Platelets are cell fragments that help form blood clots to prevent or stop bleeding. They are produced through fragmentation of large bone marrow cells called megakaryocytes. Platelets contain granules with substances important for coagulation like fibrinogen and ADP. Platelets circulate freely but activate and aggregate at sites of injury to initiate clot formation through hemostasis, a process with 5 stages: vessel constriction, platelet plug formation, coagulation, clot retraction, and clot dissolution. Disorders can cause inappropriate clotting or bleeding due to problems with platelet or coagulation factor production, function, or clearance.

1. Platelets
PREPARED BY:
MARIA CARMELA L. DOMOCMAT, RN, MSN

2. Platelets (Thrombocytes)
o Platelets are not complete cells, but fragments of
large cells called megakaryocytes.
o very small, colorless cell fragments (2-4 microns in
diameter)
o enclosed in a membrane but have no nucleus and
cannot reproduce
o have mitochondria and enzyme system (enzyme –
needed for synthesis of prostaglandin)

3. o contains 2 types of granules
alpha (ά)granules
• express P-selection on their surface:
contains fibrinogen, fibronectin, factors V
and VIII, platelet factor 4 (heparin-binding
chemokine), platelet-derived growth factor
(PDGF), transforming growth factor-alpha
(TGF- ά)
gamma (δ)granules or dense granules
• contain ADP and ATP, ionized calcium,
histamine, epinephrine

4. o must be adequate in number and
function in order to participate
optimally in hemostasis
o normally circulate as individual
cell-like structure, not attached
to each other, suspended in plasma,
and do not clump together until
activated

5. Functions
o help to prevent or stop bleeding, a
process called hemostasis
o Initiate contraction of damaged blood
vessels to minimize blood loss
o Form hemostatic plugs in injured blood
vessels to help stop bleeding
o Along with plasma, they provide
materials that accelerate blood clot
formulation, or coagulation

6. Hematopoiesis: Blood Cell Formation

7. Formation
bud off from megakaryocytes
giant multinucleate bone marrow cells derived from the
myeloid stem cell line
stem cell
Hemotocytoblast
Megakaryoblast
Promegakaryocyte
Megakaryocyte
megakaryocyte: large multilobed nucleus
platelets
platelets: anucleated parts of megakaryocyte cytoplasm

9. o develop by endomitosis
o Formation of platelets involves repeated mitoses
of megakaryocytes without cytokinesis.
Megakaryocytes undergo mitosis but not
cytokinesis thus cell does not divide
into 2 daughter cells
• Without cytokinesis – cell does not divide into
2 daughter cells but expands to accommodate the
doubling of its DNA (nuclear) content and
breaks up into fragments known as platelets

11. Blood Components: Platelets
Coagulate, form plug, prevent blood loss
Formed by fragmentation from megakaryoctyes
Figure 16-10c: Megakaryocytes and platelets

12. o newly formed platelets that are
released from bone marrow spend up
to 8 hours in the spleen before
being released into the blood
o Life Span: 10 days

13. Regulators Of Platelet Production
includes:
• GM-CSF (granulocyte-macrophage colony-
stimulating factor)
• Thrombopoietin
o source: kidney, liver, smooth muscle, bone
marrow
production and release is regulated
by the number of platelets in
circulation
stimulate committed cells and further
stages of differentiation

14. Destruction (Hemolysis)
o Senescent platelets – phagocytosed
by neutrophils and monocytes if
circulating freely
If part of thrombus or clot - phagocytosed
by neutrophils and macrophage
Can be removed also by tissue macrophages of
the MPS (mononuclear phagocyte system) in
the liver or spleen

15. Hemostasis

16. Hemostasis
Refers to the stoppage of bloodflow
• Designed to maintain integrity of
vascular compartment
• Normal
• when it seals a blood vessel to prevent blood
loss and hemorrhage
• Abnormal
• when it causes inappropriate blood clotting
or when clotting is insufficient to stop the
flow of blood from the vascular compartment

17. Control of hemostasis
o Endothelium – major site of hemostasis
o Despite the continual presence of
clotting factors and platelets in
circulation, blood normally remains
fluid
o 2 properties of normal vascular
endothelium prevent clotting
Smooth texture of endothelial lining
Negative charge of protein in endothelial cells
– which repel some negatively charged platelets
if clotting factors

18. Three hemostatic compartments

19. Damage to small blood vessels and capillaries
frequently occurs. When these vessels are damaged,
there are 5 basic mechanisms that promote
hemostasis or the stoppage of bleeding

20. 5 stages of Hemostasis
1.Vessel or vascular spasm -
(vasoconstriction at injured site)
2.Formation of the platelet plug
(plugging the hole)
3.Blood coagulation or development of an
insoluble fibrin clot (blood clotting
- complex mechanism)
4.Clot retraction
5.Clot dissolution

22. 5 stages of Hemostasis
1.Vessel or vascular
spasm(vasoconstriction at injured
site)

23. (1) Blood Vessel Spasm
• triggered by pain receptors, platelet release, or serotonin
• smooth muscle in vessel contracts

24. 5 stages of Hemostasis
1.Vessel or vascular spasm
2.Formation of the platelet plug
(plugging the hole)

25. (2) Platelet Plug Formation
• triggered by exposure of platelets to collagen
• platelets adhere to rough surface to form a plug

26. Platelet Plug Formation
14-28

29. Vasoconstriction & Plug Formation
Figure 16-12: Platelet plug formation

31. 5 stages of Hemostasis
1.vascular spasm
2.platelet plug
3.Blood coagulation or development of an
insoluble fibrin clot (blood clotting
- complex mechanism)

32. (3) Blood Coagulation
• triggered by cellular damage and blood contact with foreign
surfaces
• blood clot forms

33. Clot
Formation
& Vessel
Repair

34. Clot Stabilization
Prothrombin
Ca++
Fibrinogen
Fibrin
Polymerization

35. Blood Coagulation
14-29

36. Blood Coagulation
Extrinsic Clotting Mechanism
• chemical outside of blood triggers blood coagulation
• triggered by thromboplastin (not found in blood)
• triggered when blood contacts damaged tissue
Intrinsic Clotting Mechanism
• chemical inside blood triggers blood coagulation
• triggered by Hageman factor (found inside blood)
• triggered when blood contacts a foreign surface
14-30

37. Blood Clots
• After forming, blood clot retracts and pulls the edges of a broken vessel
together
• Platelet-derived growth factor stimulates smooth muscle cells and fibroblasts
to repair damaged blood vessels
• Plasmin digests blood clots
• thrombus – abnormal blood clot
• embolus – blood clot moving through blood
14-31

38. 5 stages of Hemostasis
1.vascular spasm
2.platelet plug
3.Blood coagulation
4.Clot retraction
5.Clot dissolution

39. 5 stages of Hemostasis
1.vascular spasm
2.platelet plug
3.Blood coagulation
4.Clot retraction
5.Clot dissolution

40. Dissolving the Clot and Anticoagulants
Bleeding stopped
Vessel repair
Plasmin
Fibrinolysis
Clot dissolved

41. Dissolving the Clot and Anticoagulants
Figure 16-14: Coagulation and fibrinolysis

45. Prevention of Coagulation
• The smooth lining of blood vessels discourages the accumulation
of platelets
• As a clot forms, fibrin absorbs thrombin and prevents the reaction from
spreading
• Antithrombin interferes with the action of excess thrombin
• Some cells secrete heparin
14-32

46. Coagulation and Disease
Hemophilia
Cardiovascular Diseases
Key problem – clots block undamaged blood vessels
Anticoagulants prevent coagulation
Keep platelets from adhering
Prevent fibrin coagulation
"Clot Busters": Prevent further clotting
Speed fibrinolysis
Limit tissue damage (heart, brain…)

47. Factor Function Coagulation disorders in children Incidence
I: Fibrinogen Afibrinogenemia, 0.1 x 106
hypofibrinogenemia
II: Prothrombin Hypoprothrombinemia 0.1 x 106
III: Tissue thromboplastin
IV: Calcium divalent cation; a cofactor for most of the enzyme-
activated processes required in blood coagulation;
enhances platelet aggregation and makes RBCs clump
together
V: Proaccelerin Parahemophilia, Factor V 0.1 x 106
deficiency
VI: discovered to be an No factor VI is involved in coagulation -
artifact
VII: Proconvertin Factor VII deficiency 0.1 x 106
VIII: Anithemophilic combined with von Willebrands factor help platelets Hemophilia A, von Willebrand 30-40 x 106
adhere to capillary walls in areas of tissue injury disease
IX: Plasma thromboplastin essential in common pathway between intrinsic and Hemophilia B 3-4 x 106
component (Christmas extrinsic clotting cascades
factor
X: Stuart-Power factor Factor X deficiency 0.1 x 106
XI: Plasma thromboplastin Hemophilia C, PTA deficiency 0.1 x 106
antecedent (PTA)
XII Hageman factor critically important in intrinsic pathway Hageman trait 0.1 x 106
XIII Fibrin-stabilizing assist in forming links among fibrin threads to form a Factor XIII deficiency 0.1 x 106
factor strong fibrin clot

48. Laboratory tests

49. Peripheral blood smear

50. platelet count
bleeding time
PT (extrinsic pathway)
activated thromboplastin time (intrinsic pathway),
thrombin time

51. Disorders of Hemostasis

52. Two main categories of disorders
of hemostasis
1. Inappropriate formation of clots
within the vascular system (i.e.,
thrombosis)
2. Failure of blood to clot in
response to an inappropriate
stimulus (i.e., bleeding)

53. Impaired hemostasis
Vitamin K deficiency
Liver disease

54. Thromboembolic Disorders
undesirable clotting
a. thrombus
b. embolus

55. Clotting Disorders
Coagulation disorders result from
defects in the clotting cascade or
fibrinolytic process. These
disorders may be inherited or
acquired
a. Hemophilias
b. Von Willebrand disease
c. Disseminated intravascular coagulation
(DIC)

56. Quantitative platelet disorders
a.Thrombocythemia
b.Thrombocytopenia

58. Petechiae and purpura

59. Large ecchymosis

60. Thrombus / embolus

61. Embolus /embolism

62. Hemarthrosis

63. Melena
Hematuria

64. Hematoma
Subdural Subungual