Blood Platelets

BLOOD PLATELETS
Dr Elizabeth S Nugraheni
PATOLOGI KLINIK FK UWKS
10/10/2012
dr Elizabeth S Nugraheni
NORMAL PLATELET
FUNCTION
Thrombocytes. Thrombocytes, also
called platelets, are essential for
coagulation.
Without an adequate number of
functioning platelets, an individual
would bleed to death.
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Variations in the Number of Thrombocytes
Thrombocyte or platelet disorders are classified as

thrombocytopenia, a decrease
in the number of platelets, or thrombocytosis, a slight increase
in the
number of platelets .
An excessive increase in the number of platelets is often referred
to as thrombocythemia
Variations in the number of thrombocytes can be the result of
bone marrow disorders.
Thrombocytopenia is the most common cause of bleeding
disorders. Thrombocytosis can be the result of a variety of
conditions such as acute blood loss, following splenectomy, some
anemias, and chronic diseases
Other causes of thrombocytosis are related to specific
hematological disorders, such as autoimmune hemolytic anemia
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Thrombocyte Count
EDTA blood is pipetted into the tubes, carefully mixed

and immediately placed in a counting chamber.
The chamber is allowed to stand for 10 minutes while
the cells settle, after which an area of 1mm2 is
counted.
The result corresponds to the number of
thrombocytes (the 1 + 100 dilution is ignored).
In an automated blood cell counter, the blood cells
are counted after they have been sorted by size.
Small cells between 2 and 20 fl (thresholds vary for
different instruments) are counted as thrombocytes.
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Thrombocyte Count
If giant thrombocytes or agglutinated
thrombocytes are present, they are not counted
and the result is an underestimate.
On the other hand, small particles, such as
fragmentocytes, or microcytes, will lead to an
overestimate. Modern analyzers can recognize
such interference factors and apply interference
algorithms to obtain a corrected thrombocyte
count.
If unexpected results are produced, it is wise to
check them by direct reference to the blood smear.
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PLATELET FUNCTION
Normal circulating platelets resemble an oblong disk.
They are essentially fragments of megakaryocyte
cytoplasm
Although lacking a nucleus, the cytoplasm contains
1. mitochondria for aerobic metabolism,
2. glycogen stores for anaerobic glycolysis, and
3. specific granules whose contents are important for
coagulation (Figure 27-1).
Almost 20% of the platelet volume comprises these
granules, whereas 25% of the protein in the platelet
is actin and myosin needed for platelet contraction.
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When flowing platelets contact

subendothelial tissue in a damaged vessel,
they adhere to the exposed collagen
through the integrin receptor GPIa/IIa and
to von Willebrand factor bound to the
collagen via another receptor, GPIb/IX-V.
This binding interaction causes platelets to
begin the early activation process and
undergo shape change with extension of
pseudopods.
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Platelet GPIb/IX-V binding to vWF causes

platelet signal transduction that is followed by
a conformational change in another integrin
receptor, GPIIb/IIIa, which then mediates firm
adhesion to vWF. Both vWF and fibrinogen
serve as bridging ligands to assist formation
of platelet thrombus. GPIa/IIa is involved in
collagen binding, but it is clearly not the most
important receptor because its congenital
absence does not result in a significant
bleeding tendency.
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By contrast, absence of GPIb/IX-V or

GPIIb/IIIa generally results in a bleeding
disorder of varying intensity.
The initial adhesion of platelets to one
another can be measured in the laboratory
as the aggregation of platelets in plasma
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High-dose ADP, thrombin, and thromboxane A 2

(through arachadonic acid stimulation) provide a
stronger stimulus
for platelet activation that results in a second
wave of irreversible aggregation.
This second wave is associated with degranulation
and release of dense granule contents (ADP and
serotonin), granule contents (platelet factor 4 and
thromboglobulin), and further generation of
thromboxane A2 through the platelet
cyclooxygenase (COX-1 isoform) pathway (Table
27-2).
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Platelets Aggregation and Adhesion

Platelet activation involves shape change with
extension of pseudopods and a release reaction
where the contents of intracellular granules are
expelled from the platelet to stimulate activation
of other, nearby platelets.
Formation of a platelet thrombus at the site of
injury requires both platelet adhesion and
aggregation.
Surface GPIa/IIa receptors bind directly to
exposed collagen. GPIb and GPIIb/IIIa receptors
interact with von Willebrand factor (vWF) to
adhere to the subendothelial tissue.
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Aggregation involves the GIIb/IIIa receptor

and fibrinogen as an essential cofactor.
The expression of the -granule receptor
P-Selectin (GMP 140) binds monocytes to
platelets and incorporates them within the
clot
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DIFFERENTIAL DIAGNOSIS
Diagnosis of a platelet abnormality

requires a high level of suspicion and a
lot of detective work. Acquired
functional abnormalities are clearly the
most common abnormality. vWD leads
the category of congenital disorders, in
terms of both incidence and severity.
Therefore, initial evaluation should
look for a disorder in these two areas.
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Acquired Abnormalities of Platelet

Function
Acuired platelet dysfunction occurs in
three clinical setting :
1. in association with hematopoietic
disease
2. as part of a systemic illness
3. as a result of drug therapy.
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Abnormalities of Platelet
Function
A. MYELOPROLIFERATIVE DISEASE
Patients with myeloproliferative disorders (ie, polycythemia
vera,myeloid metaplasia, idiopathic myelofibrosis, essential
thrombocythemia, and chronic myelogenous leukemia)
Some of these patients have very high platelet counts and
demonstrate either abnormal bleeding, or a tendency for
arterial or venous thrombosis, or even both.
Although the height of the platelet count alone does not
correlate with the bleeding or thrombotic tendency,
thrombocytosis in excess of 1 million/L is considered to be
a risk factor.
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Abnormalities of Platelet Function
MYELOPROLIFERATIVE DISEASE
At the same time, increased platelet turnover, as
measured by the reticulated platelet count, may
correlate with thrombotic risk. In patients with
polycythemia vera, expansion of the total blood
volume and an increase in blood viscosity may
also contribute to the thrombotic risk
The BT may be prolonged.
the most consistent laboratory abnormalities in
bleeding patients are defects in epinephrineinduced aggregation and dense and alpha
granule function.
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B. DYSPROTEINEMIA
Almost one-third of patients with Waldenstrom
macroglobulinemia or IgA myeloma will have a
demonstrable defect.
This condition is appears in patients with
disseminated intravascular coagulation (DIC).
Failure of platelet thrombus formation in the DIC
patient is usually multifactorial, with
thrombocytopenia, hypofibrinogenemia, and a loss
of dense and -granule function secondary to
platelet activation all playing a role.
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C. CARDIOPULMONARY BYPASS
During bypass, platelets show progressive
activation and loss of P.361 granule contents.
The aggregation response to ADP decreases and
the BT becomes prolonged.
This situation is reversible; platelet function
returns to normal within 12 to 36 hours after
surgery.
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D. UREMIA
Uremic patients consistently show a defect in platelet
function that correlates with the severity of the uremia
and anemia
It appears that the uncleared metabolic product
guanidinosuccinic acid acts as an inhibitor of platelet
function by inducing endothelial cell nitric oxide (NO)
release. Platelet adhesion, activation, and aggregation are
abnormal, and thromboxane A2 generation is decreased.
Most patients with severe uremia have a prolonged BT in
excess of 30 minutes.
This condition is corrected by hemodialysis
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E. LIVER DISEASE
Patients with liver disease have a multifaceted defect
in coagulation.
Thrombocytopenia related to hypersplenism and a
failed thrombopoietin response is common.
Platelet dysfunction, secondary to high levels of
circulating fibrin degradation products, further
increases the bleeding tendency. In addition, reduced
production of factor VII (principal cause of the
prolonged PT in liver disease patients) and low-grade,
chronic DIC with increased fibrinolysis add to the
coagulopathy.
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F. DRUG INHIBITION
Aspirin and the nonsteroidal anti-inflammatory (NSAID) drugs have
impact on platelet function.
Aspirin is a powerful inhibitor of platelet thromboxane A 2 synthesis
through its irreversible inhibition of cyclooxygenase function.
NSAID drugs (eg, indomethacin, ibuprofen, sulfinpyrazone) also
inhibit platelet cyclooxygenase,
From the clinical viewpoint, these agents are weak inhibitors of
platelet function and are usually not associated with severe clinical
bleeding. However, they will contribute to bleeding when other
aggravating factors, such as other anticoagulants, a GI disorder, or
surgery, are present
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F. DRUG INHIBITION
Most common triggers of drug-induced

immunothrombocytopenia
Analgesics
Furosemide
Antibiotics
Gold salts
Anticonvulsive drugsHeparin
Arsenic, e. g., in water Isoniazid
Quinidine
Methyldopa
Quinine
Spironolactone
Digitalis preparations Tolbutamide
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DAFTAR PUSTAKA
Hematology in Clinical Practice
Atlas of Clinical Hematologic
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Blood Platelets

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BLOOD PLATELETS

Variations in the Number of Thrombocytes

Thrombocyte or platelet disorders are classified as

EDTA blood is pipetted into the tubes, carefully mixed

When flowing platelets contact

Platelet GPIb/IX-V binding to vWF causes

By contrast, absence of GPIb/IX-V or

High-dose ADP, thrombin, and thromboxane A 2

Platelets Aggregation and Adhesion

Aggregation involves the GIIb/IIIa receptor

Diagnosis of a platelet abnormality

Acquired Abnormalities of Platelet

Abnormalities of Platelet Function

Abnormalities of Platelet Function

Abnormalities of Platelet Function

Abnormalities of Platelet Function

Abnormalities of Platelet Function

Abnormalities of Platelet Function

Abnormalities of Platelet Function

Most common triggers of drug-induced

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