Term
| myocardial is the imbalance of supply and demand of what? |
|
Definition
|
|
Term
| if a rupture occurs in plaque where does it normally occur along? |
|
Definition
|
|
Term
| what are parenteral anticoagulants-2 |
|
Definition
standard (unfactionated) heparin
LMW heparin |
|
|
Term
heparins facilitate what binding?
so what factor is not activated? |
|
Definition
thrombin to anithrombin;
fibrinogen |
|
|
Term
| what is the oral anticoagulant |
|
Definition
|
|
Term
what class of MOA is warfarin;
so what does it inhibit?
what is the overall effect of this? |
|
Definition
Vit K antagonist
vit K epoxide reductase
vit K isnt reduced to activate coagu factors |
|
|
Term
| antigcoagulants prevent what? |
|
Definition
| progression of thrombus & embolus |
|
|
Term
| anticoags also reduce recurrent episodes of what?-2 |
|
Definition
| of unstable angina and MI |
|
|
Term
| what forms the initial plug at sites of vascular injury? |
|
Definition
|
|
Term
aspririn is what class?
what does it inactivate? |
|
Definition
NSAID
Cyclooxengase 1- COX 1 |
|
|
Term
| inhibitng COX 1 prevents ___ (1 thing)from converting to ____ (2 things) |
|
Definition
arachadonic acid
thomboxane 2 and prostaglandins |
|
|
Term
| the overall effects from inhibiing COX 1 is- 2 |
|
Definition
vasodilation
prevent platelet aggregation |
|
|
Term
| COX 2 normally converts _ into _ (2 things) |
|
Definition
arachadonic acid
prostacylcins & protstaglandins |
|
|
Term
| COX 2 normally has overall effect of? |
|
Definition
vasorelaxation
antiplatelet effect |
|
|
Term
what dose range of aspirin should be used?
why? |
|
Definition
50-320 mg/day
-to permantly block COX 1 but have no effect on COX 2 |
|
|
Term
| what other NSAIDS besidies aspirin can be used to inhibit COX 1 for antithrombotic effects |
|
Definition
|
|
Term
| antiplatelet agents called thineopyridines block what? |
|
Definition
|
|
Term
|
Definition
|
|
Term
| what are the recptors for ADP-2 |
|
Definition
|
|
Term
| what is the unique thing about the ADP recptors |
|
Definition
| both are needed to activate platelets- so only have to block one |
|
|
Term
P2Y12 activated makes G_ protein and decreases what?
What does the P2Y1 do? |
|
Definition
i; cAMP
increase Gq; Increase iCa |
|
|
Term
| what are the thienopyridines-3 |
|
Definition
clopidogrel
prasugrel
ticlopidine |
|
|
Term
| the unique thing about thienopyridines is? |
|
Definition
|
|
Term
| what activates thienopyridines |
|
Definition
|
|
Term
thienopyridine metabolites bind to what recptor?
what kind of blockade is made? |
|
Definition
P2Y12
permanent for the platelet's life |
|
|
Term
| a platelet's life is how long? |
|
Definition
|
|
Term
In general for thienopyridines- how long are their half lives?
how long is thier effect? |
|
Definition
|
|
Term
| what is unique about ticlopidine's half life |
|
Definition
| first dose is 12 hrs, but then after is 4-5 days |
|
|
Term
thienopyridines are 1st/2nd prevention?
what do they prevent? |
|
Definition
2nd prevention
stroke and MI |
|
|
Term
| thienopyridines are also used to decrease events of what? |
|
Definition
|
|
Term
Main ADEs of thienopyridines- 3
which is most dangerous? |
|
Definition
bleeding
neutropenia
thrombocytopenia/leukopenia;
neutropenia |
|
|
Term
|
Definition
ulcer
bleeding
angioedema
bronchospasm |
|
|
Term
|
Definition
alopecia
bleeding/hemmorrage |
|
|
Term
|
Definition
thrombocytopenia
bleeding
increase LFTs |
|
|
Term
| what activates clopidogrel |
|
Definition
|
|
Term
| what kind of binding and link do thienopyridines make with receptor? |
|
Definition
|
|
Term
| what activates prasugrel-2 |
|
Definition
|
|
Term
what is the REVERSIBLE ADP recptor antagonist?
what recptor? |
|
Definition
|
|
Term
| why do you want a reverible blockade of P2Y12? |
|
Definition
|
|
Term
| why does Ticagrelor have more consistency? |
|
Definition
|
|
Term
| what is the bad thing about Ticagrelor?-2 |
|
Definition
inhibits 3A4 and p-glycoprotein
metabolized by 3A4 |
|
|
Term
| what dose is needed for ticagrelor if given chronically |
|
Definition
|
|
Term
|
Definition
| bleeding, increase uric acid, bradyarrthmias, increase creatine |
|
|
Term
| what preggo category is Ticagrelor? |
|
Definition
|
|
Term
daily miantence dose needed for clopidogrel?
for prasugrel? |
|
Definition
|
|
Term
what is the platelet surface protein?
what is it a recptor for? -2 |
|
Definition
glycoprotein IIb/IIIa
fibrinogen & Von Willebrand |
|
|
Term
| glycoprotein anchors platelets to each other via |
|
Definition
|
|
Term
| glycoprotein anchors the platelets to the injured vasculature thru |
|
Definition
|
|
Term
| what are some things that indirectly activate glycoprotein IIb/IIIa-6 |
|
Definition
| NE, serotonin, ADP, thrombin,collagen, TX A2 |
|
|
Term
glycoprotein IIb/IIIa inhibitors work on inhibitng what?
the overall effect is that it impairs? |
|
Definition
interactoin with fibrinogen and Von Willebrand;
platelet aggregation |
|
|
Term
| what is the monoclonal antibody that inhibits glycoprotein/platelets at rest? |
|
Definition
|
|
Term
| what are the agents that inhibit glycoproteins/platelets that are acitvited? |
|
Definition
|
|
Term
abciximab has _ half life, and _ effects?
what does it prevent? |
|
Definition
short
long
activation of glycoprotein recptors |
|
|
Term
|
Definition
in conjugation with angioplasty for thrombus
in combo wth aspirin and heparin to prevent stenosis and MI |
|
|
Term
ADEs of abciximab-2
which is more major? |
|
Definition
bleeding
thrombocytopenia;
bleeding |
|
|
Term
| what is the cyclic peptide inhibitor of GP IIb/IIIa |
|
Definition
|
|
Term
| do the agents that inhibit GP while actiavted have longerr or shorter half life than abciximab |
|
Definition
|
|
Term
| uses for the agents that inhibit activated GPS- 2 |
|
Definition
angioplasty
MI/unstable angina |
|
|
Term
ADEs of the agents that inhibit actiavted GPS-2
which is more? |
|
Definition
bleeding and thrombocytopenia;
bleeding |
|
|
Term
| are the contraindications for GP inhibitors and fibrinolytics universal? |
|
Definition
|
|
Term
| do not GP antagonists if also on? |
|
Definition
|
|
Term
MOA of thombolytic/fibrinolytic agents
-overall effect is enhanced? |
|
Definition
work as tPA to enhance plasminogen to plasmin;
fibrinolysis |
|
|
Term
what are the 3 thombolytic agents?
which have longer half life? |
|
Definition
alteplase
reteplase and tenecteplase;
reteplase and tenecteplase |
|
|
Term
|
Definition
in acute MI
thromboembo stroke |
|
|
Term
| Main ADE of thrombolytics- |
|
Definition
|
|
Term
| why is it good that thrombolytics have a very short half life? |
|
Definition
| bc of their increased risk of hemmorage |
|
|
Term
|
Definition
|
|
Term
| for ranolazine- are the effects bc of dec. in BP, or heart rate, or myocardial load? |
|
Definition
|
|
Term
ranolazine is metabolized by what?
caution with what specific drugs? |
|
Definition
3A4
Non-DHP: diltiazem, verapamil (inhibitors) |
|
|
Term
what are the ADEs of ranolazine?
most common? |
|
Definition
headache, dizzy, constipation;
constipaion |
|
|
Term
| what is a serious ADE of ranolazine |
|
Definition
|
|
Term
| caution use of ranolazine in- 3 |
|
Definition
existing QT prolong
Torsade de Pointes
hepatic and renal impairment |
|
|
Term
| contraidnicaitons for ranolazine-2 |
|
Definition
potent inhibitors or inducer of 3A4
hepatic cirrhosis |
|
|
