Acute Coronary Disease Therapy Flashcards

1
Q

What is the goal of treating ACS?

A

Increase 02 supply to the heart through:
- coronary vasodilation
Decrease oxygen demand from the heart by:
- decreasing HR
- decreasing blood pressure
- decreasing preload or myocardial contract ability

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2
Q

Describe the type of thrombosis therapy that is given and how it works.

A

Fibrinolytics:
Serine proteases that work by converting plasminogen to the natural fibrinolytic agent plasmin
Plasmin lyses clots by breaking down the fibrinogen and fibrin contained in the clot.

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3
Q

What are the 2 categories of fibrinolytic categories?

A
  1. Fibrin specific agents (all catalyst conversion of plasminogen to plasmin in the absence of fibrin.
  2. Non fibrin specific agents, such as streptokinase, catalyse systemic fibrinolysis
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4
Q

What are the contraindication of fibrinolytics? (Thrombolysis therapy)

A

Previous intra-cranial haemorrhage
Active bleeding or bleeding diathesis
Significant closed head trauma or facial trauma within 3 months
Known structural cerebral vascular lesion
Known malignant intracranial neoplasm
Ischemic stroke within 3 months
Suspected aortic dissection

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5
Q

What is the medical treatment if there is no evidence of STEMI?

A
Aspirin
Tigagrelor/ Clopidogrel
Fondaparinux (LMW heparin)
IV nitrate
Analgesia
Beta blockers
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6
Q

Why is aspirin used?

A

Aspirin is a potent inhibitor of platelet thromboxane A2 production
Thromboxane stimulates platelet aggregation and vasoconstriction

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7
Q

Why is beta blockers used?

A

Reduces the heart rate so the 02 demand decreases

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8
Q

What management is given to reduce risk of NSTEMI?

A
PCI or CABG
Aspirin
Clopidogrel, prasugrel, ticagrelor, ticlopidine, or cilostazol
Heparin
Fondaparinux
Statins
Beta blockers
GIIb/IIIa receptor blockers
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9
Q

Describe how clopidogrel works.

A

Clopidogrel is a prodrug
It irreversibly inhibits P2Y12 ADP receptor which is important in aggregation of platelets and cross linking by fibrin
It does this by blocking the activation of the GP IIb,IIIa pathway which is the final common pathway for platelet aggregation and cross linking of platelets by fibrin

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10
Q

Because clopidogrel is a prodrug, what activates it?

A

Cyp 2C19

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11
Q

What is the difference between clopidogrel and prasugrel?

A

Prasugrel inhibits ADP- induced platelet aggregation more rapidly more consistently
But the bleeding rate from prasugrel is higher

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12
Q

Name a drug which is a low molecular weight heparin.

A

Fondaparinux

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13
Q

Fondaparinux is a selective inhibitor of what?

A

Factor Xa

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14
Q

How does IV GPIIa/IIIa inhibitors work?

A

They block platelet aggregation by inhibiting fibrinogen binding to a conformationally activated form of GPIIb/IIa receptor on two adjacent platelets.
(Activated GPIIb/IIa aids in platelet aggregation as its the receptor for fibrinogen)

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15
Q

When should you avoid using beta blockers?

A

When the patient is at risk of cardiogenic shock, symptoms possibly related to coronary vasospasm or is on coccaine

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