Path: Thrombosis And Emboli

Front 1

Define thrombosis

Back 1

Pathological

Intravascular blood clot

Formed during life

Front 2

Normal haemostasis

Extravascular clots

Postmortem clots

Are all also considered to be thrombi. True or false?

Back 2

FALSE

Front 3

Layers of RBCs and then fibrin and platelets repeated are called what?

Back 3

Lines of Zahn

Front 4

Occlusion of the entire vessel during deposition of material to the thrombus is called what?

Back 4

Consecutive clot

Front 5

Virchow's triad

Back 5

1. Hypercoagulability

2. Endothelial cells damage

3. Altered blood flow

Front 6

5 anti-thrombotic properties of normal endothelium

Back 6

1. Thrombomodulin

2. Tissue factor pathway inhibitor

3. Heparin like molecule

4. tissue plasminogen activator

5. NO and PGI2

Front 7

Function of thrombomodulin

Back 7

Thrombin binds to thrombomodulin

Activates protein C

Inactivated Va and VIIIa

Front 8

Role of TFP-I

Back 8

Inactivates factors VIIa and Xa

Front 9

Role of heparin like molecules

Back 9

Binds to ATIII to inactivate thrombin, factors Xa and IXa

Front 10

How is damaged endothelium prothrombotic?

Back 10

Tissue factor expressed

Subendothelial collagen is thrombogenic

Front 11

2 changes to normal blood flow

Back 11

1. Turbulence (stress damages endothelial cells)

2. Stasis (no removal of already activated clotting factors, no bringing in of new clotting factors)

Platelets and cells contact endothelium in both cases

Front 12

3 inherited types of hypercoagulable state

Back 12

Factor V Leiden mutation (protein C can no longer cleave it)

Protein C and protein S deficiency (loss of natural anticoagulant)

Mutation in prothrombin gene (more prothrombin, more thrombin produced)

Front 13

Acquired hypercoagulable states

Back 13

Pregnancy

Burns

Sepsis

Malignancy

Oral contraceptive use

Smoking

Front 14

4 fates of the thrombus

Back 14

1. Resolution (lysis by fibrinolytic system)

2. Organisation (granulation tissue ingrowth from vessel)

3. Recanalisation (new vessel development through occlusion)

4. Embolisation (fragment broken off and carried away by circulation)

Front 15

Arterial thrombi related to...

Back 15

Turbulence and endothelial damage

Front 16

Thrombi formation in the heart related to...

Back 16

Endothelial damage and stasis

Front 17

Most important cause of venous thrombi?

Back 17

Stasis

Venous thrombi more likely to embolise

Front 18

Embolus

Back 18

Passage through venous or arterial circulation of any material that can lodge in a blood vessel and obstruct its lumen

Front 19

Types of embolic material

Back 19

MAINLY THROMBUS

Fat, air, bone marrow, nitrogen, amniotic fluid, tumour, foreign body

Front 20

Pulmonary emboli likely to have originated where?

Back 20

Most are thromoemboli from femoral, ileal and popliteal veins (goes to RHS of heart, and then to pulmonary circulation)

Front 21

Saddle embolus

Back 21

Large pulmonary embolus that blocks both pulmonary arteries, circulatory collapse

Front 22

What protects lungs from medium PE?

Back 22

Dual blood supply protects from effects of PE obstruction

Bronchial artery and adjacent pulmonary artery

Front 23

Multiple emboli with poor bronchial blood supply causes?

Back 23

Pulmonary infarct

Front 24

2 fates of pulmonary thromboemboli

Back 24

1. Resolution (reinstate original vessel lumen)

2. Organisation (granulation tissue, fibrosis and recanalisation)

Front 25

6 origins of systemic thromboemboli

Back 25

Heart

Atherosclerotic plaques

Aortic aneurysm

Prostheses

Venous thrombi

Paradoxical embolisation

Front 26

What is protective against an infarction?

Back 26

Collateral circulation

Front 27

Causes of fat embolism?

Back 27

Severe trauma including long bone fractures

Front 28

What happens in amniotic fluid embolisation?

Back 28

Fetal cells and debris enter maternal circulation via uterine and cervical veins