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69 Cards in this Set

  • Front
  • Back
what is MCV
size of the corpuscle ( RBC)
what is Hgb
hemoglobin content
what is Hct
RBC count X MCV
what is MCH
mean corpuscular hemoglobin

Hgb/RBC = # of hemoglobin per RBC
ref range for RBC counts (median)
Hgb = 15.5 m, 13.5 w
Hct= 44 m, 38 w
RBC= 5 m, 4 f
MCH= 30
MCHC= 30
wht is MCHC
Hgb/Hct = Hgb concentration per RBC
anisocytosis
dif in size
hypochromia
dec MCH
central pallor
poikilocytosis
dif in shape
polychromatophilia
young RBC c bluish tint
acanthocyte
cell with long projections
schistocyte
fragmented cell - irregular shape
stomatocyte
slit like central pallor
basophilic stippling
RNA aggregates- blue dots in RBC
Heinz body
Hgb precipitate (blue dot)
howell- jolly body
round, basophilic nuclear remnant
pappenheimer body
multiple, iron containing, granular blue dots
rouleaux
stack of RBCs
siderocyte
RBC with iron
what is the normal myeloid to erythroid ratio
1:1
what are the 3 mechs of anemia
blood loss
impaired production
increased distruction
clinical features of anemia
pale, weak, malaise
doe
brittle nails
fatty change in liver, heart and kidney
headache, faint, dim vision
what are the major features of hemolytic anemia
premature destruction of RBCs
accumulation of Hgb catabolism byproducts
inc in erythropoesis
where do hemolytic anemias usually happen
extravascular hemolysis

macs in the spleen
if it does happen, what are the features of intravascular hemolysis
hemoglobinuria
janudice
hemosidenuria
elevated bilirubin levels in the blood lead to the formation of (other than jaundice)
gallstones
what is the typical genetic defect in spherocytosis
deficiency of ankyrin protein (cytoskeletal component of RBCs)
is spherocytosis extra or intravascular
mostly extravascular
clinical factors for hereditary spherocytosis
anemia, splenomegally, jaundice
parvovirally induced aplastic crisis
gallstones
treatment for spherocytosis
splenectomy
what pathway is G6PD crucial for and what is its fxn
pentose phosphate pathway

restores NADPH supplies

this NADPH reduces glutathione which inhibits oxidative stress on the cell
what are the 2 G6PD variants that cause hemolysis
G6PD-A
G6PD - Mediterranean
what are the positive effects of G6PD deficiencies
antimalarial measure by the body
what is the inheritance pattern of G6PD deficiencies
X-linked

Males- all erythrocytes effected
Females mono or hetrozygous for it
what drugs can induce anemia in people with a G6PD deficiency
Primaquine and chloroquine
sulfas, nitrofurantoins
what type of veg should G6PD deficient people avoid
fava beans
what typy of hemolysis occures in individuals with G6PD deficiency
intra and extravascular hemolysis
what might you see in a RBC of someone with a G6PD deficiency
heinz bodies- Hgb precipitates
why do you see extravascular hemolysis in G6PD deficiency
the heinz bodies inhibit deformability of the RBC and the splenic macks bite into them, then englulf them later
which RBC are vulnerable to lysis from oxidant injury in a G6PD deficiency
the old cells are far more vulnerable
which Hgb chain is effected by sickle cell
the B-globin chain
what causes the defect in B-globin in a sickle cell person
substitution of a valine for a glutamic acid at the 6th place
what happens to the MCHC in a sickled cell
it increases
what Hgb molecule inhibits the polymerization of HbS and is used in sickle cell therapy
HbF
which Hgb molecule aggregates more readily with HbS
HbC
what does dehydration do to sickle cell pts
induces sickling by increasing the MCHC
what body sites are most affected by sickle cell
bone marrow
spleen
peripheral vascular beds
what types of hemolysis do you see in sickle cell
intravascular and extravascular
what skull effect is common in sickle cell and B-thalassemia
the crew cut look on xray due to bone marrow hyperplasia
what are the morphological effects of sickle cell
anemia
bone marrow hyperplasia
hyperbiliruibinemia, jaundice
pigment gallstones
capillary stasis and thrombosis (infarctions and ulcers)
what happens to the spleen of sickle cell pts?
enlarged in children
continued thrombosis, infarction, and scarring leads to progressive shrinking
autosplenectomy by adolescence/adulthood
clinical presentation of Sickle cell
severe anemia
vaso-occlusive crises (very painful)
chronic hyperbilirubinemia
painful bone crisis in children (hard to distinguish from osteomyelitis or hand-foot and mouth synd)
lung crisis
CNS hypoxia (stroke, seizures)
leg ulcers
parvo induced aplastic crisis
sequestration crisis (children c splenomegaly- hypovolumic/shock)
treatment of sickle cell
hydroxiuria- inc HbF concentration, inc RBC volume, anti-inflamm, NO producer
what is the difference btw B0 and B+ thalassemias
B0 has no B-globin chains in the homozygous state
B+ has a reduced amount of B-globin chains in the homozygous state
how does impared B-globin snthesis contribte to anemia
inadequate HbA formation makes MCHC low and cells are hypochromic
the imbalance affects the RBC's survival
-free chains aggrigateand form inclusions that damage the cell membrane
- apoptotic death of RBCs in the bone marrow (ineffective erythropoesis)
- inclusions in the RBCs, that make it to the blood, cause them to be destroyed in the spleen
what happens to the bone marrow in B-thalassemia pts
it expands and becomes hypererythropoetic
-crew cut appearance of the skull on xray
why is systemic iron overload a problem for B-thalassemics
ineffective erythropoesis leads to an increase in iron absorption in the diet and repeated blood transfusions add to the iron pool.

thalassemia pts receiving blood transfusions must be on iron chelators
what happens to the liver and spleen in thalassemia pts
they enlarge due to extramedullary hematopoesis and also splenomegally due to RBC destruction
what are the effects of B-thalassemia major
severe anemia c all of the conditions previously discussed
transfusions are required (death in childhood w/o it)
HbA dec, HbF inc
peripheral smear: anicytosis, microcytic hypochromic cells, target cells
facial distortion and is large
cardiac disease
ethnic predisposition for B-thalassemia
mediterranean
African
Southeast Asia
effects of B-thalassemia minor
more common, heterozygotes
malarial protection
asymptomatic/mild anemia
hypochromia, microcytosis, and target cells in blood smear
HbA2 inc, HbF norm
what are gamma4 tetramers called and what is it associated with?
barts hemoglobin
a-thalassemia
what are B-globin tetramers called and what are they associated with
HbH
a-thalassemia
what is true of a-thalassemia disease as compared to B-thalassemia
a-thal is much less severe than B-thal
what are the 4 diff a-Thalassemia classifications
Silent -a/aa
trait --/aa or -a/-a
HbH disease --/-a
hydrops fetalis --/--
clinical symptoms of silent a-thalassemia
no anemia
clinical symptoms of a-thalassemia
minimal or no anemia
clinical symptoms of HbH thalassemia
typically effects asians
HbH has extreme O2 affinity, bad for tissue perfusion
Older RBCs with HbH precipitate are removed by spleen
moderately severe anemia
clinical symptoms of hydrops fetalis
Barts Hbg forms
intrauterine death in the past
intrauterine transfusions can save the infant