Flashcards in Pathoma Chapter 6: Part 1 Deck (47)
Myeloid stem cells give rise to what?
- Erythroblasts (RBCs)
- Myeloblasts (neutrophils, basophils, eosinophils)
- Monoblasts (monocytes)
- Megakaryoblasts (Megakaryocytes)
What is a normal white cell count?
What are some causes of neutropenia?
- drug toxicity (chemo with alkylating agents)
- severe infection (gram- species)
How do chemo alkylating agents cause neutropenia?
they damage stem cells resulting in decreased production
How do severe infections cause neutropenia?
increased movement of neutrophils into tissue results in decreased circulating neutrophils
What are some causes of lymphopenia?
- immunodeficiency (DiGeorge or HIV)
- High cortisol state (Cushing's of exogenous corticosteroids)
- Autoimmune destruction (SLE)
- Whole body radiation
How does a high cortisol state cause lymphopenia?
it induces apoptosis of lymphocytes
What are some causes of eosinophilia?
- type I hypersensitivity
- parasitic infections
- Hodgkin lymphoma
What are some causes of basophilia?
- acute myeloid leukemia
What are some causes of lymphocytosis?
- viral infections
- Bordetella pertussis infection (via lymphocytosis promoting factor secreted by the bacteria which prevents them from leaving blood to enter lymph)
What is acute leukemia?
neoplastic proliferation of blasts; defined as an accumulation of 20+% of blasts in the bone marrow or peripheral blood
Why is it called "acute" leukemia?
increased blasts crowd-out normal hematopoiesis, resulting in an acute presentation
Clinical presentation of acute leukemia?
- anemia (fatigue)
- thrombocytopenia (bleeding)
- possible neutropenia (infection)
T or F. WBC is usually elevated in acute leukemia
T. due to blasts entering the blood stream
What is acute lymphoblastic leukemia defined as?
accumulation of 20+ % of lymphocytes in the bone marrow
How are lymphoblasts identified?
via positive nuclear staining for TdT, a DNA polymerase
TdT is absent in myeloid blasts and mature lymphocytes
ALL is common in what patient population?
usually kids (associated with down syndrome)
presents after 5 y/o typically
Subclasses of ALL?
B-ALL (most common) and T-ALL based on surface markers
How is B-ALL identified?
usually characterized by lymphoblasts (TdT) that express CD10, CD19, and CD20.
Clinical course for B-ALL?
requires prophylaxis to scrotum and CSF- great response
Prognosis of B-ALL?
based on cytogenetic abnormalities
i. t(12,21)-kids- has a good prognosis
ii. t(9,22)-adults- has a poor prognosis (philadelphia)
What is T-ALL characterized by?
lymphoblasts (TdT+) that express markers ranging from CD2 to CD8 (e.g. CD3/4/7).
don't express CD10
What patient population is common for T-ALL?
usually presents in teenagers as a mediastinal (thymic) mass (called acute lymphoblastic lymphoma because the malignant cells form a mass)
What is acute myeloid leukemia defined as?
20+% of immature myeloid precursors (myeloblasts) in the bone marrow
How are myeloblasts identified?
positive cytoplasmic staining for MPO (crystals of MPO commonly seen as Auer rods)
Patient population for AMLs?
older adults (avg 50-60 y/o)
High-yield subtypes of AML (based on cytogenetics, lineage of immature myeloid cells, and surface markers):
- Acute promyelocytic leukemia (APL)
- Acute monocytic leukemia
- Acute megakaryoblastic leukemia
What causes APL?
t(15,17) PML-RARa. The fusion protein causes enhancement of RARa function, which is to disrupt myeloid differentiation, but proliferation is unaffected so promyeloblasts accumulate
What is a common risk associated with APL?