Leukaemia Flashcards
how you can tell it is Acute myeloid leukaemia- (AML)
-Large nucleus- high nuclei/cytoplasmic ratio.
-No wbc/platelets. Fewer RBC.
Granules within cytoplasm.
Why does the blood film look like this? Acute myeloid leukaemia- (AML)
-Cells proliferate without maturation
- Accumulation of immature cells (myeloblasts) in bone barrow- spread to blood.
-unable to produce normal functioning cell like neutrophils, monocyte, platelet, RBC.
-gum hypertrophy
Acute lymphoblastic leukaemia (ALL). Pathological effects of clonal expansion
-lymphadenopathy: enlarged lymph nodes
-hepatosplenomegaly
-thymic enlargement
-bone pain
Child
Acute lymphoblastic leukaemia (ALL). Indirect effects of clonal expansion
-Lymphoblastic replace normal RBC- decrease- anaemia. -> Fatigue, lethargy, pallor
-thrombocytopenia -> bruising
-neutropenia ->fever from infection
Child
Acute lymphoblastic leukaemia (ALL). Treatment
-blood products -> RBC, platelets.
-systemic chemotherapy -> kill cells within leukaemia clones + allow regeneration of normal cells
-Intrathecal chemotherapy -> kill leukaemia clones in CSF.
- transplant
Chronic lymphocytic leukaemia (CLL). How can i tell?
-mature/SQUASHED lymphocyte=SMEAR/SMUDGE CELL.
-common cause of persistent lymphocytosis in elderly= raised CRP/WBC despite no infection
-lymphadenopathy
Chronic lymphocytic leukaemia (CLL). Diagnosis/management
-immunophenotyping
-FBC-> lymphocytosis, anaemia, thrombocytopenia.
-advanced-> targeted/chemoimmunotherapy
-risk of autoimmune haemolytic anaemia
Chronic myeloid leukaemia (CML). Symptoms
Splenomegaly
Epistaxis
Abdominal fullness
Chronic myeloid leukaemia (CML).
-common: 65-74y.o// 2.5x more common in Men
-increase in all granulocytes and their precursor (persistent leukocytosis).
-translocation between chromosome 9 and 22-> form BCR ABL1 gene. Uncontrolled tyrosine kinase activity(cell growth).
-treat: tyrosine kinase inhibitors prevent phosphorylation of key proteins
