FAQ - Thrombocytopenia
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Can Heperin Induced Thrombocytopenia cause you to be a poor surgical candidate and why?


Yes! Thrombocytes (platelets) are what cause your blood to clot. "Penia" means "lack of." Heparin causes your blood platelet level to drop, which means that your blood doesn't clot as fast. When people are going to cut into you you really want your blood to be ready to clot fast.  (+ info)

What is the cause of refractory thrombocytopenia?


I take it that you mean "refractory to transfusions"?

In patients who have had many platelet transfusions, a syndrome can develop in which the persons immune system develops antibodies to foreign platelets. The immune system destroys the new platelets as fast as they are run in. There is no strict algorithem for who will develop this problem, but in general: the more transfusions, the greater the risk.

Getting HLA matched platelets can be a big help if a person becomes refractory. I'm not sure if it would help to prevent it, but it is not generally done as a preventative measure (at least at my hospital).

1. Patients on chemotherapy  (+ info)

What is Chronic Thrombocytopenia? Is a type of leukemia and is it fatal?


Thrombocytopenia is a low platelet count which can be treated with medication or surgery. It the platelet count gets low then platelet transfusion would be required.

Chronic thrombocytopenia is NOT leukemia

Platelets form clots when you get a cut and thus stop bleeding. So if your platelet cound gets to low then you could bleed to death much easier  (+ info)

Thrombocytopenia (is the presence of relatively few platelets in blood) can be inherited?


If the father has the above condition what is the probability that his children will inherit it.
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Platelet production problems or defects can be inherited, that is they run in families; or non-inherited, caused or triggered by medications, drugs, or toxins, for example.  (+ info)

thrombocytopenia and prothrombin time test?


thrombocytopenia is the decreased no. of platelets in the blood, and Prothrombin Time test is done to check the effectivity of the Extrinsic pathway of clotting...any link between these two?
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These tests will detect most coagulation protein problems A relation between thrombocytopenia and time on bypass also was reported.
The clinical picture, bleeding time, prolonged partial thromboplastin time test, and plasma prothrombin time test lead to the diagnosis.

Thrombocytopenia : Relationship between platelet count and bleeding time. The bleeding time test assesses thecontribution of platelet number and function, and vessel wall. These results suggest that the severity of thrombocytopenia caused by chronic liver diseases correlates well with results of the glucagon challenge test.

Prothrombin Time : The inverse relationship between the bleeding time and the hematocrit is particularly Prothrombin Time and Activated Partial Thromboplastin Time.

If a coagulation disorder is suspected, consult a hematologist first. Routine diagnostic studies include a CBC, platelet count, sedimentation rate, blood smear for red cell morphology, urinalysis, chemistry panel, coagulation profile, rheumatoid arthritis factor, ANA test, serum protein electrophoresis, VDRL test, EKG, chest x-ray, and flat plate of the abdomen. The coagulation profile should include a platelet count, a bleeding time, a coagulation time, a partial thromboplastin time, and a prothrombin time.
If there is fever, blood cultures should be done. A bone marrow examination and bone marrow culture may be useful. If disseminated intravascular coagulation is suspected, a fibrinogen assay and estimation of fibrin degradation products should be done. Platelet function may be assessed by clot retraction tests. Spleen and liver scans and bone scans may be needed. A CT scan of the abdomen and pelvis may also be necessary. Skin, muscle, and even kidney biopsies are often done to complete the workup.
It can be seen from the above array of diagnostic tests that a hematologist should be consulted at the outset. Various forms of vasculitis may be confirmed by skin or muscle biopsy.

Initial laboratory: Complete blood count (CBC), platelet count, peripheral smear, prothrombin time (PT), activated partial thromboplastin time (APTT), and possibly a bleeding time. If the lesions appear vasculitic, consider a sedimentation rate and C-reactive protein determination. Serum creatinine and urinalysis can be ordered to screen for renal involvement. In vasculitis, the laboratory findings are often nonspecific and a skin biopsy for histology is employed  (+ info)

What is Heprin induced Thrombocytopenia type 2 ?


What are the after effects.
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here are some links...

http://www.pathology.vcu.edu/clinical/HIT_FAQ.pdf
http://en.wikipedia.org/wiki/Thrombocytopenia
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3 books on disease symptoms and treatments

you could also get these books on ebay or amazon or a half price book store. (last two are very similar)..
1.Oxford Handbook of Clinical Medicine
2.Handbook of Diseases (Lippencott)
3.Professional Guide to Diseases (Springhouse  (+ info)

I want a good picture for the backgrond of my power point about heparin induced thrombocytopenia?


Warning Graphic Image
Heparin induced thrombocytopenia
http://www.princetoncme.com/public/2005-131/slides/SL37.gif

Pathogenisis of Heparin induced thrombocytopenia
http://www.cap.org/apps/docs/cap_today/images/maycoag1.gif

Lighten one of these images up using a software photo image program and than use it as a background.  (+ info)

My son has atypical lymphocytes following thrombocytopenia.?


He is four years old and had thrombocytopenia with platelets of 5. They are now 300. Over the past few weeks of blood test we found that he has atypical lymphocytes also and they are going up from 4% to now 16% from last week.
He is four years old and had thrombocytopenia with platelets of 5. They are now 300. Over the past few weeks of blood test we found that he has atypical lymphocytes also and they are going up from 4% to now 16% from last week. Has anyone ever experienced this? Is this something you would see in luekemia? Thank you.
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Okay, so what's your question.  (+ info)

Can my mother continue on Folfox7 treatment even if she has thrombocytopenia?


One side effect of the FOLFOX treatment is a decrease in the number of platelets in your body (thrombocytopenia), making bruises easy to develop and hard to heal. This is because the chemotherapy drugs in this treatment, while stopping the growth of cancer, also stops the bone marrow from making new platelets. So most likely, your mother has thrombocytopenia BECAUSE of the FOLFOX treatment. Thrombocytopenia is an expected side effect of FOLFOX.

When thrombocytopenia is severe (less than 10,000 platelets/ul), the doctor might decide to lower the dose of the FOLFOX drugs, or delay the treatment. However, this would decrease the patient's chances of surviving the cancer.

One way for a patient with thrombocytopenia to continue the FOLFOX treatment is to give the patient platelet transfusions (add platelets into the patient's body). And if the thrombocytopenia is severe, the doctor may want to keep the patient in the hospital for the patient's safety (this is because the patient will be easily bruised, and will bleed excessively, so staying in the hospital during the treatment would be best for the patient).  (+ info)

Help me in differentiating the thrombocytopenia induced by Chemotherapy and DIC synd? What r diff diagnostics?


Could someone help me to differentiate the thrombocytopenia induced by Chemotherapy and DIC syndrome? What are the differential diagnostics?

I searched all through the literature.. Found no satisfying answers..

Would welcome suggestions from fellow colleagues and references to articles..

Thanks in advance..
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Thrombocytopenia induced by chemotherapy and DIC are different in that the former is generally caused by myelosuppression (defect in production), and the later is caused by a problem with excessive destruction. Keeping this in mind, generally, chemoinduced thrombocytopenia (CIT) should have little to no evidence of peripheral destruction on the peripheral blood smear, while DIC will show evidence of intravascular lysis of cells, this may include hemolysis (as manifested by schistocytes, rbc fragments) in addition to platelet destruction. Therefore, DIC will also show evidence of hemolysis such as elevated LDH/lowered haptoglobin (though the LDH may be elevated by tumor lysis syndrome in chemotherapy). The ultimate diagnostic test, would be a bone marrow biopsy, indicating either presence of megakaryopoiesis (in DIC) or lack there of (in CIT). Of course, a good clinical history and exam is usually helpful.  (+ info)

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