Circulation 1 -physical thrombosis and clotting in wound healing Flashcards
(32 cards)
What does the arterial system do?
takes blood away from the heart
oxygenated blood to distal organs and tissues in the body so that they can survive
Describe the arterial system?
Goes from the heart and straight into the aorta, which is a large or wide diameter, wide calibre vessel.
As it propagates through the body, it gets smaller and smaller as it branches.
Keeps getting smaller till you get to capillaries and oxygenation occurs here.
What cell lines the lumen?
endothelial cell
What do endothelial cells sit on?
basal lamina or connective tissue layer
What surrounds the basal lamina?
smooth muscle cells
What is around smooth muscle cells?
interstitial collagen fibres
What does lumen consist of?
red blood cells - carry oxygen
white blood cells - comprise immune mediated cells
platelets
plasma - fluid mixed up of water and numerous proteins other than WBC and RBC …. main constituent of that is clotting factors
What is haemostasis?
the cessation of flow of blood either within a lumen or if there’s defect in lumen stopping the flow of blood outside the lumen into the surrounding soft tissues
What are the three main steps in haemostasis?
Vasoconstriction- reduces the diameter of the lumen
-reduces blood flow
-limits blood loss
Primary haemostatic process
(initial process of trying to stop blood actually getting through the defect)
-platelet plug formation
Secondary haemostatic process
-Activation of the coagulation cascade
-fibrin meshwork
What is the parent cell of platelets?
megakaryocyte
Describe the physical appearance of a megakaryocyte?
large cell with many nuclei
What kind of division do megakaryocytes go through?
nuclear division but not cell division
How do platelets via megakaryocytes enter circulation?
megakaryocytes then produce platelets, which form little clusters on the membrane of the megakaryocytes.
Megakaryocytes in bone marrow sit over the sinusoids of bone marrow and deposit platelets into sinusoids.
-which then enters the circulation
Describe primary haemostasis?
when lumen is intact -> inactive and circulate around body
when defect in vessel- contents of vessel gets exposed to tissues and immediately body recognizes that as an abnormal event
Body reacts and platelets bind with collagen fibres and smooth muscle - become activated. Producing diff glycoproteins and molecules.
Platelets start to become sticky and they start to aggregate and stick together.
What happens in secondary haemostasia?
activation or the initiation of the coagulation cascade + the activation of clotting factors within that cascade.
Where are most clotting factors produced?
in the liver
What is the main aim of the coagulation cascade?
convert prothrombin into thrombin- which then converts water soluble molecule , fibrinogen, into an insoluble molecule called fibrin. Fibrin is the ultimate haemostatic endpoint.
Describe Extrinsic pathway?
quickest pathway
initial damage to the vessel lumen produces a mol called tissue factor. Tissue factor becomes joined to factor 7 to create a tissue factor 7A complex - which then directly acts on factor 10 , factor 5 to activate their co factors to produce thrombin, fibrin and meshwork.
Describe the intrinsic pathway?
initiated by damage to sub endothelial tissue
thrombin can act back into pathway to propagate more conversion of inactive clotting factors to active clotting factors.
How is the clotting cascade an amplification system?
so many more molecules of fibrin are produced compared to no. tissue factor mols
What is meant by initial damage?
One obvious way is trauma
Trauma leads to 1. Exposure of interstitial collagens (collagens in connective tissue between structures) and 2. Exposure of a molecule called Tissue Factor (=TF)
blood leaks out and plasma comes into contact with interstitial collagen fibres
Contact between plasma clotting factors and interstitial collagen initiates activation
tissue factor produced by smooth muscle and endothelial and initiates secondary phase of haemostasis
How do clotting factors become activated?
when come into contact with activator, activates them by allowing them to bind to co factor (12A).
When bound, becomes active complex. Can do the same in next stage of pathway
What happens when clotting factor is activated?
Many clotting factors are serine proteases
the serine mol in them is cleaved and allows co factor to bind and that active complex does same thing in next stage of pathway