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Understanding Platelets: Functions & Formation

Platelets, or thrombocytes, are non-nucleated cell fragments crucial for blood coagulation and hemostasis, with a lifespan of 8 to 10 days. They are activated by various stimuli and play essential roles in repairing capillary endothelium, forming platelet plugs, and activating coagulation. Platelet production, or thrombopoiesis, occurs in the bone marrow and is regulated by thrombopoietin, with abnormal platelet counts leading to conditions such as thrombocytosis or thrombocytopenia.

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0% found this document useful (0 votes)
5 views19 pages

Understanding Platelets: Functions & Formation

Platelets, or thrombocytes, are non-nucleated cell fragments crucial for blood coagulation and hemostasis, with a lifespan of 8 to 10 days. They are activated by various stimuli and play essential roles in repairing capillary endothelium, forming platelet plugs, and activating coagulation. Platelet production, or thrombopoiesis, occurs in the bone marrow and is regulated by thrombopoietin, with abnormal platelet counts leading to conditions such as thrombocytosis or thrombocytopenia.

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THROMBOCYTES / PLATELETS

PLATELETS are cell fragments with granules found in blood,


they play a main role in hemostasis and coagulation of blood.

MORPHOLOGY: Non-nucleated,
Disc like, round or oval.
Diameter : 2 to 4 microns.
Center dark staining – chromatomere,
periphery lighter - hylomere.
LIFE SPAN: 8 TO 10 DAYS.

DESTROYED : ½ IN CLOTS AND ½ IN SPLEEN.

NORMAL COUNT: 1.5 TO 4 lakhs per cu mm of blood

NORMAL PLATELETS ARE INACTIVE


 Until stimulated.
UNDER ELECTRON MICROSCOPE WE SEE :
[1] CELL MEMBRANE
1) Cell membrane (a) Outer glycocalyx
2) Microtubules.
(b) Phospholipids act
3) Mitochondria.
4) Granules as platelet factor.
[2] MICROTUBULES:
Have thrombosthenin
 Helps in clot retraction.

GRANULES
[4] a) ALFA GRANULES: biggest,
has: alb, Glob & Pl. gr. Fac.
[3] MITOCHONDRIA: b) DENSE GRANULES: ATP, ADP ,
Serotonin , Prostaglandin
& F- XIII.
c) GLYCOGEN GRANULES .
d) LYSOSOMAL GRANULES.
ACTIVATION OF PLATELETS:

Platelets are activated by


contact with :
[1] Subendothelial cells  collagen fibers.
[2] Rough surface.
[3] Factors from other active platelets
ATP, ADP and Thromboxane A2
(also a vasoconstrictor)
[4] Thrombin from the clot.
ACTIVATION takes place in a series of overlapping events
{1}--shape change  become irregular with pseudopodia.

{2} --increase in size.


{3} -- Platelet aggregation. get sticky,adhere to each other and tissues

{4} --Cell membrane releases lipids that form thromboxane A2

{5} --Granules secrete ADP, F-XIII, PGF, Serotonin, lysozymes etc.

{6} --cell memb. reorganised to expose Phospholipids.

{7} --contraction of microtubules causes clot retraction.


PROPERTIES OF PLATELETS:
1. Pl adhesion
2. Pl activation.
3. Pl aggregation
4. Pl agglutination.

Platelet cell membrane contains various receptors meant for


combining with specific substances like:
 • collagen
 • fibrinogen
 • Von Willebrand’s factor: a large circulating molecule produced
by endothelial cells. It plays important role in platelet adhesion
and regulates circulating level of factor VIII (and v).
 Platelet membranes also contain precursors of various substances
like: thromboxane A2, prostaglandins, and platelet factor 3 and 4 .
FUNCTIONS OF PLATELETS:
most important role in hemostasis.
1. Repair capillary endothelium: While in the circulation.
They stick to damaged endothelial lining of the capillaries
and bring about a speedy repair.
If platelet count falls (below 50,000 per cu mm) capillary
bleeding occurs.
(2) Releases vasoconstrictors - serotonin and thromboxane- A2.
This helps hemostasis. (NOTE: Platelets cannot synthesize 5-HT,
they obtain their 5-HT while passing through the GIT.)

(3) Forms platelet plug which stops bleeding before clots forms.
this is due to its properties of ----

(4) Stores and transports granular contents liked ----


(5) Activates coagulation – surface activation of F-XII.

(6) Releases Platelet Phospholipid for thromboplastin formation.

(7) Platelet growth factor stimulates endothelial cells,


muscle fibers and fibroblasts to make new cells to
repair vessel wall.
(8) Contraction of microtubules and release of F-XIII causes
clot retraction. Speed of clot retraction (syneresis) is directly
proportional to the number of platelets present and is
dependent upon the thrombosthenin (contractile protein)
in presence of ATP and magnesium ions.
THROMBOPOIESIS or MEGAKARYOCYTOPOIESIS
DEVELOPMENT OF PLATELETS
DEVELOPMENT: IN BONE MARROW.

from PHSC (Pluripotent hemopoiotic stem cell)

Committed White cell line (polyploid precursor cell)

 Megakaryoblast (Stage I)
 Pro-megakaryocyte (Stage II)
 Granular megakaryocyte (Stage 111)
 Platelets.
Megakaryocytes 
are giant granulated cells
(dense granular cytoplasm )
( Diameter - 35-160 µm )
The cytoplasm forms micro-
vesicles which have a unit cell
membrane covering.
megakaryocytes introduces
pseudopodia through the
walls of the sinusoids and
platelets are formed by
pinching off bits of cytoplasm.
 ultimately the full cell
disintegrates to form 1000 to
5000 platelets.
CONTROL / REGULATION OF THROMBOPOIOSIS
When platelet number decreases
OR there is infections–
 the liver & kidneys secrete
 a factor called
THROMBOPOIETIN (TPO)
TPO  bind with circulating
platelets,
when platelets are destroyed
TPO is released
 and stimulates production of
new platelets.
COUNTING PLATELETS:
( I ) BLOOD FILM WITH EDTA:
number of platelets per high power field or per no of RBC.

(II) NEUBAUERS CHAMBER--- Brechers method


a) WBC pipette -- Ammonium Oxalate as Diluting fluid,
b) RBC center square, high power,
c) Microscope adjusted to phase contrast,
 Platelets look like small shiny dots.
APPLIED:
INCREASE IN PLATELETS  THROMBOCYTOSIS, THROMBOCYTHEMIA.
will cause intravascular coagulation.
DECREASE IN PLATELETS  THROMBOCYTOPENIA.
will cause bleeding.
CAUSES OF THROMBOCYTOSIS:- over production : is seen in 

* *

* *
CAUSES OF THROMBOCYTOPENIA: decreased production or more destruction.

*
CAUSES OF THROMBOCYTOPENIA: decreased production or more destruction.

v
CLINICALLY CALLED PURPURA 
causes bleeding from small capillaries in mucus membranes , skin ,
urinary tract and gastro-intestinal tract.
Forms small red - purple - blue spots and bruises.
DRUGS THAT INHIBIT PLATELET ACTIVATION:
Used for prevention of thrombosis and cardio vascular disorders.
# Aspirin / salicylic acid: can increase bleeding time from normal of
1 to 4 minutes to up to 6 minutes,
by stopping formation of thromboxane A2 .
# ADP receptor inhibitors like clopidogrel and ticlopidine
stop action of ADP.

THANK YOU

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