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78 Cards in this Set

  • Front
  • Back
Myocardial ischemia.
Imbalance between oxygen supply and myocardial oxygen demand in the heart.
Causes of Myocardial ischemia
Low coronary blood flow
High oxygen demand(Demand)
Main cause of ischemia
Low coronary blood flow
Determinants of mycocardial oxygen demand
Heart rate
Wall stress or tension(preload, and afterload)
Demand is the target for
Biochemical consequences of ischemia
naerobic shift
decrease high energy phosphate
decrease atp
increase adp
decrease creatinine phosphate
increase lactic acid
Increase intercelluler calcium
Functional consequences of ischemia
Decrease ventricle relation
decrease venticle contraction
increase fillng pressures
Ecg abnormalities
Chest pain
Myocardial stunning
Brief period of myocardial ischemia causeing a prolonged impairment of myocardial dysfunction with a gradual return to normal fx
Myocardial hibernation
Reduction in myocardial contractility causing oxygen consuption to match a reduced oxygen supply
Where does myocardial necrosis occur first
Subendocardium. Takes 4-6hrs to get to subepicardium
Myocardial necrosis is signaled by
appearance in circulating blood proteins normaly found in intact cardiac cells
Silent ischemia
Not benign, increase in SI, increase risk
Chronic stable angina
Coroanry atherosclerosis.exertional exercise problems.
Bile Acid Binding Resins
Hypercholesterolemia.Offset.Increase of cholesterol.liver.
Whats good to use with Bile Acid Binding Resins
Statins mechanism
decrease HMG-CoA reductase
Which is most popular?
What are statins pleiotrophic effects?
Lipids, improve endothelial cells, enhance plaque stability
reduce inflammation.
Niacin Mechanism
Inhibits lipolysis of triglycerides by hormone sensitive lipase.
What should you not use NIACIN with?
Statins, will cause myopathy
Cholesterol absorption blockers
Inhibits processes in jejunum. Inhibit NPC1L1.
What are CAB's used with?
What shouldnt CABs be paired with?
Bile Acid binding resins
Bind to ppar
Increased lipoprotein lipase
Reduced expression of ApoIII
Increased ApoIandII
What should you not do with fibrates?
Mainline use
Sideffects of Fibrates?
GI, hair loss, uticaria
Dont use fibrates with
Unfortunatley, Fibrates sometimes cause?
Increase in LDL levels
Use of fibrates?
Hypertriglyceridemia, and low HDL Levels associated with metabolic syndrome(type 2 diabetes)
Beta adrenergic blockers
Block catecholamines from binding adrenergic receptors
Used for unpredictable effects in variant angina
B-adrenergic blockers
Adverse effects of B-adrenergic blockers.
Bronchoconstriction, cardiac effects, lethargy, fatigue, nightmares
Fibrates should not be used if
Pt have cardiac conduction problems or obstructive lung disease.
Fibrates work for
Stable angina, NOT VARIANT
Name 2 types of calcium channel blockers.
Cardio Selective
Which can be used with B-antag
Which is stronger? Dihydropyridine or Cardio Selective?
Cardio Selective
Name cardioselective drugs
Diltiazem, verapamil
Cardio Selectives should not be used in pt with
Cardiac conduction disorders
How do cardiac conduction blockers work
Decrease heart rate and contractility
Cardiac selective and Dihydopyridine work by
decreasing systemic atrial conduction and decrease coronary artery conduction.
What do Calcium channel blockers treat?
Variant angina
Calcium channel blocker mechanism
NON COMPETITIVLY inhibit mvnt of ca through L-type membrane calcium channels.
Which of the two ca blockers have slow recovery time?
Cardiac Selective
ADP inhibitors
Inhibit the binding of ADP to its receptor on platelets.
Which ADP inhibitor has fewer adverse effects
What are the two ADP inhibitors?
Clpidogrel and Ticlopidine
What kind of drug are ADP inhibitors?
Adp inhibitors are used with?
Duration of action for ADP inhibitors
4-8 days
ADP Inhibitor sideffects
Neutropenia, Thrombotic thrombocytopenia, purpera, GI bleeding
Why is clopidogrel more popular
Less neutropenia,rapid onset of action.
Permanently acetylates COX-1
Blocks thromboxane at platelet.
What does aspirin do
decrease the risk of MI by fiftey percent.
How long does aspirin last?
Some pts develope resistance to anti platlet effects of aspirin
5-8%. these pt are at more risk for adverse events
GP IIb/IIIa receptor inhibitors
These are recepters on platelets.
GP Molecular mechanism
Prevent fibrinogen mediated cross linkage of platelets through GP receptors on platelets
Decreases aggregation.
How is GP given
How long is GP duration?
What is GP used with?
Aspirin and Heparin
Adverse effects of GP
Thrombocytopenia, bleeding
When is Gp more effective
When used prior to percutaneous coronary interventions than in unstable angina.
GP stands for
Direct thrombin inhibitor
Bind to the catalytic site of thrombin and prevent substrate access.
Intergrated response of thrombin inhibitor
Produce stable level of anticoagulation but not yet proven to be usefull
How are thrombin inhibitors administrated?
Which drug is like leeches/
Dircet thrombin inhibitor
Main problem with thrombin inhibitors?
Inhibition of coagulation proteases by antithrombin.
Which protease does heparin typicaly work on
The new type of heparin
Called LMWH(low molecular weight heparin). Better half life. Better absorption.
LMW Heparin is
Resistance can occur with long term use of
LMWH is given