Drugs To Treat Myocardial Ischemia.

Front 1

Myocardial ischemia.

Back 1

Imbalance between oxygen supply and myocardial oxygen demand in the heart.

Front 2

Causes of Myocardial ischemia

Back 2

Low coronary blood flow
Hypoxia(supply)
High oxygen demand(Demand)

Front 3

Main cause of ischemia

Back 3

Low coronary blood flow

Front 4

Determinants of mycocardial oxygen demand

Back 4

Heart rate
contractility
Wall stress or tension(preload, and afterload)

Front 5

Systole

Back 5

Aferload

Front 6

Diastole

Back 6

Preload

Front 7

Demand is the target for

Back 7

treatment

Front 8

Biochemical consequences of ischemia

Back 8

naerobic shift
decrease high energy phosphate
decrease atp
increase adp
decrease creatinine phosphate
increase lactic acid
Increase intercelluler calcium

Front 9

Functional consequences of ischemia

Back 9

Decrease ventricle relation
decrease venticle contraction
increase fillng pressures
Ecg abnormalities
Chest pain

Front 10

Myocardial stunning

Back 10

Brief period of myocardial ischemia causeing a prolonged impairment of myocardial dysfunction with a gradual return to normal fx

Front 11

Myocardial hibernation

Back 11

Reduction in myocardial contractility causing oxygen consuption to match a reduced oxygen supply

Front 12

Where does myocardial necrosis occur first

Back 12

Subendocardium. Takes 4-6hrs to get to subepicardium

Front 13

Myocardial necrosis is signaled by

Back 13

appearance in circulating blood proteins normaly found in intact cardiac cells

Front 14

Silent ischemia

Back 14

Not benign, increase in SI, increase risk

Front 15

Chronic stable angina

Back 15

Coroanry atherosclerosis.exertional exercise problems.

Front 16

Bile Acid Binding Resins

Back 16

Hypercholesterolemia.Offset.Increase of cholesterol.liver.

Front 17

Whats good to use with Bile Acid Binding Resins

Back 17

Statins

Front 18

Statins mechanism

Back 18

decrease HMG-CoA reductase

Front 19

Which is most popular?

Back 19

Satitins

Front 20

What are statins pleiotrophic effects?

Back 20

Lipids, improve endothelial cells, enhance plaque stability
reduce inflammation.

Front 21

Niacin Mechanism

Back 21

Inhibits lipolysis of triglycerides by hormone sensitive lipase.

Front 22

What should you not use NIACIN with?

Back 22

Statins, will cause myopathy

Front 23

Cholesterol absorption blockers

Back 23

Inhibits processes in jejunum. Inhibit NPC1L1.

Front 24

What are CAB's used with?

Back 24

Statins

Front 25

What shouldnt CABs be paired with?

Back 25

Bile Acid binding resins

Front 26

Fibrates

Back 26

Bind to ppar
Increased lipoprotein lipase
Reduced expression of ApoIII
Increased ApoIandII

Front 27

What should you not do with fibrates?

Back 27

Mainline use

Front 28

Sideffects of Fibrates?

Back 28

GI, hair loss, uticaria

Front 29

Dont use fibrates with

Back 29

Statins

Front 30

Unfortunatley, Fibrates sometimes cause?

Back 30

Increase in LDL levels

Front 31

Use of fibrates?

Back 31

Hypertriglyceridemia, and low HDL Levels associated with metabolic syndrome(type 2 diabetes)

Front 32

Beta adrenergic blockers

Back 32

Block catecholamines from binding adrenergic receptors

Front 33

Used for unpredictable effects in variant angina

Back 33

B-adrenergic blockers

Front 34

Adverse effects of B-adrenergic blockers.

Back 34

Bronchoconstriction, cardiac effects, lethargy, fatigue, nightmares

Front 35

Fibrates should not be used if

Back 35

Pt have cardiac conduction problems or obstructive lung disease.

Front 36

Fibrates work for

Back 36

Stable angina, NOT VARIANT

Front 37

Name 2 types of calcium channel blockers.

Back 37

Dihydropyridine
and
Cardio Selective

Front 38

Which can be used with B-antag

Back 38

Dihydropyridine

Front 39

Which is stronger? Dihydropyridine or Cardio Selective?

Back 39

Cardio Selective

Front 40

Name cardioselective drugs

Back 40

Diltiazem, verapamil

Front 41

Cardio Selectives should not be used in pt with

Back 41

Cardiac conduction disorders

Front 42

How do cardiac conduction blockers work

Back 42

Decrease heart rate and contractility

Front 43

Cardiac selective and Dihydopyridine work by

Back 43

decreasing systemic atrial conduction and decrease coronary artery conduction.

Front 44

What do Calcium channel blockers treat?

Back 44

Variant angina

Front 45

Calcium channel blocker mechanism

Back 45

NON COMPETITIVLY inhibit mvnt of ca through L-type membrane calcium channels.

Front 46

Which of the two ca blockers have slow recovery time?

Back 46

Cardiac Selective

Front 47

ADP inhibitors

Back 47

Inhibit the binding of ADP to its receptor on platelets.

Front 48

Which ADP inhibitor has fewer adverse effects

Back 48

Clopidogrel

Front 49

What are the two ADP inhibitors?

Back 49

Clpidogrel and Ticlopidine

Front 50

What kind of drug are ADP inhibitors?

Back 50

Prodrugs

Front 51

Adp inhibitors are used with?

Back 51

Aspirin

Front 52

Duration of action for ADP inhibitors

Back 52

4-8 days

Front 53

ADP Inhibitor sideffects

Back 53

Neutropenia, Thrombotic thrombocytopenia, purpera, GI bleeding

Front 54

Why is clopidogrel more popular

Back 54

Less neutropenia,rapid onset of action.

Front 55

Aspirin

Back 55

Permanently acetylates COX-1
Blocks thromboxane at platelet.

Front 56

What does aspirin do

Back 56

decrease the risk of MI by fiftey percent.

Front 57

How long does aspirin last?

Back 57

7-10days

Front 58

Some pts develope resistance to anti platlet effects of aspirin

Back 58

5-8%. these pt are at more risk for adverse events

Front 59

GP IIb/IIIa receptor inhibitors

Back 59

These are recepters on platelets.

Front 60

GP Molecular mechanism

Back 60

Prevent fibrinogen mediated cross linkage of platelets through GP receptors on platelets

Front 61

Gp

Back 61

Decreases aggregation.

Front 62

How is GP given

Back 62

IV

Front 63

How long is GP duration?

Back 63

Short

Front 64

What is GP used with?

Back 64

Aspirin and Heparin

Front 65

Adverse effects of GP

Back 65

Thrombocytopenia, bleeding

Front 66

When is Gp more effective

Back 66

When used prior to percutaneous coronary interventions than in unstable angina.

Front 67

GP stands for

Back 67

Glycoprotein

Front 68

Direct thrombin inhibitor

Back 68

Bind to the catalytic site of thrombin and prevent substrate access.

Front 69

Intergrated response of thrombin inhibitor

Back 69

Produce stable level of anticoagulation but not yet proven to be usefull

Front 70

How are thrombin inhibitors administrated?

Back 70

IV

Front 71

Which drug is like leeches/

Back 71

Dircet thrombin inhibitor
Lepirudin

Front 72

Main problem with thrombin inhibitors?

Back 72

BLEEDING

Front 73

Heparin

Back 73

Inhibition of coagulation proteases by antithrombin.

Front 74

Which protease does heparin typicaly work on

Back 74

Xa

Front 75

The new type of heparin

Back 75

Called LMWH(low molecular weight heparin). Better half life. Better absorption.

Front 76

LMW Heparin is

Back 76

Safer

Front 77

Resistance can occur with long term use of

Back 77

Heparin

Front 78

LMWH is given

Back 78

SUBQ