coagulation of blood

Question 1

coagulation

Answer 1

coagulation or clotting is defined as the process in which blood looses its fluidity and becomes jelly like mass few minutes after it is shed out or collected in a container
Formation of a clot on top of the platelet plug strengthens and supports the plug, reinforcing the seal over a break in a vessel
The clotting mechanism involves a cascade of reactions in which clotting factors are activated.
Most of them are plasma proteins synthesized by the liver (vitamin K is needed for the synthesis of factor II, VII, IX and X)
They are always present in the plasma in an inactive form
When activated they act as proteolytic enzymes which activate other inactive enzymes
Several of these steps require Ca++ and platelet phospholipid.

Question 2

thirteen clotting factors

Answer 2

-fibrinigonen
-prothrombin
-thromboplastin
-calcium
-labile factor
-stable factor
-antihemophilic
-christmas factor
-staurt-prower factor
-plasma thromboplastin antecendent
-hageman
-firbrin stabilizing factor

Question 3

haemostasis

Answer 3

The term haemostasis means prevention of blood loss
Hemostasis is the process of forming clots in the walls of damaged blood vessels and preventing blood loss, while maintaining blood in a fluid state within the vascular system

Question 4

steps of haemostasis

Answer 4

Vascular spasm
Formation of platelet plug
Blood coagulation

Question 5

vascular spasm

Answer 5

Reduces flow of blood from injured vessel
Causes
Sympathetic reflex
Release of vasoconstrictors
(TXA2 and serotonin) from platelets that adhere to the walls of damaged vessels

Question 6

platelet plug formation

Answer 6

Platelet adherence
Platelet activation
Platelet aggregation

Question 7

platelet adherence

Answer 7

Platelet adhesion: When a blood vessel
wall is injured, platelets adhere to the
exposed collagen and von Willebrand
factor in the wall via platelet receptors →

Question 8

platelet activation

Answer 8

Platelet activation →Activated platelets release the contents of their
granules including ADP and secrete TXA2 →
activates nearby platelets to
produce further accumulation of more
platelets (platelet aggregation) and forming
a platelet plug

Question 9

platelet aggregation

Answer 9

The aggregated platelet plug not only physically seals the break in the vessel but also performs three other important roles
The actin–myosin complex within the aggregated platelets contracts to compact and strengthen what was originally a fairly loose plug
The platelet plug releases several powerful vasoconstrictors that induce profound constriction of the affected vessel to reinforce the initial vascular spasm
(3) The platelet plug releases other chemicals that enhance blood coagulation, the next step of hemostasis

Question 10

steps of blood clot formation

Answer 10

The ultimate step in clot formation is the conversion of fibrinogen, a large, soluble plasma protein produced by the liver and normally always present in the plasma into fibrin, an insoluble, threadlike molecule
This conversion into fibrin is catalyzed by the enzyme thrombin at the site of the injury
Fibrin molecules adhere to the damaged vessel surface, forming a loose, netlike meshwork that traps blood cells, including aggregating platelets
The resulting mass, or clot, typically appears red because of the abundance of trapped RBCs
The original fibrin web is rather weak, chemical linkages rapidly form between adjacent strands to strengthen and stabilize the clot meshwork and
Catalyzed by a clotting factor known as factor XIII (fibrin-stabilizing factor), which normally is present in the plasma in inactive form

Question 11

role of thrombin

Answer 11

Convert fibrinogen into fibrin
Activates factor XIII to stabilize the resultant fibrin mesh
Acts in a positive-feedback fashion to facilitate its own formation
Enhances platelet aggregation, which in turn is essential to the clotting process
Thrombin exists in the plasma in the form of an inactive precursor called prothrombin
Prothrombin, is converted into thrombin by fator X

Question 12

factor X can be activated by

Answer 12

An Intrinsic system
An Extrinsic system

Question 13

intrinsic pathway

Answer 13

The initial reaction is the conversion of inactive factor XII to active factor XIIa
Factor XII is activated in vitro by exposing blood to foreign surface (glass test tube)
Activation in vivo occurs when blood is exposed to collagen fibers underlying the endothelium in the blood vessels

Question 14

extrinsi patway

Answer 14

Requires contact with tissue factors external to blood
This occurs when there is trauma to the vascular wall and surrounding tissues
The extrinsic system is triggered by the release of tissue factor (thromboplastin from damaged tissue), that activates factor VII
The tissue thromboplastin and factor VII activate factor X

Question 15

clot retraction

Answer 15

Clot formation is fully developed in 3-6 min
Contraction of platelets trapped within the clot shrinks the fibrin meshwork pulling the edges of the damaged vessel closer together
During clot retraction serum is squeezed from the clot

Question 16

vessel repair

Answer 16

The aggregated platelets secrete a chemical that helps promote the invasion of fibroblasts (“fiber formers”) from the surrounding connective tissue into the wounded area of the vessel
Fibroblasts form a scar at the vessel defect

Question 17

clot dissolution

Answer 17

Clot is slowly dissolved by a fibrinolytic (fibrin-splitting) enzyme called plasmin
If clots were not removed after they performed their hemostatic function, the vessels would eventually become obstructed by clots
Plasmin, like the clotting factors, is a plasma protein produced by the liver and present in the blood in an inactive precursor form, plasminogen
Plasmin is activated in a fast cascade of reactions involving many factors, among them factor XII (Hageman factor), which also triggers the chain reaction leading to clot formation
In addition to removing clots, plasmin functions continually to prevent clots from forming inappropriately
Throughout the vasculature, small amounts of fibrinogen are constantly being converted into fibrin, triggered by unknown mechanisms
Clots do not develop, however, because the fibrin is quickly disposed of by plasmin activated by tissue plasminogen activator (tPA) from the tissues, especially the lungs

Question 18

anti-coagulation drug- aspirin

Answer 18

Aspirin
inhibits the cyclooxygenase enzyme in the eicosanoid pathways that generate prostaglandins and thromboxane
Because thromboxane A 2 , produced by the platelets, is important for platelet aggregation, aspirin reduces both platelet aggregation and the ensuing coagulation
Importantly, low doses of aspirin cause a steady-state decrease in platelet cyclooxygenase (COX) activity but not endothelial-cell cyclooxygenase; so the formation of prostacyclin —the prostaglandin that opposes platelet aggregation—is not impaired
Platelets, once formed and released from megakaryocytes, have lost their ability to synthesize proteins. Therefore, when their COX is irreversibly blocked, thromboxane A 2 synthesis is gone for that platelet’s lifetime
In contrast, the endothelial cells produce new COX molecules to replace the ones blocked by the drug
Aspirin appears to be effective at preventing heart attacks
In addition, the administration of aspirin following a heart attack significantly reduces the incidence of sudden death and a recurrent heart attack

Question 19

warafin

Answer 19

interferes with the action of vitamin K, which in turn reduces the synthesis of clotting factors by the liver

Question 20

heparin

Answer 20

Heparin
the naturally occurring endothelial-cell cofactor for antithrombin III, can also be administered as a drug, which then binds to endothelial cells and inhibits clotting

Question 21

xanbans

Answer 21

Xanbans
Another type recently developed includes drugs that specifically inactivate factor Xa

Question 22

recombinant t-PA

Answer 22

Recombinant t-PA
Intravenous administration of recombinant t-PA within a few hours after myocardial infarction significantly reduces myocardial damage and mortality
Recombinant t-PA has also been effective in reducing brain damage following a stroke caused by blood vessel occlusion