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67 Cards in this Set
- Front
- Back
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What is CHF?
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condition in which the heart is unable to pump enough blood to meet the peripheral tissues' needs
- fluid accumulation - nearly any other CV disease will eventually lead to CHF |
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Why is CHF described as a vicious cycle?
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decrease in cardiac function, then other changes tend to occur that further decreases cardiac function (treat early so this vicious cycle doesn't occur)
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What are the pharmacological goals for treating CHF?
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1. increase heart's ability to pump blood
2. decrease cardiac workload (decrease volume heart has to pump, decrease pressure heart has to work against) |
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What are the 2 categories of druges used for CHF?
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1. agents that increase myocardial contraction force: positive inotropic agents
2. agents that decrease cardiac workload |
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What is an example of an agent that increases myocardial contraction force?
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- digitalis
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What are examples of agents that decrease cardiac workload? (5)
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1. ACE inhibitors
2. angiotensin II receptor blockers 3. beta adrenergic blockers 4. diuretics 5. vasodilators (Prazosin, Minipress, alpha 1 blockers, nitrates) |
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What is inotropy?
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musclar contractility
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What is a positive inotropic effect?
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increase heart's ability to pump
increase contractility force |
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What is the mechanism of Digitalis?
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1. inhibits Na+/K+/ATPas activity
2. increases sodium in cell 3. decreases Ca+/Na+ exchanger activity 4. increase Ca+ in cell 5. allows increase in muscle contractility |
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What is the mechanical effect of Digitalis?
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increases contractile force
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What is the autonomic/electrophysiological effect of Digitalis?
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- directly inhibits sympathetic activity
- used to treat arrhythmias (decreased abnormal excitation of cells) |
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What are pros of using Digitalis (digoxin, Lanoxin)? (2)
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1. increases CO (resting and exercise), which improves exercise tolerance
2.decreases symptoms of heart failure and number of hospitalization associated with CHF |
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What are cons of using Digitalis (digoxin, Lanoxin)? (3)
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1. not clear whether it improves life expectancy
2. long 1/2 life (takes longer to build up theraputic concentration) 3. narrow therapeutic window |
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What are adverse side effects seen when using Digitalis?
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1. toxicity (low TI)
2. arrhythmias (drugs used to treat them can also cause them) 3. GI, cardiac disturbances 4. CNS manifications |
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What should be monitored when taking Digitalis?
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blood plasma levels
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What are 2 examples of "others" (positive inotrophic agents)?
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1. phosphodiesterase inhibitors (PDE)
2. Dopamine (Intropin), dobutamine (Dobutrex) |
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When is Phosphodiesterase (PDE) inhibitor used?
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for ACUTE or SEVERE heart failure (not for chronic use)
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When are Dopamine (Intropin) or dobutamine (Dobutrex) used?
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- for ACUTE or SEVERE heart failure
- used if Digitalis or derivative is not effective |
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Does Dopamine/dobutamine increase HR?
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it is a Beta 1 agonist and does not increase HR
- only changes cardiac contractility |
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What is hemostasis and what is its function?
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blood coagulation
prevents hemorrhaging |
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What happens if there is too much/too little clotting?
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too little: results in too much blood loss
too much: results in abnormal clot formation (thrombogenesis) |
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Describe the bare-bone basics to the intrinsic system/extrinsic system for coagulation.
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The intrinsic and extrinsic come together
1. prothrombin changes into thrombin to bring pathways together 2. turns fibrinogen into fibrin 3. CLOT! |
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How does breakdown of the clot occur?
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1. plasminogen is turned into plasmin when tissue plasminogen activator is added
2. plasmin = fibrinolysin and that breaks down or lyses fibrin clot |
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What are 3 treatments for overactive clotting?
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1. anticoagulants
2. antithrombotics 3. thrombolytics |
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What is the function of anticoagulants used for overactive clotting?
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control function and synthesis of clotting factors
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When are anticoagulants used?
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used to prevent, treat abnormal venous clot formation (venous thrombosis)
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What are 2 primary drugs used as anticoagulants?
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1. heparins
2. oral anticoagulants |
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How are heparin anticoagulants administered? When are they used?
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- administered parenterally
- used initially for DVT and for pregnant patients |
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What is the mechanism of heparin anticoagulants?
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potentiates activity of antithrombin III
by binding to clotting factors, antithrombin III inactivates them (clotting factors) increased antithrombin III activity reduces the tendency to clot |
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What are adverse effects of heparin anticoagulants?
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hemorrhage, death
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What is the difference between true heparin administration and heparin derivatives?
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some heparin derivatives (enoxaparin, Lovenox) may be injected subQ and have lower risk of adverse effects than true heparin
- can self administer heparin derivatives |
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What is the mechanism of oral anticoagulants?
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impairs vitamin K-dependent synthesis of clotting factors
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What are examples of oral anticoagulants?
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warfarin, Coumadin
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What are advantages/disadvantages of oral anticoagulants (warfarin, Coumadin)?
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advantages: taken orally
disadvantages: contraindicated during pregnancy, not effective for several days |
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What are adverse effects for oral anticoagulants?
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hemorrhage
death |
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What are some reasons for having a slow clotting factor production?
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- not eating enough vitamin K
- not absorbing enough - not synthesizing enough - newborns can't synthesize vitamin K, could be given after birth |
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What is the difference in routes between heparins vs. warfarin?
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heparins: parenteral, IV, subQ
warfarin: oral |
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What is the difference in onset of action between heparins vs. warfarin?
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heparins: fast
warfarin: slow |
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What is the difference in mechanism between heparins vs. warfarin?
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heparins: increase antithrombin III (inactivates clotting factors)
warfarin: impairs vitamin K-dependent synthesis clotting factors |
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What is the difference in reasons for using heparins vs. warfarin?
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heparins: acute, DVT (prevention or breakdown), PREGNANT WOMAN can take these
warfarin: long term DVT prevention |
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What does the American College of Chest Physicians recommend for patients with acute DVT?
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early mobility in preference to initial bed rest when feasible
after treatment: (24 hours and INR levels) |
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What is a summary of the American College of Chest Physicians studies about early ambulation?
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anticoagulation and early ambulation with leg compression leads to faster pain/swelling reduction (similar with PEs) as compared to immobilization
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What is the function of antithrombotics for overactive clotting? What are indications for use?
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- inhibit platelet formation
- used to prevent thrombus formation in arteries (prevent and treat MI and prevent ischemic CVA) |
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What are antithrombotic drugs?
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aspirin
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What are adverse effects of antithrombotics used for overactive clotting?
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- increased risk of hemorrhage (including hemorrhagic CVA)
- possible GI irritation |
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What are examples of thrombolytics for overactive clotting?
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tissue plasminogen activtator (t-PA), alteplase
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What are 2 functions of thrombolytics?
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1. facilitate the destruction of blood clots
2. reestablish blood flow through vessels that have been occluded by thrombi |
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What are indications for using thrombolytics for overactive clotting?
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treating acute MI (12 hours)
ischemic CVA (3 hours) |
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How are thrombolytics administered? What are their mechanism?
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IV
convert plasminogen to plasmin |
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What are adverse effects associated with thrombolytics?
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risk of hemorrhage
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How is hemophilia treated?
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replace missing clotting factors
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How do you treat vitamin K-dependent clotting factor deficiencies?
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administer exogenous vitamin K
(can be oral or pareneral -- can bypass GI tract as necessary) |
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How is excessive bleeding due to excessive plasmin breakdown of clots treated?
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administered antifibrinolytics/antiplasmin agents
decrease activity of plasmin system |
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What should a PT be careful of with a patient who has a clotting deficiencies? (4)
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1. falls/bumps
2. deep tissue massage 3. small knicks or bleeds becomes more of a problem 4. avoid plyometric and high impact |
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What are people at risk for?
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intrajoint hemorrhaging (hemarthrosis)
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What are 3 examples of clotting deficiencies?
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1. hemophilia
2. vitamin K-dependent clotting factor deficiencies 3. excessive bleeding due to excessive plasmin breakdown of clots |
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What is hyperlipidemia? What can it lead to?
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increased plasma lipids
leads to atherosclerosis, leading to increased clotting and related diseases |
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What are lipoproteins?
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- some remove cholesterol from arterial walls (HLDs)
- some transport and deposit cholesterol on the arterial wall (LDLs, VLDLs) |
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What does pharamocological treatment emphasize in respect to lipoproteins?
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increasing HDLs and decreasing LDLs and VLDLs
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What are characteristics of all 4 major types of antihyperlipidemia drugs? (2)
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- used in combination with diet changes
- each can sometimes be used in combination with other antihyperlipidemic drugs |
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What are indications for using an antihyperlipidemic drug?
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decrease cholesterol levels which decreases the risk of CV disease
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What are adverse side effects associated with antihyperlipidemic drugs?
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- serious side effects are rare
- myopathy is rare but a potentially serious side effect of statins (cause muscle weakness, pain, inflammation) |
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What are the 4 categories of antihyperlipidemia drugs?
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1. statins (Lipitor)
2. fibric acids (fibrates) 3. niacin (Niaspan) 4. Ezetimibre (Zetia) |
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What is the primary effect of statins (lipitor) and what are contraindications?
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- decreases total cholesterol and LDL
- avoid grapefruit products - avoid use in pregnancy and young children |
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What is the primary effect of fibric acid (fibrates)?
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decrease triglycerides and VLDL
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What is the primary effect of Niacin (Niaspan)?
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broad spectrum benefits to cholersterol profile
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What is the primary effect of Ezetimibre (Zetia)?
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decrease cholesterol absorption from GI tract (decreasing total cholesterol)
**excreted out of the bloodstream |
