Haemostasis and Blood Coagulation I

Question 1

define Haemostasis.

Answer 1

sequence of responses that stops bleeding when vessels are injured

Question 2

state the three mechanisms to prevent blood loss.

Answer 2

– Vascular spasm
– Platelet plug formation
– Blood clotting (coagulation)

Question 3

The vascular spam.

Answer 3

during blood vessel injury- smooth muscle in the wall contract-reduces blood flow from the ruptured vessel

Question 4

what causes contraction during vessel injury?

Answer 4

Contraction is due to local myogenic spasm; local autacoid (hormone-like) factors from damaged tissues, vascular endothelium, and blood platelets; nervous reflexes (initiated by pain impulses).

Question 5

which substance is released by the platelets in small vessels to cause vasoconstriction?

Answer 5

Thromboxane A2

Question 6

define Autacoid

Answer 6

are biological factors which act like local hormones, have a brief duration, and act near their site of synthesis

Question 7

A small cut in the blood vessel is sealed by a ———-rather than a blood clot.

Answer 7

platelet plug

Question 8

The platelets cytoplasm consists of :

Answer 8

a) contractile proteins (actin, myosin & thrombosthenin)

b) endoplasmic reticulum&Golgi apparatus(synthesize various enzymes & store Ca2+ ions)

c) mitochondria & enzyme systems (form ATP & ADP; prostaglandins)

d) fibrin-stabilizing factor

e) growth factor(causing vascular endothelial cells, vascular smooth muscle cells, & fibroblasts to multiply & grow cellular growth  helps repair damaged vascular walls).

Question 9

———————–a group of lipids with hormone-like actions that your body makes primarily at sites of tissue damage or infection.
Prostaglandins are produced by the enzyme systems.

Answer 9

prostaglandins

Question 9

Platelet cell membrane surface have:

Answer 9

Glycoproteins: i) repulses/resist adherence to normal endothelium
ii) causes adherence toinjuredareas of the vessel wall, especially to injured endothelial cells, and even more so to any exposed collagen from deep within the vessel wall.

b) Phospholipidsthat activate multiple stages in the blood-clotting process.

Question 10

The Haemostatic event

Answer 10

Plateletscontacts damaged vascular surface platelets begin to swell their contractile proteins contract forcefully cause the release of granules containing multiple active factors they become sticky they adhere to collagen in the tissues & to a protein calledvon Willebrand factor(vWF=leaks from plasma into traumatized tissue).

Question 11

what does the platelet surface glycoproteins bind to?

Answer 11

von Willebrand factor(vWF) in the exposed matrix below the damaged endothelium.

Question 12

Then platelets secret——and——— and their enzymes form———–

Answer 12

a). ADP.
b). Platelet -activating factor.
c). thromboxane A2.

Question 13

When more and more platelets accumulate on the damage vessel they form a——

Answer 13

platelets plug.

Question 14

Once platelets plug is formed, they are stabilized by——–then ——–occurs

Answer 14

fibrin clot
clot retraction

Question 15

Factors that prevent blood clotting in normal vascular system.

Answer 15

More than 50 substances causing/affecting coagulation are found in blood & tissues

Some promote coagulation> procoagulants

Some inhibit coagulation> anticoagulants

Blood coagulation depends on the balance of both

Anticoagulants normally predominate in blood stream

Hence blood doesn’t coagulate while circulating in blood vessels

In vessel rapture, procoagulants override anticoagulants at area of tissue damage
Then a clot develops

Question 16

Blood coagulation factors in Ruptured blood vessel

Answer 16

1. Thrombin
2. Fibrin
3. Plasmin
   Thrombin Formation

Question 17

3 essential steps that place in clotting

Answer 17

1. Blood vessel injury  cascade reaction resulting in Prothrombin activator
2. Prothrombin activator catalyzes conversion Prothrombin (in presence of Ca2+) to thrombin
3. Thrombin acts as enzyme to convert fibrinogen to fibrin fibers.

Question 18

Fibrin formation

Answer 18

1. Fibrinogen= plasma protein, prod. by liver.

*Thrombin (enzyme) acts on fibrinogen  fibrin monomer  polymerize with other fibrin monomer  fibrin fiber  polymerized to longer fibrin fibers.
Fibrin molecules held by weak hydrogen bond & not cross-linked
2. Fibrin clots are weak & get stabilized by fibrin-stabilizing factor= cross-linkages.

*Fibrin-activating factor is activ. by thrombin  operate as enzyme to form covalent bonds btwn more & more fibrin monomer molecule  multiple cross-linkages btwn adjacent fibrin fibers adding strength to fibrin meshwork

Question 19

Blood clot and Retraction

Answer 19

Blood clot= fibrin threads, trapped RBCs, platelets, plasma
Clot retract.=clot contracts expresses serum (since fibrinogen & other clotting factors have been removed)—-Failure of clot retraction Platelet deficiency
*Platelet attached to fibrin fibers in clot release fibrin-stabilizing factors
*Platelets activ. platelet contractile proteins strong contraction by platelets attached to fibrin compresses fibrin meshwork.
*This platelet contract. is activ. by thrombin + Ca2+
*Edges of broken vessels pull together= further contributing to hemostasis.

Question 20

define Serum

Answer 20

is the fluid that comes from in the cut after the blood ha oozed out.

Question 21

Positive feedback of clot formation:

Answer 21

Blood clotting at injury site extends into the surrounding blood  positive feedback to promote more clotting.

Thrombin  promote clot formation

Thrombin  prothrombin  more thrombin

Thrombin  acts on blood-clotting factors formation of prothrombin activator

Thrombin  increase prod. of factors VIII, IX, X, XI, and XII and aggregation of platelets.

The blood clot continues to grow until blood leakage ceases.

Question 22

The extrinsic pathway for initiating clotting:

Answer 22

The extrinsic pathway for initiating the formation of prothrombin activator begins with a traumatized vascular wall or traumatized extravascular tissues that come in contact with the blood.

This condition leads to the following steps:

1.Release of tissue factor:

Traumatized tissue releases a complex of several factors calledtissue factorortissue thromboplastin (consist of from the membranes of the tissue) plus alipoprotein complexthat functions mainly as aproteolytic enzyme.

Question 23

The extrinsic pathway for initiating clothing :

Answer 23

2.Activation of factor X—dependent on factor VII and tissue factor:

Tissue factor complexes with blood coagulation factor VII in the presence of calcium ions activ. factor X activated factor X(Xa).

3.Effect of Xa to form prothrombin activator—dependent on factor V:

Factor Xa combines with tissue phospholipids (released by tissue factors or by platelets) as well as with factor V, to form the complex calledprothrombin activator.

In the presence of Ca2+, prothrombin thrombin, and the clotting process takes place as already explained.

Question 24

The intrinsic pathway for initiating clotting:

Answer 24

1.Blood trauma causes  activation of factor XII  release of platelet phospholipids:

Trauma to the blood or exposure of the blood to vascular wall collagen alters two important clotting factors in the blood:

a) Factor XII

b) Platelets

When factor XII is disturbed, such as by coming in contact with collagen, becomes activated factor XII (XIIa).

Simultaneously, the blood trauma also damages the platelets because of adherence to collagen; this releases platelet phospholipids that contain the lipoprotein calledplatelet factor 3.

2.Activation of factor XI.
Factor XIIa activ. factor XI  factor XIa, This reaction also requireshigh-molecular-weight kininogen(HMWK) and is accelerated by prekallikrein.

Activation of factor IX by activated factor XI.
Factor XIa activ. factor IX  factor IXa.
4.Activation of factor X—role of factor VIII.
Factor IXa + factor VIIIa + platelet phospholipids + factor III from the traumatized platelets, activ. factor X  factor Xa.

Factor VIII is the factor that is missing in a person who has classichemophilia, so it is calledantihemophilic factor.

Action of activated factor X to form prothrombin activator—role of factor V.

Factor Xa combines with factor V and platelet or tissue phospholipids to form the complex calledprothrombin activator.

The prothrombin activator, in turn, initiates the cleavage of prothrombin to form thrombin within seconds, thereby setting into motion the final clotting process.

Question 25

The role of Ca2+ in intrinsic and extrinsic pathways:

Answer 25

Promotion or acceleration of all blood-clotting factors.

No Ca2+ no blood clotting by either pathway

Question 26

the plasmin formation

Answer 26

A plasma protein Plasminogen, when activ. plasmin (fibrinolysin)
Plasmin = digest fibrin fibers + protein coagulants (fibrinogen, factors V, VIII, XII, prothrombin).

When clot is formed large [plasminogen] is trapped inside clot

Damaged tissue + vascular endothelium release tissue plasminogen activator (t-PA) very slowly.

When bleeding stops t-PA converts plasminogen plasmin removes blood clot.

Question 27

Conditions for Excessive Bleeding in Humans:

Answer 27

Deficiency of vit K
Less prothrombin, factor 7,9,19

Question 28

Production of which factors is increased by thrombin

Answer 28

8,9,10,11,12

Question 29

Haemophilia

Answer 29

genetic clotting of blood unproperly

Question 30

Haemophelia A
Haemophilia B

Answer 30

Factor 8 deficiency
Factor 9 deficiency

Question 31

Thrombycytopenia

Answer 31

Less platelests i the blood due to infections

Question 32

Extrinsic pathway factors

Answer 32

5,7,10

Question 33

Plasmin formation factors

Answer 33

V, VIII, XII

Question 34

What removes blood clot

Answer 34

Plasmin

Question 35

What converts plasminogen to plasmin

Answer 35

tissue plasminogen activator (t-PA)

Question 36

Conditions for excessive bleeding

Answer 36

Vitamin K deficiency
Haemophilia
Thrombocytopenia (decrease in number of platelets due to infections)