last lot Flashcards
cytogenetic change in most follicular lymphomas
bcl-2 oncogenet
t(14;18)
CLL- what kind of cell?
asians- T cell
westerns- B cell
CLL bad
Zap 70
del 17q13
p53
Hodgkins- lymphocyte deplete or predominant best prog?
lymphocyte deplete worse prognosis
NK flow cytom
16, 56, 57
B cell flow
19,20,22
also follicular often CD10- immature B cells
some indolent lymphomas often pinch some T cell markers to confuse you - CD5, CD43
T cell flow
CD 2,3,5,7
and 4 and 8
Mantle flow
CD 5 pos
CD 23 neg
CLL flow
CD 23
CD5
myeloid flow
CD 13
CD33
MDS presentation
rarely present with opportunistic infection as B and T cells work fine
improve survival in MDS
azacitadine
how does deferasirox work?
oral, binds Fe3+
acquired vs inherited factor VIII def
in inhibitor acquired will not correct study
in congen haemophilia will correct
VWD usual inheritance
AD
VW factor in haemophilia
factor 8 in VWD
in VWD factor 8 is low
in haemophilia, VWfactor is normal
How do you bypass a factor 8 inhibitor
give factor VIIa
can also try immune tolerance induction/desensitisation
desmopressin which haemophilia
A only
not b
What is peak HIT onset?
5-10 days or one day if previous exposure in last 30 days
drop over 50 percent from highest reading post starting hep, still over 20 count
no other reason
new thrombosis
Why no warfarin in acute HIT
risk skin necrosis and venous gangrene during initiation
wait until plt over 150 , and overlap for 5 days
if with thrombosis- 3 months
if wihtout thrombosis - 1 month
if down track need PCI- use bivalirudin or argatroban
if down track totally recovered and immuno assay neg- can use UFH intra op for cardiac and valve surgery. If assay positive, use bivalirudin
DIC chronic vs acute
both have high fibrin deg products and d dimer up
THROMBIN TIME normal to slight increase in chronic- up in acute
factor levels and PT and APTT normal in chronic
