Coagulation and Bleeding Disorders Flashcards Preview

SP 16 - Path Test 2 > Coagulation and Bleeding Disorders > Flashcards

Flashcards in Coagulation and Bleeding Disorders Deck (49)
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1

What are the 3 major components of the hemostatic system?

Vascular wall
Platelets
Coagulation Proteins

2

What are the 3 phases of primary hemostasis?

Adhesion
Activation
Aggregation

3

Adhesion

Adhesion of platelets to the damaged endothelial wall
Adhesion activates surface membrane receptors and adhesive proteins (vWF)

4

von Willebrand Factor

Mediates the adherence of platelets to the subendothelial colalgen

5

Activation

In order to effectively form a hemostatic plug, additional platelets are recruited to the local site
As platelets are activated by binding to vWF, there is release of second messenger molecules within the platelet

6

What does platelet activation lead to?

Shape change of platelet from discoid to spheroid
Secretion of cytoplasmic ADP
Activation of the glycoprotein IIb/IIIa receptor
Contraction of the platelet mediated through actin fibers

7

Activation

Platelets interact with other platelets
The release of cytoplasmic ADP causes the activation of adjacent platelets, and platelet-platelet binding through fibrinogen

8

Secondary Hemostasis / Fibrin clot formation

Soluble coagulation proteins within the plasma are activated to generate thrombin in an amplification reaction
Thrombin converts fibrinogen to fibrin, which adds stability to the clot after fibrin monomers are cross-linked by Factor XII

9

Intrinsic Pathway

Sequence of activation of Factor XII
XII --> XIIa (via kallikrein)
XI --> XIa (via XIIa)
IX --> IXa (via XIa)

10

Extrinsic Pathway

Sequence of activation of Factor VII by TF:
VII --> VIIa (via TF)

11

The Common Pathway

X --> Xa
Prothrombin --> Thrombin (via Xa)
Fibrinogen --> Fibrin (via thrombin)

12

What proteins are responsible for regulating hemostasis?

Antithrombin
Protein C
Plasminogen

13

How does Antithrombin regulate hemostasis

Inhibits the activity of thrombin and other serine proteases of the coagulation cascade, but forming an inactive enzyme-inhibitor complex

14

What is the most well known Antithrombin and how does it work?

Antithrombin III
In the presence of heparin, it becomes activated so that it can form a complex with thrombin, thus destroying the ability of thrombin to participate in the coagulation cascade

15

Protein C

Regulates major cofactors of the coagulation cascade (Va and VIIIa)
Activated Protein C (APC) plus Protein S (its cofactor) together inactivate factors Va and VIIIa

16

Plasminogen

Gets activated by tissue plasminogen activator from the endothelium (tPA) into Plasmin
Plasmin trims fibrin, thus controlling the degree of secondary coagulation

17

Prothrombin time (PT)

Time needed for plasma to form a clot in the presence of added tissue thromboplastin
Screens for the activity of proteins in the extrinsic pathway
Used to measure anticoagulation of pts using oral anticoagulants

18

Partial Thromboplastin Time (PTT)

A measurement of the time needed for plasma to form a clot in the presence of added ground glass or kaolin (these activate Factor XII)
Screens for activity within the Intrinsic Pathwys

19

Platelet count

A measurement of platelet number in anticoagulated blood
Normal: 150,000-400,000/uL

20

Thrombocytopenia

Decrease in platelet number

21

Thrombocytosis

Increase in platelet number

22

Thrombocythemia

Increase in platelet number

23

Mixing Studies

Measures platelet function
If pt has prolonged PT or PTT, you mix their blood with normal blood in a 1:1 ratio
If the problem is corrected - a deficiency exists
If the problem persists - there is an inhibitor present

24

von Willebrand disease symptoms

Mucocutanous bleeding is the predominant clinical manigestation:
Nosebleeds
Ecchymosis (bruising)
Bleeding with trauma or surgery
Excessive menstrual flow

25

von Willebrand Disease

Autosomal dominant abnormal vWF
Most common inherited bleeding disorder
Symptoms often improve after adolescence

26

Type I vWF disase

Most common form
Decreased production in the amounts of vWF

27

Type II wWF disease

Qualitatively abnormal vWF

28

Type III vWF disease

Complete lack of vWF
This form is autosomal recessive

29

What are the laboratory manifestations of vWF disease?

Prolonged PT
Prolonged PTT

30

What are the therapeutic options for vWF disease?

Desmopressin
Antifibrinolytic agents in mild cases
Factor VII concentrates containing vWF and cryoprecipitate in severe cases