Ischaemic Heart Disease Flashcards

0
Q

Anti-coagulant drugs

A

Heparin
Bivalirudin
Fondaparinux

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1
Q

Anti platelet therapy drugs

A

Aspirin
Clopidogrel
Newer - prasugrel/ticagrelor

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2
Q

Anti-ischaemic agents

A

Beta-blockers
Nitrates
Calcium channel blockers

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3
Q

Haemostatic plug formation

A

Platelet aggregation

Coagulation - thrombin&fibrin

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4
Q

Platelet action in ACS

A

Circulating platelets activated by binding to exposed collagen and vWf at site of plaque rupture
Activation of platelets results in release of soluble agonists - TXA2 and ADP
ADP activates surrounding platelets

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5
Q

ADP release…

A

Activates surrounding platelets by binding P2Y12 and P2Y2
Then intracellularmsignallimg activates integrin (GP IIb/IIIa) receptor
Causing sustained platelet aggregation by binding fibrinogen and vWf

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6
Q

TXA2

A

Produced by platelets in response to stimuli (ADP, thrombus, collagen)
Increases platelet aggregation
Vasoconstriction

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7
Q

Aspirin:

A

Irreversible COX inhibitor
So platelets produce less prostanoids, less TXA2
Rapid onset of action

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8
Q

Aspirin loading dose in acute MI

A

300mg
Significant decrease in cardiovascular mortality
Reduction in progression from unstable angina to MI

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9
Q

Secondary aspirin prevention MI

A

75md od

Reduction in cardiovascular events

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10
Q

Theinopyridines

A

Antiplatelet agents
Clopidogrel & prasugrel - inhibit ADP mediated stimulation of P2y12 receptor
So inhibition of platelet activation and aggregation
Prodrugs metabolised by cytochrome p450
Active metabolised irreversibly bind P2y12 receptor
(Clopidogrel limited by metabolisation)
Ticagrelor binds reversibly and doesn’t require activation

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11
Q

GP IIb/IIIa receptor

A

Activation leads to cross linking fibrinogen so platelets aggregate
Inhibitors indicated if a visible thrombus on angioplasty
Eg abciximab

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12
Q

Abciximab

A

Glycoproteins IIb/IIIa receptor antagonist
Platelet aggregation inhibitor
During and after coronary angioplasty
Short half life

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13
Q

Heparin

A

Inhibits coagulation cascade
(Vs anti platelet drugs inhibiting aggregation)
Enhances anti thrombin activity

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14
Q

Mechanism of ischaemia

A

Imbalance between myocardial oxygen supply and demand

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15
Q

Haemodynamic changes induced by ischaemia:

A

Increased LV end-diastolic pressure
Increased diastolic stiffness
Decreased cardiac output
Development of LV wall motion abnormalities

16
Q

Mechanism of anti-ischaemic medications

A

Decrease demand or increase supply myocardial oxygen
Do not correct underlying cause
Inc. nitrates & beta-blockers

17
Q

Nitrates

A

Relief of a final symptoms
Decrease demand by venodilatation (high dose arterial vasodilatation)
Improve coronary blood flow - dilate coronary arteries, improve collateral flow, revse CA spasm

18
Q

Nitrate treatment types

A

Sublingual GTN/tablets - fast acting
IV ISDN infusion if nitrate tolerance (isosorbide dinitrate)
Long acting ISMN - near 100% bio available, bypassing hepatic metabolism

19
Q

Beta-blockers

A

Reduce ischaemia
Competitive inhibition of b-adrenergic receptors in cardiac tissue
Negative chronotropic and inotropic effects
Decrease myocardial oxygen demand
34% reduction in inhospital mortality

20
Q

Beta- blocker contraindications

A
Hypersensitivity
Acute heart failure & cardiogenic shock
AV block
Severe asthma or COPD
Late stave PAD or sever raynauds
Untreated phaeocgromocytoma
Metabolic acidosis