Anticoags and hemmorhage dissorders Flashcards

1
Q

What sort of chemical is heparin, where is it produced and what function does it have?

A

Naturally occuring produced by basophils and mas cells to prevent formation and extension of blood clots
Important to note that heparin does NOT disentregrate clots that have already formed.

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2
Q

What is the mechanism of heparin?

A

Binds and activates antithrombin III inhibiting
Thrombin
Factor 9a
Factor 10a

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3
Q

What is warfarin derived from and how does it work?

A

Warfarin (Coumadin) is a synthetic derivative of coumarin and decreases blood coagulation by interfering with K metabolism.

Helps to stop the formation of clots, the extension of clots, and helps to prevent clots from breaking off.

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4
Q

What are the vitamin K-dependent clotting factors?

A
Vitamin K effects the production of clotting factors 
2
7
9
10
Also: protein C and protein S.
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5
Q

What is Dabigataran?

A

A direct thrombin Inhibitor

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6
Q

What are rivaroxaban and apixaban?

A

These are both direct Factor Xa inhibitors.

In other words these inhibit the common pathway.

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7
Q

What is Fonaparinux?

A

Synthetic pentasaccharide inhibitors of Factor Xa

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8
Q

What does activated Protein C do?

A

Breaks down clotting factors 5a and 8a

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9
Q

What does Tissue Factor Pathway Inhibitor do?

A

Inhibits the extrinsic pathway in the clotting system.

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10
Q

What would you administer to reverse the effects of too much coumadin (Warfarin)?

A

Vitamin K!

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11
Q

What is the INR, International normalized ration?

A

This is the PT of the patient devided by a normalized PT and is used to compensate the differences in tissue factor.

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12
Q

How would one test for deficient clotting factor?

A

Mix the patients plasma with normal plasma and test for PT. The PT should normalize if the patient has a clotting factor deficiency.

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13
Q

What factors can increase the partial thromboplastin time? (PTT)

A

Prolonged by heparin, hemophilia, and antiphospholipid antibody.

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14
Q

All clotting factors are taken into consideration when testing for coagulation except for which?

A

VII
and
13

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15
Q

Which test is more specific to a low dosage of Heparin?

A

PTT

as it will be prolonged.

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16
Q

Which test is more specific to a low dose of Warfarin (coumadin)

A

Pt

as it will be prolonged.

17
Q

Where are the effects of warfarin Necrosis most commonly seen?

A

Thighs, breasts, and buttocks displaying blue/blackening of the skin with a painful eskar.

18
Q

What causes warfarin necrosis?

A

The patient has a deficiency in protein C which normally inhibits clotting.

Because of this, the other clotting factors 9 and ten are able to continue and thrombosis of the dermal vessels occur.

19
Q

To help avoid Warfarin necrosis, what is done?

A

Heparin is given first with an anticoagulant, the patient is then transfered to warfarin later.

20
Q

What causes Heparin-induced Thrombocytopenia?

A

Rarely seen, caused by Platelet factor 4 from platelets binding heparin and blocking its action promoting coagulation.

Antibodies then bind these platelet/heparin complexes leading to endothelial injury leading to even more platelet activation.

Seen most commonly in unfractionated heparin!

21
Q

What is Bernard-Soulier disease?

A

Defect of platelet adhesion due to missing glycoprotein Ib

These platelets are really large.

22
Q

What is Glanzmann’s Thrombasthenia?

A

Defects of platelet aggregation due to missing
glycoprotein IIb (Binds platelet to Von willebrands)
and
glycoprotein IIIa (Binds fibrinogen between platelets)

23
Q

What is Thrombotic Thrombocytopenic Purpura?

A

Antibodies directed against the von Willebrand factor cleaving protease, ADAMTS-13

24
Q

What is von Willebrands disease?

A

Deficiency of Von willebrands antigen leading to inability to coagulate with hemmorhages.
Seen with easy bruising, nose bleeds, etc.

25
Q

What causes Hemophilia A?

A

Factor VIII deficiency

Is x-linked recessive

26
Q

What causes hemophilia B?

A

Factor IX deficiency, is X-linked recessive

27
Q

What causes hemophilia C?

What is the risk population

A

Milder form in which there is a Factor XI deficiency
Seen in mostly autosomal recessive with some heterozygotes.

Danger population in Ashkenazic Jewish,

28
Q

What are some possible morbidities seen in Hemophilia?

A
Deep internal bleeding
Joint damage
Transfusion transmitted infection
Adverse reactions to clotting factor treatment
Intracranial haemorrhaging
29
Q

What are two bodily issues that will lengthen PT time, PTT time, Bleeding time, and Platelet count (lower)?

A

Liver failure

Disseminated intravascular coagulation (DIV)

30
Q

What is the definition of Disseminated Intravascular Coagulation (DIC)?

A

Acute, subacute, chronic onset of widespread activation of the coagulation system resulting in tiny fibrin thrombi through the entire body,

This depletes platelets leading to patient bleeding to death.

31
Q

What is thrombocytopenia?

A

Lack of platelets, frequently seen in DIC.

32
Q

What is Consumptive coagulopathy?

A

This is seen in diseminated intravascular coagulation in which all of the platelets are used up and the patient is at risk of bleeding.

33
Q

Why are cut RBC seen so typically in Disseminated intravascular coagulation?

A

Strands of fibrin cut the RBC as they pass through causing small infarctions.

34
Q

How can D-DIMER be a sign of Disseminated Intravascular coagulation?

A

D-DIMER assay measures plasmin-cleaved insoluble cross-linked fibrin.
Thus it is an INDIRECT measure of plasmin and thrombin activity.

35
Q

What are two biochemical markers for disseminated intravascular coagulation?

A

Plasmin and thrombin

Tested for by the D-DIMER test.