mechanism of hemostasis & function of the platelets Flashcards

1
Q

def the natural hemostasis

A

is the spontaneous prevention of blood loss by physiological process . it effective in stopping bleeding from small vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

list mechanisms of natural hemostasis

A
  1. local vasoconstriction
  2. formation of temporary platelet plug (1ry hemostasis)
  3. formation of definitive blood clot (2ry hemostasis)
  4. repaired of injured blood vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what’s the role of local VC in hemostasis?

A

contraction of the injured vessel slows the flow of blood causing dec blood loss .

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what’s the mechanism that stimulate local VC ?

A
  1. nervous reflex :
    induced by pain impulses due to trauma
  2. local myogenic spasm :
    induced by direct damage to vascular wall
  3. chemicals released by endothelial cells and platelets :
    thromboxane A2 & serotonin , which cause VC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

formation of temporary platelet plug (1ry hemostasis) occur through ………………..

A

platelet adhesion , platelet activation & platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

illustrate the mechanism of 1ry hemostasis

A
  1. damage of blood vessels causes disruption of endothelium and exposure of the underlying collagen
  2. the platelet adhere to the collagen (platelet adhesion)and such adhesion is potentiated by von Willebrand factor
  3. binding of platelets to the collagen induces platelet activation
  4. the activated platelets change their characteristic , they swell , become irregular in shape with numerous irradiating pseudopods and become sticky
  5. they secrete ADP and thromboxane A2 which in turn act on nearby platelets activate them and more platelet aggregation occur forming platelet plug
  6. the plug is more effective in preventing blood loss in small vessel
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

illustrate the role of aggregated platelet plug

A

it physically seals the break in the vessels.
1. the actin-myosin protein complex within the aggregating platelet contract to compact and strengthen the originally loose plug
2. the chemicals released from the platelet plug include several powerful vasoconstrictors as , serotonin, epinephrine, & thromboxane A2 which induce profound constriction to reinforce the initial self induced vascular spasm
3. it releases other chemical substances that enhance blood coagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

list important chemical affecting platelet aggregation

A
  1. adenosine diphosphate (ADP)
  2. von Willebrand factor (VWF)
  3. thromoxane A2 (TxA2)
  4. prostacyclin (PIG2)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what’s the role of ADP in platelet aggregation ?

A

it cause the surface of nearby circulating platelets to become sticky so that they adhere to the first layer of aggregated platelets .
more ADP is released from newly aggregated platelets , which cause more platelets to aggregate (+ve feed back ) building up a plug of platelets.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what’s the role of VWF in platelet aggregation?

A

-it’s a protein secreted by endothelial cells
- form bridge between vessel wall & the first layer of platelets
- it binds to collagen, and then platelet bind to it , so it facilitates the adherence of platelets to damaged vessel wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what’s role of TxA2 in platelet aggregation ?

A
  • adherence platelets to collagen causes the conversion of arachidonic acid in the platelet plasma membrane to TxA2 which stimulate platelet aggregation and secretion of platelet granules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what’s role of PGI2 in platelet aggregation ?

A

the normal endothelium contains an enzyme that converts arachidonic acid intermediates into a specific prostaglandin (PGI2) that inhibits the platelet aggregation, so the platelet plug is limited to the defect and doesn’t spread along normal endothelium in both directions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

formation of blood clot or blood coagulation called ………….

A

2ry hemostasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what’s 2ry hemostasis?

A

it’s transformation of blood into a solid gel termed a clot or thrombus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

where the 2ry hemostasis occur?

A

around the original platelet plug when the plasma protein fibrinogen is converted to fibrin molecule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

in response to rupture of vessels , a complex cascade of chemical reactions occurs in the blood involving …………………………. clotting factor are ………………. enzymes which activate each other

A

-many blood coagulation factor (clotting factor)
- proteolytic

17
Q

the net result is formation of complex of activated substances called …………. that catalyze the conversion of …………to ………… which then convert ………to ………

A

-prothrombin activator
- prothrombin to thrombin
- fibrinogen to fibrin

18
Q
  • the fibrin is initially ………..
  • it’s converted to …….stabilized by ……
A
  • a loose mesh of interlacing strands
  • dense tight aggregate
    activated factor XIII & ca++
19
Q

the prothrombin activator is formed by …………………

A

the 2 clotting pathways :
extrinsic pathway
intrinsic pathway

20
Q

illustrate extrinsic pathway of blood clotting pathways

A
  1. it begin with trauma to the vascular wall and the surrounding tissue
  2. traumatized tissues release tissue or tissue thromboplastin (factor III)
  3. tissue factor (factor III) activate factor VII (VIIa)
  4. then the tissue factor combine with VIIa & ca++ = activate factor X (Xa)
  5. Xa with tissue phospholipid with active factor V = prothrombin activator
  6. prothrombin activator splits prothrombin into thrombin in presence of ca++ & tissue phospholipid
21
Q

illustrate the intrinsic pathways

A
  1. it begin :
    - in vivo with:
    I. exposure of the blood to collagen from traumatized vascular wall (causes activation of factor XII)
    II. trauma to the blood (causes damage to the platelet & release of platelet phospholipids.
    - in vitro with :
    III. when the blood becomes into contact with a wettable surface such as glass (cause activation of factor XII)
  2. these cause activation of factor XII
  3. XIIa activate XI, requiring (HMW-k) high molecular weight kininogen & is accelerated by prekallikrein
  4. XIa activate factor IX in presence of Ca++
  5. IXa acting with VIIIa , platelet phospholipids , ca++ to activate factor X
  6. then Xa combine with Va and phospholipid to form prothrombin activator as the last step in the extrinsic pathway
22
Q

illustrate the interaction between extrinsic & intrinsic pathways

A

1- both start at the same time
2- extrinsic is much more rapid
3- extrinsic potentiate intrinsic by :
- trace amount of thrombin formed by extrinsic activate factor V &VIII which are involved in the intrinsic pathway
- activated factor VII share in activation of factor IX
* factor V , VIII act as cofactor but don’t form link in the chain

23
Q

what’s role of vit K in blood coagulation?

A
  1. cause conversion of fibrinogen to fibrin
  2. acts in a +ve feed back to facilitate its own formation through the activation of factors VIII & V
  3. enhance platelet aggregation
  4. activate factor XIII to stabilize the resulting fibrin meshwork
  5. activates plasminogen to plasmin (anticlotting)
24
Q

list sources of vit K in the human body

A
  • diet
  • bacteria including human intestinal normal flora
25
Q

what’s the importance of vit K in blood coagulation?

A

necessary for liver formation of prothrombin , factor VII, IX ,X & protein C, S

26
Q

deficiency of vit K lead to deficiency of factors (VII, IX, X) & protein C, S from blood leads to ……………..

A

bleeding tendency

27
Q

within few minutes after the fibrin clot is formed it begins to ………. and a ……………………………… is squeezed out . as the clot retracts it pulls the edge of ……………..together.

A

-contract
-clear non coagulable fluid called serum
-the broken vessels

28
Q

what’s the role of platelet in clot retraction ?

A
  1. attach to fibrin fibers in such a way that they bond the fibrin fiber together
  2. platelet release fibrin stabilizing factor (XIII)cause more linking bonds between fibrin fibers
  3. platelet activate thrombasthenia, actin, myosin (contractile protein) cause contraction of platelet that are attached to fibrin . help in compress the fibrin meshwork
29
Q

illustrate clot dissolution (fibrinolysin)

A
  • after few days
  • allow blood flow to be reestablished after the clot has stopped the bleeding
  • allow tissue repair to take place
30
Q

illustrate repair the injured blood vessels

A
  • it’s eventual growth of fibers tissue into the blood clot to close the hole in the vessels permanently
31
Q

illustrate the function of platelets

A
  1. formation of hemostatic plug
  2. platelet plug release chemicals (platelet release reaction) :
    - ADP = platelet aggregation
    - serotonin, epinephrin, & TxA2 = VC
    - platelet factor 3 (PF3)
  3. stabilization of blood clot as platelets have cytoplasmic granules contain fibrin stabilizing factor (factor XIII)
  4. induce clot retraction
  5. release of platelet derived growth factor (PDGF) that stimulates wound healing