Cardio L18 Thrombosis Flashcards Preview

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Flashcards in Cardio L18 Thrombosis Deck (56)
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1

Thrombosis

Formation of a solid mass from the constituents of the blood within the living circulation.

!!!Distinction from blood clot!!!

2

Blood clot

When blood solidifies outside the living circulation the solid and fluid components separate and form blood clots.

3

When a thrombus forms

The cellular and serum phases are mixed and form a series of alternating layers of cell poor and cell rich zones.

4

Layers of thrombus

Lines of Zahn

5

Arterial site thrombus type

Tiny, consisting largely of platelets (Very small dimension)

6

Venous site thrombus type

Small and pale; platelet and fibrin rich (Fast local blood flow)

7

Capillaries thrombus type

Large and red; Red cell rich (Slow local blood flow)

8

Virchow’s triad →

The conditions, which predispose to thrombosis, were first addressed by Virchow in the mid 19th Century.
Changes in the vessel wall
Changes in local blood flow
Changes in co-agulative qualities of the blood

9

Changes in the vessel wall

Loss of endothelial integrity (most common: atheroma)

10

Changes in local blood flow

Nature of blood flow – laminar vs. turbulent
Disturbance of blood flow allows large numbers of platelets to come into contact with endothelium.

11

Changes in co-agulative qualities of the blood

Alteration in coagulability of the blood
Increased platelet numbers:
1. Major injury
2. Surgery
3. Post partum
Increased fibrinogen concentration

12

→ Thrombus forms at

sites of endothelial injury.

13

Intact endothelium tend to discourage thrombosis by 3

1. Expressing sulphated mucopolysacchardies (heparin and heparin like molecules)
2. Expressing tissue plasminogen activator (TPA)
3. Synthesizing prostacyclin (PGI2)

14

The endothelial cell surface is covered by and are potent activators ok

covered by sulphated mucopolysaccharides, which carry a large negative charge.

These molecules are potent activators of circulating antithrombotic enzymes such as anti-thrombin 3.

15

Heparin causes

A conformational change in the anti-thrombin molecule which enhances its activity a hundredfold.

16

Endothelium expresses

Tissue plasminogen activator (TPA)

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Plasminogen is the

Circulating, inactive, precursor of the enzyme Plasmin which destroys thrombus.

18

Endothelial TPA activates

Plasminogen with the result that there is active destruction of thrombus at the endothelial surface.

19

Damaged endothelial cells generates

Prostacyclin (PGI2)

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PGI2 function

Dilates vessels
Disaggregates platelets

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Opposition to PGI2

Prostaglangin generated by platelets

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Platelets description

Circulating anuclear fragments of the cytoplasm derived from megakaryocytes (multinucleate bone marrow cells, each of which will generate between 2000 & 4000 platelets).

23

Platelets structure

3 microns diameter
Conc – 200-400 x 10 to the 9/L
Approx 10 day life span

24

Platelets Contain two sorts of cytoplasmic granules

Alpha granules
Dense bodies

25

Alpha granules

Coagulation factors
Platelet derived growth factors
Fibrinogen

26

Dense bodies

Unique to platelets
Adenine nucleotides (ADP)
5 Hydroxytryptamine
Calcium

27

Platelet Adhesion

Rapid adherence to collagen exposed by endothelial damage

28

Platelet releases reaction

Degranulation of the platelets

29

Platelet aggregation

1. Platelets rapidly clump together to cover the area of endothelial cell loos
2. Mediated by ADP and Ca2+

30

Prostaglandins Generated from

Cell wall phospholipids, which are released when cells are injured.

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