Platets And Coagulation

Front 1

What is the most common thrombocytopenia in adults and children ?

Back 1

ITP

Front 2

2ry Hemostasis ?

Back 2

Front 3

What is the most common thrombocytopenia in adults and children ?

Back 3

ITP

Front 4

What is ITP ? What is the cause of ITP ?

Back 4

Autoimmune production of IgG against platelet GPIIb/IIIa by plasma cells in the spleen

Front 5

What are the Platelets disorders?

Back 5

Back (Definition)

Front 6

What is the rule of spleen in ITP ?

Back 6

1/Production of igG antibodies against GPIIb/IIIa by plasma cells in the spleen.

2/antibody pound platelets are consumed by splenic macrophages resulting in thrombocytopenia

Front 7

Types of ITP ?

Back 7

1/ acute --> children --> weeks after viral infection or immunization. Self limited and usually resolve within weeks. Response well to steroids.

2/chronic --> adults ( women of child bearing age ) --> 1ry or 2ry ( SLE ) 1st manifestation of it. May cause short lived thromcytopenia in offering since igG cross placenta. Response to steroids early but often relapse.

Front 8

What is MAHA ?

Back 8

Pathological formation of platelet microthrombi in small vessels --> platelets are consumed in the formation of microthrombi --> RBCs are sheared as they cross microthrombi --> hemolytic anemia with schistocytes

Front 9

What are the MAHA diseases ?

Back 9

HUS

TTP

Front 10

Most common inherited coagulation disorder ?

Back 10

vWF disease

Front 11

Coagulation factor inhibitors? Most common affected factor ? Diagnosis ?

Back 11

Back (Definition)

Front 12

What is vWF disease ? Presentation ? Lab ? Diagnosis ? Treatment ?

Back 12

Front 13

Vit K affect which factors

Back 13

disco 1972

Protein C and S

Factors 10, 9, 7, 2

Front 14

Vit k function on coagulation ?

Back 14

Vit K is activated by epoxied reductase in the liver, activated vit k. Gamma carboxylates factor 10,9,7,2 and proteins C and S. Gamma carboxylation is necessary for factor function.

Front 15

How does liver failure affects coagulation ?

Back 15

1/ decrease production of coagulation factors

2/ decrease activation of vit k by epoxide reductase

It is followed by PT

Front 16

How does liver failure affects coagulation ?

Back 16

1/ decrease production of coagulation factors

2/ decrease activation of vit k by epoxide reductase

It is followed by PT

Front 17

How does large volume transfusion affect 2ry Hemostasis?

Back 17

Dilutes coagulation factors results in relative deficiency

Front 18

Heparin induce Thrombocytopenia?

Back 18

Development of IgG antibodies against heparin bound platelet factor 4 (PF4) __> antibody heparin PF4 complex activates platelets causing thrombosis and thrombocytopenia.

Front 19

What is Virchow triad ?

Back 19

1/ disruption of blood flow

2/endothelial cell damage

3/ HyperCoagulation

Front 20

What causes disruption of blood flow ?

Back 20

1/ immobilization

2/ cardiac wall dysfunction ( arrythmias, MI )

3/aneurysms

Front 21

What is Hypercoagulable state ? Causes ?

Back 21

Excessive procoagulant protein and decrease anticoagulant. It could be inherited or acquired.

1/protein c or s def. 2/ factor V Leiden 3/prothrombin 20210A 4/anti-thrombin def. III 5/OCPs

Front 22

Mechanism of fibrinolysis ?

Back 22

Fibrinolysis removes thrombus after damaged vessel heals.

1/ tissue plasminogen activator (tPA) converts plasminogen to plasmin--> plasmin cleaves fibrin and serum fibrinogen , destroy coagulation factors and blocks platelet aggregation.

2/ A2-antiplasmin inactivate plasmin

Front 23

What are disorders of fibrinolysis?

Back 23

They are due to plasmin over activity :-

1) radical prostatectomy--> release of urokinase activate plasmin

2) liver cirrhosis--> reduce production of a2-anti plasmin

Front 24

What are the labs in fibrinolysis disorders ?

Back 24

Increase PT, PTT, bleeding time, normal platelet counts. Increase fibrinogen split product

Front 25

What are disorders of fibrinolysis?

Back 25

They are due to plasmin over activity :-

1) radical prostatectomy--> release of urokinase activate plasmin

2) liver cirrhosis--> reduce production of a2-anti plasmin

Front 26

What are the labs in fibrinolysis disorders ?

Back 26

Increase PT, PTT, bleeding time, normal platelet counts. Increase fibrinogen split product

Front 27

Treatment of fibrinolysis disorders ?

Back 27

Aminocaproic acid which blocks activation of plasminogen

Front 28

What are the procoagulant factors ?

Back 28

1/ TXA2 from platelets

2/decrease blood flow

3/ increase platelet aggregations

Front 29

Anti aggregation factors ?

Back 29

PGI2

NO

Increase blood flow

Decrease platelet aggregation

Protein c

Protein s

Anti thrombin III

Front 30

Most common cause of Hypercoagulability in whites ? What is the cause and explain it ?

Back 30

Factor V Leiden. Mutation at the site of cleavage by protein c and s --> resistant to degradation

Front 31

Anti-thrombin III job ? Deficiency causes ?

Back 31

It is activated by heparin like molecules produced by the endothelium. Then ATIII inactivate thrombin and coagulation factor.

Deficiency causes HyperCoagulation.

Front 32

Thrombosis vs post mortem clot ??

Back 32

Back (Definition)

Front 33

What is Virchow triad ?

Back 33

1/ disruption of blood flow

2/endothelial cell damage

3/ HyperCoagulation

Front 34

What causes disruption of blood flow ?

Back 34

1/ immobilization

2/ cardiac wall dysfunction ( arrythmias, MI )

3/aneurysms

Front 35

How does endothelium prevent thrombosis ??

Back 35

1/ block the subendothelial collagen and underlying tissue factor

2/ produce and secret:

1. Prostacyclin ( prostaglandin I2)

2. NO

Both vasodilate and inhibitor platelet aggregation

3. Heparin like molecule --> augment ATIII which inactivates thrombin and coagulation factors

4. tPA ( converts plasminogen to plasmin)

5.thrombomodulin --> redirect thrombin to activated protein C which inactivates factor V & VIII

Front 36

Causes of endothelial damage ?

Back 36

Atherosclerosis

Vasculitis

High levels of homocysteine ( vit B12, folate def. or cyststhionine beta synthase def. )

Front 37

What is cyststhionine beta synthase deficiency ? And what are the consequences of it ?

Back 37

It converts homocysteine to cyststhionine. If it is deficient then lead to build up of homocysteine and homocysteinuria--> 1/ vessel thrombosis 2/mental retardation 3/lens dislocation 4/ long slender fingers

Front 38

HUS vs TTP ?

Back 38

Back (Definition)

Front 39

Cyststhionine beta synthase def ??

Back 39

Back (Definition)

Front 40

Which hormone increase the production of coagulation factors ?

Back 40

Estrogen

Front 41

Causes of fat embolism ? And what is the characteristics of it ? What is composed of ?

Back 41

1/ bone fracture (specially long) while fracture is still present or shortly after repair.

2/ soft tissue trauma.

Characterized by dyspnea and petechia r on the skin overlying the chest

The emboli have fat and bone marrow elements.

Front 42

What are the cases of gas embolism ?

Back 42

1) decompression sickness

[ joint and muscle pain " bends" and respiratory symptoms "chokes"]

2)laparoscopic surgeries

Front 43

What is the composition of emboli ?

Back 43

Cholesterol cleft in it

Front 44

What is the composition of amniotic fluid embolus and what is the symptoms of it ?

Back 44

Composed of squamous cells, keratin debris from fetal skin.

Present with Sob, DIC and neurological symptoms

Front 45

Why is most of PE's are Asymptomatic ?

Back 45

1/ dual blood supply of the lung

2/ the emboli usually small --> self resolves.

Front 46

When does Pulmonary infarction happen in PE ?

Back 46

If a large or medium sized artery is obstructed in pts with pre-existing cardiopulmonary compromise; only 10% of PEs cause infarction

Front 47

What causes sudden death from PE ?

Back 47

Large saddle embolus that blocks both left and right pulmonary arteries OR significant occlusion of a large pulmonary artery.

Death usually due to electromechanical dissociation.

Front 48

What may arise from chronic emboli ?

Back 48

When they reorganized over time they may cause pulmonary HTN.

Front 49

Systemic embolism where due they arise from ?

Back 49

Left heart