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46 Cards in this Set
- Front
- Back
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What are glycosides do to the heart
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improve cardiac contractility
Inotropic prototype : digoxin |
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what do we use glycosides for
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Prototype: digoxin
positive inotropic negative chronotropic(heart rate) negative dromotropic(conduction) increase sodium and water excretion |
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what does digoxin toxicity look like (signs and symptoms)
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early: n/v, vision changes
Late: dysrhythmias due to progressive heart block; see halos around lights, see green/yellow tint to white objects |
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what do we use to reverse digoxin toxicity
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1. hold dose
2. give immune Fab( Digibind) bind with molecule and then is excreted by kidney. as more tissue molecules are released into the bloodstream(diffusion), more binding takes place 3. Hasten elimination by binding (charcoal, cholestyramine) |
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what drugs can increase the likelihood of digoxin toxicity
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diuretic
1. the most common cause of digoxin overdose: hypokalemia 2. even therapeutic levels may be too high if K is low |
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how is digoxin first dose given
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digitalization (loading)
Higher doses at first, then typical doses -can do IV or PO -Does depend on body weight |
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what do we check before giving digoxin
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1. see pt periodic drug levels
2. electrolyte level 3. must take apical pulse for 1 full min 4. watch HR, dysrhythmias 5. electrolyte imbalance: hypokalemia and hypomagnesemia increase risk of toxicity, hyperkalemia and may produce dysrhythmias 4. renal insufficiency pt: decrease excretion of digoxin and easier toxic |
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difference in treating chronic angina and acute angina
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chronic angina is ischemia of heart tissue, not death
if remove trigger pain subsides |
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how do we give nitroglycerin(NTG)
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1. oral: time-released with heavy first pass effect, not good for emergent need
2. oral mucous membranes : quick 3. ointment, remember to wear glove 4. transdermal patches for sustained release longer term(12 hr on , 12hr off) |
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what are two side effects of NTG
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1. headache, lessens over first 2 wks
2. Hypotension-does dependent, if BP falls too fast or too much, get poor perfusion(can trigger reflex tachycardia) |
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What are glycosides do to the heart
|
improve cardiac contractility
Inotropic prototype : digoxin |
|
|
what do we use glycosides for
|
Prototype: digoxin
positive inotropic negative chronotropic(heart rate) negative dromotropic(conduction) increase sodium and water excretion |
|
|
what does digoxin toxicity look like (signs and symptoms)
|
early: n/v, vision changes
Late: dysrhythmias due to progressive heart block; see halos around lights, see green/yellow tint to white objects |
|
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what do we use to reverse digoxin toxicity
|
1. hold dose
2. give immune Fab( Digibind) bind with molecule and then is excreted by kidney. as more tissue molecules are released into the bloodstream(diffusion), more binding takes place 3. Hasten elimination by binding (charcoal, cholestyramine) |
|
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what drugs can increase the likelihood of digoxin toxicity
|
diuretic
1. the most common cause of digoxin overdose: hypokalemia 2. even therapeutic levels may be too high if K is low |
|
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how is digoxin first dose given
|
digitalization (loading)
Higher doses at first, then typical doses -can do IV or PO -Does depend on body weight |
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what do we check before giving digoxin
|
1. see pt periodic drug levels
2. electrolyte level 3. must take apical pulse for 1 full min 4. watch HR, dysrhythmias 5. electrolyte imbalance: hypokalemia and hypomagnesemia increase risk of toxicity, hyperkalemia and may produce dysrhythmias 4. renal insufficiency pt: decrease excretion of digoxin and easier toxic |
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|
difference in treating chronic angina and acute angina
|
chronic angina is ischemia of heart tissue, not death
if remove trigger pain subsides |
|
|
how do we give nitroglycerin(NTG)
|
1. oral: time-released with heavy first pass effect, not good for emergent need
2. oral mucous membranes : quick 3. ointment, remember to wear glove 4. transdermal patches for sustained release longer term(12 hr on , 12hr off) |
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what are two side effects of NTG
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1. headache, lessens over first 2 wks
2. Hypotension-does dependent, if BP falls too fast or too much, get poor perfusion(can trigger reflex tachycardia) |
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pt education regarding storage and use of Nitroglycerin (NTG)
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stored in airtight light resistant (brown) glass bottles or air tight aluminum spray
bottles expire 6 moth after opened |
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what do we use antidysrhythmics for
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restore the cardiac rhythm to normal:
Block adrenergic stimulation of the heart Depress myocardial excitabitliy and contractility decrease conduction velocity in cardiac tissue increase recovery time (repolarization-resting) of the myocardium Suppress automaticity (Spontaneous depolarization to initiate beats |
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what are the big side effects of antidysrhythmics
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1. potential to worsen dysrhythmias
2. QT prolongation 3. Toxicity/low margin of safety for many |
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lidocaine toxicity-what does it look like
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Lidocaine has low margin of safety
tremors, twitching, blurred vision, tinnitus, dyspnea, sever dizziness, fainting, bradycardia, convulsions (esp in elder) |
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bad side effects of amiodarone
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1. pulmonary fibrosis
2. thyrotoxicosis 3. dizzness, bitter taste, tremors, blue-gray skin color |
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What are the three main types of lipid lowering drugs?
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1. bile acid sequestraints
2. cholestrerol synthesis inhibitors 3. HMG-CoA inhibitors (satins) |
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How does each type work to reduce cholesterol?
Bile Acid Sequestrants |
Prototype: cholestyramine (Questran)
Effects sequesters or binds with the bile so it cannot be reabsorbed excreted in feces body responds by making more cholesterol and bile than before loss is greater than gain so decreases cholesterol. |
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How does each type work to reduce cholesterol?
Cholesterol Synthesis Inhibitors |
Prototype: lovastatin (Mevacor)
Effect most effective drugs to lower LDL inhibits critical enzyme in formation of cholesterol (HMG-CoA) thus decreasing total cholesterol, LDL, and triglycerides while also increasing HDL |
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How does each type work to reduce cholesterol?
Lower serum triglycerides (fibrates) |
Prototypes: gemfibrozil (Lopid)
Action--inhibits synthesis of VLDL, the biggest carrier of triglycerides |
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what is the big side effect of statins
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Muscle Degeneration
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what do we monitor when someone is on a statin
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??
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Risks of anticoagulation?
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Risk of bleeding is life-threatening
Active hemorrhage Recent hemorrhagic stroke Recent surgery Hemophilia Pregnancy Recent abortion/miscarriage |
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three different types anticoagulation drug, their uses, and their difference
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1. heparin
2. warfarin 3. dabligatran |
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Heparin
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Prototype: heparin (administered SC or IV)
mfg in the liver, lungs, gut--obtained from slaughterhouse animals Action direct blocking of intrinsic pathway clotting cascade, helps antithrombin inactivate factor Xa and thrombin |
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Oral Anticoagulant
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Prototype: warfarin (Coumadin)
Action does not work in the blood but in the liver to inhibit synthesis of vitamin K dependent clotting factors (VII, IX, X, and prothrombin) ADME highly protein bound long t 1/2 of 36 hr |
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Dabigatran (Pradaxa)
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Direct, reversible thrombin inhibitor
Prevention of VTE, Atrial fibrillation New oral agent- Launched October 2010 No monitoring Consistent dosing Hemorrhage (especially in elderly) |
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How do we monitor Heparin, Warfarin and dabigatran
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Heparin- aPTT
Warfarin-PT/INR Dabigatran-no need to monitor |
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Antiplatelet drugs-what are they used for
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Prototype: aspirin
Action blocks enzyme necessary to create the stickiness of the vessel walls so it inhibits platelet aggregation, permanently alters the platelet one 325 mg tablet can double bleeding time for up to 7 days--it takes that long to make new platelets |
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HIT-what is it and how do we find it? what else do we use instead?
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Growing problem of heparin induce thrombocytopenia
Generate antibiodies against the foreign drug Incidentally creates issues for platelets Not use heparin if can for routine IV flushes If HIT develops can never get heparin again |
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Thromolytics-how do they differ from the above drug>
big contraindicaitons |
Prototype: streptokinase (Streptase)
comes from beta hemolytic strep Action reacts with plasminogen found in clots and converts it to plasmin which dissolves the clot ADME the protein destroyed by gastric acid, only given parenterally (duration 4 hr) |
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Dabigatran (Pradaxa)
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Direct, reversible thrombin inhibitor
Prevention of VTE, Atrial fibrillation New oral agent- Launched October 2010 No monitoring Consistent dosing Hemorrhage (especially in elderly) |
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How do we monitor Heparin, Warfarin and dabigatran
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Heparin- aPTT
Warfarin-PT/INR Dabigatran-no need to monitor |
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Antiplatelet drugs-what are they used for
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Prototype: aspirin
Action blocks enzyme necessary to create the stickiness of the vessel walls so it inhibits platelet aggregation, permanently alters the platelet one 325 mg tablet can double bleeding time for up to 7 days--it takes that long to make new platelets |
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Patient education regarding use of any blood thinners
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?
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HIT-what is it and how do we find it? what else do we use instead?
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Growing problem of heparin induce thrombocytopenia
Generate antibiodies against the foreign drug Incidentally creates issues for platelets Not use heparin if can for routine IV flushes If HIT develops can never get heparin again |
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Thromolytics-how do they differ from the above drug>
big contraindicaitons |
Prototype: streptokinase (Streptase)
comes from beta hemolytic strep Action reacts with plasminogen found in clots and converts it to plasmin which dissolves the clot ADME the protein destroyed by gastric acid, only given parenterally (duration 4 hr) |
