120814 intro to anemia Flashcards
(24 cards)
anemia
decreased circulating RBC mass (can’t directly measure, so use surrogates)
compensatory mechanisms in anemia
increased RBC production increased 2,3-DPG shunting of blood from non-vital to vital areas increased cardiac output increased pulmonary fxn
signs and symptoms of anemia
weakness, fatigue (tissue hypoxia)
marrow expansion with potential bony abnormalities (increased RBC production)–in severe, chronic anemia
pallor (shunting of blood)
tachycardia (increased cardiac output)
dyspnea on exertion (increased pulmonary fxn)
functional classification of anemia
blood loss
decreased production
accelerated destruction
investigation of anemia-what to look at
clinical history and PE get you 90% of the way CBC reticulocyte count examination of peripheral blood smear specific diagnostic tests
most important parameter in CBC for assessing O2 carrying capacity of blood
hemoglobin
hematocrit provides what kind of information?
RBC volume out of total blood volume, but it’s redundant if you have hemoglobin
RBC count
number of RBCs per unit volume
generally correlates well with Hb and hematocrit in CBC so adds little independent info
MCV
mean cellular volume
very useful in differential diagnosis of anemia (microcytic, normocytic, macrocytic)
microcytic anemia differential diagnosis
iron deficiency
thalassemia
anemia of chronic disease
other (rare)
macrocytic anemia differential diagnosis
megaloblastic (impaired DNA synthesis):
B12 and folate deficiency
some drugs
myelodysplastic syndromes
non-megaloblastic (other mechanisms): reticulocytosis liver disease hypothyroidism some drugs
MCH
mean corpuscular hemoglobin
calculated as Hb/RBC
high correlation with MCV
obsolete in utility
MCHC
mean corpuscular hemoglobin concentration
measure of how chromic RBCs are
calculated as Hb/(MCVxRBC)
it’s decreased in hypochromic anemias and vice versa
RDS
red cell distribution width
measure of variability of red cell volume
useful for separation of anisocytotic anemias (Fe deficiency) from non-anisocytotic anemias (anemia of chronic disease)
bite cells represent
increased oxidant stress
Howell Jolly bodies are
nuclear fragments
rouleaux
single file stack of coins-RBCs
agglutination
3-D clumps of RBCs due to Ig cross-linking RBCs
in acute blood loss anemia, when does reticulocyte count peak?
after 7-10 days
what happens in chronic blood loss anemia?
no anemia initially because bone marrow compensates
eventual development of IRON DEFICIENCY with resultant iron deficiency anemia
reticulocyte%’s problem
reticulocyte percent varies depending on total RBC count
so need to correct for it
or another solution-get absolute reticulocyte count
decreased RBC production types
ineffective erytropoiesis
decreased RBC precursors (marrow failure)–stem cell defects with adequate erythropoietin, marrow replacement, decreased erythropoietin
anemia of chronic disease
intravascular free Hb goes on to
be combined with haptoglobin. goes to liver and is cleared
sometimes you get free heme. free heme combines with hemopexin and goes to the liver as well
hemolysis-general features
reticulocytosis
increased indirect bilirubin from heme catabolism
increased LDH released from destroyed RBCs
decreased haptoglobin (no feedback mechanism)
morphologic abnormalities of red cells in specific disorders
spenomegaly in chronic cases (spleen works hard to clear RBCs)
bony abnormalities in severe chronic hemolytic anemias
