Lymphoid and Myeloid Disorders Flashcards
Normal blood film
Erythrocytes
Bi concave discs
Thinner parts appear transparent as more light can get through
Lymphocytes and neutrophils and small platelets dotted throughout
Acute leukaemia
Mechanism
Leads to
Proliferation of primitive precursor cells usually only found in bone marrow
Proliferation w/out differentiation
Primitive cells replace normal bone marrow cells
No space for normal cells to mature
Anaemia - Palor and lethargy
Neutropenia - immunocomprised
Thrombocytopenia - bleeding
Bone pain due to marrow infiltration
Leukaemia Acute
Lymphoid
Acute lymphoblastic leukaemia
Myeloid
Acute myeloid leukaemia
Leukaemia chronic
Lymphoid
Chronic lymphatic leukaemia
Myeloid
Chronic myeloid leukaemia
Histology of acute leukaemia
Leukaemic cells are abundant
Acute lymphoblastic leukaemia
Treatment
Common in children
Proliferation of lymphoblasts in bone marrow
85% survival rate - esp in girls, 1-10, low WBC and certain morphology
Poor prognosis in adults
Induction
Consolidation chemo and or craniospinal irradiation
Maintenance chemotherapy
Bone marrow transplantation only if relapse
Acute myeloid leukaemia
Relevant subtype
Treatment
Malignant proliferation of myeloblasts in bone marrow Affects adults Poor prognosis 15-50% 5 year survival Most relapse 6 subtypes
Gum infiltration in acute monocytic subtype M5
Cyclical high dose chemo (induction and consolidation with no maintenance)
Sometimes transplant
Chronic lymphatic leukaemia
Histology
Proliferation of mature lymphocytes usually B cells Most common Affects elderly >65 years Presents with anaemia, infections, lymphadenopathy and splenomegaly Lymphocytosis Good prognosis Survival > 10 years is norm Treats only advanced disease
Dense nuclei of lymphocytes
Chronic therefore
Chronic myeloid leukaemia
Treatment and mechanism of it
Histology
Gradual onset
High WBC and splenomegaly
Chromosome translocation between 9-22 BCR-ABL oncogenes 3 phases - chronic -accelerated - blast crisis
Treatment
- imatinib
blocks abnormal oncogene activity
molecular remission can occur
Bone marrow cell transplant
Myeloblasts with open DNA
Myelodysplasia
Mechanism
Who does it affect
Presenting condition
Treatment
Premalignant condition of heamopoietic precursors i.e. bone marrow cells
disease of elderly
asymptomatic sometimes
may present with anaemia, thrombocytopenia and pancytopenia
several subtypes
variable course
can transform to acute myeloid leukaemia
treatment - supportive, bone marrow transplantation in the young
Lymphoma
Types
Hodgkin
Non-hodgkin
Hodgkin lymphoma
Types
Diagnostic cell
Treatment
Painless lymphadenopathy B symptoms - sweats, weight loss, fever Two peaks 15-35 years, >55 10 year survival 90% rate 4 subtypes
Reed-Sternberg cell
Chemo, radiotherapy, stem cell transplantation
Non-Hodgkin lymphoma
Two grades
Indolent/low grade e.g follicular lymphoma
Gradual onset
May be asymptomatic
Incurable, median survival 10 years
Chemotherapy, radiotherapy, transplantation
Aggressive, high grade e.g diffuse large B cell lymphoma
Rapidly progressive
Usually symptomatic
Potentially curable
Treatment - chemotherapy, radiotherapy, transplantation
Myeloproliferative disorders
Polycythaemia rubra vera
- red cell proliferation
Chronic myeloid leukaemia
- white cell proliferation
Essential thrombocythaemia
- platelet proliferation
Myelofibrosis
- marrow stroma proliferation
Polycythaemia is
11.50-14 haemoglobin - females
12-16 - haemoglobin - males
Erythrocytosis Increase in circulation of red cells Primary - PRV - thrombosis - splenomegaly, hepatomegaly - venesection, aspirin and myelosuppression treatments - myelofibrosis and AML can result Secondary - hypoxia - inappropriate erythropoietin secretion - renal tumour
