly
2. urinary retention in men with prostatic hyperplasia 3. hyperthermia in infants |
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hexamethonium
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nicotonic antagonist, can prevent reflex vagal responses, like reflex bradycardia caused by NE
side effects = severe orthostatic hypotension, blurred vision, sexual dysfunction, constipation (anti-cholinergic side effects) |
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hits up B1 and B2 receptors used rarely for AV block
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isoproterenol
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dobutamine mechanism and indications
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Mainly hits up B1 > B2
inotropic (increases contractility) but NOT chronotropic used for heart failure, cardiac stress testing |
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what symphathomimetic can be used to dilate pupil before eye exam
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phenylephrine
can also vasoconstrict, cause nasal decongestion |
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mechanism of amphetamines, ephedrine
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indirect general sympathetic agonist, releases stored catecholamines
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cocaine mechanism
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indirect sympathetic agonist + reuptake inhibitor
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alpha 2 agonist rx for hypertension with renal disease
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clonidine
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rx for pheochromocytoma
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phenoxybenzamine (irreversible) - use before removing tumor
reversible form is phentolamine |
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name the 3 alpha1 blockers
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prazosin, terazosin, doxazosin
rx for hypertension, mainly used for urinary retention in BPH 1st dose see orthostatic hypertension |
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alpha 2 blocker that treats depression
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mirtazapine
can also cause sedation, increase serum cholesterol, appeptite increase |
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Nonselective Beta blockers
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propanolol (it's a pro just hits em all up) timolol (glaucoma), nadolol, pindolol
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B1 selective antagonists
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metoprolol (moderate metoprolol- "i will only take Beta 1...", acebutol, atenolol, betaxolol, esmolol (short acting)
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Beta blocker used in glaucoma
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timolol - decrease aqeous humor secretion
*also betaxolol, carteolol |
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3 types of people who shouldn't take beta blockers
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1. people who like sex- impotence
2. asthmatics - B2 antagonist --> bronchoconstriction 3. diabetics - B2 increases insulin release, thus B2 blocker can decrease insulin release *other side effects - sedation, bradycardia/AV block/CHF |
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Rx for malignant HTN that causes cyanide toxicity
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nitroprusside
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dopamine D1 receptor agonist
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fenoldopam
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K+ channel opener that relaxes vascular smooth muscle in malignant HTN
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diazoxide
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What are the effects of nitrates on:
EDV BP Contractility HR Ejection time MVO2 |
Nitrates decrease PRELOAD
EDV: down BP: down Contractility:up (reflex) HR: up (reflex) Ejection time: down MVO2: down *the reduction in stroke work from the low EDV reduces the O2 more than the reflex contractility, HR |
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What are the effects of beta blockers on:
EDV BP Contractility HR Ejection time MVO2 |
EDV: increase (decrease HR = increase filling)
BP: low (less renin, less CO, skeletal muscle vasodilation) Contractility: low (less Ca2+) HR: low (prolonged phase 4) Ejection time: high MVO2: low |
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side effects of lovastatin
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hepatotoxicity, rhabdomyolysis
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how does niacin increase HDL
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niacin has two functions:
1. inhibits lipolysis in adipose 2. reduces VLDL secretion by decreasing VLDL, and thus LDL formation you prevent cholesterol transfer from HDL to LDL (via CETP). Thus, more HDL stays in the serum and less is cleared. |
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3 side effects of niacin
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1. red flushed face (decreased by aspirin)
2. hyperglycemia - acanthosis nigricans 3. hyperuricemia (exacerbates gout) |
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effect of cholestyramine on LDL, HDL, and triglycerides
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cholestyramine prevents intestinal reabsorption of bile acids- liver must use cholesterol to make more.
thus it decreases LDL, increases HDL slightly, but has the adverse effect of slightly increasing triglycerides |
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side effects of cholestyramine
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1. GI discomfort
2. dereased fat soluble vitamine 3. cholesterol gallstones (because liver is making more cholesterol to compensate for the lack of reabsorption) |
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ezetimibe - mechanism and rare side effect
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ezetimibe is a cholesterol absorption blocker in the small intestine
*has no effect on LDL, HDL rarely can cause hepatoxicity |
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best drug for decreasing cholesterol
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"fibrates" gemfibrozil, clofibrate, bezafibrate, fenofibrate
*upregulate LPL --> increased TG clearance upregulates LPL causing increased TG clearance. effects = decreases TG, increase HDL, decrease LDL |
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3 side effects of fibrates
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myositis
hepatoxicity cholesterol gallstones |
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what is the effect of class IA, IB, IC antarrhythmics on AP duration?
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IA = longer AP, longer QT interval, longer effective refractory period
IB = shorter AP IC = same AP |
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side effects of quinidine
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cinchonism - headache, tinnitus, torsades de poines (because of prolonged QT interval)
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used for both atrial and ventricular arrhythmias, esp. reentrant and ectopic SVT, VT.
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Type IA antarrhythmics
quinidine, procainamide, disopyramide |
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side effects of procainamide
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SLE-like syndrome (reversible)
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best antiarrhythmic for post-MI
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Type IB antiarrhythmics
Lidocaine, Mexiletine, Tocainide |
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contraindicated post-MI, but used for last resort in refactory tachycardia
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Type IC antiarrhythmics
Flecainide, Encainide, Propafenone |
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8 side effects of amiodarone
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hepatoxicity
pulmonary fibrosis hyper/hypothyroid (amiodarine is 40% iodine by weight) corneal deposits blue/gray skin deposits - photodermaitis neurologic effects constipation CV effects (bradycardia, heart block, CHF) |
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side effects of K+ channel blockers:
sotalol ibutilide bretylium |
sotalol = torsades de pointes, excessive beta block
ibutilide = torsades bretylium - new arrhythmias, hypotension |
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difference of Beta blocker, K+ channel blocker, and Ca2+ channel blocker on ECG
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beta blockers = inrease PR interval (AV node is most sensitive to Beta blockers, which decrease slope of phase 4)
K+ blockers- increase AP duration by blocking K+ exit, increase QT interval (risk for torsades) by elongating phase 3 (repolarization) of ventricular AP Ca2+ channel blocker = increase PR by decreasing AV nodal phase 0 depolarization. *remember, verapamil is used primarily for atrial tachy because it slows conduction through AV node |
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drug of choice for diagnosing/abolishing SVT.
this drug can be blocked by? |
Adenosine (increases K+ out of cells) --> hyperpolarizing, and also decreases Ca2+ in.
*very short acting ~15 sec tox = flushing, hypotension, chest pain effects blocked by THEOPHYLLINE |
