platelets

Introduction

Structure and
composition

agenda Mechanism of action and

Platelets disorders

Management
 Introduction
platelets, or thrombocytes are the smallest
components of blood and play a crucial role in stop
bleeding. They are cell fragments that cluster
together to form a plug and then a clot when blood
vessel is damaged. Platelets help in wound healing
and can indicate various health conditions when
their level are abnormal, such us cancer and
autoimmune disease. A normal platelet count range
from 150.000 to 400.000 per microliter of blood.
Formation
In bone marrow from
megakaryocytes stimulated
by thrombopoietin secreted
by kidneys & liver.
70% of the platelets
extruded from the bone
marrow pass to the blood
and 30% are stored in the
spleen.
Structure and composition
Platelets, the smallest blood cells, are anucleate
fragments essential for hemostasis. Their structure
is complex, comprising various organelles and a
unique arrangement that facilitates their function in
vascular
Platelet integrity and clot formation
Composition
Size and Shape: Platelets typically measure 2-5
μm in diameter and are biconvex discs in their
resting state, which aids in smooth circulation
through blood
Plasma vesselsThe membrane is a
Membrane:
phospholipid bilayer with embedded proteins,
featuring a smooth surface with invaginations that
form the open canalicular system (OCS)
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Cytoplasmic Components
•Granules:
Platelets contain α-granules and
dense bodies, which store various
proteins and signaling molecules
crucial for activation and
aggregation.
•Cytoskeleton:
The cytoskeleton, primarily
composed of microtubules and
filaments, undergoes significant
reorganization upon activation,
allowing shape change and
pseudopod formation.

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Platelets granules
Dense Bodies: Alpha Granules:
•Alpha granules are larger and contain a
•These granules store small variety of proteins, including growth
molecules such as adenosine factors and clotting factors.
diphosphate (ADP), calcium ions, •Key secretions from alpha granules
and serotonin. include:
•Upon activation, dense bodies • Platelet-derived growth factor
release these substances, which (PDGF)
are vital for platelet activation • Platelet factor 4 (PF4)
and aggregation, enhancing the • Fibrinogen
clotting process • von Willebrand factor (VWF)
•These proteins are essential for promoting
healing and facilitating the aggregation of
platelets at the site of injury

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Mechanism of action
Platelet Adhesion
•Circulating platelets detect the injury site.
•Platelets stick (adhere) to the exposed collagen through a
protein called von Willebrand factor (vWF).
•vWF binds to GPIb receptors on the platelet surface, acting
like Velcro.
Platelet Activation
•Once platelets are adhered, they become activated.
•They undergo a shape change: from smooth disks → spiky,
irregular forms.
•Activated platelets release chemical signals stored in their
granules:
• ADP: activates other nearby platelets.
• Thromboxane A₂ (TXA₂): promotes more platelet
activation & vessel narrowing.
• Calcium ions: important for activating clotting
factors. 8
Platelet Aggregation
•Activated platelets now start sticking to
each other, forming a platelet plug.
•This is done through the GPIIb/IIIa
receptors on platelets, which bind to
fibrinogen (a bridging molecule).
•Fibrinogen connects multiple platelets
like glue.
Clot Stabilization
(Secondary Hemostasis)
•The soft platelet plug needs to be
reinforced.
•This is done by the coagulation
cascade, which produces fibrin (a
strong protein thread).
•Fibrin forms a mesh that stabilizes
the clot and traps red blood cells.

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Function of platelets
1. Hemostasis
(Stopping
Bleeding)
This is the primary
function of platelets.
When a blood vessel is
injured, platelets:
•Adhere to the injury site
•Activate and release
chemicals
•Aggregate to form a
temporary platelet plug
•Work with clotting
factors to form a stable
blood clot

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2. CLOT FORMATION (THROMBUS
FORMATION)
• PLATELETS HELP INITIATE AND AMPLIFY THE COAGULATION
CASCADE
• THEY RELEASE SUBSTANCES LIKE CALCIUM, ADP, AND
PLATELET FACTOR 3, WHICH ARE NECESSARY FOR
ACTIVATING CLOTTING FACTORS
• HELP CONVERT FIBRINOGEN → FIBRIN, WHICH REINFORCES
THE CLOT

3. WOUND HEALING & TISSUE REPAIR

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 Platelets disorders
Platelet disorders are conditions affecting the
number or function of platelets, which play a
critical role in blood clotting and maintaining
vascular integrity. they can be classified into
quantitative (abnormal platelet counts) and
qualitative (abnormal platelet function)
disorders.
Quantitative platelets disorders
Thrombocytopenia
Decrease in platelet count is
called thrombocytopenia. It leads
to thrombocytopenic purpura
Purpura is a reddish-blue or
purplish discoloration of skin or
mucosa from spontaneous
extravasation of blood
May be due to a defect or
deficiency in blood platelets
Blood may ooze from gingival
margins.
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Thrombocytosis
• It is increase in platelet count
• It could be primary and secondary

1. Primary
thrombocytosis
This type is typically caused by a bone
marrow disorder where the bone marrow
produces too many platelets. It can be
associated with conditions like essential
thrombocythemia.
It may lead to complications such as
abnormal blood clotting or bleeding due to
the excessive number of platelets.
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2. Secondary thrombocytosis
• This is the more common type and occurs as
a result of another condition, such as
infection, inflammation, anemia, or after
surgery. In this case, the high platelet count
is typically a reaction to an underlying issue
rather than a primary problem with platelet
production.
• Conditions like rheumatoid arthritis, cancer,
and iron deficiency anemia can trigger
reactive thrombocytosis.

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3. Thrombocythemia
 It is a myeloproliferative blood
disorder.
 It is characterized by the
production of too many platelets in
the bone marrow. Too many
platelets make normal clotting of
blood difficult
 Etiology is idiopathic
 Thrombocythemia occurs in the
following conditions:
i. Carcinoma
ii. Chronic leukemia
iii. Hodgkin’s disease.

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Qualitative platelet disorders
• Glanzmann’s Thrombasthenia
Is a rare inherited bleeding disorder that affects the ability of
platelets (thrombocytes) to function properly in blood clotting.
It is caused by defects in the platelet surface receptors that are
critical for platelet aggregation
• Bernard-Soulier Syndrome (BSS)
Is a rare inherited bleeding caused by a deficiency or
dysfunction of the Glycoprotein Ib-IX-V complex
(GPdisorderIb-IX-V) on the surface of platelets.
This complex is essential for platelets to bind to von
Willebrand factor (vWF), which helps platelets adhere to
the blood vessel wall at the site of injury.
Without proper binding to vWF, platelets cannot adhere
and form the initial plug for clotting.

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• Storage Pool Disorders
Storage Pool Disorders are a group of platelet
function disorders caused by defects in the
storage or release of granules (storage
compartments) inside platelets.
These granules contain important substances,
such as adenosine diphosphate (ADP), calcium,
serotonin, and fibrinogen, which are released
when platelets are activated.
In storage pool deficiency, there is a defect in the
dense granules, leading to a lack of release of
ADP and calcium, which impairs platelet
aggregation and clot formation.

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Acquired disorders
• DRUG INDUCED
ASPIRIN AND NSAIDS INHIBIT CYCLOOXYGENASE,
IMPAIRING THROMBOXANE A2 PRODUCTION.
• UREMIA
TOXINS IN RENAL FAILURE AFFECT PLATELET
FUNCTION
• LIVER DISEASE
REDUCES SYNTHESIS OF CLOTTING FACTORS AND
PLATELETS

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Treatment
• Thrombocytopenia: Platelet transfusion,
immunosuppression (e.g. corticosteroids), or
splenectomy.
• Thrombocytosis: Antiplatelet drugs (e.g. aspirin),
cytoreduction therapy for myeloproliferative causes.
• Qualitative Disorders: Avoidance of antiplatelet drugs,
use of desmopressin (DDAVP) to stimulate platelet
release, though it's generally more effective in disorders
involving the vWF or primary aggregation defects as
DDAVP increases the amount of factor VIII and von
Willebrand factor circulating in your blood by around
three to five times your normal level.

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General principles of management
Control of Moderate severe bleeding
Minor bleeding
bleeding bleeding

Pressure and Seek immediate

Platelet
Transfusion or
Hemostatic agents Clotting Factor
Infusion

Topical agents Surgical

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Hemostatic agents
Hemostatic Agents comprise
bone wax, sutures, gelatin
of animal origin,
regenerated oxidized
cellulose, collagen, platelet
rich plasma, thrombin, fibrin
sealants, electric or laser
scalpels, antifibrinolytic
agents such as tranexamic
acid (Kapron mouth
wash use 10ml 5%) .

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Restore circulatory volume
1. Fluid resuscitation
Use crystalloids (ringer lactate, normal
saline) for volume replacement
2. Blood transfusion for sever blood
loss
Packed red blood cells for anemia
Platelets for thrombocytopenia
Fresh frozen plasma for clotting factors
deficiency

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Hemostatic support
1. PLATELET TRANSFUSION: FOR PLATELET COUNT
<50,000/ΜL IN ACTIVE BLEEDING OR <20,000/ΜL
IN HIGH-RISK PATIENTS.
2. CLOTTING FACTOR REPLACEMENT:
•FFP FOR MULTIPLE FACTOR DEFICIENCIES.
•CRYOPRECIPITATE FOR FIBRINOGEN
REPLACEMENT.
•SPECIFIC FACTORS (E.G., VIII, IX) FOR
HEMOPHILIA.
3. VITAMIN K: FOR WARFARIN-INDUCED BLEEDING
OR VITAMIN K DEFICIENCY.

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Specific cases
Surgical bleeding
• Pre-surgical evaluation of bleeding
risk.
• Use of electrocautery or sutures for
ligation of blood vessel.

Bleeding in Anticoagulated
Patients
Reversal Agents:
• Protamine sulfate for heparin.
• Vitamin K or prothrombin complex
concentrates (PCC) for warfarin.

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Meran seuleiman

Ahmad alfares
Maxillofacial
department

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