how big is the cell? Best way to classify is with MCV (mean corpuscular volume) Small, normal or big?
The machine has the RBC’s pass through an aperture and sizes it. And then takes an average; this is the
best way for classifying an anemia
MCV: < 80, it is microcytic (if you play odds, its Fe def)
MCV (normal): 80 -100 =; have Normocytic anemia;
MCV above 100 = macrocytic (b12 or folate)
If you have small and large cells (dimorphic popcorn of RBC’s) it will be Normocytic
(Like the met acidosis, and resp alk, but normal pH). So, how could you have a Fe def anemia and a
folate def anemia at the same time? Know where these things are reabsorbed – Fe reabsorbed in
the duodenum, Folate is reabsorbed in the jejunum, and B12 is reabsorbed in the terminal ileum. So
if you have all these, you have small bowel dz (ie celiac dz); pt has malabsorption that affects diff
areas of the bowel. Example: celiac sprue (MCC malabsorption) – involves duodenum and jejunum,
therefore will have def of Fe and folate, and will have small cells and large cells. Example: if it
involves the jejunum and terminal ileum, you will have folate and B12 def.
RDW – RBC Distribution Width
This machine looks at the RBC’s and tells if the RBC’s coming out of the aperture are all uniformly
small, normal, macrocytic, or different in size. So, the RDW detects a change in size of the RBC’s and
it reports it as a number. Example: microcytic anemia, with an increased RDW; this tells us that is
microcytic, and there are different sized microcytic cells. Example: if you develop microcytic anemia
overnight and all the cells are Fe def, the cells don’t become microcytic immediately; they are
normocytic first before they become microcytic, and there will be a size variation picked up by the
Here’s the trick: when you look at the CBC, and it shows decreased MCV with an increased RDW,
this is Fe def anemia (not thalassemias b/c that is genetic and ALL the cells are microcytic).
Slide with high RDW – has large and small cells. Another slide with spherocyte (have too little
membrane, and therefore cannot hold a biconcave disk - an anorexic cell), and target cell (has too
much membrane and too much Hb collects in there and looks like a bull’s-eye – an obese cell).
Target cells are imp markers for alcoholics b/c they have altered cell membrane due to an altered
cholesterol concentration of the membrane and markers for hemoglobinopathies (ie thalassemias,
Mature RBC looks like biconcave disk and is thin in the middle b/c there is less Hb there, and more is
concentrated at the edges; this is why there is a central area of pallor in a normal RBC when it lying
flat. All microcytic anemias have one thing in common: decreased Hb synthesis; with less Hb, the
redness of the cell with decrease and see greater area of pallor will increase (and if you play odd it’s
IDA). Spherocyte – too lil mem, therefore it’s a sphere; NO central area of pallor! (All red, no central
area of pallor). Microcytic anemias all have a PALE, blank color to them; therefore, it is very easy to
ID spherocyte and microcytic cells with hypochromia and IDA of chronic dz.
Audio Day 3: Hematology File 2
Normocytic Anemia: For normocytic anemia, you need to look at the reticulocyte count. First, you have to correct for the
degree of anemia (Hct/45 X ret ct). Then look to see if there is polychromasia, if there is
polychromasia (then divide by 2); 3% or higher = BM responding normally, and 2% or lower = not
Physical signs of anemia: – spoon nails = Fe def (aka kelosis), riboflavin def
Pallor of conjunctiva = have 6 grams or less of Hb
Palmer crease – works for white people – if don’t see red, pt is anemic
Ie women, often due to Fe def
Lead line – discoloration in gums due to lead poisoning
Neurologic exam very imp in B12 def b/c the posterior columns are knocked off and lateral
corticospinal tract, therefore have propioception abnormalities and decreased vibration
sensation and babinski (lateral cortical).
Fe studies – four Fe studies:
1. Serum Fe (normal = 100, like the alveolar O ),
2. Serum ferritin. best test – this is a soluble, circulating form of Fe storage; it rep the amount
of Fe stored in the BM, so, if you had to pick one test for dx of Fe def, anemia of a chronic dz, or
Fe overload, you would pick serum ferritin b/c this is the best screening test.
3. TIBC (total Fe binding capacity); the carrying protein for Fe is transferrin (trans = ‘carrys’) and
it is made in the LIVER.
4. % saturation= serum Fe divided by TIBC
1. Transferrin and the TIBC is the SAME! (Remember transferrin is what carries Fe).
2. There is a relationship of Fe stores in BM with the transferrin synthesized in the liver. When
the Fe stores in the BM are deficient (ie Fe def anemia), that is the signal for the liver to make
more transferrin, so it’s increased; therefore, TIBC will also be increased in Fe def. Therefore,
low Fe stores = increased transferrin synthesis and increased TIBC (an inverse relationship); also,
if Fe stores increase, transferrin and TIBC will decrease (ie Fe overload – hemochromatosis,
3. % saturation is a calculation = serum Fe/TIBC (normal serum Fe is 100 and normal TIBC is 300,
therefore, the % sat’n is normally 100/300 = 33% - therefore, 1/3 of the binding sites are
occupied with Fe.
These are the terms and Fe studies we use, esp for microcytic anemias (related to Fe problems).
Pathogenesis of microcytic anemias
All microcytic anemias are microcytic (b/c they have a problem making Hb). When the RBC is
developing in the marrow, it’s the Hb concentration within the RBC that determines the number
of cell divisions. Therefore, if the Hb synthesis is decreased, it is a signal in the marrow to
increase the number of mitoses. When cells mitoses, they go from something originally big to
something small. So b/c of the decrease in Hb syn, there are extra divisions and therefore the
cell is smaller.
All four groups of microcytic anemias have a decrease in Hb. Hb = heme + globin; Heme