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Small Animal Medicine > Hematology - Levine Hemostasis SG > Flashcards

Hematology - Levine Hemostasis SG Flashcards

1
Q

What are the two key cellular players in primary hemostasis:

A

Endothelial cells and platelets

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2
Q

What is the end result of primary hemostasis?

A

The formation of a platelet plug

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3
Q

What are some clinical signs that you would you expect if a patient had a defect in primary hemostasis?

A

Petechiae, ecchymoses, epistaxis, hemoptysis, hematuria, hematemesis, melena, hematochezia, ocular bleeding, and CNS bleeding

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4
Q

What are 4 main abnormalities that can lead to defective primary hemostasis?

A

Thrombocytopenia

Impaired platelet function

Von Willebrand factor deficiency

Impaired Von Willebrand function

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5
Q

What is the most common acquired disorder of primary hemostasis?

A

Thrombocytopenia

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6
Q

What is the most common hereditary disorder of primary hemostasis?

A

Von Willebrand factor deficiency

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7
Q

List 4 possible causes of a prolonged BMBT.

A

Thrombocytopenic

Thrombopathic (platelets don’t work)

vWF deficient/abnormal

Abnormal vasculature

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8
Q

What 3 tests would you want to perform to rule out secondary triggers of ITP?

A

Tick panel, imaging, and thorough drug history

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9
Q

Explain how vincristine works to treat ITP:

A

It prevents microtubule polymerization

It promotes accelerated megakaryocyte fragmentation and platelet release from bone marrow

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10
Q

True or False: Vincristine is an effective treatment for IMHA.

A

False

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11
Q

Explain the basic idea behind IVIG therapy for ITP:

A

It blocks mononuclear phagocyte Fc receptor so that macrophages cannot engulf Ab coated platelets

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12
Q

What are three blood products that contain platelets?

A

Fresh whole blood, platelet rich plasma, and fresh platelet concentrate

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13
Q

What are three indications for a platelet transfusion?

A

Severe thrombocytopenia

Suspect pulmonary or CNS hemorrhage

Acquired or hereditary thrombopathias

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14
Q

When would you give a platelet product transfusion to a dog with a platelet function problem (thrombopathia) that is not actively bleeding?

A

If they are going to surgery

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15
Q

How does Clopidogrel (Plavix) work?

A

Inhibiting the platelet ADP receptor

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16
Q

What cell surface is coagulation initiated on?

A

Fibroblast

17
Q

What cell surface is coagulation amplified and propagated on?

A

Platelets

18
Q

Give an example of one factor deficiency that is better represented by the cell-based model of coagulation than the traditional cascade/waterfall coagulation model and briefly explain why.

A

Hemophilia A because it better explains what is going on in the body

The traditional cascade/waterfall coagulation model helps better to determine laboratory testing and what is happening in the test tube

19
Q

What is the target of tissue factor pathway inhibitor?

A

TF-FVIIa

20
Q

What is the target of antithrombin?

A

Thrombin, Factor Xa

21
Q

What is the target of protein C?

A

Factors V and VIII

22
Q

What are the two main factors/cofactors in the extrinsic pathway?

A

TV and VIIa

23
Q

If you have a delay in aPTT, but normal PT, what factors could be deficient?

A

Factos VIII, IX, XI, and XII

24
Q

What is the end result of the common coagulation pathway?

A

fibrin formation

25
Q

Spud, one of your favorite patients has Hemophilia A. If Spud were to bleed, which of the following signs would not be expected?

  1. Petechiae
  2. Joint bleed
  3. Hemoabdomen
  4. Hemothorax
  5. Large ecchymoses
A

a. Petechiae

Petechiae is associated with primary hemostasis. Hemophilia A is a disorder of coagulation factors which are associated with secondary hemostasis

26
Q

What inhibitor does heparin work with to inhibit secondary hemostasis and what clotting factors does it inhibit?

A

Inhibitor: Antithrombin

Clotting factor: Factor II

Clotting factor: Factor Xa

27
Q

Name two diseases where you might have reduced antithrombin, which would in turn lead to hypercoagulability (i.e. increased risk of clots forming where you don’t want them)?

A

Protein losing enteropathy (PLE) and Protein losing nephropathy (PLN)

28
Q

Your patient comes in with a hemoabdomen. You perform clotting times and both PT and aPTT are markedly prolonged. Which of the following could explain this result:

  1. Deficiency in FVIII (Hemophilia A)
  2. Anti-coagulant rodenticide toxicity
  3. Patient was given too much heparin, which inhibited factor X and II
  4. Deficiency in FVII
  5. B and C
A

e. B and C

29
Q

True or False: D-dimer elevation alone is diagnostic for DIC.

A

False

30
Q

What do you measure to try to diagnose DIC?

A

Primary hemostasis - platelets

Secondary hemostasis – screening coagulation tests

Secondary hemostasis - fibrinogen

Fibrinolysis – D-dimer or FDP

Inhibitors - AT

31
Q

Name a drug that is given to inhibit fibrinolysis, thereby stabilizing clots and (hopefully) preventing bleeding in cases like dogs with hemoabdomen from cancer or in trauma.

A

E- aminocaproic acid or tranexamic acid

32
Q

Describe two reasons why there is loss of control of coagulation in DIC so that clotting happens at places other than where vessels are actually injured.

A

Decreased inhibitors

Expression of TF by cells that don’t normally express TF

33
Q

Give three examples of diseases that can be associated with DIC.

A

Sepsis, severe inflammatory disease, and metastatic cancer

34
Q

What is the best way you can treat DIC?

A

Treat the underlying disease

35
Q

The most comment acquired disorders of secondary hemostasis are:

A

Rodenticide toxicosis and DIC

36
Q

The most common hereditary disorder of secondary hemostasis is what?

A

Hemophilia A

37
Q

What is the first test to do when you suspect primary hemostatic disorder?

A

platelet count

38
Q

What tests do you do when you suspect a disorder of secondary hemostasis?

A

Prothrombin time (PT), activated partial thromboplastin time (aPTT) and thrombin clot time (TCT)

Small Animal Medicine (100 decks)

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