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24 Cards in this Set
- Front
- Back
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Hypertension treatment
What are the 5 general drug categories for treatment? |
Diuretics, Sympathoplegics, Vasodilators, ACE inhibitors, A II receptor blockers
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Diuretics for HTN
1)Name and Side effects |
1)Hydrochlorothiazide- hypokalemia, hyperlipidemia, hyperuricemia, hypercalcemia,hyperglycemia
2)Loop Diuretics- K+ wasting, metabolic alkalosis (volume contraction), ototoxic |
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Clonidine
1) MOA 2) side effects |
1)central agonist at alpha2 to prevent further release
2) dry mouth, sedation, rebound hypertension |
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Methyldopa
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same as clonidine
Causes (+) Coomb's test |
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Hexamethonium
1)MOA 2)Side effects |
1) Blocks Vasovagal response to increase HR and BP
2) Orthostatic Hypotension |
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Reserpine
1)MOA 2)Side Effects |
1) Blocks Dopamine uptake into vessicles ---> decreases NE stores
2) Sedation, Depression |
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Prazosin
1)MOA 2)Side Effects |
1) selective alpha 1 antagonist
2) 1st dose hypotension |
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Beta Blockers
1) MOA 2)Side Effects |
1) Drugs that start with A-M selectively block increased HR to drop CO. The rest act on Beta2 as well to prevent bronchodilation
2)Impotence, Asthma exacerbation, Sedation, CHF, bradycardia |
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Hydralazine
1)MOA 2)Use 3)Toxicity |
1)Vasodilator in arteries via cGMP
2)Severe HTN, CHF 3) SLE like syndrome, reflex tachy (use B blocker) |
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Nifedipine, Verapamil, Diltiazem
1)MOA 2)side-effects 3)uses |
1) Block voltage gated L-type Ca+ channel to reduce contractility
Vascular muscle-nifedipine>diltiazem>nifedipine Heart muscle- Verapamil>Diltiazem>Nifedipine 2)Dizziness, flushing, nausea, constipation (verapamil) 3)HTN,Angina, Arrythmias (not nifedipine) |
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Nitroprusside
1)MOA 2)Side Effects |
1)increase NO release and vaso/veno dilates, but it is metabolized into cyanide.
2)Causes cyanide poisoning |
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Captopril
1)MOA 2)Side Effecs |
1)ACE inhibitor to block Renin/Angiotensis system
2) CAPTOPRIL Cough, Angioedema (decreases C1 Esterase), Proteinura, Taste Change, hypOtension, Pregnancy problems (renal damage to fetus), Rash (erythema multiforma, Stevens Johnson), Increase Renin, Low AT II |
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Nitroglyceride, isosorbide
1)MOA 2)Use 3)Side Effects |
1) vasodilates veins via cGMP to decrease preload (decrease cardiac work)
2)Angina 3)Headache, Tachy (due to decrease CO), Hypotension Tolerance develops Monday Disease- if exposed to nitratse in industry, tolerance develops through work week, but showing up on Monday will cause Headache, Hypotension, and Tachy |
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Anginal Therapy
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Goal is to decrease O2 consumption of myocardium via decreasing EDV, Afterload, Contractility, or HR
Nitrates- decrease Preload with reflex increase HR/ B-Blockers- decrease afterload by decreasing contraction and HR Combo- drastically decrease O2 consumption via decreased HR and BP |
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Cardiac Glycosides - Digitalis, Digoxin
1)Facts 2)MOA 3)Use |
1) 75% bioavailable, 20-40% protein bound, and t1/2 = 40 hours, urinary excretion
2)Inhibits Na/K pump which builds up Na inside cell --> lowers Na/Ca exchanger so that intracelluar Ca+ increases --> (+) inotropy Also increases PR interval 3) used in CHF (inc inotropy), and Afib (dec conduction AV node) |
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Digoxin
4) Toxicity 5) Antidote |
4) Nausea, Vomiting, Yellow Vision, Arrythmias
Risk increases with Renal Failure (less excretion), hyokalemia (synergistic effect), and Quinidine (displaces from Plamsa Protein to increase levels) 5) Stop Dig, give K+, use Lidocaine for arrhythmia, anti-Dig Fab fragments |
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Class I Antiarrhythmics
-What channels do they all block?? |
They are Na Channel blockers, specifically the fast Na+ channels involved in Phase 0 upstroke.
They can also slow Phase 4 upstroke Na+ funny channels in abnormal pacemaker cells. |
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Class Ia
1)Names 2)Effect 3)Uses 4)Toxicity |
1) Quinidine, Procainamide, Amiodarone (also Class III), and Disopyramide
2) Moderate blockade of upstroke, and Prolongs the Repolarization --> net increase in Refractory Period to slow down abnormal re-entry circuits (long QT) 3) Afib, SVT, Vfib 4) Quinidine- cinchonism (headache, tinnitus, thrombocytopenia), and Torsades de Pointe Procainamide- SLE like syndrome |
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Class Ib
1) Names 2) Effect 3) Use 4) Toxicity |
1) Lidocaine, Tocainide
2) Weakest block of Na fast channels, and shortens repolarization to cause a decrease in Refractory Period. Only works on infarcted tissue 3)Post-MI arrythmias and digitalis induced 4) Local anesthesia, CNS depression, |
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Class Ic
1) Names 2) Effects 3) Uses 4) Toxicity |
1) Flecainide, Ecainide, Propafenone
2) Strongest slow down of Na fast channels, but no effect on Repolarization (same Refractory Period) 3) Used in life threatening Vtachs, SVT (last resort) 4) Can induce arrythmias |
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Class II - Beta Blockers
1)MOA 2)Toxicity |
1) Decrease cAMP which prevents phosphorylation of Rianodine receptors --> less Ca+ for contraction
Prolongs upstroke of Phase 4 in pacemaker cells (long PR interval) 2) Impotence, exacerbate asthma, bradycardia, sedation, may mask hypoglycemia (because it releases Glucagon) |
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Class III - K+ Blockers
1)Names 2)MOA 3)Uses 4)Toxicity |
1) Sotalol, Amiodarone, Ibutilide
2) Prolongs the time for K+ to leave the cell -->increase Refractory Period (QT) 3)Used in SVT and Vtach when other drugs fail 4) Sotalol- torsades de pointe Amiodarone- Pulmonary Fibrosis, Hepatotoxic, Hyper/hypothyroid (check PFTs, LFTs, and TFTs). Also visual changes, and skin deposits 4) |
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Class IV- Ca+ Blockers
1)Names 2)MOA 3)Uses 4)Toxicity |
1) Verapamil, Diltiazem (Nifedipine not used)
2) They block Ca+ currents, which are the fast channels in Pacemaker cells. Prolong ERP and conduction velocity of AV node 3) Prevention of nodal Arrhythmias (SVT) 4) Constipation, flushing, edema, CHF (decreases contraction force), AV block |
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Adenosine
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Causes flat line for 15 seconds --> abolishes AV node arrhythmia (cardioversion)
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