TEG is a non-invasive test that quantitatively measures the ability of whole blood to form a clot. The thromboelastogram is a graphical image of the recorded amplitude of movement of the pin as a function of time.
Deviation of each of these TEG parameters from the reference values suggests specific disturbances of hemostasis and coagulation. Prolongation of the R time reflects a quantitative or qualitative deficiency of coagulation factors that may be corrected by fresh frozen plasma (FFP) transfusion, prothrombin complex, or anticoagulant reversal. Prolongation of the K time, or a decrease of the alfa angle, suggests a deficiency of fibrinogen and may be corrected by cryoprecipitate or lyophilized fibrinogen concentrate. Low MA indicates a quantitative or functional deficiency of platelets and could be corrected by platelet concentrate transfusion or desmopressin. Finally, an increased LY value implies activated fibrinolysis that may be treated by fibrinolysis inhibitors (aminocaproic or tranexamic acid). The opposite changes in TEG parameters suggest a prothrombotic state.
Older Questions
25/11/2020 – Attempt by selecting one of the options and clicking on the vote button.
The patient presents with refractory anemia and the presence of hypolobated micromegakaryocytes in this marrow aspirate (there are multiple of these in the image below). This suggests the diagnosis of Myelodysplastic Syndrome (MDS) with Isolated 5q Deletion ((5q –Syndrome).
MDS with isolated 5q deletion cases typically present with persistent anemia that has no other identifiable cause ie it can present as refractory anemia. They present with striking macrocytic anemia and are generally transfusion-dependent. Haploinsufficiency of the ribosomal gene RPS14 is known to cause the erythroid defect in the 5q- syndrome and leads to anemia via both p53-dependent and p53-independent tumor suppressor effects, p21, and cell cycle arrest.
24/11/2020 –Attempt by selecting one of the options and clicking on the vote button.
The aspirate here shows spindle-shaped mast cells in a symptomatic patient. Although the data in question is not sufficient to make a diagnosis of systemic mastocytosis the fact that the patient is symptomatic and bone marrow has spindle-shaped morphology is sufficient evidence to think for a possibility of systemic mastocytosis and in the case KIT mutation would be found.
Not that Mast cells having spindle morphology, expression of CD25 with or without CD2 are considered atypical and if these have KIT mutation then these are considered clonal.
Read about diagnostic criteria of MASTOCYTOSIS from WHO 2017 book.
22/11/2020 –Attempt by selecting one of the options and clicking on the vote button.
(B) Macrothrombocyte. The platelet depicted (arrow) is larger than the average erythrocyte.
(C) Microthrombocytes (arrows) are typical of those seen in Wiskott-Aldrich syndrome or X-linked thrombocytopenia.
(D) Dohle-like bodies in the cytoplasm of neutrophils (arrows) are seen in the May-Hegglin anomaly
In any male child with thrombocytopenia or immunodeficiency, the diagnosis of WAS should be considered. The presence of microthrombocytes (As in smear C) increases the likelihood of this diagnosis. Affected individuals with classical WAS are generally
recognized within 1 year of life due to bruising and bleeding as well as recurrent infections (bacterial more than viral). Diagnosis of patients with XLT may not be made until later in life. Eczema develops after the first year of life, and dermatologic evaluation to assess the severity and treatment of eczema should be undertaken. Confirmatory sequencing of the WAS gene to detect mutations should be performed in families without a prior diagnosis.
20/11/2020 – Attempt by selecting one of the options and clicking on the vote button.
The image here shows hemophagocytosis as the macrophase cytoplasm shows engulfed neutrophil.
There are inherited and non-inherited (acquired) causes of hemophagocytic lymphohistiocytosis (HLH). Primary HLH is caused by loss of function, (i.e. inactivating) mutations in genes that code for proteins cytotoxic T cells and NK cells. Secondary HLH (sHLH) is associated with and thought to be promoted mostly by infectious and malignant diseases.
The five subtypes of Familial HLH are each associated with a specific gene:
FHL1: HPLH1
FHL2: PRF1 (Perforin)
FHL3: UNC13D (Munc13-4)
FHL4: STX11 (Syntaxin 11)
FHL5: STXBP2 (Syntaxin binding protein 2)/UNC18-2
Nearly half of the cases of type 2 familial hemophagocytic lymphohistiocytosis are due to bi-allelic PRF1 mutations.
