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(HGC) ACNP804 Exam 2 > Harrison's Ch 118: Antiplatelets, anticoagulants, fibrinolytics > Flashcards

Harrison's Ch 118: Antiplatelets, anticoagulants, fibrinolytics Flashcards

1
Q

What is the most common cause of MI, ischemic stroke, and limb gangrene?

A

Arterial thrombosis

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2
Q

What is the danger of DVT?

A

Pulmonary embolus

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3
Q

Where do venus thrombi usually originate?

A 
#Valve cusps of the calf
#Muscular sinuses

They’re triggered by stasis so get to walkin’!

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4
Q

What are 3 classifications of anti-thrombotic drugs?

A

1) Antiplatelets
2) Anticoagulants
3) Fibrinolytics

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5
Q

In vascular injury, what activates platelets?

A

Exposure of subendothelial collagen & von Willebrand factor (vWF)

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6
Q

The most widely-used anti-platelet agent in the world is…

A

…ASPIRIN! Yay!

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7
Q

What does aspirin do that makes it all antiplatelet & stuff?

A

Irreversibly acetylating & inhibiting platelet cyclooxygenase (COX-1)!

Platelets need COX-1, but aspirin gets in the way. Does that make it a COX block?

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8
Q

Indications for aspirin as a SECONDARY anti-platelet?

A 
Secondary prevention of cardiovascular events in patients with:
#coronary artery disease
#cerebrovascular disease
#peripheral vascular disease
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9
Q

Indications for aspirin as a patient’s PRIMARY anti-platelet?

A 
Patients whose annual risk of MI is > 1%. This basically means:
#Pts > 40 yrs with 2 or more major risk factors for CAD
#Pts > 50 yrs with 1 or more risk factors
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10
Q

Aspirin is more effective in men or women?

A

Neither! Aspirin is equal opportunity awesome.

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11
Q

Women get another benefit from aspirin, though. What is it?

A

In women, it lowers the risk of stroke!

The COX-block is more helpful to the ladies. :)

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12
Q

Aspiring: the higher dose the better, right?

A 
NOPE!
#Doses are 75-325 PO daily
#Bigger is NOT better: higher doses are not more effective
#Side effects are dose-dependent though
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13
Q

When you want RAPID antiplatelet effect, what dose?

A

Initial dose of AT LEAST 160 mg.

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14
Q

Aspirin side effects

A 
GASTROINTESTINAL! Ew.
#Erosive gastritis
#Peptic ulcers (possibly bleeding!)
#Side effects are dose-related, so keep it low when you can
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15
Q

But we can use enteric-coated aspirin to eliminate that risk?

A

No, buffering aspirin does not completely eliminate the risk

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16
Q

Aspirin’s side effects are particularly worrisome when you combine it with another specific drug. Which one?

A

Warfarin! Patients be bleeding all over the place.

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17
Q

When a patient must be on dual warfarin-aspirin therapy, what do we know about the aspirin dose?

A

KEEP IT LOW, Y’ALL. 75-100mg daily.

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18
Q

Hard question: if someone has aspirin allergy with bronchospasm, should we be giving them aspirin?

A

That is a negative, captain. This is most common in patients with chronic urticaria or asthma, particularly those with nasal polyps or chronic rhinitis.

So: asthma+chronic stuffy nose? BEST KEEP AN EYE ON THAT TROUBLEMAKER.

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19
Q

What is aspirin resistance, anyway? Is it a helpful thing to know about?

A 
#Clinically: failure of aspirin to protect patient from ischemic events
#Biochemically: failure of aspirin to produce expected inhibitory effects
#Pretty much not useful, as we only ever know about it after the fact
#No good standardized tests for it
#Aspirin resistance is a research tool basically
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20
Q

What are the thienopyridines?

A 
#Ticlopidine
#Clopidogrel
#Prasugrel
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21
Q

How do the thienopyridines work?

A

Block P2Y12, a key ADP receptor on platelets

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22
Q

True or false: the thienopyridines are prodrugs.

A

True. All must be metabolized by the CYP450 enzyme system in the liver before they become active.

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23
Q

Prasugrel has one major benefit over the other 2 drugs in its class. What is it?

A

It’s waaaaaaay faster. Even though it also requires metabolism by the CYP450, its quickly & completely absorbed in the gut & it has more efficient activation pathways.

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24
Q

How long might it take for ticlopidine & clopidogrel to start working at their usual doses?

A

Several days. Ain’t nobody got time for that!

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25
Why don't we use ticlopidine much anymore?
Clopidogrel is more potent & has a better safety profile
26
What are some considerations when choosing between aspirin & clopidogrel?
``` #Clopidogrel reduced the risk of CV death, MI, & CVA by 8.7% compared with aspirin #Aspirin is a LOT cheaper ```
27
Should we ever combine aspirin & clopidogrel?
``` Yes! This combo is recommended: #For 4 weeks after implantation of a bare metal coronary stent #Longer than that in a drug-eluting stent #Patients with unstable angina: 9.3% risk on the combo, but 11.4% risk with aspirin alone ```
28
Okay, so what is the catch when you combine aspirin & clopidogrel?
It's BLEEEEEEEEDING! Of course it's bleeding.Increases the risk of major bleeding to about 2% yearly. Even when you drop the aspiring dose to 100 mg.
29
So when is it NOT worth it to combine aspirin & clopidogrel?
``` #Not proven superior to clopidogrel alone in acute ischemic CVA #Not proven superior to aspirin alone for PRIMARY prevention for those at risk for CV events. ```
30
Okay then, prasugrel or clopidogrel? Which one is better?
Composite of CV death, MI & CVA significantly lower with prasugrel than with clopidogrel.
31
If prasugrel decreases risk more significantly, why aren't we using it in everyone?
Again with the BLEEDING! Prasugrel has significantly higher rates of fatal & life-threatening bleeding.
32
Who should be careful to avoid prasugrel?
``` #Generally avoid it in older patients #Contraindicated in those with history of cerebrovascular disease ```
33
When would we give a very large dose of clopidogrel?
When rapid ADP receptor blockade is required. Loading doses of 300, 600, even 900 may be given before coronary stenting (normal daily doses are 75 mg).
34
Can you give a loading dose of prasugrel?
Yes, it's about 60 mg (daily type doses are 10mg)
35
Side effects of ticlodipine:
``` #Gastrointestinal #Hematologic: neutropenia, thrombocytopenia, thrombotic thombocytopenic purpura #Need some serious blood count monitoring here ```
36
Side effects of clopidogrel & prasugrel:
#GI & hematologic side effects are rare.
37
True or false: thienopyridines are totally effective for everyone.
False! Genetic polymorphisms can make a huge difference.
38
What specific CYP450 enzyme may cause issues with prasugrel & clopidogrel?
Patients with the loss-of-function CYP2C19*2 allele show much less platelet inhibition & a much higher rate of CV events when treated with clopidogrel, compared to those with the wild-type CYP2C19*1 allele.
39
How many people are at risk for this genetic resistance to clopidogrel?
``` #25% of whites #30% of African-Americans #50% of Asians ```
40
Can PPI & clopidogrel be administered at the same time?
``` #PPIs inhibit CYP2C19, producing a small reduction in clopidogrel effectiveness #The extent to which this increases CV events is controversial ```
41
Since genetic polymorphisms may influence clinical outcomes with clopidogrel...
...pharmacogenetic profiling might be useful to identify our clopidogrel-resistant patients!
42
In what form is dipyridamole used for antiplatelet purposes?
Extended-release dipyridamole in combination with low dose aspirin, called Aggrenox
43
Who gets Aggrenox?
Patients with TIA, for prevention of CVA
44
How does dipyridamole work?
``` #Blocks the breakdown of cyclic AMP, which reduces intracellular calcium & inhibits platelet aggregation #Blocks update of adenosine by platelets & other cells ```
45
Are Aggrenox or dipyridamole used to prevent CV events in coronary artery disease?
No! It has vasodilatory effects, and it should not be used for stroke prevent in patients with CAD.Use clopidogrel instead!
46
Heparin! How does it work?
Activating antithrombin & accelerating the rate at which antithrombin inhibits clotting enzymes.
47
How is heparin administered?
Either subcutaneous or IV infusion. DO NOT EAT THE HEPARIN.
48
What alters clearance of heparin?
Heparin clearance is dose-dependent! It binds to the endothelium. When the endothelium is saturated, suddenly your half-life is gonna get loooooooonger!
49
How 'bout that heparin half-life?
30-60 minutes with bolus IV doses of 25-100 units/kg, respectively.
50
Does heparin bind ONLY to antithrombin?
NOPE! It can bind to other proteins as well, which is what makes it so variable from person to person. Everyone's got different amounts of heparin-binding proteins in there, so everyone's gonna have a different response.
51
So since everyone responds differently to heparin administration, what do we do? What are the labs used to monitor it?
``` We keep close tabs on it! #aPTT #anti-factor Xa level ```
52
Up to 25% of patients need > 35,000 units per day of heparin to achieve therapeutic aPTT! What do we do for these "heparin-resistant" patients?
We monitor using anti-factor Xa levels. They're usually "resistant" because of elevated serum fibrinogen & factor VIII, which shorten aPTT.
53
IV Heparin dosing
#BOLUS: 5000 units, or 70 units/kg #INFUSION: 12-15 units/kg/hour
54
Which requires more heparin: venous thromboembolism or acute coronary syndromes?
The DVT. Probably because DVTs are relatively more HUUUUGE than tiny little coronary thrombi.
55
Limitations of Heparin
``` #Poor availability at low doses #Dose-dependent clearance #Variable anti-coag response #Reduced activity in vicinity of platelet-rich thrombi #Limited activity against factor Xa incorporated into the prothrombinase complex, and thrombin bound to fibrin ```
56
Side effects of heparin
``` #Bleeding. (I know you're shocked.) #Thrombocytopenia ```
57
How do we reverse heparin? How much of that drug do we give?
Protamine sulfate!Typically, 1mg of protamine sulfate neutralizes 100 units of heparin.
58
What can be a serious problem with protamine sulfate?
Oh, just that people can have anaphylactoid reactions to it. NO BIG DEAL, RIGHT?
59
What is low-molecular weight heparin?
A drug consisting of smaller heparin fragments
60
Advantages of LMWH over heparin
``` #Better bioavailability #Dose-independent clearance #Predictable anti-coagulation response #Lower risk of heparin-induced thrombocytopenia #Lower risk of osteoporosis ```
61
Warfarin was first used as...
...rat poison! Your little old farmer patients will look at you all crazy if you tell them they need to start warfarin. That might warrant some patient education.
62
How does warfarin work?
Keeps vitamin K from being reduced, which decreases the effectiveness of clotting factors that use reduced vitamin K in their synthesis: II, VII, IX, and X
63
Why is there a delay in warfarin's onset of action?
It's delayed while the newly synthesized clotting factors (with reduced activity) gradually replace their fully active counterparts
64
What should we know about warfarin, genetics, & the CYP450 system?
Warfarin is metabolized in the liver, SO, patients with variants of CYP2C9*2 AND CYP2C9*3 or VKORC1 will need LOWER MAINTENANCE DOSES. These genetic polymorphisms decrease the warfarin requirement!
65
What should we tell patients re: warfarin & diet?
Warfarin is easily affected by fluctuations in dietary vitamin K intake!If you're gonna eat spinach, eat the same amount each day!
66
How do we monitor warfarin?
INR
67
Target INR for various purposes
``` #For most: INR 2-3 #Mechanical heart valve: 2.5-3.5 #Atrial fib: > 1.7 #Bleeding risk increases: > 4.5 ```
68
How can we reverse warfarin if needed?
Vitamin K administration
69
Newest oral anticoagulants:
``` #Dabigatran #Rivaroxaban ```
70
What are the newest oral anticoagulants licensed for in the US & Canada?
CVA prevention in patients with ATRIAL FIB!
71
What are the fibrinolytics?
``` #Streptokinase #Anistreplase #Urokinase #tPA or alteplase (tissue-type plasminogen activator) #Tenecteplase #Reteplase ```
72
What are fibrinolytic drugs for?
Used to degrade thrombi
73
How are fibrinolytic drugs administered for treatment of acute MI?
Systemically!

(HGC) ACNP804 Exam 2 (7 decks)

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