Thrombotic And Fibrinolytic Disorders

Front 1

Fibrinolytic disorders

cause

Back 1

increased plasmin activity

Front 2

Functions of Plasmin

Back 2

• Inactivates Factors Va and VIIIa

• Degrades Factor XIIa

• Lyses Fibrin and Fibrinogen

Front 3

Fibrinogenolysis (Primary Fibrinolysis)

definition

Back 3

Over activation of plasmin

• Plasmin breaks down fibrinogen

Front 4

Fibrinolysis

definition and cause

Back 4

Can be normal

Can be pathological

• over activation of plasmin
• overwhelms plasmin inhibitors

Front 5

Activators of fibrinolysis

Back 5

Liver Disease

• decreased inhibitors of fibrinolytic system

  
  

  • Alpha 2 anti-plasmin

Exogenous activators

• streptokinase, urokinase, tPA

Front 6

Alpha 2 Anti-plasmin deficiency

Back 6

plasmin can attack not only fibrin, but fibrinogen, factors V & VIII, causing bleeding

Front 7

Thrombosis
(Thrombophilia)

definition

Back 7

clot occurring in a major vessel

Front 8

Emboli

definition

Back 8

thrombus broken free from original site and lodges in capillaries of an organ

Front 9

Factors Implicated in Causing Thrombosis

Back 9

• Major tissue trauma and Surgery

• Obesity

• Complications of pregnancy

• Oral contraceptives

• Anti – Thrombin Deficiency

Front 10

Anti – Thrombin Deficiency

cause and pathology

Back 10

Hereditary - often family history of pathological thrombi and emboli

normally neutralizes IIa, lXa- XIIa and plasmin

Front 11

Protein C and Protein S Deficiencies

Back 11

• normally inactivates Va and VIIIa

  
  
  • Also liberates tPA from endothelial cells – therefore defic. = no clot breakdown

Front 12

Activated Protein C Resistance (APC -R)

(also known as Factor V Leiden)

Back 12

APC resistance – factor V resistant to inactivation by APC

Front 13

Factor XII Deficiency

Back 13

decreased activation of plasminogen (Needed for activation of plasminogen to plasmin)

Front 14

Dysfibrinogenemia

Back 14

Dysfibrinogenemia – can’t be lysed by plasmin

Front 15

Lupus inhibitor

Back 15

inhibits prostacyclin production or release from endo cells – normally inhibits plt adhesion

Front 16

Prothrombin mutation

Back 16

increased Factor II levels

Front 17

HMWK and PK deficiency

Back 17

both decrease amount plasminogen activation

Front 18

Plasminogen Deficiency

Back 18

• Type I - decrease in activity and antigen

• Type II - dysfunctional

Front 19

tPA deficiency

Back 19

Results in decreased activation of plasminogen to plasmin

Front 20

Increased Plasminogen Activator Inhibitor
(PAI)

Back 20

increased – inhibits tPA, therefore results in decreased activation of plasminogen to plasmin

Front 21

Thrombin activatable fibrinolytic inhibitor (increased)

Back 21

alters clot – to inhibits fibrinolysis

therefore if it's increased = thrombosis

Front 22

Homocysteine increased

Back 22

theory – damage to endothelial cell

Front 23

Heparin Cofactor II Deficiency

Back 23

Results in decreased neutralization of thrombin

Front 24

TTP

Back 24

• unusually large vWF stimulates expression of TF3

Front 25

HITTS

Back 25

• Possible plts and microparticles released occlude microvasculature