Coagulation of blood L9 Flashcards

1
Q

what is the Hemostasis ?

A

The physiological process of stopping blood from flowing out of blood vessels by changing blood from a liquid to a gel, forming a blood clot.

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2
Q

Why do we need hemostasis?

A

We need it in order to stop blood from flowing out of damaged vessels.

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3
Q

even when the vessels are not damaged, coagulation takes place why ?

A

due to presence of coagulating factors , This process is called latent coagulation.

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4
Q

what is latent coagulation. ?

A

is when the vessels are not damaged, and coagulation takes place due to presence of coagulating factors

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5
Q

what is the amount of latent coagulation per day due the presence of factors ?

A

2 g of fibrin per day

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6
Q

what is the fibrin ?

A

fibrin, an insoluble protein that is produced in response to bleeding and is the major component of the blood clot.

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7
Q

what are two types of hemostasis ?

A

1] Thrombocytic / Platelet clotting

2] Plasmic coagulation

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8
Q

Thrombocytiс clotting is realizing due ?

A

due to platelet factors which are contained in thrombocytes (platelets).

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9
Q

what is the main platelet factors:

A
  • thromboplastin (No3)
  • antiheparin(No4)
  • fibrinogen(No5)
  • thrombostenin(No6)
  • serotonin(No10)
  • factor of thrombocytic aggregation (No11)
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10
Q

What does thrombocytic coagulation do?
and why they call it platelet coagulation?
and Why it also calls as microcirculatory coagulation?

A

-What does thrombocytic coagulation do?
This coagulation may stop bleeding in those vessels which have low blood pressure

-why they call it platelet coagulation ?
bcs It happens due to presence of platelets factors.

-Why it also calls as microcirculatory coagulation?
Because it has most importance in microcirculatory vessels (capillaries).

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11
Q

what are the stages of realizing the thrombocytic coagulation ?

A

1) vasospasm;
2) platelet adhesion after platelet activation (3-10 sec);
3) platelet aggregation (plug formation) (for few seconds);
4) retraction of a platelet thromb (for few seconds).

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12
Q

what is the final results of thrombocytic coagulation?

A

is the formation of a platelet plug (clot, thromb, thrombus).

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13
Q

explain the all steps of platelet coagulation

A

1 - Vasospasm is constriction of vessels that causes decrease in blood flow to the injured area. Happens due to factor no. 10 - Serotonin.
Note: even vasospasm may stop bleeding that’s mean some time no need to go through all the steps

2- platelet adhesion
Happens due to factor no. 3( thromboplastin) and 4 ( antiheparin)
in the endothelium. Factor 3 has three active biochemical centers.
Two of them bind to sub-endothelian collagen fibers due to Willibrant factor.
This lasts 3-10 sec. After this occurs platelets activation.
- platelet activation
Happens in presence of factor no. 5 – Thrombocytic fibrinogen
Activation of platelet is associated with the appearance of high concentration of ADP from ATP.
ADP is released from active platelets, as well as from damaged endothelium, which induces the next phase – aggregation.

3- platelet aggregation (platelet plug formation)
Happens in presence of factor no. 11 – Platelet aggregation factor.
It begins almost simultaneously with adhesion and consists of twisting the platelets and adhering them to the site of damage.

4-retraction of a platelet thrombus
Happens in presence of factor no.6 – Thrombostenin. Retraction is the compaction and fastening of a blood clot on a damaged vessel.
It is carried out under the influence of thrombostenin of platelets, due to the active reduction of their actin-myosin complex. Results of platelet coagulation is formation of platelet thromb. It is not strongly fixed on vessel, so it may be flown away. Since, the thromb flows away plasmic coagulation is followed.

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14
Q

What plasmic coagulation needs for ?

A

It helps to stop bleeding from high pressure vessels (arteries).

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15
Q

what is the main Plasmic factors?

A

I – Fibrinogen
II – Prothrombin
III – Thromboplastin (tissue factor)
IV – Ca2+
V – Proaccelerin (labile factor),
VI – Accelerin (active factor)
VII – Proconverting (stable factor)
VIII – Antihaemophilic globulin A
IX – Antihaemophilic globulin B (Christmas factor)
X – Autothrombin (Stuart prower factor)
XI – Antihaemophilic globulin C
XII – Hageman factor (glass factor, contact factor)
XIII – Fibrinase (Fibrin stabilizing factor, Laki-Lorand factor)
XIV– Prekallikerin (Fletcher factor)
XV – Fitzgerald factor

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16
Q

explain the phases of plasmic coagulation

A
  • There are 3 main phases of plasmic coagulation, but 2 more supplementary (pre- and post-) phases are also exist.
  • / PRE-PHASE
    1. The formation of prothrombinase.
    2. The formation of thrombin.
    3. The formation of fibrin.
  • / POST–PHASE
17
Q

explain the PRE-PHASE

A
  • Since, platelet clotting does not help in stopping of blood bleeding from high pressure vessels, processes may realize to continuation by plasmic coagulation.
    So we call platelet coagulation as pre-phase of plasmic coagulation.
18
Q

explain the FORMATION OF PROTHROMBINASE

A

-During this phase the active enzyme complex, prothrombinase is formed, which will further activate prothrombin.
It proceeds by two pathways:
-1-EXTERNAL
-2- INTERNAL
The formation of prothrombinase is only possible by both of the pathway went to the utmost
1- INTERNAL pathway
Factor XII (hageman factor, contact factor ) is typically activated. It is called as “contact” because, it works only when a physical external influence (e.g. injury) happens.
Factor XII sets off a series of cascade proteins activation reactions that in turn activates factor XI(Antihaemophilic globulin C)
then factor IX( Antihaemophilic globulin B (Christmas factor) )
and then X (Autothrombin (Stuart prower factor)
2- EXTERNAL pathway
It is initiated by tissue damage.
Then factor III is released from the membrane of damaged cells of the vessel and surrounding tissues.
Factor III (tissue factor) goes on to activate factor VII.( Proconverting (stable factor))
- Finally, factor VIII (Antihaemophilic globulin A)
combines with factor IX( Antihaemophilic globulin B (Christmas factor) ) to form an enzyme complex
that activates factor X, ( Autothrombin (Stuart prower factor) leading to the common pathway.
- Factor VII Proconverting (stable factor) a goes on to activate factor X into factor Xa.
-Xa further forms as prothrombinase

19
Q

What is prothrombinase? What is it made up of?

A

It is a complex made up of:
some active plasmic factors (X, IX, VII);
7-Proconverting (stable factor)
9-Antihaemophilic globulin B
10-Autothrombin (Stuart prower factor)
active platelet factor (3) thromboplastin
and Ca2+ (IV) and phospholipids and some other factors, for example, Willebrand factor

20
Q

what is Willebrand factor

A

It is a large molecule, which acts as matrix for activation of prothrombin, following to this processes as next stage.

21
Q

explain the Prothrombinase general idea

A
  • is most multifactorial and lengthy process (5-10 min) compared to other stages, because it is completed only due to influence of both external and internal pathways.
    Also it will form only when all the factors are activated, and this may happens only under specific circumstances of critical mechanical influences on tissues, vessels and blood.
22
Q

what conclusion that appearance of Prothrombinase ?

A

its indicates the occurrence of injury.

23
Q

explain FORMATION OF THROMBIN ?

A
  • The appearance of prothrombinase results into the starting of the next phase of coagulation – the formation of thrombin from prothrombin in the presence of calcium ions (Ca2+).
  • If prothrombinase is formed, organism “understands” that the vessel has been damaged. Therefore, the subsequent phases proceed quickly.
  • Thrombin formation process lasts 2-5 s.
24
Q

explain Formation of fibrin ?

A
  • In the third phase – the formation of fibrin from fibrinogen. Initially, soluble fibrin monomer is formed under the influence of thrombin. Thrombin also activates the fibrin-stabilizing factor (XIII). Then, with the participation of calcium ions, a soluble fibrin polymer is formed, which is then converted by the fibrin-stabilizing factor into an insoluble fibrin polymer. In such a fibrin network, blood cells, in particular erythrocytes, settle and a red blood clot forms, which clots the wound
  • At the stage of soluble fibrin thromb it is
    1) loose,
    2) with a high plasma content,
    3) the blood formed elements in it retain their structure,
    4) it is poorly fixed to the site of damage and can easily be washed off by blood flow or removed mechanically
25
Q

what is retraction and how its happened ?

A
  • its Transferring from soluble to insoluble fibrin
    It happens under influence of not only XIII(Fibrinase (Fibrin stabilizing factor, Laki-Lorand factor) but also platelet factor no.6 (Thrombostenin) and Ca2+.
    -Factor XIII is an actinomyosin complex, which, like muscle sarcomere, in the presence of Ca2+, is contracted and significantly reduces its length.
26
Q

explain the conditions of plasmic thromb ?

A
  1. Primary thromb. It is loosely fixed on injury,
    with high plasma content,
    can easily be washed off by blood flow or removed mechanically.
  2. Secondary thromb. It is hardly fixed on injury,
    with no plasma content,
    cannot be removed at any case.

Result of plasmic coagulation – formation of fibrin thromb.

27
Q

what is Result of plasmic coagulation

A

– formation of fibrin thromb.

28
Q

explain POST-PHASE

A
  • Includes the processes of fibrinolysis and vessels recanalization.
    Cause the normal condition of vessel is its passability of blood the thromb finally must be removed. This realises by process of restoration of damaged vessel by lysis of fibrin. It is lengthy process which lasts for somewhere 10 days or more.

-They may call this process as the post-phase but need to understand that it is not a process of coagulation. Coagulation finishes by appearance of secondary fibrin thromb.

29
Q

what is the FACTORS INCREASING COAGULATION

A
  1. Vitamin K: with the presence of vitamin K only majority of plasmic factors are synthesised in liver. Vitamin K containing drugs increases plasmic factor synthesis. And the result is increased coagulation
  2. Calcium: calcium is one of the plasmic factor (IV).
    Calcium is widely contained in many drugs. Applying them, you should always take into account its great (!!!) influence on increasing of blood coagulation and a risk of thrombosis

3.Hypoxia, hypercapnia, acidosis and temperature increase:
all this processes and changes realize during physical stress, and any physical stress is a risk of vessels damage.

30
Q

what is the Thrombosis ?

A

Thrombosis occurs when blood clots block your blood vessels. There are 2 main types of thrombosis: Venous thrombosis is when the blood clot blocks a vein. Veins carry blood from the body back into the heart. Arterial thrombosis is when the blood clot blocks an artery.

31
Q

what is the FACTORS DECREASING COAGULATION ?

A
  1. Heparin and Plasmin: strong anticoagulant drugs.
  2. Antibiotics: increases danger of microcirculatory haemorrhage.
  3. Aspirin: also increases danger of microcirculatory haemorrhage.
  4. Hirudin : obtained from leechs.
  5. Decrease in temperature: because of less activity of enzymes.
  6. Alkalosis: the same reason.