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53 Cards in this Set

  • Front
  • Back
clinical signs of accumulation of hg degradation products
jaundice
gallstones
dark red urine
acute exacerbation of hemolysis due to activation of MACs
hemolytic crisis
impairment of BM red cell production
aplastic anemia
depletion of nutrients, folic acid, or iron
marrow exhaustion
causes hemoglobinemia and hemoglobinurea
intravascular RBC destruction
causes of intravascular RBC destruction
toxic substances in the red cell or environment (infection, drugs)
mechanism of intravascular RBC destruction
complement activation
physical trauma (march hemoglobinemia, artificial heart valves, thermal burns)
mechanism of extravascular hemolysis
Ig bind to RBC and they get trapped in the red pulp of spleen by MACs Fc binding
corrected reticulocyte count in rapid red ell turnover
>4% (hallmark of acc red cell turnover)
what is a spherocyte and what disease is it indicative of
small, hyperchromic red cell; hereditary spherocytosis, autoIg hemolytic anemias, or burns
diseases that cause schistocyte formation
HUS
TTP
DIC
prosthetic heart valves
three types of autoimmune hemolytic anemias
warm
cold
paroxysmal cold
most common type of autoimmune hemolytic anemia
warm
Ig subtype that mediates warm hemolytic anemia
IgG
antibody in warm hemolytic anemia is directed at what
Rh factor
Ig subtype that mediates cold hemolytic anemia
IgM
type of autoimmune hemolytic anemia that usually follows an infection
cold
mechanism of RBC destruction in warm antibody
extra and intravascular
mechanism of RBC destruction in cold antibody
extravascular
Ab against I antigen on RBC
cold agglutinins
biphasic autoimmune hemolytic anemia where IgG fixes in the cold and activates complement upon warming
paroxysmal cold agglutinins
alloimmune hemolytic anemia of fetus due to Rh incompatibility with mother
erythroblastosis fetalis (hydrops)
prophylaxis of hydrops fetalis
Rh Ig
what is the direct coombs test
marker Igs are added to patient serum to look for Igs to RBC
what is the indirect coombs test
patient serum is added to lab red cells and look for reaction
enzyme deficiency that causes hemolyic anemia
glucose 6 phosphate dehydrogenase deficiency
heinz bodies
G6PD
clinical signs of G6PD
asymptomatic until drug or illness
tx of G6PD deficiency
remove agent and it resolves
most common enzyme deficiency in glycolysis
pyruvate kinase
pyruvate kinase deficiency results in what changes to the RBC
membrane deformity and extravascular destruction
etiology of hereditary spherocytosis
deficiency in cytoskeleton protein spectrin
only cell that has elevated MCHC
spherocytes
therapy to hereditary spherocytosis
splenectomy
two types of hereditary hemolytic anemias
hereditary spherocytosis
hereditary elliptocytosis
hemolytic anemia that is exacerbated by sleep
paroxysmal nocturnal hemoglobinuria
RBC membrane disorder caused by deficient complement regulation and abnormal sensitivity to complement lysis
paroxysmal nocturnal hemoglobinuria
tests for paroxysmal nocturnal hemoglobinuria
flow cytometry for CD55/59
acanthocyte
hemolytic anemia due to hepatocellular disease
what is march hemoglobinemia
hemolysis due to RBC trauma
three most common thrombotic microangiopathies
DIC
TTP
HUS
tetrad of sx seen in HUS
seizures
hemolytic anemia
acute renal failure
thrombocytopenia
etiology of diarrhea positive HUS
shigella toxin e.coli
pentad of sx in TTP
fever
ARF
thrombocytopenia
microangiopathic HA
neurologic sx
etiology of TTP
absence of ADAMTS which leaves large vWF multimers
fever
chills
headache
low back pain
acute hemolysis
less severe form of mother fetal hemolytic anemia that causes mild anemia
ABO compatibility where mother is O and child is A or B
sex linked enzyme deficiency hemolytic anemia
G6PD
anemia
venous thrombosis
increased infection
increased leukemia
PNH
membrane disorder caused by an acquired mutation in PIG gene
PNH
tx of TTP
plasma exchange
peripheral smear findings in hemolytic anemias
spherocytes
schistocytes
reticulocyte levels in all hemolytic anemias
elevated (reticulocytosis is way to differentiate hemolytic anemias)