Wednesday, March 18, 2009


Dear Sharifah

Salam! As far as I know, only acute promyelocytic leukemia (AML3) can primarily cause DIC. Correct me if I’m wrong. Basically DIC in AML resulting from infiltration of myeloid cells in bone marrow which leads to thrombocytopenia.

Promyelocytic leukemia is an accumulation of immature granulocyte (could be lineage of myeloblast or megakaryoblast)

So when the immature granulocyte increase, it means that less functional platelet can be formed.

DIC is devided into two steps which are

1) Abnormal activation of coagulation (microthrombosis formation)

2) Exhaustion of coagulating factor (bleeding)

So (simple pathophysiology for us to remember is)

Disorder in hematopoiesis --> APL --> Infiltration of immature granulocyte in bone marrow --> decrease production of platelet --> thrombocytopenia --> abnormal activation coagulation pathway --> microthrombus production --> exhaustion of coagulating factor --> bleeding


sharifah on March 18, 2009 at 12:33 PM said...

accumulation immature granulocyte tu bkn ke kat pheripheral blood film kan?
bkn kat bone marrow...btol x?
immature granulocyte tu refer pd cell apa?
akan mature jd wbc apa?

Miss Independent on March 18, 2009 at 1:00 PM said...

mau tnya,

cara kamu explain sbb BM tu byk hasilkan leukemic cells so reduce platelet synthesis sbb dorg dr stem cell yg sama, kan?

hbs tu, kalo dlm case laen, apa2 case yg menyebabkan BM failure, kenapa tader pon DIC?

one more thing, ada lgi neoplasm laen yg cause DIC, tp dlm AML hnya M3. (ref: internal medcine of harrison)

Jacknaim on March 18, 2009 at 1:01 PM said...

1) Definition of AML

Acute myeloid leukaemia (AML) is a cancer that affects immature blood cells on myeloid cell line.

AML causes an overproduction of abnormal blast cells which crowd the bone marrow and prevent it from making normal blood cells.

The blast also infiltrate other tissue@ organ...

2) Dah da tulis kat atas. immature granulocyte (could be lineage of myeloblast or megakaryoblast) --> Tp dlm m3 mostly Megakaryoblast......

Jacknaim on March 18, 2009 at 1:17 PM said...

to miss independent

the keypoint is thrombocytopenia.. M3 lineage hasilkan platelet...

BM failure sila check explaination dlm emedicine. BM failure leh sebabkan thrombocytopenia.. perlu ingat yg DIC ialah condition dan bukannya diagnosis.refer kpd dua keadaan; microthrombosis bila activation of coagulation cascade then bleeding bile exhaustion of coagulating factor........

of course la neoplasma lain pun bleh sebabkan DIC. but i just explain DIC dalam AML khususnya M3 sebab jawa soalan.. ape2 shaja disease yg boleh activate coagulation pathway bleh sebabkan secondary DIC.... kk

Ibnu Shaukani on March 18, 2009 at 1:26 PM said...

yup, naim jwb based on AML.thnx naim.

tp, soalan kak pa general : how malignancy lead to DIC kan..

Ibnu Shaukani on March 18, 2009 at 5:40 PM said...

tumpang tnya, mcmana thrombocytopenia lead to abnormal activation of coagulation pathway?

yg aku tahu, sebab reduce platelet, akan menyebabkan bleeding takde sapae control utk clot, so akan jd terus bleeding. x tahu reduce platelet akan activate abnormal activation coagulation pathway. bleh terangkan x?

haidarrealm on March 20, 2009 at 1:43 AM said...

salam..kitorang ade bincang psal aml dlm stdy grup td...mcm ade pcnggahan sket ngan ape yg jacknaim bgtau..
1. M3 bkn lineage megakaryoblast tp promyelocyte (myeloblast lineage)..M7 yg megakaryoblast
2. thrombocytopenia tjadi sbab supression ator lineage
3. DIC tjadi dlm M3 sbb leukemic cell tu produce fibrinolytic factor n procoagulant
untuk tau lbh lanjut bkak robbins patho yg besar 694..
good luck

Anonymous said...

The mechanism of DIC induction in patients with AML-M3 appears to involve the primary granules of the transformed promyelocytes. These primary granules contain a thromboplastin-like substance capable of activating the extrinsic system of coagulation as well as cancer procoagulant, a factor X activator.5,6,15-- 17 The release of these substances sets the abnormal clotting phenomenon in motion such that the greater the release of primary granules, the greater the clotting, and the more severe the symptoms, M3 produces increased numbers of promyelocytes, which results in a large degree of cell death and the release of massive amounts of granule contents.



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