The Megakaryocytes' Clinical Significance, Tetralogy of Fallot, Nail Clubbing, Cardiology 

For my own reference Diseases: * = Myeloproliferative neoplasms (MPNs) 1:37 - *Alcoholism* - (Low megakaryocytes -> Low platelets -> Bleeding / Petichiae) 1:58 - **Essential Thrombocytopenia* - (Clonal malignancy -> High megakaryocytes -> High platelets) 2:50 - **Polycythemia Vera* - (Clonal malignancy -> Increased proliferation of ALL cell lines -> High megakaryocytes -> High platelets) 4:35 - *Right-to-left shunts*, _e.g. Tetralogy of Fallot_ - (Megakaryocytes bypass pulmonary circulation and get trapped in sinusoids and secrete PDGF -> Clubbing + Hypertrophic osteoarthropathy + Periostitis) 9:39 - *Megaloblastic anemia* - (Low B12/folate -> Decreased DNA replication -> Large hematopoietic cells with open chromatin -> All lines giant) 11:33 - *Aplastic anemia* - (Poor bone marrow -> Decreased proliferation of ALL cell lines -> Low megakaryocytes -> Low platelets) 13:29 - **Primary myelofibrosis* - (Clonal malignancy -> High atypical megakaryocytes -> Monoclonal proliferation of fibroblasts in bone marrow -> Increased bone marrow fibrosis -> Initial panmyelosis with subsequent pancytopenia) 14:57 - *Myelodysplastic syndrome (MDS)* _AKA mini AML_ - (Defective maturation of all myeloid cell lines -> WBC hyperproliferation -> Low and abnormally sized megakaryocytes -> Low platelets) 17:18 - *MDS with 5q deletion (5q-syndrome)* - (Subtype of MDS with High megakaryocytes -> High platelets) 15:57 - **Myelofibrosis with myeloid metaplasia (MMM)* - (Clonal malignancy -> Dysplastic megakaryocytes) 18:21 - *Immune throbocytopenic purpura (ITP)* - (Immune mediated platelet destruction -> Low platelets -> Compensatory increase in TPO -> High megakaryocytes) 18:36 - *Thrombotic thrombocytopenic purpura (TTP) / Hemolytic uremic syndrome (HUS)* - (Large vWF multimers -> Excessive platelet aggregation -> Low platelets -> Compensatory increase in TPO -> High megakaryocytes) 19:55 - *Acute uncompensated deseminated intravascular coagulation (DIC)* - (Tissue factor released into circulation -> Widespread fibrin deposition -> Fibrin microthrombi -> Platelet (and coagulation factor) consumption -> Low platelets -> Compensatory increase in TPO -> High megakaryocytes) 20:39 - *Acute megakaryocytic Leukemia (AML)* - (High megakaryocytes -> Monoclonal proliferation of fibroblasts in bone marrow -> Increased bone marrow fibrosis) 20:54 - *Gray-platelet symdrome-like disorder* - (X-chromosome-linked mutation of GATA1 -> Absence of alpha granules in platelets -> Large agranular platelets + Fibrinogen (and other alpha granule proteins) accumulate in Bone marrow -> Bone marrow fibrosis)

we always get taught to check for clubbing in lung disease but NO ONE ever explained why it happen. Thank you for clarifying the theory behind this finding, 'it makes so much sense' when you know what you are looking for and why!!!!

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1) Megakaryocytes can be found in the spleen at Primary Myelofibrosis due to extramedullar hematopoiesis in advanced stage. 2) Underproduction = low Megakaryocytes and/or enlarged (folate/B12 deficiency) in bone marrow. Overdestruction = high number of Megakaryocytes in bone marrow to compensate by more platelet production. 3) Clonal thrombocytosis has morphologycaly abnormal nuclei of Megakaryocytes.

can you add subtitles please?

A great video! Thank you ❤️

Could u plz explain mds in a video if possible .... Also the point about hypercellularity yet pancytopenia

thank you thank you thank you thank you

Sir isn't M2 more common than M7?

Why would a bone marrow biopsy show rare megakaryocytes and light hemodilution

I blame you to describe obese large cells as Egyptian parliament I think you have wrong idea about us I would like to invite you to visit Egypt And I am sure you will change your mind