Leukemias Flashcards
What do abnormal CBC patterns indicate
Leukocytosis: reactive vs cancer or BM d/o
Leukopenia: meds, splenic sequestration, BM d/o
Polycythemia: dehydration, BM d/o
Thrombocytosis: reactive vs BM do
Thrombocytopenia: consumptive vs BM d/o
What are the WBC
Neutrophils Eosinophils Basophils Monocytes Lymphoctes
What do different leukocytosis findings indicate
Blasts: AML/ALL
Bands: infection
High neuts, low lymphs, no abn cells: Corticosteroids
If you find polycythemia vera (high H&H), inquire about these
Dehydration Tobacco use OSA Pickwickian (very obese= high risk OSA) JAK2 mutation High EPO levels
If you find thrombocytosis, inquire about these
Co-existing anemia
infection
removed spleen
non-infx inflammatory condition
What are Myeloproliferative Neoplasm
Acquired clonal abnormalities, can lead to MDS
Basically, the thermostat that control blood cell production is turned UP!
MPN and MDS are on a continuum as part of chronic myeloid neoplasms and can progress to acute leukemia*
Compare MPN vs MDS
MPN: terminal myeloid expansion= too much blood!
MDS: cell dysplasia= not enough blood!
What are the chronic myeloproliferative neoplasms
CML polycythemia vera essential thrombocytopenia primary myelofibrosis non-classic MPN
What are the types of polycythemia
Primary: 2/2 acquired or inherited mutation; polycythemia vera, chuvash polycythemia, idiopathic erythrocytosis
Secondary: 2/2 elevated Epo; Epo secreting tumor, Hypoxia
Combined: decreased plasma volume + increased RBC mass; tobacco use
What is polycythemia vera
JAK 2 mutation (exon 14&12) causes increased RBC mass, with a low Epo level
Dx w/ BM Bx: hypercellular with absent Fe stores (overproducing RBC but not iron)
MC in 60+ y/o
How does polycythemia vera present
Hgb: 18 Pruritis after warm shower HA, dizziness blurred vision tinnitus fatigue early satiety PUD Sx Erythromelalgia of hands and feet Facial plethora plenomegaly HTN Excoriated skin Thrombosis or hemorrhage
How do you treat PV
Phlebotomy! Want Hct <45%
Low dose aspirin
Cytoreductive agents: Hydroxyurea* (brings all cell counts down!)
-Prevent it from progressing to primary myelofibrosis
What is essential thrombocythemia (primary thrombocytosis)
Plt: 1 million! (can dx at >450)
BM Bx: normocellularity w/ prominent megakaryocytes
JAK2 mutation
-R/o iron deficiency
-Increased risk for hemorrhage and thrombosis
How do you treat Essential Thrombocythemia
Low dose ASA
Hydroxyurea
What is CML
Overproduction of myeloid cells (WBC 100-200)
MC in middle aged
*Philadelphia chromosome associated
What are the phases of CML
Chronic stable: MC. if not Tx, can progress to blast phase
Accelerated: increased blasts. will progress to blast phase in 4-6 months
Blast phase (crisis): survive 1-2 years. May see ALL or AML
How does CML present
Fatigue
night sweats
low grade fever
abd pain (2/2 splenomegaly)
CML labs will show
High WBC (100-200) low LAP score Presence of BCR or ABL gene <5% blasts Dont need BM Bx, but it is strongly required
How do you treat CML
Allogenic stem cell transplant may cure if pt is really sick!
Tyrosine Kinase Inhibitors for disease control: Gleevec* (imatinib) may decrease need for transplant in CML pts
Palliative care w/ cytotoxics: Hydroxyurea (IF + cytarabine have more ADE)
What are the types of transplant you can get
Allogenic: from others
Autologous: from yourself after it has been cleaned
How does Gleevec work in CML
Inhibits tyrosine kinase which may be an abnormal defect in philadelphia chromosome
What is non-classic MPN
Chronic neutrophilic leukemia
hypereosinophilic syndrome (HES)
chronic eosinophilic leukemia (CEL)
-Basically MPN W/O: BCR-ABL gene
What do you need to rule out in HES/CEL
Parasitic infection!
You suspect it because both have elevated eosinophils, which indicate parasite infx
What happens to cells in acute leukemia
Progenitor cells lose the ability to differentiate
The worse acute leukemia prognosis is if it arises from MDS or MPN
Can also be caused by benzene and cytotoxic agents (melphalan, etoposide- chemo drugs)
