Top 10

Anemias

to Know for Boards

Kristine Krafts, M.D.
PathologyStudent.com
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Table of Contents
Introduction
1
2
3
4
5
6
7
8
9
10

Iron-deficiency anemia
Megaloblastic anemia
Hereditary spherocytosis
Glucose-6-phosphate-dehydrogenase deficiency
Sickle cell anemia
Thalassemia
Autoimmune hemolytic anemia
Microangiopathic hemolytic anemia
Anemia of chronic disease
Aplastic anemia

Introduction
Clinical stuff
Anemia (from an-, without, and -emia, blood) is a reduction below normal in hemoglobin or red blood cell
number. Patients with anemia can present in different ways, depending on what kind of anemia they have
and how severe it is. The general signs and symptoms of anemia relate to the underlying lack of oxygencarrying capacity: fatigue, weakness, dizziness, tachycardia, pallor of skin and mucous membranes. Its
important to remember that if an anemia is fairly mild, symptoms will not be present. Also, if the anemia is
chronic and slowly-progressive, the cardiovascular system adjusts to the new diminished level of oxygen,
and symptoms will only appear when the anemia becomes quite severe.
In addition to the general symptoms of anemia, some specific findings may be present. If the anemia is
hemolytic, the patient may be jaundiced. Patients with iron-deficiency anemia may show spoon-shaped
nails (koilonychia), a smooth tongue, or pica (a craving to eat dirt and other non-food items). And patients
with megaloblastic anemia may develop a big, beefy tongue.

The Complete Blood Count (CBC)

The CBC is comprised of a bunch of different indices. You get all of these on every report, whether you
ask for them specifically or not (thats just the way the machine does it!). Some of these indices are really
useful (like the hemoglobin, MCV and RDW), and some of them are rarely if ever used (like the mean
platelet volume). You should know what each one measures, and be able to recognize the normal range.
Red blood cell count (RBC)
Total number of red blood cells in blood
Normal ranges: male 4.5-6.0 x 1012/L, female 3.8-5.2 x 1012/L
Hemoglobin (Hgb)
Concentration of hemoglobin in blood
Normal ranges: male 13-18 g/dL; female 12-16 g/dL
Hgb below normal = anemia

The most useful red cell indices

are the hemoglobin, MCV and RDW.

Hematocrit (Hct)
Volume of packed red blood cells.
In the old days, was performed by spinning a tube of blood and estimating the amount of total
blood volume taken up by the red cells (not a great method because if the cells are of unusual
shape, they may not pack as well as normal red cells, producing an artificially elevated Hct)
Now calculated by machine (MCV x RBC)
Normal ranges: male 40-52%, female 35-47%

Mean red blood cell volume (M CV)

Average size of red blood cells
Normal range: 80-100 fL (1 fL = 10-15 L)
Differentiates between microcytic (MCV < 80), normocytic (MCV 80-100) and macrocytic (MCV >
100) anemias
Mean cell hem oglobin (MCH)
Weight of Hgb in the average red blood cell
Normal range: 26-34 pg (1 pg = 10-12 g)
Not a frequently used parameter
Mean cell Hgb concentration (MCHC)
Concentration of Hgb in the average red blood cell
Normal range: 32-36 g/dL
Calculated by machine (Hgb/Hct)
Differentiates between hypochromic (MCHC < 32) and normochromic (MCHC 32-36) anemias
There is no such thing as a hyperchromic red cell (you cant put excess hemoglobin into a cell, or it
would burst!)
You can see this nicely on a blood smear: normochromic cells have a zone of central pallor (that
white dot in the middle of the cell) that is no more than 1/3 the diameter of the red cell.
Hypochromic red cells have just a thin rim of hemoglobin.
Red cell distribution width (RDW )
Standard deviation of the MCV
Tells you how much the red blood cells differ from each other in size. If they are all pretty similar in
size, the RDW is low. If some are little and some are big, the RDW is high.
Normal range = 12-13.5%
Differentiates between anemias with minimal anisocytosis (difference in cell size) (RDW 12-13.5%)
and those with increased anisocytosis (RDW > 13.5%).

W hite blood cell count (W BC)

Total number of leukocytes in blood
Normal ranges: adult: 4.5-11 x 109/L, newborn: 9 -30, child over 1: 5.0-17.0
A high WBC is seen in many conditions. Some are benign, such as infection and inflammation.
Others are malignant, such as leukemia.
Differential (diff)
Amounts of each white blood cell type in blood
Normal ranges:

Percentage of WBC
Neutrophils
45-75
Lymphocytes
20-50
Monocytes
1-8
Eosinophils
0-6
Basophils
0-1

Absolute (x 109/L)
2-8
1-4
0.1-0.8
0-0.5
0-0.3

Platelet count (Plt)

Total number of platelets in blood
Normal range = 150-450 x 109/L
Causes of a low platelet count are numerous and include splenomegaly, idiopathic
thrombocytopenic purpura, disseminated intravascular coagulation, and bone marrow failure.
Causes of a high platelet count are also numerous, and include reactive thrombocytosis (as seen in
iron-deficiency anemia) and essential thrombocythemia.
MPV (mean platelet volume)
Average size of platelets
Normal range depends on the platelet count! (Normally, if the platelet count falls, the body
compensates a little by trying to make bigger platelets.)
Not used all that often.

The Blood Smear

There are three main things you need to look at when youre faced with a blood smear: the red
cells, the white cells, and the platelets. It helps if you have a plan that you follow every time, kind of
like radiologists do when they look at imaging studies. That way youre not tempted to just start
looking at the exciting stuff and forget about all the other stuff. Heres your plan for the red cells.
1. Estim ate num ber (just eyeball it; make sure there arent a lot of holes between the cells).
2. Look for variation in size (anisocytosis).

Oval macrocytes (B12/folate deficiency)

Microcytes (iron deficiency anemia, thalassemia)

The size range can often help you narrow down which type of anemia is present
(for example, in iron-deficiency anemia, there is usually a big range of sizes)
3. Look for variation in shape (poikilocytosis).

Schistocytes (microangiopathic hemolytic anemia)

Spherocytes (hemolytic anemia, hereditary spherocytosis)

Teardrop cells or dacryocytes (myelofibrosis or myelophthisic processes)

Target cells or codocytes (hemoglobinopathies, thalassemias, liver disease)

Sickle cells (sickle cell anemia)

Echinocytes and acanthocytes (liver disease)

4. Estim ate the average am ount of hem oglobin in each cell (chrom asia).

Normochromic (zone of central pallor comprises 1/3 of the cell diameter)

Hypochromic (zone of central pallor comprises >1/3 of the cell diameter)

5. Estim ate num ber of reticulocytes (look for polychrom atophilic cells).

Normal: one or two polychromatophilic cells per field.

The lower the Hgb, the higher the reticulocyte count should be.
6. Look for anything else weird.

Nucleated red blood cells

Inclusions (Howell-Jolly bodies, Pappenheimer bodies, bugs)

When looking at blood smears,

it helps to follow the same plan
every time.

Reticulocytes vs. polychromatic cells

Reticulocyte and polychromatophilic cell are
two names for the same thing immature red
cells that still contain a little ribosomal RNA.
When you do a supravital stain on a blood smear,
the RNA stains blue, and the cells are called
reticulocytes. When you do a normal WrightGiemsa stain, the cells look big and slightly
basophilic,
and
they
are
called
polychromatophilic cells. This is one of those
fine points that, when casually mentioned on
rounds your third or fourth year, will make you
look very smart.

One. Iron-Deficiency Anemia

Pathogenesis
Blood loss (e.g., GI bleed or menses) or really bad diet (rare)

Morphology

Iron-deficiency anemia is a
microcytic, hypochromic anemia with
oval macrocytes
increased
anisocytosis and poikilocytosis.

Hypochromic, microcytic anemia

Increased anisocytosis (some little cells, some bigger cells)
Increased poikilocytosis (elliptocytes are present, for some reason)
Decreased reticulocyte number (because theres not enough iron around!)
Platelet count usually increased for some reason

Iron studies

serum iron
TIBC (total iron binding capacity)
ferritin

Treatment
Figure out why patient is iron deficient (don't just treat the anemia, or you might miss something really
important, like a GI bleed due to colon cancer). Then give iron (orally).

Iron-deficiency anemia

Two. Megaloblastic Anemia

Pathogenesis
Vitamin B12 and/or folate deficiency (from bad diet, absorption problems, folate-antagonist drugs)
makes it hard to make DNA (you need both B12 and folate to make DNA). RNA production runs
smoothly though. So the nucleus (full of DNA) lags behind the cytoplasm (full of RNA) in
development, and the cell divides more slowly (because its waiting for signals from the slowmoving nucleus).

macrocytic anemia

Morphology
Blood

Macrocytic anemia (MCV >100)

Oval macrocytes.

Hypersegmented (more than 5 lobes) neutrophils.

Megaloblastic anemia is a
with oval macrocytes

and hypersegmented neutrophils.

Bone marrow

Megaloblastic cells: giant red cell or neutrophil precursors with nuclear-cytoplasmic

asynchrony (mature cytoplasm, immature nucleus).

Treatment
Treatment depends on the cause of the anemia. You cant (or shouldnt) just replace the B12 and/or
folate without knowing whats wrong with the patient.

Megaloblastic anemia

Three. Hereditary Spherocytosis

Pathogenesis
Patients with HS have defects in the membrane cytoskeleton (in spectrin, ankyrin, band 3, or band
4.2). The red cell membrane is unstable, leading to increased fragility and the formation of
spherocytes, which get eaten by macrophages.

Hereditary spherocytosis:
Lots of spherocytes due to
a spectrin defect.

Morphology

Mild normochromic, normocytic anemia.

Numerous spherocytes.

Treatment
If the disease is mild, patients dont need treatment. In severe cases, splenectomy can be useful
(because thats where the red cells get destroyed).

Hereditary spherocytosis

Four. G6PD Deficiency

Pathogenesis
Glucose-6-phosphate dehydrogenase (G6PD) helps reduce nasty free radicals made during cell
metabolism. Patients who have a deficiency of G6PD are usually okay until they encounter some
sort of oxidizing substance (like a drug, or fava beans). Without G6PD, free radicals attack the
molecular bonds between heme and globin, and globin becomes denatured, forming a little blob
called a Heinz body. The spleen bites out these Heinz bodies, leaving what look like actual bite
marks in the cell.

Without G6PD,
free radicals accumulate
and Heinz bodies form.

Morphology
Without exposure to offending agents, most patients have no anemia. After exposure, though,
patients get an acute hemolytic episode, with cell fragments, microspherocytes, and bite cells
(caused by recent pitting of Heinz bodies). Supravital staining reveals Heinz bodies (these decrease
in number as Hgb bottoms out, because younger cells have greater G6PD activity).

Treatment
Avoid exposure to known oxidants. Usually the hemolysis is self-limiting, with spontaneous
resolution in a week or so.

Bite cell

Five. Sickle-Cell Anemia

Pathogenesis
Sickle cell anemia is a type of hemoglobinopathy (diseases with point mutations in one of the
globin chain genes). The abnormal hemoglobin (called HbS) in sickle cell anemia changes shape
when it releases oxygen. The HbS molecules then aggregate and polymerize, forming the cell into
a fragile, non-deformable, sickle shape. Sickle cells bust open more easily; they also stick together
in small vessels, leading to ischemia (often occurring in hands, feet, lungs, and spleen). The spleen
may undergo massive enlargement (due to red cell sequestration) in early childhood. By early
adulthood, however, the spleen is reduced to a small, fibrotic remnant (due to recurrent
hemorrhage and fibrosis); this is called autosplenectomy.

Sickle cell anemia is a

qualitative abnormality
of hemoglobin

Morphology
In the blood, particularly during crises, sickle cells are present. After autosplenectomy occurs, there
is whats called a "post-splenectomy blood picture": nucleated red blood cells, targets, HowellJolly bodies, Pappenheimer bodies, and a slightly increased platelet count (the platelets love to
hang out in the spleen, so when you take away their little home, they have no choice but to hang
out in the blood).

Treatment
Its important to prevent triggers (things that makes the red cells want to give up oxygen, like
infection). Vaccination against encapsulated bugs is given in patients who have undergone
autosplenectomy.

Sickle-cell anemia

Six. Thalassemia
Pathogenesis
The thalassemias are characterized by a quantitative decrease in one of the hemoglobin chains. In
-thalassemia, there is a decreased amount of chain. In -thalassemia, there is a decreased
amount of chain. You end up with a two-fold problem:
1. Decreased hemoglobin production (because of the decrease in globin chains)
2. Excess unpaired chains (in thalassemia) or , , and chains (in thalassemia), which
form tetramers and lead to premature red cell destruction.

Thalassemia is a

quantitative abnormality
of hemoglobin

Morphology
In mild thalassemia, patients have a mild microcytic, hypochromic anemia. Sometimes there are
target cells, or cells with basophilic stippling. Patients with severe thalassemia have a whopping
anemia marked anisocytosis and poikilocytosis.

Treatment
Patients with mild thalassemia dont require treatment. Patients with severe anemia may need
repeated red cell transfusions or even bone marrow transplantation.

Moderate thalassemia

Seven. Autoimmune Hemolytic Anemia

Pathogenesis
There are two flavors of autoimmune hemolytic anemia, warm and cold. In warm autoimmune
hemolytic anemia (WAIHA), the patient makes IgG anti-red-cell antibodies which bind best at 37 C
(warm). Macrophages think these antibody-coated red cells are yummy, and they nibble them up
(or gobble them whole). In cold autoimmune hemolytic anemia (CAIHA), the patient makes IgM
anti-red-cell antibodies that bind best at temperatures <37 C (cold). This means they bind in
distal body parts but fall off in warm body parts. Because the antibodies are IgM in nature, they
bind a bunch of red cells together, forming clumps. In addition, complement binds to the red cells,
causing intravascular hemolysis.

Morphology
In WAIHA, the blood smear shows prominent spherocytosis. In CAIHA, if you make the blood
smear at a cool temperature, you can see nice big red blood cell agglutinates (clumps)!

WAIHA:

IgG
spleen
spherocytes

CAIHA:
IgM/complement
intravascular hemolysis
agglutination

Important lab test

Direct antiglobulin test (DAT)
Also called the Coombs test. Mix patient's red cells with anti-human globulin (an antibody against
human immunoglobulins). If the red cells are coated with antibodies (as they are in some immune
processes, see later), the anti-human globulin will attach to those antibodies, bridging the red cells
and making them clump together. So, a positive result (red cell clumping) means the patient's red
cells are coated with antibodies, and the hemolysis is probably immune-related.

Treatment
Treat underlying cause, if there is one. In WAIHA, steroids can be useful, and if all else fails,
splenectomy might be necessary. In CAIHA, its helpful to keep the patient warm.

CAIHA

Eight. Microangiopathic Hemolytic Anemia

Pathogenesis

If a patient has MAHA,

you must find out why!

Red cells are ripped apart by physical trauma (fibrin strands snag them or mechanical devices bash
them). There are a ton of possible causes, including disseminated intravascular coagulation,
hemolytic-uremic syndrome, thrombotic thrombocytopenic purpura, and artificial heart valves.

Morphology
The blood smear shows schistocytes, which are small, pointy red cell fragments.

Treatment
The important thing is to figure out whats causing the MAHA and then treat that.

Schistocyte

Nine. Anemia of Chronic Disease

Pathogenesis
Anemia of chronic disease happens in a ton of different diseases, from infections, to inflammatory
conditions, to malignancies. There is a complex disturbance in iron metabolism which prevents iron
from making it into normoblasts.

ACD is bland-looking

Morphology
The blood shows a normochromic, normocytic anemia with minimal anisocytosis and poikilocytosis
(its a bland-looking anemia). Some cases (about 25%) are microcytic, but the MCV rarely gets
below 72 fL.

Iron studies

serum iron
TIBC
ferritin (ferritin is an acute phase reactant! It goes up in the types of conditions that cause ACD)

Treatment
ACD is usually so mild that no treatment of the anemia is required. The underlying disease is the
focus of the patients treatment.

Anemia of chronic disease

Ten. Aplastic Anemia

Pathogenesis
In aplastic anemia, there are very few hematopoietic precursor cells in the bone marrow (and
therefore, decreased numbers of red cells, white cells, and platelets in the blood). The causes are
numerous (like drugs, viruses, or hereditary conditions), but in most cases, no specific cause can
be identified.

In aplastic anemia, there is a

pancytopenia

and an empty marrow

Morphology
The blood is pancytopenic, meaning that the red cells, white cells, and platelets are all decreased.
The bone marrow is markedly hypocellular, or "empty".

Treatment
Treatment includes transfusion of blood components as needed, drug therapy to stimulate
hematopoiesis and suppress the immune system, and if necessary, bone marrow transplant.

Aplastic anemia: bone marrow

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Everything you need to know about hematopathology, illustrated with tons of
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Chronic Leukemias
Chronic leukemias are very different from acute leukemias. Chronic leukemias are for the most part
diseases of older adults (acute leukemias occur in both children and adults). They appear in an
insidious fashion and have a relatively good prognosis (as opposed to acute leukemias, which have
a stormy onset and poor prognosis). In addition, chronic leukemias are composed of fairly matureappearing hematopoietic cells (as opposed to acute leukemias, which are composed of blasts).
There are two kinds of chronic leukemias: myeloid and lymphoid. Instead of being reasonable, and
calling them chronic myeloid leukemias and chronic lymphoid leukemias, the powers that be
dubbed the two divisions chronic myeloproliferative disorders and chronic lymphoproliferative
disorders. These names are not so great, in my opinion, since these are not just disorders they
are real leukemias! But no one asked me.

Pathophysiology
The chronic leukemias are malignant, monoclonal proliferations of mostly mature myeloid or
lymphoid cells in the bone marrow (and blood). These leukemias progress more slowly than acute
leukemias. So early on, the marrow is involved but not totally replaced by malignant cells. Still, it
is hard for the normal white cells to function properly. The lymphoid cells, in particular, have a hard
time making normal immunoglobulin in certain chronic lymphoproliferative disorders. One of the
major causes of mortality in these patients is infection. As the chronic leukemias evolve, more and
more of the marrow is replaced by tumor, and eventually there is little room for normal white cells to
grow.

- Vivian H.
Sample:
Pages 6366

Clinical Features
Chronic leukemias present in over a period of weeks or months. Patients might have splenomegaly
(which shows up as a dragging sensation or fullness in the left upper quadrant of the abdomen),
lymphadenopathy, or a general feeling of malaise and fatigue. Some patients are asymptomatic at
diagnosis, and the disease is picked up on a routine blood smear or CBC. Likewise, the clinical
course is different in chronic leukemia. In many cases of chronic leukemia, patients can live for years
without treatment at all.

Chronic Myeloproliferative Disorders

The chronic myeloproliferative disorders are malignant clonal proliferations of a pluripotent stem cell
that lead to excessive proliferation of myeloid cells in the blood and bone marrow. What that means
in plain English is that a stem cell somewhere way back (before its even committed to the
neutrophil line, or red cell line) goes bad and starts proliferating like crazy so you wind up with a
marrow packed with cells from all the myeloid lineages (the official name is panhyperplasia).
Usually, one particular myeloid lineage predominates in this growth fest so youll see a ton of all
the myeloid cells, but the majority are neutrophils, or red cells, or megakaryocytes. So the chronic
myeloproliferative disorders have been divided into four types according to what is proliferating
most:

Chronic myeloid leukemia (tons of neutrophils and precursors)

Polycythemia vera (tons of red cells and precursors)
Essential thrombocythemia (tons of platelets and megakaryocytes)
Chronic myelofibrosis (tons of everythingthen nothing! See below.)

Well consider each of these separately because they are very different clinically and
morphologically. But they do have some common features: all of them have a high white count with
a left shift, a hypercellular marrow, and splenomegaly.

Chronic myeloproliferative disorders:

CML, PV, ET, and

chronic myelofibrosis

Chronic myeloid leukemia

Chronic myeloid leukemia (CML) is a chronic myeloproliferative disorder characterized by a marked
proliferation of neutrophils (and precursors) in the bone marrow and blood. All cases have a t(9;22),
also known as the Philadelphia chromosome (its the 22 thats officially the Philadelphia
chromosome).
Clinical Features

CML has a t(9;22).

CML frequently occurs in patients who are around 40 or 50. It does not occur in children (though
there is a separate disease similar to CML, called juvenile CML, that does occur in kids). Usually, the
onset is slow, with a long asymptomatic period, followed by fevers, fatigue, night sweats and
abdominal fullness. On physical exam, patients usually have an enlarged spleen. Hepatomegaly and
lymphadenopathy may also be present.
There are three clinical stages, or phases, of CML: chronic phase, accelerated phase and blast
crisis. Patients generally present in chronic phase and then progress to one or both of the other
phases.
Chronic phase

High but stable number of neutrophils and precursors.

Stable hemoglobin and platelet count.

Easily controlled by therapy.

With traditional treatment (not imatinib, see below), usually lasts 3-4 years; is then followed
by accelerated phase and/or blast crisis.
Accelerated phase

Characterized by a change in the patient's previously stable state.

Usually see increasing leukocytosis, decreasing hemoglobin and platelet count.

May terminate in this stage, or may progress to blast crisis.

Usually fatal within several months.

Blast crisis

Characterized by a marked increase in blasts (myeloblasts or lymphoblasts).

Usually fatal within a few weeks or months.

Chronic myeloid leukemia:

marked neutrophilia,

left shift, and basophilia

Morphology
Blood
The blood smear shows a marked neutrophilia with a left shift. The left shift is a little weird in that it
is not evenly distributed between all the neutrophil stages. There are tons of neutrophils at all stages
of development, but there are relatively more myelocytes and segmented neutrophils (and relatively
less of the other stages). There are a few myeloblasts around (which you dont see in normal blood,
of course) but they dont number more than 2 or 3%.
Heres an interesting thing: patients with CML almost always have a basophilia. Thats actually one
of the first things that happens in the development of the disease! There are few if any other reasons
for a basophilia. So if you see this in a patient, even if they dont have the typical findings of CML
(big white count with lots of neutrophils and precursors), you should rule out CML!
The platelet count may be increased (because of all the megakaryocytes around in the bone
marrow).

CML: blood

Bone marrow
The bone marrow is hypercellular, with a pan-myeloid hyperplasia (all the myeloid cells are increased
neutrophils and precursors, red cell precursors, megakaryocytes). However, if you look closely,
youll see that the neutrophils and precursors make up the bulk of the cells. Later in the course of
the disease, the marrow may become fibrotic. You can detect this using a reticulin stain. This is not
a good sign.
Pathophysiology
All cases of CML have a translocation between chromosomes 9 and 22, resulting in whats
commonly known as the Philadelphia chromosome (Ph). This designation refers to the new
chromosome 22 that results from the translocation. Nobody talks about poor chromosome 9. The
translocation places the c-abl proto-oncogene on chromosome 9 next to the bcr gene on
chromosome 22. A new, fusion gene is created: the bcr-abl gene. The bcr-abl gene encodes a
protein called p210, which increases tyrosine kinase activity and disrupts the cell cycle.
Heres a weird fact: the Philadelphia chromosome is found not only in the myeloid cells, but also in
some B lymphocytes! Thats weird, considering that this is a myeloid lesion with no apparent
changes in the lymphoid cells. This probably means that the initial bad cell (the one that became

CML: bone marrow

malignant) was a very early stem cell, one that hadnt even committed itself to myeloid or lymphoid
lineage yet, and the Philadelphia chromosome is present in all the descendents of that cell. Further
supporting this idea is the fact that when patients enter blast crisis, the blasts can be lymphoid!
Treatment and Prognosis
In the old days, CML was treated with myelosuppressive agents like hydroxyurea, and then if the
patient had a match and could tolerate it, allogeneic bone marrow transplant was performed. That
was the only hope for a cure.
Recently, a new drug called imatinib (or Gleevec) was developed that targets the messed-up
tyrosine kinase receptor activity in CML. It has been like a miracle for many patients even patients
in the later stages of the disease. In fact, we dont even know what the typical prognosis of CML is
anymore, because these patients are still living with the disease. This drug has turned CML into a
chronic but treatable disease, like diabetes, for many patients. Its one of the happiest leukemia
research stories ever.