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CRP- Cardiology > Coagulants, Anticoagulants, and Thrombolytics > Flashcards

Coagulants, Anticoagulants, and Thrombolytics Flashcards

1
Q

What are 3 general causes of coagulation deficiencies?

A
  1. genetic disorders (ex. hemophilia)
  2. acquired disorders (ex. decubitus ulcer; aka bed sores)
  3. trauma/surgery
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2
Q

For what can we use fresh blood and plasma?

A

replacement and supplement

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3
Q

What do we use factor 8 to treat?

A

this is a plasma precipitate (fresh or frozen) or made via recombinant DNA (8-12 hour half-life) and used for hemophilia A.

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4
Q

What do we use factor 9 to treat?

A

this is purified human factor (from plasma) that is heat treated, or made via recombinate DNA and used to treat hemophilia B.

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5
Q

What do we use facto 7a to treat?

A

hemophilia A and B because it activates coagulation factor 10 as well as coagulation factor 9.

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6
Q

What are the 4 vitamin K-dependent clotting factors?

A

2, 7, 9, and 10. Thus, if vitamin K is missing, the clotting cascade would not progress.

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7
Q

From where does thrombin (that we use to treat) come?

A

bovine (cattle) plasma. It is available to use topically and comes in a powdered form that you shake over the laceration to arrest severe bleeding.

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8
Q

What is absorbable gelatin (GELFOAM)?

A

denatured collagen that activates platelets to form a clot. It comes in a powder or sponge form and is nonantigenic :) This is used in surgery and trauma. You leave it there when you are done because the clot forms around it. It will then be reabsorbed by the body.

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9
Q

What can cause unwanted coagulation?

A
  1. thromboembolic diseases
  2. extracorporeal devices (renal dialysis)
  3. prophylactic treatment for previous thrombotic event
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10
Q

What are the injectable anticoagulants?

A
  • heparin
  • lepirudin
  • bivaliruden
  • argatroban
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11
Q

Can you give heparin intramuscularly?

A

NO. It will cause a hematoma at the site.

Only give it IV or SC.

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12
Q

What does heparin do?

A

potentiates antithrombin III, leading to more inactivated thrombin

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13
Q

What are the side-effects of heparin?

A

unwanted bleeding from mucous membranes, unwanted wounds, intracranially, or GI areas.

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14
Q

For what is heparin used?

A

prevention and treatment of DVT, PE, and arterial thrombosis

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15
Q

What are the in vitro (outside of the body) uses of heparin?

A

hemodialysis, indwelling vascular catheters, laboratory blood samples

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16
Q

What is the antagonist to heparin?

A

protamine sulfate

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17
Q

What is Lepirudin?

A

highly specific direct IRREVERSIBLE inhibitor of thrombin. Used when heparins are contra-indicated because of HIT (heparin inducted thrombocytopenia)

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18
Q

What are the side effects and what must you monitor with Lepirudin?

A
  • hemorrhage can occur at any site in patients.
  • an unexpected fall in hemoglobin, fall fall in BP or any unexplained symptom should lead to consideration of hemorrhage.
  • must closely monitor anticoagulation status via PTT
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19
Q

What is Bivaliruden?

A

specific direct REVERSIBLE inhibitor of thrombin, thus inhibiting platelet activation. It has a rapid onset and rapid offset.

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20
Q

When are the direct thrombin inhibitors used?

A

percutaneous coronary angioplasty

21
Q

What is warfarin?

A

oral anticoagulant that inhibits vitamin K decreasing synthesis of factors 2, 7, 9, and 10

22
Q

**What factors DECREASE the effect of warfarin?

A
  • p450 induction because this enzyme metabolizes warfarin
  • increased production of clotting factors (leafy green vegetables).
  • increased vitamin K absorption
  • inhibition of biotransformation
23
Q

**What factors INCREASE the effect of warfarin?

A
  • decrease vitamin K absorption
  • drugs that displace warfarin from plasma proteins (NSAIDS like piroxicam, indomethacin, diflunisal)
  • inhibition of platelet aggregation
  • decreased production of clotting factors
24
Q

What is Dibigatran?

A

direct inhibitor of thrombin, used to prevent venous thromboembolic events in adults following total hip or total knee replacement surgery. Better than warfarin in pts with atrial fibrillation.

25
Q

What is Idarucizumab?

A

reversal agent for dabigatran, by binding to it and its acylglucuronide metabolites with higher affinity than the binding affinity of dabigatran to thrombin, neutralizing its anticoagulant effect.

26
Q

What is Rivaroxaban (Xarelto)?

A

inhibits free factor 10a and clot-bound 10a prothombinase activity, thus inhibiting platelet aggregation.
It is used for thromboembolism prevention after orthopedic surgeries. and pts with non-valvular atrial fibrillation.

27
Q

Does Rivaroxaban have a reversing agent?

A

NO. Currently lots of law suits for excessive bleeding.

28
Q

What is edoxaban?

A

selective factor 10a inhibitor for prevention of thromboembolism; simialr to rivaroxaban.

29
Q

Does edoxaban have a reversing agent?

A

NO

30
Q

Is aspirin use recommended to prevent the risk of a SECOND heart attack?

A

YES

31
Q

Is there evidence that taking aspirin prophylactically will reduce the risk of a FIRST heart attack?

A

NO

32
Q

What is Clopidogrel (plavix)?

A

IRREVERSIBLE (covalent binding) of the ADP receptor on platelets, thus inhibiting ADP-induced binding of fibrinogen to platelet.

33
Q

For what is clopidogrel used?

A

cardiovascular conditions prone to clot formation.

34
Q

What major side effect does clopidogrel have?

A

TTP

35
Q

What is Ticlopidine?

A

inhibits platelet function by inducing a thrombasthenia-like state. It irreversibly inhibits ADP-induced platelet-fibrinogen binding and subsequent platelet-platelet interactions (same as clopidogrel).

36
Q

What is the main use for Ticlopidine?

A

acute cerebral ischemia

37
Q

What is Prasugrel?

A

inhibits platelet activation and aggregation mediated by the P2Y ADP receptor.

38
Q

What is the main use for Prasugrel?

A

to prevent clots in angioplasty patients.

39
Q

What is Ticagrelor?

A

REVERSIBLE antagonist of P2Y ADP receptor and does NOT require bioactivation; faster onset. Used for cardiovascular conditions prone to clot formation.

40
Q

What is dipyridamole?

A

increases cellular concentration of cAMP in platelets via inhibition of phosphodiesterase. Used in combination with warfarin as prophylaxis of thromboemboli for prosthetic heart valves.

41
Q

What is prostacyclin (PGI2)?

A

increases intra-platelet cAMP by stimulating adenylate cyclase and thus blocks platelet adhesion and aggregation.

42
Q

So, what happens anytime you increase cAMP?

A

you decrease platelet adhesion and aggregation

43
Q

When would we want fibrinolysis?

A

for venous or arterial thromboembolism

44
Q

What is streptokinase?

A

activates plasminogen to plasmin to break up clots. (NOT CLOT SPECIFIC; it will do this all over the body, duh).

45
Q

What is urokinase?

A

comes from humane urine or kidney cells and cleaves arg-arg 560-561 peptide bond in plasminogen, thus activating it to plasmin. Again NOT CLOT SPECIFIC.

46
Q

What is tissue plasminogen activator (t-PA)?

A

binds to fibrin and activates bound plasminogen, cleaving its arg-arg 560-561 bond. This is CLOT SPECIFIC :)
Usually is directed via a catheter to be given directly at the site of the clot.

47
Q

What is aminocaproic acid?

A

This is the antidote to the fibrinolysis drugs (streptokinase, urokinase, t-PA). It binds to lysine binding sites on plasminogen and plasmin blocking the binding of plasmin to target fibrin. This is a potent inhibitor of fibrinolysis; aka it keeps clots around.

48
Q

What is important to remember about treating bleeding disorders?

A

whether you are treating to increase or decrease coagulation, if you overdo it, you can cause the reverse to occur :(

CRP- Cardiology (49 decks)

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