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29 Cards in this Set

  • Front
  • Back
What are clinical conditions of hematologic malignancy?
*Leukemia
*Lymphoma
*Benign Lymph node disorder
*Multiple Myeloma
*Polycythemia
what are four types of leukemia?
Acute Lymphoblastic
Acute Myelogenous
Chronic Lymphoblastic
Chronic Myelogenous
what is difference of cells that leukemia is derived from?
lymphoblastic is from lymphoid precursors

myelogenous is from neutrophilic and monocytic precursor cells
what is the major key of dx acute leukemia?

how can you tell which acute leukemia it is?
acute leukemia has predominance of BLASTS

if the blasts are lymph or myelo

also lymphoblastic has unique CNS involvment and lymphadenopathy
what is typical age of Acute lymphoblastic?

acute myelogenous?
lymphoblastic is kids and teens (3-7)

myelogenous is 50
what are s&S of acute leukemia?
bone pain
hepatosplenomegaly
signs of anemia
signs of thrombocytopenia (petech, purp, ecchy, nose bleed)
what are the majority of blasts in acute lymphoblastic leuk?

what are major subtypes of acute myelogenous?
most are type B (rest are T)

myelo=8 major subtypes (M0-M7)
what is key dx feature of chronic leukemia?

which leukemia has the philly chromosome?
chronic has mature differentiated B/T cells or neutrophils

Chronic Myelogenous has philly chromosome
what is the most common leukemia in US and estern europe?

what lab finding is consistent with this?
Chronic Lymphocytis is most common leukemia

Periph Smear shows smudge cells (and absolute lymphocyte count >5000)
what are typical signs of chronic leukemia?
weight loss, fatigue, fever, night sweats

early satiety and LUQ pain assoc with splenomegaly
what condition needs to be ddx's from CML?

how can you differentiate?
leukemoid rxn needs to be distinguished

leukemoid has INCREASED lap and absent philly chromosom
what is tx of ALL?

what is treatment of CML?
ALL is indcution, consolidation and maintenance

CML=Gleevac(imatinib mesylate)
what is prognosis of AML?
CLL?
CML?
AmL has 40-60% rate if they have a bone marrow or stem cell transplant from HLA identical sibling

CLL=prolonged survival but not curable

CML has 90% 5 year follow up with gleevac and 83% overall(very promising)
what are two types of Lymphoma?

what is lymphoma
Non Hodgkins and Hodgkins

malignant proliferation of lymphocytes usually presenting as painless lymphadenopathy
what are follicular and small lymphocytic lymphomas?
low grade non hodkings

the rest are high grade
what is the major difference b/w non hodge and hodge?
NHL is localized or generalized and has internodal LESS predictable spread
what is presentation of follicular low grade NHL?

what is presentation of small lymphocytic?
follicular is painless peripheral lymphadenopathy

small lymphocytic is similar to CLL
what is treatment of follicular low grade NHL?

what is prognosis
tx with rituximab(rituxan) antibody therapy (traditional CHOP as well)

prognosis is not cureable yet
what is age of onset of High grade NHL?
acute lymphoblastic is kids
burkitts is kids and immunocompromised
Diffuse large cell is middle age and elderly
which type of high grade NHL is the most invasive?

what is tx?

what is prognosis?
diffuse large cell

tx is chemo for generalized and local radiation

prognosis is 70% cure rate general and 85-90 local
what are peak ages of hodgkins lymphoma?

what are major presenting sx?
bimodal 15-35 then >50

more common in males

majority are asymptomatic but can have B symptoms (fever, night sweat, weight loss)
what is tx of Hodgkins?

what is prognosis?
CHEMO and readiation

prognosis is very good (>90%)
what is multiple myeloma?

when does it occur?
malignant proliferation of plasma cells

middle age and elderly
what is the classic triad of the multiple myeloma?

what are other impt findings?
1. marrow plasmacytosis
2. lytic bone lesions
3. serum and/or urine PARAPROTEIN

other's include:
bone pain, back and chest pain, anemia and hypercalcemia
what causes relative polycythemia?

is there an increase in RBC mass?
dehydration

no increase in RBC mass
what is absolute polycythemia?

what are causes?
increase in RBC mass

primary cause (VERA) from excessive proliferation of RBC's

*hyperviscosity and hypervolemia

secondary is from increased serum erythropoietin
what are causes of secondary absolute polycythemia?
hypoxia or erythropoietin
what is classic presenation of poly vera?

what are other common s&s?
ITCHINESS afte warm shower or bath is classic

other includes hyperviscosity and splenomegaly
what is a complication of poly vera?

what is treatment of poly vera?
complication is life threatening thrombosis or hemorg of upper GI

tx with periodic phlebotomy to decrease RBC

possible hydroxyurea and splenectomy