Hematology - Levine Hemostasis SG Flashcards Preview

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Flashcards in Hematology - Levine Hemostasis SG Deck (38)
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1

What are the two key cellular players in primary hemostasis:

Endothelial cells and platelets

2

What is the end result of primary hemostasis?

The formation of a platelet plug

3

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

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

4

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

Thrombocytopenia

Impaired platelet function

Von Willebrand factor deficiency

Impaired Von Willebrand function

5

What is the most common acquired disorder of primary hemostasis?

Thrombocytopenia

6

What is the most common hereditary disorder of primary hemostasis?

Von Willebrand factor deficiency

7

List 4 possible causes of a prolonged BMBT.

Thrombocytopenic

Thrombopathic (platelets don’t work)

vWF deficient/abnormal

Abnormal vasculature

8

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

Tick panel, imaging, and thorough drug history

9

Explain how vincristine works to treat ITP:

It prevents microtubule polymerization

It promotes accelerated megakaryocyte fragmentation and platelet release from bone marrow

10

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

False

11

 Explain the basic idea behind IVIG therapy for ITP:

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

12

What are three blood products that contain platelets?

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

13

What are three indications for a platelet transfusion?

Severe thrombocytopenia

Suspect pulmonary or CNS hemorrhage

Acquired or hereditary thrombopathias

14

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

If they are going to surgery

15

How does Clopidogrel (Plavix) work?

Inhibiting the platelet ADP receptor

16

What cell surface is coagulation initiated on?

Fibroblast

17

What cell surface is coagulation amplified and propagated on?

Platelets

18

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.

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

What is the target of tissue factor pathway inhibitor?

TF-FVIIa

20

What is the target of antithrombin?

Thrombin, Factor Xa

21

What is the target of protein C?

Factors V and VIII

22

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

TV and VIIa

23

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

Factos VIII, IX, XI, and XII

24

What is the end result of the common coagulation pathway?

fibrin formation

25

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. Petechiae

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

26

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

Inhibitor: Antithrombin

Clotting factor: Factor II

Clotting factor: Factor Xa

27

 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)?

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

28

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

e. B and C

29

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

False

30

What do you measure to try to diagnose DIC?

Primary hemostasis - platelets

Secondary hemostasis – screening coagulation tests

Secondary hemostasis - fibrinogen

Fibrinolysis – D-dimer or FDP

Inhibitors - AT

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