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Cardiovascular Medicine > Anticoagulant > Flashcards

Flashcards in Anticoagulant Deck (42)
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1
Q

What are the two types of clots?

A

White and Red

2
Q

What is the main component of white clots, patho of the clot, what types of vessels do we find them in, what pathological condition is most associated with white clots?

A

Platelets. Platelets adhere to damaged endothelium. High pressure arteries. Local ischemia.

3
Q

Main component of red clots, what types of vessels do we most commonly find red clots, and what pathological condition do we get from red clots?

A

Fibrin trapping RBCs, low pressure veins and heart, embolism.

4
Q

What are the three families of drugs to treat clots?

A

Anticoagulants, anti-platelets, and thrombolytics

5
Q

Big picture, when do we use anticoagulants?

A

To prevent clot formation in the veins and heart, so red clots.

6
Q

Big picture, when do we use antiplatelet drugs?

A

To prevent clots in the arteries, so white clots.

7
Q

Big picture, when do we use thrombolytics?

A

Restore blood flow after a clot has formed. Bust up the clot.

8
Q

Big picture what is the MOA for anticoagulants?

A

Regulate function and synthesis of clotting factors

9
Q

Two groups of anticoagulants?

A

Parenteral (indirect and direct thrombin blockers) and oral

10
Q

What drug are we talking about with indirect thrombin inhibitors and what is its MOA?

A

Heparin. Increases AT3 activity by 1000 fold.

11
Q

What are the three types of indirect thrombin and 10 inhibitors and what are their differences in their effects?

A

HMW: inhibits both thrombin and factor 10
LMW: inhibits factor ten mostly, a little of thrombin
Fonda: only factor 10

12
Q

What are the two ways we can monitor patients on heparin?

A

aPTT (intrinsic pathway) and anti 10 assay

13
Q

2 adverse effects of heparin?

A

Bleeding and HIT

14
Q

What is the big picture patho of HIT?

A

Antibodies attack the heparin-platelet factor 4 complex and activates the platelets, and lead to a pro thrombotic state.

15
Q

Two big indications for these indirect thrombin inhibitors?

A

DVT and PE

16
Q

How does Lepirudin and Bivalirudin bind to thrombin?

A

Bind at both the active site and the substrate site.

17
Q

How does Argatroban bind to thrombin?

A

Only at the active site.

18
Q

What is the route of administration for indirect thrombin inhibitors and direct thrombin inhibitors?

A

Parenterally

19
Q

2 clinical indications for direct?

A

HIT and angioplasty

20
Q

What is the most commonly prescribed anticoagulant in US?

A

Warfarin

21
Q

What is the MOA for warfarin, 2 things?

A
  1. Inhibits vitamin K epoxide reductase

2. Inhibits GGCX from carboxylating clotting factors

22
Q

What clotting factors are affected by not being able to carboxylate?

A

2,7,9,10

23
Q

Which Warfarin isomer is more potent?

A

S

24
Q

3 indications for Warfarin?

A

Treat clots, A fib, and patients with prosthetic heart valves.

25
Q

What is the adverse effect of warfarin that is specific to a specific patient population?

A

Teratogenic effect in fetus. Bleeding disorder.

26
Q

What is the bioavailability of warfarin and what is its state in the blood?

A

100% bio and mostly bound to albumin.

27
Q

High chance of thrombosis INR, Normal, chance of bleeding, and warfarin patients INR?

A

.5, .9-1.3, 4-5, and 2-3

28
Q

What is responsible for the most variation of Wafarin? What ethnicity is more resistant to warfarin? What ethnicity is less resistant to Warfarin?

A

The individuals unique reductase. AA. Asians.

29
Q

4 advantages of using warfarin?

A

Oral, long action, don’t need kidneys for drug clearance, and reversed by giving vitamin K.

30
Q

2 main drawbacks to using Warfarin?

A

Doing incredibly variable which leads to problems and required INR monitoring.

31
Q

What are the direct oral anticoagulants blocking and what are their 3 clinical uses?

A

Factor 10 And thrombin

Prevent embolism, treat embolism, and prevent stroke in Afib.

32
Q

3 advantages of DOAC?

A

Fixed doses so don’t need monitoring
Equal in efficacy of warfarin
Rapid onset of action

33
Q

1 drawback of DOAC?

A

Excreted by kidney so you have to adjust dose for patients with kidney disease

34
Q

What is the only oral direct thrombin blocker?

A

Dabigatran

35
Q

2 clinical indications for dabigatran?

A

Reduce the risk of embolism in a fib patients and treat venous clots.

36
Q

What is the disadvantage of dabigatran?

A

Mostly excreted by the kidneys

37
Q

What is the antidote for DOAC for factor ten?

A

A Alfa

38
Q

What is the antidote for DOAC for thrombin?

A

Idarucizumab

39
Q

What blood coag test do we do to monitor heparin?

A

APTT and anti10

40
Q

What test do we do to monitor warfarin?

A

PT based INR

41
Q

What test do we do to monitor DOAC ten blockers?

A

Anti 10

42
Q

What blood test do we do to monitor DOAC thrombin blockers?

A

Diluted TT