• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/52

Click to flip

52 Cards in this Set

  • Front
  • Back
What is the definition of stable angina pectoris?
Chest discomfort on exertion, relieved by rest, most commonly due to CAD
What is the definition of unstable angina pectoris?
Chest discomfort both on exertion and at rest
Define a STEMI
MI due to TOTAL coronary occlusion, almost always involving a thrombus
Define a NSTEMI
MI due to PARTIAL/ TEMPORARY coronary occlusion, may or may not involve a thrombus. Due to an excess of demand
What other drug should you prescribe with unfractionated heparin (UFH)?
Antiplatelet therapy - heparin activates platelets
How fast does UFH work, and how fast is its half-life?
IV - minutes, SubQ - 1-2hrs

IV Half life = 2 hours
What can you give to a patient who starts bleeding after a heparin infusion to reverse its effects?
Protamine sulfate (but this can cause hypotension, so don't be too ready to use it)
Apart from bleeding, what is another major risk of UFH?
HIT - heparin-induced cytopenia, a hypersensitivity in which antibodies are produced to heparin
Who should NOT receive heparin?
Active bleeders, recent surgery, trauma, or known history of HIT
How does UFH work?
Binds to AT-3, inhibiting thrombin, Factor IIa and Factor Xa
What is the difference in mechanism of action between UFH and low-molecular weight heparin?
UFH targets AT-3, thrombin, IIa and Xa
LMWHeparin targets Xa predominately
What are the advantages of low-molecular weight heparin over UFH?
LMWHeparin inhibits circulating thrombin, AND accesses thrombin/fibrin clots already formed
longer half-life, and effective with 1-2 subQ injections daily
less platelet activation than UFH,
less likely to cause HIT/osteoporosis
What are the disadvantages of LMWH over UFH?
LMWH = $$$
Difficult to reverse with protamine sulfate
Renal excretion - higher risk in renal insufficiency
What is LMWH's generic or trade name?
enoxeparin/Lovenox
How do direct thrombin inhibitors (DTIs) work?
By binding either thrombin's active, catalytic site, OR
by binding the fibrinogen binding site
What are the high molecular weight direct thrombin inhibitors?
hirudin, bivalirudin (=Angiomax, hirulog)
What are the low-molecular weight direct thrombin inhibitors?
argatroban, efegatran
What is an advantage of direct-acting thrombins over heparin?
less bleeding
How do fibrinolytic drugs work
Convert plasminogen into plasmin, which busts up fibrin, fibrinogen, and any protein with an arginyl-lysine bond hanging around
How do fibrin-specific agents work?
They work on fibrin-bound plasminogen ONLY, producing fibrin-bound plasmin to bust up clots
What are the generations of fibrinolytic drugs?
G1: Streptokinase, urokinase
G2: recomb tPA (fibrin-specific)
G3: rPA (reteplase) TNK-ase (tenecteplase)
What complication is high rate in administering fibrinolytics?
Stroke - 1% ICH rate
What must we absolutely know about the details of aspirin's MOA?
Aspirin IRREVERSIBLY DEACTIVATES COX-1, preventing thromboxane A2 synthesis, and therefore platelet activation.
Effects last 7-10 days until all of the COX-1 in platelets circulating when you took the aspirin has been replaced
What cardiovascular disease patients should take aspirin.
Trick question! Pretty much everyone with CVD should take aspirin.
What do clopidogrel (Plavix) and ticlopidine (Ticlid) have in common with aspirin?
They are oral antiplatelet agents, but clopidogrel/ticlopidine block platelets via ADP-dependent pathway instead of COX-1.
How long does it take for clopidogrel (Plavix) or ticlopidine (Ticlid) to work with vs. without a loading dose?
2 hours, no matter what loading dose you give.
What are the side effects of ticlopidine (Ticlid) use?
neutropenia, TTP (purpura)

unless patient is contraindicated, clopidogrel is usually preferred. Ticlid is banned in parts of Europe because of toxicity
How is clopidogrel (Plavix) administered?
Oral, once daily. Everyone gets 75mg, regardless of weight.
Who should get clopidogrel (Plavix)?
Anyone with a drug-eluting stent, or percutaneous coronary intervention.
ACS (less recurrence of ischemia)
Secondary prevention of CVD
What are clopidogrel (Plavix)'s limitations?
Takes hours to work
CYP polymorphisms cause people respond differently, and poor antiplatelet response = adverse outcomes
May increase bleeding
May be inhibited by other meds
What oral anti-platelet agents are more effective than clopidogrel?
prasugrel, ticagrelor

*but higher bleed risk, too, so don't give to the elderly, prior strokes, or really thin people
What are common side effects of ticagrelor that need to be monitored?
dyspnea (14% and bradycardia 6%)
What is the most effective oral anti-platelet regimen for people who can't take clopidogrel (e.g., get Plavis drug rash)? Hint: 2 meds
Ticagrelor + low dose aspirin
How is clopidogrel (Plavix) metabolized?
hepatic - 85% is inactivated in first step of metabolism by CYP
Why is Glycoprotein (Gp) IIb/IIIa important in platelet aggregation?
The Gp IIa/IIIb receptor is the landing pad for fibrinogen on activated platelets.

This represents another interaction to block platelet activation, later in the process than COX-1 (aspirin) or ADP-dependent (clopidogrel/ticlopidine/prasugrel/ticagrelor) pathways
What is the prototype for Gp IIb/IIIa antagonists?
Abciximab (ReoPro), indicated only in percutaneous intervention (PCI)

But $$$ and difficult to reverse, less effective in absence of PCI
What are the more reversible, small molecule GpIIb/IIIa antagonists?
tirofibran (Aggrastat) and eptifibitide (Integrilin)
How do nitrates work?
2 ways:
1) Vasodilate coronary arteries = increased supply
2) Reduce systemic blood pressure -> LV volume, decreasing O2 demand
Who should NOT take nitrates?
LBP, hypovolemia, RVMI, or Viagra/Cialis (phosphodiesterase inhibitors - remember the drug commercials "Those who are taking nitrates should not take Viagra")
How long does SL nitroglycerin take to work?
1-3 minutes
What is one side effect of taking nitrates long term?
Tolerance! This is a vasoconstrictive episode when you are taken off of continuous nitro. Can avoid this by having pre-planned time off of nitrates (12hrs on/12hrs off)
What are the common side effects of nitrates?
Hypotension and syncope

Also headache and can be potentiated by Viagra/Cialis
How do beta blockers work to help ACS/Angina?
Lower heart rate, blood pressure and contractility.

This does not affect supply, but does decrease demand.
What are the calcium channel blockers?
Nifedipine, amlodipine
Verapamil, diltiazem
Which calcium channel blocker works predominately by slowing the heart and increasing contractility?

-Amlodipine
-Verapamil
-Diltiazem
Verapamil

VERapamil = VERy strong and slow (heart contractions)
Which calcium channel blocker works predominately by vasodilation?

-Nifedipine
-Amlodipine
-Diltiazem
Nifedipine

NifedIPINe = NifedOPEN (vessels)
How do diltiazem and amlodipine work?
By both chronotropic/ionotropic AND vasodilation.
Who should not get verapamil or diltiazem?
Anyone with bradycardia, heart block, heart failure or liver failure

Do not give Dig or Ranexa with verapamil!
Who should not get nifedipine / amlodipine?
Hypotensive patients
How does Ranexa work?
Another trick, nobody knows! It's just an anti-anginal.
Who should get Ranexa?
Only patients refractory to triple therapy.
What is "triple therapy" for angina?
Nitrate + Ca channel block + beta block