Haematology Flashcards
What is pancytopenia?
Low RBC + Low WBC + Low Platelets
- think malignancy
Raised MCV + Raised bilirubin consider what…
Haemolytic process!
What is seen on a haemolytic blood test screen?
Haptoglobin low <0.03, LDH raised, DAT + Ve (Coombs test), Raised reticulocytes 330 (25-75)
How should haemolysis be managed?
- Call haematology (it’s an emergency).
- Start folic acid
- Start steroids
What is a positive Coombs test?
An abnormal (positive) direct Coombs test means you have antibodies that act against your red blood cells. This may be due to: Autoimmune hemolytic anemia. Chronic lymphocytic leukemia or similar disorder.
Epidemiology of acute lymphoblastic leukaemia
Acute lymphoblastic leukaemia (ALL) is the most common malignancy affecting children and accounts for 80% of childhood leukaemias. The peak incidence is at around 2-5 years of age and boys are affected slightly more commonly than girls.
What is the difference between myeloid and lymphocytic leukaemias?
Myeloid comes from myeloid precursors (neutrophils)
Lymphocytic comes from lymphoid precursors (B cells)
What is ALL?
Acute lymphoblastic leukaemia
ALL is the most common cancer of childhood (2-5yrs peak). It is caused by the abnormal clinical proliferation of lymphoid progenitor cells. These lymphoid precursors infiltrate normal haematopoietic cells of the bone marrow and other organs of the body.
Chronic myeloid leukaemia (CML) epidemiology and associations
CML is most common in middle-aged patients, with males slightly more affected.
It is classically associated with the Philadelphia chromosome.
What is CLL?
CLL is most common in male patients over the age of 60. It is caused by the proliferation of functionally incompetent malignant B cells.
What is the difference between acute vs chronic leukaemia’s?
The difference between acute and chronic leukaemia is that acute leukaemia is a result of impaired cell differentiation, resulting in large numbers of malignant precursor cells in the bone marrow; on the other hand, chronic leukaemia is the result of excessive proliferation of mature malignant cells, but cell differentiation is unaffected.
How does AML present?
It typically presents with symptoms of bone marrow failure (anaemia, bleeding, infections) and signs of infiltration, including: hepatomegaly, splenomegaly, and gum hypertrophy.
How is AML diagnosed?
Blood tests commonly show leucocytosis, but white cells can sometimes be normal or low. For this reason, diagnosis is dependent on bone marrow biopsy, as well as other molecular analyses.
What is seen on bone marrow biopsy in AML?
Auer rods
Treatment of AML:
AML is commonly treated with chemotherapy regimens or bone marrow transplant.
AML prognosis:
Without treatment: Dead in 2 months
With treatment: 20% 3-year survival rate.
Pathophysiology of ALL - read to understand
Abnormal proliferation of lymphoid progenitor cells. Lymphoid precursors infiltrate normal haematopoietic cells of the bone marrow and other organs of the body.
ALL epidemiology
2-5yrs peak!
(Accounts for 80% of childhood leukaemia’s).
Symptoms of ALL
Bone marrow failure = pancytopenia = anaemia, bleeding, infections).
Symptoms may also be caused by organ infiltration, such as bone pain.
Signs on examination in ALL
Signs include painless lymphadenopathy, hepatosplenomegaly, CNS involvement (e.g. cranial nerve palsies, meningism) or testicular infiltration (resulting in painless unilateral testicular enlargement).
Diagnosis of ALL
Blood results show leucocytosis and blast cells on blood film and bone marrow analysis.
Treatment and prognosis of ALL
Chemo
Children have a cure rate of 70-90%.
CML pathophysiology
Proliferation of functionally incompetent malignant B cells.
Philiadelphia chromosome translocation.
- commonly pt aged 60-70
Symptoms of CML?
Symptoms: weight loss, tiredness, fever, and sweating, bleeding (thrombocytopenia), and gout.
