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54 Cards in this Set

  • Front
  • Back
What is CDA
-inherited, refractory anemias characterized by both
abnormal and ineffective erythropoiesis
-the red cell precursors in the bone marrow exhibit multinuclearity
CDA type I
- characterized by mild macrocytosis but prominent anisocytosis and poikilocytosis in the blood
- bone marrow has multilobated erythroid precursors with megaloblastoid changes
CDA type II
-erythroblasts show bizarre changes, but no megaloblastic features
-normocytic, normochromic anemia present
-positive Ham’s test (acidified serum test with cells susceptible to hemolysis in acidified serum)
-red cells also have increased blood group antigen i
CDA type III
- erythroblasts are giant and multinucleated; in fact, some may have as many as 12 nuclei and are called gigantoblasts
- megaloblastoid changes are not prominent, but the anemia is nevertheless macrocytic
What is PNH
PNH is a rare, acquired disorder of the red cell membrane characterized by the membrane’s abnormal sensitivity to complement and caused by an abnormal clone of hematopoietic stem cells.
PNH type I
cells display absent to minimal lysis
PNH type II
cells show intermediate susceptibility to lysis
PNH type III
cells excessively sensitive to complement lysis
clinical features of PNH
1. most often seen in the third to fifth decade
2. insidious onset
3. the classic presentation from which the name of the disorder is derived is not common
4. hemosiderinuria is present in most patients
5. venous thrombosis severe complication
6. infections common when leukopenia present
lab findings of PNH
1. characteristically see anemia, leukopenia, and thrombocytopenia
2. usually see normocytic, normochromic blood smear
3. reticulocytosis
4. NRBC may be seen
5. decreased RBC membrane acetylcholinesterase
6. decreased LAP (leukocyte alkaline phosphatase)
7. positive urine hemosiderin
8. bone marrow shows erythroid hyperplasia
tests for PNH
a. sugar water test (sucrose hemolysis test)
b. Ham’s test (acidified serum test
c. detection of GPI anchored cell surface antigens using monoclonal antibodies and flow cytometry
CO bound to heme instead of O2
formed when iron of Hgb molecule is oxidized to ferric state
inherited methemoglobin
deficiency of enzyme NADH-methemoglobin reductase
-this enzyme reduces cytochrome b5, which converts naturally occurring ferric iron back to the ferrous state
acquired methemoblobin
occurs in healthy individuals when drugs or other toxic substances oxidize Hgb in circulation
formed when a situation or condition, such as ingestion of a sulfur-containing drug or chronic constipation, causes a build up of the sulfur content of the blood
American blacks commonly express HbDPunjab which is the same as
HbDLos Angeles
glutamine-->glutamic acid @ position 121 on beta chain
HbS and HbG at alkaline pH
second most common hemoglobinopathy
results from the substitution of lysine for glutamic acid at the 26th position on the beta chain
migrates with HbA2, HbC and HbOArab at alkaline pH
-results from a substitution of lysine for glutamic acid at position 121 on the beta chain
-migrates with HbC, HbE and HbA2 at alkaline pH
Hb Constant spring
-31 extra amino acids on alpha chains
-inefficient alpha chain synthesisj
-mild micro/hypo
-Hb Barts xs delta chains floating around
Hb Lepore
-classified as a variant of beta thal because the non-alpha chain is actually a hybrid beta chain
-HbS at alkaline pH
-hybrid delta-beta chains
-xs alpha chains
-decreased Hb
-smear is a mess (like beta thal)
HPFH hereditary persistence of fetal Hb
-decreased delta and beta chain synthesis is compensated for by increased gamma chain production in adult life
-only HbF produced, no xs alpha chains
-no clinical symptoms (no anemia)
delta-beta thal
-no production of delta and beta chains
-mild anemia micro/hypo
-delta chain production can fully compensate for loss of beta chain synthesis
forward scatter
detects cell size
side scatter
detects cell granulation and nuclear structure
B cell markers
CD 10, 19, cytoplasmic Ig chains
M0 markers
CD 13, 33, 34
M1/M2 markers
CD 15
M3m markers
CD 13, 33 no HLA-DR
M6 markers
glycophorin A
M7 markers
CD 41, 42, 61
PLL marker
no CD 5
Hairy Cell Leukemia marker
expresses CD 103
Why iron is toxic
iron can take a proton from oxygen or hydrogen peroxide to become Fe 3+ and create free radicals
moves iron across the gut lumen
DCYTB reductase
reduces iron from 3+ to 2+ so it can be transported from gut lumen to cytoplasm
storage form of 2+ iron in cells
move iron 2+ out of cell into plasma
-only binds 3+
-tranfers iron in blood stream because free iron floating is bad
oxidase converts 2+ into 3+ in plasma
transferrin receptors
retics have lots, mature RBC do not
-malregulation of iron absorption leads to disease, iron deposition in the liver
-causes ferroportin internaliztion
-synthesis increased by inflammation/iron stores and decreased by hypoxia/anemia
refractory cytopenia with unilineage dysplasia
-no myeloblasts in PB and <5% in BM
-survive 66 months
-low chance AML
refractory anemia with ringed sideroblasts
-15% or more of erythroblasts are ringed sideroblasts
-dimorphic anemia
-survive 6 years, low chance AML
refractory cytopenia with multilineage dysplasia
-one or more PB cytopenia
-BM myeloblasts at least 5%
-survive 20 months, AML progression is variable
5-9% BM blasts and 2-4% PB blasts
10-19% BM blasts and 5-19% blasts in PB
myelodysplastic syndrome with isolated deletion
-deletion of chrom. 5
-anemia (often macrocytic)
-elderly women, survive 12 years
-<5% blasts in BM and <1% blasts in PB
chronic myelomonocytic leukemia
-Ph' and BCR-ABL neg.
-dysplasia of one or more myeloid lineages
blasts <5% in PB and <10% in BM
blasts 5-19% in PB and 10-19% in BM
atypical chronic myeloid leukemia
-no Ph' of BRC-ABL fusion gene
-dysplasia in erythroid and megakaryocytic lineages may be seen in BM
-seen in middle aged people
juvenile myelomonocytic leukemia
-abnormal proliferation of granulocytic and monocytic cells
-75% of cases in children <3 years old
-cases with an abnormal karyotype have bee linked to markedly elevated levels of HbF