This presentation delves into the crucial role of platelets in the human body's hemostatic system. Explore the structure and function of platelets, their role in blood clotting, and the significance of platelet disorders. Gain insights into platelet production, regulation, and the impact on overall health. Discover the latest research and advancements in platelet-related medical interventions.

1. BLOOD
PLATELETS
F R AG M E N T S O F C Y TO P L AS M .

2. INTRODUCTION OF THROMBOCYTES
Platelets/ Thrombocytes
are small, colorless,
non nucleated and
moderately refractile
formed elements of the
blood.
Diameter = 2 to 4 μ
Shape = spherical or
rod shaped.

3. STRUCTURE
AND
COMPOSITION
Platelets are constituted
by:
1. Cell membrane =
contains lipids
(phospholipids*,
cholesterol and
glycolipids) and
carbohydrates
(glycocalyx,
glycoproteins*) and
proteins.
[*=functionally imp]
2. Microtubules = Made
up of polymerised
protein called TUBULIN.
Forms a ring around
cytoplasm below the cell
membrane. Provide
structural support to
inactivated platelets.
3. Cytoplasm =
Contains cellular
organelles, Golgi
apparatus, endoplasmic
reticulum, mitochondria,
micro tubeles, micro
vessels, filaments and
granules. Also contains
proteins, enzymes and
hormones.

4. NORMAL
COUNT AND
VARIATION
• NORMAL PLATELETS COUNT = 2,50,000/cu
mm of blood
• PHYSIOLOGICAL VARIATIONS :-
• 1.Age = platelets are less in infants and
reaches Normal level at 3rd month after birth.
• 2.Sex = No difference in males and females.
During menstruation it’s reduced in females.
• 3.High Altitude = platelets count increases.
• 4.After meals = It increases.

5. PROPERTIES
OF
PLATELETS
• 1. ADHESIVENESS : Sticking to a rough surface.
During injury of blood vessels, endothelium is
damaged and endothelial collagen is exposed.
While coming jn contact with collagen, platelets
are activated and adhere to collagen.
• 2. AGGREGATION : Grouping of platelets.
Adhesion is followed by activation of many
platelets by substances released from dense
granules of platelets.
• 3. AGGLUTINATION : Clumping together of
platelets. Aggregated platelets are agglutinated by
the actions of agglutinins and platelets activating
factor.

6. FUNCTIONS
OF
PLATELETS
• 1. Role in Blood clotting: Platelets are responsible for
the formation of the intrinsic prothrombin activator,
which helps in clotting.
• 2. Role in clot retraction : Platelets contains contractile
proteins namely actin, myosin, thrombosthenin, which
are responsible in clotting retraction.
• 3. Role in Haemostasis : platelets prevents blood loss
by constriction of blood vessels and by forming
temporary plug.
• 4. Role in Repair : platelets derived growth factors in
cytoplasm of platelets is useful in repair of endothelial
and blood vessels.
• 5. Role in defense mechanism : By agglutination,
platelets encircle foreign bodies and destroy them.

7. ACTIVATION OF PLATELETS
During activation, the
platelets change their
shape with elongation of
long fillamentous
pseudopodia called
FILOPODIA.
Filopodia helps in
aggregation. Activation and
aggregation of platelets is
accelerated by ADP,
thromboxane A2 and
platelets activating factor
(PTA).

8. DEVELOPMENT
OF PLATELETS
1. Platelets are formed
from bone marrow.
2. Pleuripotent stem cells
give rise to
Magakaryocytes, which
forms pseudopodium.
3. A Portion of
pseudopodium is
detached, which gets
entered in circulation.
4. Production of platelets
is influenced by Colony
stimulating factors
(secreted by T
lymphocytes and
monocytes)and
Thrombopoetin(secreted
by liver and kidneys).

9. LIFE SPAN AND FATE
OF PLATELETS
• Average life span = 10 days
• Platelets are destroyed by tissue macrophage system
in spleen.
• Splenomegaly : enlargenlargement of spleen,
decrease platelets count.
• Splenectomy : removal of spleen, increases platelets
count.

10. APPLIED
PHYSIOLOGY
• 1. Thrombocytopenia: Decrease in
platelets count.
• 2. Thrombocytosis : Increase in platelets
count.
• 3. Thrombocythemia: persistent and
abnormal increase in platelets count.
• 4. Glanzmann’s thrombasthenia :
Inheritant hemorrhagic disorder, caused
by structural or functional abnormalities of
platelets.

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