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Flashcards in Dixon cardiovascular system Deck (26):
1

what are the main components of blood

plasma
platelets
erythrocytes
leukocytes

2

what does plasma contain

water
electrolytes
organic solutes
proteins (albumins, immunoglobulins, fibrinogen and clotting factors)

3

platelets:
nucleated?
lifespan?
function?

non nucleated
contains granules
5-9 day lifespan
used in haemostasis, blood vessel repair, inflammation

4

erythrocytes:
nucleated?
lifespan?
function?

non nucleated
red bi-concaved disc
120 days lifespan
oxygen transport

5

leukocytes:
nucleated?
lifespan?
function?

nucleated
variable life span
important for defence

6

what is haemostasis?
what are the three mechanisms

arrest of blood flow from damaged vessel.

vascular spasm, coagulation cascade
platelet activation and plug formation

7

describe vascular spasm

damage to vessel wall
vasoconstriction of vessel wall
decrease in blood flow through damaged vessel.

8

role of coagulation in haemostasis

solidifcation of blood (clot formation) through amplifying cascade.

soluble fibrinogen is converted to insoluble fibrin by thrombin. the fibrin forms a mesh which traps blood cells and platelets.

9

what are the differences between the extrinsic and intrinsic part of the coagulation cascade?

extrinsic:
needs extravascular tissue factor
activated after tissue trauma
in vivo mechanisms
very fast (seconds)

intrinsic:
all components are available in blood
contact activation
in vivo AND in vitro
slower (minutes)

10

what factors are involved in the intrinsic pathway/contact pathway?

factor 2 is cleaved to factor 2a.
factor6 is cleaved by factor2a into factor6a
factor 9 is cleaved by factor 6a into factor 9a.

factor 9a, with factor 8a/ca2+ is used in the extrinsic pathway

11

what factors are used in the extrinsic pathway?

factor7 is cleaved by tissue factor into factor7a
factor 10 is cleaved by factor 9a/ca2+/factor8a into factor 10a.

prothrombin (factor2) is cleaved by factor 10a/ca2+/5a into thrombin (factor 2a)

12

what are the coagulation factors? (generic overview)

present in blood as inactive precursors
formation of precursors require reduced form of vitamin K.
theyre activated by proteolysis (factor 2 to factor 2a)
they are proteolytic enzymes when activated
amplification is built into the cascade

13

what is the role of thrombin in haemostasis?

converts fibrinogen into fibrin

factor13 is cleaved by thrombin into factor13a which causes fibrin monomers to form stronger bonds with eachother

activates platelets

induces platelet aggregation and gp2b/3a expression

inhibited by antithrombin 3 and fibrin

14

how does the body prevent uncontrolled coagulation and removal of clots?

coagulation checkpoints and fibrinolysis

15

what are the coagulation checkpoints?

1) fibrin inhibits thrombin

2) protein C from plasma is activated by thrombin and proteolytically inhibits factor 5a and 8a

3)antithrombin3 from plasma inhibits thrombin and other factors

4) heparin from endothelium , mast cells and basophils are a cofactor for at3

16

what is the purpose of fibrinolysis

clot dissolution
activated simultaneously with coagulation cascade.

17

what is the process of fibrinolysis

a clot is formed that contains inactive plasminogen

plasminogen activators convert plasminogen to plasmin (digests fibrin, factor 2, 5 and 8)

protein c inhibits factors 2, 5 and 8 while the clot dissolves

18

what is platelet plug formation

process that is integrated with coagulation pathway in which platelets go through three stages to form a clot

19

what are the three stages of platelets plug formation?

adhesion
activation
aggregation

20

discuss platelet adhesion

when blood vessel wall is damaged platelets will undergo adhesion to collagen.

the platelet surface have adhesive receptors which interact with the collagen directly or indirectly.

21

discuss platelet activation

platelets are activated and will change shape from round to spikey?
they release granules of mediators which promote the clotting cascade, platelet activation and aggregation, wound repair, and inflammation.

thromboxane A2 (txa2) is released and causes the activation and activation of more platelets.

22

discuss platelets aggregation

glycoprotein 2b/3a receptors bond with fibrinogen which bonds with more platelet receptors and forms bonds and eventually a clot.

23

how is thromboxane synthesised?

membrane phospholipids are cleaved by phospholipase A2 into arachidonic acid and lyso-PAF (converted to PAF)

cyclo-oxygenase (COX) induces arachidonic acid to be converted to cyclic endoperoxides

cyclic endoperoxides is cleaved by thromboxane synthase into TXA2.

TXA2 acts as a vasoconstrictor and promotes platelet aggregation.

OR// cyclic endoperoxides is cleaved by prostacyclin synthase into prostacyclin.

prostacyclin is a vasodilator and inhibits platelets aggregation.

24

what is the function of GP2B/3A receptors?

1) binds fibrinogen, von Willebrand's factor and other proteins

2)expressed only on activated platelets

3) final common pathway in stimulation for platelet aggregation

4) functional antagonists are used as drugs e.g. tirofiban

25

how is the coagulation cascade integrated with the platelet process?

platelets are activated by thrombin

activated platelets provide surface for coagulation cascade to occur

26

what is the summary of haemostasis?

vessel wall damage = activation of coagulation cascade and platelet plug formation

= clot formation
= cessation of blood loss
= vessel wall healing
= clot dissolution