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103 Cards in this Set
- Front
- Back
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What is Congestive Heart Failure (CHF) |
heart doesn't pump blood as well as it should The failing heart has reduced work output per unit of O2 consumption not all blood pumped out of heart: accumulation of blood in the heart: leads to enlarged heart |
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How do the drugs that treat CHF work on the heart? |
reduce the O2 demands of the heart OR by increasing the function/strengthen the heart |
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What group of drugs treat CHF? What are these derived from? |
Cardiac Glycosides (Digitalis) foxglove plants |
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The cardiac glycoside that is used in the treatment of CHF? |
digoxin (Lanoxin) |
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What is the primary use of digitalis? Secondary use? |
Congestive Heart Failure
Atrial Flutter and Fibrillation |
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How does digitalis work? |
-Increases cardiac output without an increase in O2 consumption. LV failure: fluid accumulate in lungs RV failure: fluid accumulates in systemic vessels-leads to edema. cant put enough blood through kidneys for excretion |
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Why does digitalis depress the conductal system? |
So that every impulse does not reach the ventricles. |
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How does digitalis act on the heart? |
Receptor is an enzyme in the cell membrane called NA/K ATPase. Blocks Na/K uptake, more calcium retention. Increase contraction, stronger contraction. |
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Digitalis has a positive inotropic effect which means it does what? |
increases force of contraction increases influx of Ca2+ contraction phase enhanced |
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Digitalis does what to the refractory period?
(this does what 4 things) |
Decreases refractory period: atrial and ventricular muscle more loss of K+ decreases repolarization time can induce fibrillation |
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Digitalis increases cardiac output and causes what effect on the heart? |
-decreases size of distended congestive heart -diuresis from improved CV dynamics |
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Digitalis Increases the refractory period of the ___ Node and _________ fiber system due to ____________ stimulation (PsANS). (What three things does this do?) |
AV Purkinje Vagus Nerve - decreases conduction velocity - can lead to heart block or other arrhythmias - this is why digitalis is used in Afib |
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Digitalis can cause slowing of the heart rate at what does? (this is due to what 2 things?) |
Low doses - vagus nerve stimulation - decreases SANS activity due to restoring cardiac output |
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Therapeutic index of digoxin |
Low therapeutic index -hospital administration -need to individualize doseage |
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Toxic cardiac reactions to digoxin |
-heart block -ectopic systoles of ventricular origin -arrhythmias |
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Toxic Extra Cardiac reactions to digoxin
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Visual: yellow-green, white dot, double vision CNS: headache, drowsy, dizzy GI: nausea/vomit (CTZ), anorexia, increase salivation, cramps, diarrhea |
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Treatment of digoxin toxicity (4) |
-ECG -digiband (Ab to digitalis) -Potassium supplements -Lidocaine for ventricular arrhythmias |
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The drugs used first for treating CHF? |
ACE inhibitor ARB Diuretic |
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CHF drugs that cause a decreased Preload pressure |
Venule Dilators: -nitroglycerine -diuretics -salt restriction |
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CHF drugs that cause an increased contractabilty |
Inotropics -digoxin |
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CHF drugs that cause a decreased afterload pressure |
Arteriole dilators: -ACE inhibitors -ARB -Calcium channel blockers -alpha channel blockers |
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What is a cardiac arrhythmia? |
an abnormal heart beat |
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Drugs for cardiac arrhythmias are used to: |
used to modify or restore the rhythm of the heart toward normal |
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What is the action of cardiac arrhythmia drugs? |
Cardiac Depressants! |
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The mechanism of action of cardiac depressants (drugs for cardiac arrhythmias) |
- decrease in cardiac activity -increase in refractory period -decrease in pacemaker activity |
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What is the classification for antiarrhythmic drugs |
Vaughan-Williams Classification |
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What is the Vaughan-Williams Classification of antiarrhythmic drugs? |
Type I: Na+ blocker (membrane stabilization blocks conduction) Type II: beta receptor blocker (reduce SANS activity) Type III: K+ blocker (prolong action potential & repolarization) Type IV: Ca++ blocker (slow conduction velocity at AV node) |
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Type I drugs: |
antiarrhythmic, Na+ channel blocker. membrane stabilization blocks conduction. decrease conduction and depolarization. increase repolarization time. |
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Type I antiarrhythmic drug used in Dentistry? |
lidocaine (xylocaine) |
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lidocaine (xylocaine) |
Na+ channel blocker (stabilize membrane and block conduction) decreases responsiveness, conduction increases repolarization time. |
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How is lidocaine delivered to body? |
parenterally (but effective oral derivatives are available) |
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lidocaine may be used in emergency situations during what? |
during transport following an acute myocardial infection, this may be used. |
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How does lidocaine affect ventricular function |
decreases automaticity in purkinje fibers therefore used for treatment of ventricular ectopic rhythms
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What arrhythmia does lidocaine treat? |
ventricular fibrillation |
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Toxicities of myocardial depressants (3) |
excessive cardiac depression leading to drowsy and lethargy nausea and vomit various CNS disturbances |
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Type II antiarrhythmic drugs? |
beta receptor blockers reduce SANS activity |
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Type III antiarrhythmic drugs? |
K+ channel blockers prolongs the action potential and repolarization |
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Type IV antiarrhythmic drugs? |
Ca++ channel blockers slows conduction velocity at AV node. |
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used to manage life-threatening recurrent ventricular fibrillation or unstable ventricular tachycardia- assists to convert atrial fibrillation to normal sinus rhythm |
Type III antiarrhythmic drugs |
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Side effect of Type IV antiarrhythmic drugs |
gingival hyperplasia |
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What is angina pectoralis |
severe substernal pain in chest due to inadequate blood flow insufficient oxygen to the heart=pain coronary muscles are spasming |
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Three types of Angina pectoralis? |
-Chronic Stable Angina (Classic Angina of Effort) -Variant Angina -Unstable Angina |
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Chronic stable angina (classic angina of effort) |
presence of atheromatous obstruction in the coronary arteries goal: increase myocardium perfusion, decreases O2 demand |
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Variant Angina |
coronary artery spasm goal: prevent vasospasm |
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Unstable Angina |
thrombi near atherosclerotic plaque goal: correct tendency to form thrombi |
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Normal coronary flow |
-myocardium has a smaller blood supply in relation to O2 requirement -normal flow is regulated by physical factors such as transmural pressure during systole -some autoregulation-adenosine |
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Myocardial O2 supply is determined by:
and compromised by: |
coronary blood flow atherosclerosis, arterial spasm, and platelet-fibrin thrombi |
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Myocardial O2 demand is influenced by: and influenced by: |
heart rate, contractability, and wall tension exercise, smoking, cold, and eating |
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THe pain of angina pectoris (3) |
acute attack long-term prophylaxis short-term prophylaxis |
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Classification of drugs used to treat angina pectoris |
Negative Inotropic Vasodilators |
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Negative inotropic vasodilators: |
inorganic nitrites and organic nitrates |
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Selected pharmacology of nitrites and nitrates: Examples |
nitroglycerine (Nitrostat) amyl nitrite (Amyl Nitrite Aspirols) |
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nitroglycerine (Nitrostat) |
treat angina pectoris, emergency drug, sublingual, vasodilator, immediate onset
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amyl nitrite (Amyl Nitrite Aspirols) |
treat angina pectoris, ammonia inhalant, immediate response, causes vasodilation |
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Negative inotropic vasodilators: Mechanism of Action |
produce nitric oxide (NO) in vascular smooth muscle. |
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Why are negative inotropic angina pectoris drugs only taken as needed? |
Tolerance development |
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Adverse reactions and precations of negative inotropic drugs |
throbbing vascular headaches (Nitrates) methemoglobinemia (Nitrites) face flushing hypotension reflex tachycardia (palpations) fainting nausea/vomit visual disturbance (dilate retinal vessels) |
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Drug interaction that can occur with negative inotropic vasodilators |
-hypotensive effects of narcotics and antihypertensive agents -increase intraocular pressure of anticholinergic agents NOT TO BE USED WITH ATROPINE in glaucoma -drop in BP enhanced with PDE-5 (Viagra) |
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Antianginal agents in dentistry |
prophylactic use of nitroglycerin in angina pt. emergency use of nitroglycerin or amyl nitrite in treating an acute anginal attack |
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precautions with the use of antianginal agents in dentistry |
use patients prescription and dose know nonspecificity of drug and overdose response short shelf life- frequently update |
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Beta blocker used to treat angina pectoris |
Proranolol (Inderal) decreases demand of O2 on the heart. |
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Calcium blocking agents used to treat angina pectoris |
directly inhibit Ca++ -relaxes effect on vascular smooth muscle arterial dilation in coronary and systemic beds |
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amlodipine (Norvasc) |
Ca++ entry blocking agent relaxes the vascular smooth muscle and dilates arterioles in coronary and systemic beds |
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What drugs are used to treat thromboembolic disorders |
Anticoagulant drugs |
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Blood coagulation cascade phases |
1. coming together of many factors to activate factor 10 2. factor 10 convers prothrombin to thrombin 3. thrombin converts fibrinogin to fibrin |
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What ion is essential for coagulation? |
Calcium |
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Chemistry of Heparin: |
Large, highly polar molecules |
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Heparin mechanism of anticoagulant action: |
mediated by endogenous component of plasma- heparin cofactor (antithrombin III) neutralizes thrombin so it cannot act (antithrombin action) |
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what decreases the levels of antithrombin III? |
estrogen (birth control decreases antithrombin III and can cause blood clots) |
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Naturally occurring, prevents microclots from appearing in our blood. |
Heparin |
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Onset and half life of Heparin |
immediate
t1/2= 1-3 hours |
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Route of administration: Heparin |
parenteral (NOT orally) |
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Clinical use of heparin |
"Heparin Lock"- draw blood, put some heparin in it to prevent coagulation |
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Heparin anticoagulant is antagonized by what? |
protamine sulfate (use if there is a heparin overdose) |
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What is the adverse effect of Heparin |
hemmorhage |
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Oral anticoagulants |
Coumarin derivatives |
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Example of an oral anticoagulant |
warfarin (Coumadin) |
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warfarin (Coumadin) mechanism of action: |
antagonize the utilization of Vitamin K by the liver depresses the synthesis of plasma clotting factors (2, 7, 9, 10) decreases platelet adhesiveness |
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Pharmacokinetics of oral anticoagulants: |
oral, but high variability in amount absorbed highly bound to plasma protein metabolized in liver |
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adverse effect of oral anticoagulats |
hemmorhage |
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Coumarin derivatives (oral anticoagulants) are antagonized by what? |
Vitamin K |
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Newer orally administered anticoagulants are different how? |
more predictable don't need to monitor INR can inhibit -Thrombin -Factor 10a |
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Blood has the capacity to dissolve clots by means of what? |
fibrinolytic system |
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When activated ______forms ______ to break clots |
plasminogen plasmin |
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activators of the fibrinolytic system may be used in the treatment of |
victims of a heart attack |
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Example of activators of the fibrinolytic system |
tissue plasminogen activator [t-PA, alteplase (Activase)] |
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tissue plasminogen activator: |
natural enzyme made available by genetic engineering. prevents tissue damage by opening vessel sooner used less tissue damage from blood clot |
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What is the most common complication associated with activators (thrombolytics) |
bleeding |
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If body has excessive amounts of t-PA what happens |
the body doesn't clot and at a surgical risk |
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Platelets provide: |
the initial hemostatic plug at site of injury to the vascular. |
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Platelet inhibitors used to prevent: |
thrombosis and to alter the natural history of atherosclerotic vascular disease |
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Example of a platelet inhibitor |
asprin |
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Drugs used to lower plasma lipoproteins: |
high levels of lipids (cholesterol) can lead to CV disease |
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High cholesterol can accelerate what |
development of atherosclerosis which may lead to thrombosis (blood clot) and infarction (heart attack) |
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LDL? |
bad cholesterol put lipids on tissues |
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HDL |
good cholesterol takes lipids to liver |
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Therapeutic approach to lower plasma lipoproteins: Diet |
diet low in cholesterol and saturated fats diet high in fiber |
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Lower plasma lipoproteins, need to reduce all other risk factors: |
smoking, hypertension, obesity, poor physical condition, diabetes |
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Drug therapy (last case scenerio) to lower plasma lipoproteins: |
HMG-CoA reductase inhibitors (statins) |
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HMG-CoA reductase inhibitors AKA |
"statins" |
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How do statins work? |
synthesis in liver. inhibit exyme "rate limiting step" to decrease LDL and increase HDL |
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atorvastatin (Lipitor) |
lower plasma lipoproteins decrease LDL increase HDL by inhibiting the enzyme |
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side effects of HMG-CoA reductase inhibitors (statins) |
elevate liver enzymes muscle pain (myopathy) memory loss (cognitive problems) dpse-related depletion of Coenzyme Q10 |
