ACS and AMI - Therapy

Question 1

what are the acute coronary syndrome diseases?

Answer 1

unstable angina
non-STEMI
STEMI
sudden cardiac death

Question 2

what is the pathogenesis of acute coronary syndrome?

Answer 2

atherosclerotic plaque rupture or erosion
superimposed platelet aggregation and thrombosis
vasospasm and vasoconstriction
subtotal or transient total occlusion of vessel

Question 3

what is the goal of therapy?

Answer 3

increase myocardial oxygen therapy through coronary vasodilation

decrease myocardial oxygen demand

• decrease in HR
• decrease blood pressure
• decrease preload or myocardial contractility

Question 4

when would you do thrombolysis?

Answer 4

when PCI isnt used in 2 hours

Question 5

how does thrombolysis work?

Answer 5

converting plasminogen to the natural fibrinolytic agent plasmin.

Plasmin lyses clot by breaking down the fibrinogen and fibrin contained in a clot.

Question 6

what are the two catogaries that fibrinolytics are divided into?

Answer 6

fibrin specific agents such as
-alteplase, 	
-reteplase, 
-tenecteplase 
All catalyse conversion of plasminogen to plasmin in the absence of fibrin. 

Non–fibrin-specific agents such as streptokinase catalyse systemic fibrinolysis.

Question 7

what are contraindication for thrombolysis?

Answer 7

Prior intracranial hemorrhage (ICH)

Known structural cerebral vascular lesion

Known malignant intracranial neoplasm

Ischaemic stroke within 3 months

Suspected aortic dissection

Active bleeding or bleeding diathesis (excluding menses)

Significant closed-head trauma or facial trauma within 3 months

Question 8

what are the benefits of thrombolysis?

Answer 8

23% reduction in mortality

39% when used with aspirin

Question 9

if no evidence of a STEMI what treatment would you do?

Answer 9

Aspirin
Tigagrelor/Clopidogrel
Fondaparinux/LMW heparin
Intravenous nitrate
Analgesia
Beta Blockers

Question 10

what is the management to reduce the risk from NSTEMI?

Answer 10

PCI or CABG
Aspirin
Clopidogrel, prasugrel, ticagrelor, ticlopidine or cilostazol
Heparin (LMWH)
Fondaparinux
GIIb/IIIa receptor blockers
Statins
B blockers

Question 11

what is the effect of aspirin on MI and unstable angina?

Answer 11

reduce mortality by 23%

reduce MI and death by 50%

reduces reinfarction by 32% and combined vascular events by 25%

Question 12

what is clopidogrel?

Answer 12

prodrug

Question 13

what is the function of clopidogrel?

Answer 13

inhibits ADP receptor activated platelet aggregation

Question 14

what is clopidogrel used in combination with?

Answer 14

aspirin

Question 15

what treatment is used post MI?

Answer 15

beta blockers
I.V. atenol or metoprolo
oral beta blockade started weeks or months post MI

Question 16

what is aspirin a potent inhibitor for?

Answer 16

platelet thromboxane A2 production

Question 17

what does thromboxane stimulate?

Answer 17

platelet aggregation and vasoconstriction

Question 18

What is The IIb/IIIa complex

Answer 18

a receptor for fibrinogen, fibronectin and von WF

Question 19

whats the function of the IIb/IIIa complex

Answer 19

Activation of this receptor complex is the “final common pathway” for platelet aggregation and cross-linking of platelets by fibrin.

Question 20

what part of the population is resistant to CYP2C19?

Answer 20

14% of population have low CYP2C19 levels and demonstrate resistance to clopidogrel

Question 21

what is prasugrel?

Answer 21

Member of the thienopyridine class of ADP receptor inhibitors, like clopidogrel

Question 22

whats the difference between prasugrel and clopidogrel?

Answer 22

Compared to clopidogrel prasugrel inhibits ADP–induced platelet aggregation more rapidly, more consistently,

Question 23

what is low molecular weight heparin?

Answer 23

an integral component of the ACS protocol

Question 24

what is GPIIb/IIIa?

Answer 24

an integrin complex found on platelets

Question 25

what is the major adverse effect of GPIIb/IIIa?

Answer 25

bleeding