The most common cause of an ACS is:

A. gradual narrowing of a CA decreasing CA blood flow

B. increased myocardial O2 demand

C. atherosclerotic plaque rupture with superimposed clot

D. activation of the coagulation cascade leading to plaque rupture

troponin is more specific for myocardial cell necrosis than CK

65yo, NSTEMI, 6h post onset, BP 130/80, hr 88, S3, rales, ST-depression

What do you use to treat symptoms, prevent death, stroke and reinfarction?

A. clopidogrel, fondaparinux, metoprolol, furosemide

B. clopidogrel, enoxaparin, eptifibatide, furosemide

C. reteplase, unfractionated heparin, metoprolol, enalapril

D. alteplase, bivalirudin, furosemide, captopril

B.

Clopidogrel

Enxoaparin

Eptifibatide

Furosemide

65yo male, 3h post onset, HTN*10y, hemorrhagic stroke, BP 90/50, HR 98bpm. Treat with ASA, IV NTG, what else to prevent death, stroke, and reinfarction?

A. unfractionated heparin and clopidogrel

B. reteplase, unfractionated heparin, metoprolol

C. enoxaparin and metoprolol

D. enoxaparin and abciximab

Which of the following antithrombotic drug therapy regimens is preferred for a patient undergoing primary PCI?

A. asa, UFH, abciximab, reteplase

B. clopidogrel, enoxaparin, UFH, tirofiban

C. clopidogrel, ASA, streptokinase, abciximab

D. clopidogrel, ASA, UFH, abciximab

D. Clopidogrel, ASA, UFH, Abciximab

no fibrinolytics and abciximab is preferred over tirofiban

Which of the following best describes pts who should receive eplerenone following MI?

A. all pts

B. all pts with LVEF<40% and SCr<2.5mg/dL

C. all pt with HF symptoms and serum K <5.5mEq/L

D. all pt with DM and LVEF<40%

Which of the following best describes a pt with NSTEMI who is a candidate for treatment with diltiazem?

A. HF while receiving metoprolol

B. continued chest discomfort despite nitrates and atenolol

C. HR of 55bpm while on propranolol

D. stable COPD

Poor adherence to which of the following meds is associated with stent thrombosis following PCI?

A. lovastatin

B. clopidogrel

C. captopril

D. warfarin

Which of the following therapies reduces the risk of stroke following MI?

A. warfarin

B. ASA

C. simvastatin

D. all of the above

Which of the following reduces mortality following NSTEMI?

A. ramipril

B. reteplase

C. clopidogrel

D. isosorbide dinitrate

What is plasmin?

What is plasmin's inactive precursor?

How is it activated?

How is tPA inhibited?

a protease that cleaves fibrin

plasminogen

tPA is released from endothelial cells during conditions of low blood flow

PAI-1 and PAI-2

ASA is irreversible inh of COX-1 (converst AA--> TXA2)

Clopidogrel and ticlopidine - irreversible inh of platelet ADP receptors (stronger stimulus of platelet agg than TXA2)

thrombin

collagen

ADP

TxA2

1. fibrinogen 

2. von Willebrand factor

inh gamma carboxylation of glutamic acid sidechains on vit K-dependent clotting factors:

prothrombin (2)

factor 7

factor 9

factor 10

and the anticoagulant protein - protein C

blocks vitamin K epoxide reductase (the enzyme needs the reduces form)

Prothrombin 2

Thrombin 2a

Thrombin converts fibrinogen to fibrin

converts 5-5a and 8-8a on surface of platelets

enh activity of 10a and 9a

8a/9a is additional pathway for factor 10

factor 13a is a stabilizer

Haparin - antithrombin 3 to inactivate thrombin, 10a, 9a 

(more sp for thrombin)

LMWH cannot bind antithrombin 3 and thrombin (higher specificity for factor 10a than thrombin)

Lepirudin

Bivalirudin

bind to the catalytic site and substrate binding site on the surface of thrombin

bivalirudin is susceptible to very slow cleavage by thrombin which slowly inactivates the drug