QUANTITATIVE PLATELET

DISORDER

Hannie M. Sacatan
• THROMBOCYTOPENIA
• Decreased production
• Dilutional loss
• Nonimmune destruction
• Immune platelets destruction
• sequestration
 THROMBOCYTOPENIA

• Is a common clinical disorder and results from one or any combination of mechanisms including
production defects, accelerated loss or destructions and splenic sequestration.
 DECREASED PRODUCTION

• Pathophysiology
• The severity of bleeding is related to the degree of thrombocytopenia.
• Haemostatic defects are said to be more severe when the platelet count fall rapidly rather than
gradually.
• Clinical presentation
• Small vessel bleeding attributed to thrombocytopenia results in PETECHIAE,PURPURA or
ECCHYMOSES ( haemorrhages into the skin of different sizes < 3mm , 1cm and > 3cm
respectively.
• Significant bleeding usually does not occur until the platelet count id less than 60X109L.
• The central nervous system id the most serious site of spontaneous bleeding which may be fatal.
• Laboratory findings:
• Platelet counts is DECREASED
• Clot retraction usually is ABNORMAL when the platelet count is below 60x109/L
• ETIOLOGIES:
• Generalized bone marrow suppression leading to a DECREASE in all cell types is
characteristic of plasma anaemia.
• Selective suppression of the megakaryocytes is associated with chlorothiazide(diuretic) and
other drugs
• Myelophthisic process is a space occupying lesion in the bone marrow such as metastatic tumor
,fibrosis or leukaemia.
 DILUTIONAL LOSS

• Extensive blood transfusion is accompanied by thrombocytopenia, the degree of which is

directly proportional to number of units transfused.
 NONIMMUNE DESTRUCTION

• My result from exposure of platelets to nonendothelial surfaces, activation of the coagulation

process or platelet consumption by endovascular injury with no measurable depletion of
coagulation factor.
==
Artificial surface
Activition of the coagulation system
Hemolytic uremic syndrome
Thrombotic thrombocytopenic purpura
• Pathopysiology
• TTP affects many organs whereas in HUS, it predominantly involves the efferent arterioles and
glomeruli of the kidneys.
• It is possible that causative agents act on boyh the platelet and the endothelial surfaces.
• Clinical presentation:
• vomiting or diarrhea is the most common symptoms preceding the anaemia and renal failure characteristics of
HUS.
• The patient frequently is pale and slightly jaundiced and may present with purpura and bleeding from the
mucous membranes. Thrombotic thrombocytopenic purpura is diagnosed most frequently in patients between
the ages of 10 and 40 with peak incidence in the third decade of life ,women being affected more frequently
than men.
• FEVER, PALLOR , PETECHIAE , NEUROLOGIC MANIFESTATIONS , and RENAL DESIASE are the
chief clinical features.
• Laboratory findings:
• Increased variation of red blood cell size
• Urine contains ( casts ,erythrocytes , leukocytes and large quantities of albumin because of
lesions in the kidneys.
• Serum level, creatinine and urea nitrogen are increased
• Treatment:
• Therefore , treatment tend to be based on the practical experience of the clinician. In addition no
single therapeutic approach is likely to be effective in all patients because of the heterogeneity of
pathogenesis in these disorders.
• Exchange plasmapheresis , whole blood exchange transfusion or plasma infusion are indertaken
to remove , reduce , or modify the effect of soluble immune complexes and to replace plasma
factors.
 IMMUNE PLATELET DESTRUCTION

• Increased platelet destruction by immune mechanism os associated with increased level of

immunoglobulin's or complement on the platelet surface.
• Immune thrombocytopenia's may caused by ALLOANTIBODIES, AUTOANTIBODIES or
DRUGS.
 POST TRANSFUSION PURPURA

• Is a rare complication characterized by sudde ,rpfound, and selflimited thrombocytopenia ( less

than 20x109/L).
• The mechanism responsible for the destruction of the patient negative is unkown.
• Plasmapheresis apperars to be most effective I resolving bleeding complication, with an
increased in the platelet count with in 48hours.
 NEONATAL ISOIMMUNE
THROMBOCYTOPENIA
is caused by TranSplacental passage of maternal igG antibodies directed against fetal platelet
antigen INHERITED from the father and absent on the mothers platelets.
Usually al hematologic parameter are normal except the platelet count which may be 30x109/L.
THE TREATMENT OF CHOICE IS TRANSFUSION WITH MATERNAL PLATELETS
WASHED WITH ABO COMPATINLE PLASMA TO REDUCE THE LIKELIHOOD OF
FURTHER TRANSFER OF MATERNAL ALLOANTBODY TO THE INFANT.
• Primary immune thrombocytopenia is an autoimmune disorder of unknown cause affecting both
children and adults. The low peripheral blood platelet count is caused by premature platelet
destruction by self-reacting antibodies in addition to an impairment of platelet production.
• PATHOPHYSIOLOGY
• Total platelet mass in the body is regulated by the balance between production and clearance of
platelets. In hypoplastic thrombocytopenias, such as aplastic anemia or chemotherapy-induced
thrombocytopenia, platelet counts are decreased due to reduced platelet production.
• CLINICAL PRESENTATION
• Petechiae
• Ecchymoses
• Mucosal bleeding
• Chronic ITP is longer and includes easy BRUISINF and abnormal menstrual bleeding.
• Treatment
• Purpose of therapy is to raise the platelet count to a level that will maintain hemostasis.
• Chronic ITP may be treated with splenectomy to remove a major site of platelet storage and
destruction and antibody synthesis or eith immunosuppressant's such as corticosteroids.
• causes of secondary ITP are the human immunodeficiency virus (HIV) and the hepatitis C virus
(HCV).
• If a medicine causes your body to produce antibodies, which seek and destroy your platelets, the
condition is called drug-induced immune thrombocytopenia. Heparin, a blood thinner, is the
most common cause of drug-induced immune thrombocytopenia.
• Heparin, a blood thinner, is the most common cause of drug-induced immune thrombocytopenia.
If a medicine prevents your bone marrow from making enough platelets, the condition is called
drug-induced nonimmune thrombocytopenia. Chemotherapy drugs and a seizure medicine called
valproic acid may lead to this problem.
• Laboratory findings:
• lab results are similar to those describes for other immune thrombocytopenia's.

• Therapy:
• The most important aspects of treatment is to discontinue the drugs suspected of triggered the
immune thrombocytopenia. Corticosteroids may be administered because of their positive effects
on vascular integrity.
 SEQUESTRATION

• The spleen may be responsible for thrombocytopenia either by increased phagocytosis and
destruction of damaged platelets or by increased sequestration of normal undamaged platelets.
 THRPMBOCYTOSIS
• Is an abnormal INCREASED in the number of circulating platelets as a result of physiologic or
pathologic processes.
• Two types of thrombocytosis:

• Primary thrombocytosis - also known as essential thrombocythemia (or ET), is a disease in

which abnormal cells in the bone marrow cause an increase in platelets.
• Secondary thrombocytosis - is excess platelets in the bloodstream that develops as a result of
another disorder and rarely leads to excessive blood clotting or bleeding.