HEMATOLOGY - PLATELETS AND ITS FUNCTIONS

1. PLATELETS

2. CHARACTERISTICS OF PLATELETS
• Platelets are DISC shaped.
• Platelets are formed in bone marrow by FRAGMENTATION of
MEGAKARYOCYTES.
• Normal plasma concentration - 150,000 to 300,000 / microlitre.
• Half life - 8-12 days.

3. CHARACTERISTICS OF
PLATELETS
CYTOPLASM CONTAINS ACTIN ,
MYOSIN ,
THROMBOSTHENIN
(contractile proteins)
contract platelets

4. CHARACTERISTICS OF
PLATELETS
CYTOPLASM CONTAINS Residuals of
GOLGI BODIES
AND
ENDOPLASMIC RETINACULUM
synthesis enzymes and store Ca2+

5. CHARACTERISTICS OF
PLATELETS
CYTOPLASM CONTAINS MITOCHONDRIA AND ENZYMES
ATP and ADP production

6. CHARACTERISTICS OF
PLATELETS
CYTOPLASM CONTAINS Enzymes for PROSTAGLANDIN
synthesis
prostaglandin is local hormone.

7. CHARACTERISTICS OF
PLATELETS
CYTOPLASM CONTAINS FIBRIN STABILIZING PROTEINS

8. CHARACTERISTICS OF
PLATELETS
CYTOPLASM CONTAINS GROWTH FACTORS
FOR
vascular endothelial cells
vascular smooth muscles
fibroblasts

9. CHARACTERISTICS OF
PLATELETS
CELL
MEMBRANE
SURFACE
CONTAINS coat of GLYCOPROTEIN
THAT
REPEL normal endothelium
ADHERE injured vascular wall

10. CHARACTERISTICS OF
PLATELETS
CELL
MEMBRANE
SURFACE
CONTAINS PHOSPHOLIPIDS ,
that
ACTIVATES
multiple stages of blood clotting.

11. HEMOSTASIS
prevention of blood loss

12. 4 main steps of hemostais
①Vascular contriction
②Platelet plug formation
③Blood clot formation
④Fibrous tissues grows into blood clot

13. Vascular contriction
• when blood vessel ruptures, trauma causes smooth muscle of vessel
wall to contract.
• contraction of vessel reduces the blood flow.
• Contraction results due to
• local myogenic spasm
• local autacoid factors
• nervous reflexes

14. Platelet plug formation
• PLATELETS then changes their physical characteristics on exposure to
damage vessel
①they swells
②they develops irridating pseudopodia
③contraction of contractile proteins , that releases the granules
containg activating factor for clotting.
④they become sticky , so they attaches to collagen and Vol
willebrand factor.
⑤they secretes ADP
⑥synthesis Thromboxane A2

15. Platelet plug formation
• ADP and Thromboxane a2
• act on nearby platelets and activates them,
• additional activated platelets stick over those originally activated platelets.
• At the site of puncture,
• more and more platelet attaches to form platelet plug.
• then fibrin thread form and attaches platelets more tightly.

16. Blood clot formation
• ACTIVATOR SUBSTANCES are released from,
• traumatized vessel wall
• platelets
• blood proteins
• Activator substances, adhere to the traumatized vessel then initiate
clotting process.

17. Fibrous organization or Dissolution of clot
• once blood clot form , it can
invaded by fibroblasts
usually when clot is formed
in a small hole,
then connective tissue
fromation occurs.
dissolve
when clot are formed at
those places where it was
not needed

18. BLOOD COAGULATION

19. Basic theory
• BODY have procogulants and anticoagulants.
• normally anticoagulant are more, so blood flows freely in vessels
without clotting.
• in INJURED VESSEL , procoagulants become more , so clot formation
happens.

20. GENERAL MECHANISM
• Formation of PROTHROMBIN ACTIVATOR in response to injured vessel
wall.
prothrombin thrombin
PROTHROMBIN ACTIVATOR
fibrinogen fibrin fibres
THROMBIN ( Ca2+)

21. APPLIED
• PROTHROMBIN CONCENTRATION - 15mg/dl.
• Formed in liver by using VITAMIN K
• PROTHROMBIN CONCENTRATION DECREASES and lead to
bleeding tendencies :-
• deficiency of VITAMIN K
• liver diseases

22. Conversion of fibrinogen to fibrin
• Form in liver.
• Plasma concentration : 100 to 700 mg/dl
• normally it doesn't leaks to interstitial fluid.
• THROMBIN act on FIBRINOGEN and convert it to FIBRIN
MONOMERS,
• Fibrin monomers polymerize and form fibrin polymer.
• FIBRIN POLYMER constitute the RETICULUM of blood clot.

23. Conversion of fibrinogen to fibrin
initially fibrin monomers are loosely bond with weak hydrogen bonds.
FIBRIN - STABILIZING FACTOR activated by thrombin.
formation of srong covalent bond btween fibrin monomers and cross linking
between fibres,
this give tremendously 3 dimensional strength to fibrin meshwork.

24. COMPOSITION OF CLOT
FIBRIN MESHWORK,
entrapping ,
 blood cells
 platelets
 plasma
fibrin fibres adhere to damage vessels and stop blood loss.

25. CLOT RETRACTION
-AND EXPRESSION OF SERUM.
clot begins to contracts
expresses most of the
fluid with in 20 to 60
minutes known as SERUM
With in few
minutes of clot
formation,

26. CLOT RETRACTION
-AND EXPRESSION OF SERUM.
PLATELETS
ARE
NECESSARY,
they bonds different
fibres together
release procogulants
like fibrin stabilizing
factor
platelets contributes to clot
retraction by activating
CONTRACTILE PROTEINS
 thrombosthenin
 actin
 myosin
ALSO ACTIVATED BY
THROMBIN WITH Ca2+

27. CLOT RETRACTION
-AND EXPRESSION OF SERUM.
CONTRACTION
OF CONTRACTILE
PROTEINS
Strong contraction of platelets
spicules attached to fibrins
that compresses fibrin
meshwork into small mass
CLOT RETRACTS
edges of broken vessel come
together leading to hemostatis
1
2
3
4

28. POSITIVE FEEDBACK OF CLOT FORMATION
Thrombin have proteolytic effect on fibrinogen as well as other
clotting factor like:
 thrombin act on PROTHROMBIN
 thrombin act on FACTORS RESPONSIBLE FOR FORMATION OF
PROTHROMBIN ACTIVATOR
when critical
amount of clot
formed
it causes more and more
blood clot to form by
formation of more and
more thrombin.
continues untill the
blood leakage
ceases

29. INITIATION OF COAGULATION
INITIATED BY
TWO PATHWAYS
EXTRINSIC PATHWAY
INTINSIC PATHWAY
FORMATION OF
PROTHROMBIN
ACTIVATOR
 trauma to vascular wall
 trauma to blood
 exposure of blood to
damaged endothelial
cell or to collagen

30. EXTRINSIC PATHWAY FOR INITIATING
CLOTTING
TRAUMA TO VASCULAR WALL
tissue factor/ tissue thromboplastin
VII
VIIa
X
Xa
Ca++
V
Ca++
prothrombin
activator
prothrombin
thrombin
activates
platelet
phospholipids

31. ENTRINSIC PATHWAY FOR INITIATION OF
CLOTTING
BLOOD TARUMA OR CONTACT WITH COLLAGEN
XII XIIa
HMW kininogen, prekalikrein
XI XIa
Ca++
IX IXa

32. IXa
IX
VIIIa
Ca++
TISSUE PHOSPHOLIPDS
(released from platelets on
exposure to trauma)
VIII
X Xa
prothrombin activator
V
Va
Ca++
prothrombin thrombin
Ca++
thrombin
thrombin

33. PREVENTION OF BLOOD CLOTTING IN
NORMAL VASCULAR SYSTEM.
Endothelial surface factors
smoothness of endotethelial surface
layer of glycocalyx on the endothelium
Protein bound with endothelial membrane , Thrombomodulin
THROMBOMODULIN
binds thrombin
Thrombomodulin-
thrombin complex
activates plasma
protein PROTIEN C
PROTEIN C inactivates factor Va and VIIIa

34. PREVENTION OF BLOOD CLOTTING IN
NORMAL VASCULAR SYSTEM.
• Antithrombin action of Fibrin and antithrombin III
During formation of clot,
90% of fibrin is absorbed
by fibrin fibres
it prevent spread of
thrombin and formation
of clot
remaining 10%
thrombin combines
with Antithrombin III
which further block
the effects of thrombin

35. • HEPARIN
• COMBINES with Antithrombin III , increases the effectiveness by 100
to 1000 times.
PREVENTION OF BLOOD CLOTTING
IN NORMAL VASCULAR SYSTEM.
HEPARIN - ANTITHROMBIN III COMPLEX
remove several activated coagulation factors,
like XII,XI,X,IX

36. PREVENTION OF BLOOD CLOTTING
IN NORMAL VASCULAR SYSTEM.
Basophilic Mast cell
HEPARIN
produce largest quantities of HEPARIN
they are abundent near capillaries of lungs and liver
that prevent clotting in small capillaries allowing free flow of blood

37. • PLASMIN causes lysis of blood clots,
• Plasma proteins , contains euglobin called plasminogen , when
activated form plasmin
PREVENTION OF BLOOD CLOTTING
IN NORMAL VASCULAR SYSTEM.
PLASMIN DIGESTS
FIBRIN FIBRES
FIBRINOGEN
FACTOR V, VIII,XII
PROTHROMBIN

38. • Activation of plasminogen to form plasmin then lysis of clots.
PREVENTION OF BLOOD CLOTTING
IN NORMAL VASCULAR SYSTEM.
during clot formation,
plasminogen is
entrapped in clot.
injured tissue very slowly release
TISSUE-PLASMINOGEN ACTIVATOR
(t-PA)
few days later when clot stops bleeding,
t-PA converts plasminogen to plasmin
important function of the plasmin system, to remove minute clots,
from millions of tiny peripheral vessels

39. DISEASES RELATED TO BLOOD COAGULATION
• VITAMIN K DEFICIENCY
• HEMOPHILIA
• THROMBOCYTOPENIA
• DISSEMINATED INTRAVASCULAR COAGULATION

40. VITAMIN K DEFICIENCY
• Decrease in prothrombin
factor VII
factor IX
factor X
blood clotting factors are produced in liver,
Liver diseases decreases clotting factors and increases bleeding
tendencies

41. Vit K + Liver carboxylase
VITAMIN K DEFICIENCY
adds carboxyl group to the
glutamic acid residues on
clotting factors:
PROTHROMBIN
Factor VII, IX, X
PROTEIN C
AFTER adding carboxyl group on glutamic
acid residues Vit K oxidized (inactive)
VITAMIN K EPOXIDE REDUCTASE
COMPLEX 1
(VKORc1)
again activates vitamin K ( reduced Vit K)

42. • Vitamin K synthesis is done by gut flora
• then absorption occurs with absorption of fat.
• in case of GIT disease , Vit K absorption decreases and deficiency can
occur.
• failure of liver to secreate Bile in GIT , decreases absorption of fat, hence
decrease Vit k absorption.
VITAMIN K DEFICIENCY
Vit K injection is administered before major surgeries to prevent
exessive bleeding tendencies

43. HAEMOPHILIA
• Usually occurs in males
• X linked recessive disorder.
• Deficiency of Factor VIII , Known as CLASSICAL HEMOPHILIA ,
• Also known as HEMOPHILIA A
• Can also occur due to deficiency of Factor IX.
• Patient is normal utill have any trauma.

44. HAEMOPHILIA
FACTOR VIII
SMALL
COMPONENT
LOST
HAEMOPHILIA A
LARGE
COMPONENT
LOST
VON WILLEBRAND
DISEASE

45. THROMBOCYTOPENIA • Deficiency of platelets.
Lack of repair of
vascular damages
in small vessel.
Small punctate
hemorrhages
occurs in all body
tissues
Small purplish
blotches appears
on skin
Known as
THROMBOCYTOPENIC
PURPURA

46. THROMBOCYTOPENIA
BLEEDING usually occurs
when
Platelets < 50,000
If less than 10,000 platelets
,
It would be lethal.
TREATMENT
1. BLOOD
TRANSFUSION
2. SPLENECTOMY

47. THROMBOEMBOLIC CONDITION
Thrombus
Abnormal clot
that develop in
vessel wall
Sticked to the
vessel wall
Continues
strike by
flowing blood
It break off ,
then known as
embolus.

48. THROMBOEMBOLIC CONDITION
EMBOLI
(free floating clot in blood)
IF ORIGINATE IN LEFT
SIDE OF HEART
Plug arterioles in brain ,
kidney.
IF ORIGINATE IN RIGHT
SIDE OF HEART
Plug arterioles in lungs causing
pulmonary artries embolism

49. • Rough endothelial surface of Blood vessel.
• Arteriosclerosis
• Infection
• Trauma
THROMBOEMBOLIC CONDITION- CAUSES
• When blood flow slow, as in small capillaries
t-PA is used for treating intravascular clot in case of stroke ,
coronary artery blockage, etc.

50. Femoral venous thrombosis leading to
Massive pulmonary emobolism
immobile bed
ridden patient
blood flow is
slow in leg veins
for hours
clot form in
leg vein
that thrombus can be upto iliac vein or
IVC
SOMETIMES , a part of thrombus breaks
in the direction of moving blood.
emobli flows to right side of heart, can
cause blokage of pulmonary artries
leading to "MASSAIVE PULMONARY
EMOLISM"
1
2
3
4
5
6

51. Massive pulmonary
emobolism
IF both pulmonary artries are
blocked , then immidiate
death can occur.
TREATMENT
t-PA theray