PLATELETS: ENGINEERS
FROM HUMAN BLOOD
DEFINITION: Platelets, or thrombocytes, are small,
colourless cell fragments in our blood that form clots and
stop or prevent bleeding.
SITE OF FORMATION: Produced are megakaryocytes,
they are produced in spongy bone marrow from
Pleuripotent Stem Cells.
SHAPE: Platelets appear as Colourless, flat, Spherical
discs. When stained in Leishmann stain they appear as
tiny, faint purple structures
SIZE: 2-4micrometres
NORMAL COUNT: 1,50,000-4,00,000/mm^3
LIFE-SPAN: 8-11 days
FATE: Destroyed by ‘Macrophage System’ of Spleen
CELLULAR STRUCTURE:
(i) Trilaminar, 6nm thick cell membrane
(ii) Cytoplasm contains Microtubules (to maintain
their shape), Microfilaments (useful in clot
retraction), and membrane-bound granules
(alpha & dense type)
PROPERTIES:
1. Platelet adhesion: When a blood vessel is injured,
platelets get adhered to the exposed collagen.
2. Platelet Activation: Adhesion to collagen gets them
activated, which causes changes in their shape, size,
and contact with other platelets, and also release
granules called ‘Platelet Release’
3. Aggregation: Activated factors release Ca++,
serotonin, ATP, fibrinogen and Platelet Activating
factor, all responsible for aggregation of platelets at
the site of injury.
3. Diagrammatic Representation:
FUNCTIONS:
!. Primary haemostasis
2. Transport and storage
3. Vasoconstriction
4. Secondary Haemostasis
5. Clot retraction
6. Repair of capillary endothelium
7. Defence mechanism
8. Growth factors
9. Regulation of local blood flow
1. Primary Haemostasis/Plug formation:
Platelets form a plug by adhesion and aggregation, which
seals the injured vessel temporarily.
2. Transport & Storage:
Platelets pick-up serotonin while passing through GIT
and store it until further usage
3. Vasoconstriction:
Platelets during breakdown release serotonin and
thromboxane A2 which promote vasoconstriction which
takes place along with platelet plug formation.
4. Secondary Haemostasis:
Platelets arrest bleeding by definitive clot formation with
the help of clotting factors I, V, XI, XIII, III, and IV.
5. Clot Retraction:
After the healing of injury, the volume of clot reduces,
and is called ‘Clot Retraction’ which is carried out by
thrombostenin and myosin present in platelets.
6. Repair of Capillary Endothelium:
Platelets adhere to injured surface of the blood vessel
start the healing process immediately, with the help of
‘Von Willebrand factor’. Absence of this factor causes
low platelet count and fragile platelets which causes
Haemorrhagic spots under skin on small capillaries;
leading to ‘Purpura’.
7. Defence mechanism:
By Phagocytosis, and by sometimes Agglutination,
platelets destroy carbon particles, protein complexes
and pathogens which bring about defence of the body.
8. Growth factors:
These factors in platelets help in multiplication of
endothelial cells and fibroblasts which helps in healing of
injured blood vessels.
9. Regulation of blood flow: This is brought about by
Endothelium-Derived Relaxing Factor (EDRF).
DIAGRAMMATIC REPRESENTATION OF FORMATION OF A BLOOD CLOT
(TYPICAL ACTION OF ACTIVE PLATELETS)
MALFUNCTIONS AND DISORDERS:
1. Thrombocytopenia
2. Aplastic anaemia
3. Pernicious anaemia
4. Splenomegaly
5. X-ray irradiation
6. Allergies
7. Idiopathic Thrombocytopenia
8. Drug actions
9. Thrombocytosis
10. Thrombocythaemia
11. Thromboasthermia
1. Thrombocytopenia: Decreased amount of or
production of thrombocytes due to excessive
destruction (possibly below 40,000/mm^3)
2. Aplastic Anaemia: Decrease in formation of new
thrombocytes
3. Pernicious Anaemia: Decreased production of
platelets due to lack of Vitamin B12 either due to
malasorbtion of inadequate intake
4. Splenomegaly: Excessive destruction due to
enlarged spleen.
5. X-ray irradiation: Megakaryocytes (which help in
formation and maturation of platelets) are damaged
and destructed by high radioactivity
6. Allergies: Allergies cause alterations in normal
functions and formations of platelets
7. Idiopathic Thrombocytopenia: It may be caused due
to presence of ‘Antiplatelet Antibodies’ in the blood.
8. Drug actions: Certain drugs like Quinine, Methyl
Dopa, Ethanol derivatives destroy platelets in large
amounts.
9. Thrombocytosis: It is the increase in platelet count
below the normal ranges (4,00,000 mm^3), mainly
due to conditions like leukaemia, Splenomegaly,
Polycythaemia Vera, Hodgkin’s disease, adrenaline
level imbalance, etc.
10. Thrombocythaemia: Explosive elevation in
levels of platelets (beyond 10,00,000 mm^3).
Usually a rare and medically attentive condition.
11. Thromboasthaemia: Also called as
‘Glanzmann’s Thromboasthaenia’ is the deficiency
in normal functioning of thrombocytes (meanwhile
levels remain optimal). [Further divided into type I,
II, III and Acquired Thromboasthaenia].
FUN FACTS:
(i) Endothelium of platelets also provide Anti-
clotting roles which inhibits action of clotting
factors by certain ‘Anti-clotting factors’ (e.g.
Thrombomodulin blocks the action of factors
VIII and V, Tissue factor pathway inhibitor
blocks the action of factor III, etc.)
(ii) Excessive number of platelets may contribute
to ‘Thrombosis’, which is the unwanted
coagulation of blood even in unharmed blood
vessels which may cause blockages in blood
supply
(iii) If blood is lost from the body in some way,
platelets get restored within 72 hours after
cessation of blood loss.
(iv) Platelets can be donated through a process
called plateletpheresis, and donations are
needed regularly to meet the demand.
(v) Under some circumstances, platelets also
contribute to immunological defensive
response against tumour cells in the body.
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