BLS overview
GESHAN GUNAWARDANA
-RBC life span – 120d
-Plt life span – 7 – 10 d
-Neutrophil life span – 2d (in
inflammation – 6-8h) =early
manifestation of BMF
Haematology
Deficiency anemia s (Fe, B12)
Haemolytic anemias
Pancytopenias
Neoplasms in WBC (ALL, AML, CLL, CML, MM etc…)
Platelet defects (reduced number or functional) and DIC
Thrombophilia
Defects in coagulation
Transfusion medicine
Pharm (deficiency anemias, anticoagulants)
Haematology
Deficiency anemia s (Fe, B12)
Haemolytic anemias
Pancytopenias
Neoplasms in WBC (ALL, AML, CLL, CML, MM etc…)
Platelet defects (reduced number or functional) and DIC
Thrombophilia
Defects in coagulation
Transfusion medicine
Pharm (deficiency anemias, anticoagulants)
Point 1 – deficiency anemias
Fe deficiency
B12 and folate deficiency
Point 2 – Haemolytic anemia
Haemolytic profile
Point 4 –neoplasms in WBC
Lymphoid neoplasms
Lymphoid neoplasms
Precursor B cell
leukaemia/lymphoma
(Pre B ALL)
Peripheral B cell
neoplasia
CLL/SLL
Hairy cell leukaemia
Burkitt s lymphoma
Precursor T cell or NK cell
neoplasia
(pre T ALL or lymphoma)
Peripheral T cell or NK
cell neoplasia
Hodgkin lymphoma
Hodgkin vs non-hodgkin
Non- Hodgekin(B cell)
Multiple
myeloma
Myeloid neoplasms(AML/CML)
Causes for AML,
1ry – de novo gene mutation (ionizing radiation, chemicals like benzene, viruses like HTLV 1,
genetic sx like fanconi, down s)
2ry – From MDS, myeloproliferative diseases
Myelo-proliferative disorders
In PV, PMF, ET there s V617F mutation causing activation of JAK 2 kinase which
stimulate erythropoietin & thrombopoietin Receptors causing increased RBC and
plts. But GM-CSF (so not huge rise in WBC). CML has different gene mutations
Myelodysplastic syndrome
Point 4 - Pancytopenia
Pancytopenia
Reduced
production
Infiltration of BM
AML/MF
MDS(can progress
from BMF)
Increased
consumption
B12/FA deficiency
MM
Metastasis
TB
True BMF
AA
Inherited
Fanconi anemia
Dyskeratosis
congenita
Splenomegaly
PNH
Idiosyncratic
SLE
Infections(TB,AIDS
Point 5 – Causes of Macrocytosis
Physiological – pregnancy, neonates
PathologicalWith megaloblastosis (anything which
disrupts DNA synthesis)
Without megaloblastosis
B12/FA deficiency
Alcohol (most common cause)
Methotrexate (inhibit DHF reductase)
Hypothyroidism (erythropoiesis becomes
slow)
5-flurouracil
Liver diseases (cirrhosis) macrocytosis
with target cells
Haemolytic anemias (due to
reticulocytosis)
In BM infiltrations (MM, Metastasis)
Point 6 – Leuco-erythroblastic blood
picture (megaloblastosis)
M – Myelofibrosis
M – megaloblastic anemia
M – metastasis
M – Multiple myeloma
M – Marble bone disease(osteogenesis imperfecta)
H – Haemorrage (severe)
H – Severe haemolysis
Point 7 – Different types of RBC
Point 8 – causes of splenomegaly
In aplastic anemia liver,
spleen,LN are not enlarged (if
pancytopenia present with
organomegaly look for other
cuases for BMF rather than
AA like myelofibrosis
Platelet disorders
Thrombophilia
Coagulation disorders
Transfusion medicine
THANK YOU & GOOD LUCK !!!