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The Top Ten Anemias to

Know for Boards
A Quick Review of High-Yield Anemias

Kristine Krafts, M.D.

2nd Edition

Table of Contents
Introduction ............................................................................3
Important basic stuff ...............................................................4
Iron-Deficiency Anemia ..........................................................9
Megaloblastic Anemia ...........................................................10
Hereditary Spherocytosis ......................................................11
G6PD Deficiency ..................................................................12
Sickle-Cell Anemia ................................................................13
Thalassemia ...........................................................................14
Autoimmune Hemolytic Anemia ..........................................15
Microangiopathic Hemolytic Anemia ...................................17
Anemia of Chronic Disease ..................................................18
Aplastic Anemia ...................................................................19
Preview: The Complete Hematopathology Guide ...............20

Introduction
Thanks for downloading The Top Ten Anemias to Know for Boards. This short study guide
covers the anemias most often covered on board exams (and on pathology course exams). It
quickly summarizes the most high-yield points about pathogenesis, morphology and treatment
for each anemia, and gives you a nice image of each type. We'll also take a quick look at some
important clinical features of anemias, and we'll discuss the meaning of CBC indices as well as
how to look at a blood smear.

Getting Started
You can click on any of the anemia titles in the table of contents to go straight to that anemia.
Or just read the whole thing straight through - it should only take 15 - 20 minutes.

If you like this book

You might find some of our other guides useful. Here's a summary of Pathology Student stuff:
The Complete (But Not Obsessive) Hematopathology Guide
A concise but thorough review of benign and malignant hematopathology.
Clot or Bleed: A Painless Guide for People Who Hate Coag
Coag made understandable! Covers basic mechanisms and bleeding and thrombotic diseases.
Path Bites Anthology: A Collection of Short, Easy and Strangely Fun Pathology
Lessons
Over 500 quick, high-yield essays that cover all major areas in general and systemic pathology.
Anatomic Pathology Compendium
A collection of our best Pathology Student essays on difficult anatomic pathology topics.
Hematopathology Compendium
A collection of our best Pathology Student essays on hematopathology.
General Pathology Compendium
A collection of our best Pathology Student essays on general pathology topics.
Neuropathology Mini-Course
A 4-week course that covers 12 high-yield neuropath topics, with memory strategies you can put
to use right away.

www.PathologyStudent.com

Top 10 Anemias page 3

Important basic stuff

Clinical Information
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.

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The Complete Blood Count

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
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 (MCV)
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

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Mean cell hemoglobin (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 cells 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%).
White blood cell count (WBC)
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.

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Differential (diff )
Amounts of each white blood cell type in blood
Normal ranges:
Percentage of WBC

Absolute (x 10

Neutrophils

45-70

2-8

Lymphocytes

20-50

1-4

Monocytes

1-8

0.1-0.8

Eosinophils

0-6

0-0.5

Basophils

0-1

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.

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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. Estimate number (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. Estimate the average amount of hemoglobin in each cell (chromasia).

Normochromic (zone of central pallor = 1/3 of the cell diameter)
Hypochromic (zone of central pallor >1/3 of the cell diameter)
5. Estimate number of reticulocytes (polychromatophilic 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)

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Iron-Deficiency Anemia
Pathogenesis
Blood loss (e.g., GI bleed or heavy menses) or really bad diet (rare).

Morphology
The red cells are hypochromic and microcytic. There is increased anisocytosis
(each successive wave of new red cells is smaller, because there's less and less iron
around!) and poikilocytosis (elliptocytes are often present). Reticulocytes are
decreased, because the lack of iron leads to decreased red cell production. The
platelet count is often increased, for some reason.

IDA: hypochromic red cells and anisocytosis

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 oral iron
supplements.

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Megaloblastic Anemia
Pathogenesis
Vitamin B12 and/or folate deficiency (from bad diet, absorption problems, folateantagonist 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 slow-moving nucleus).

Morphology
Blood
The red cells are macrocytic, and you often see great big oval macrocytes.
Hypersegmented neutrophils (with more than 6 nuclear lobes) are also present.

Megaloblastic anemia: hypersegmented neutrophil

Bone marrow
The bone marrow shows "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.

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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.

Morphology
The red cells are normochromic and normocytic, and depending on the patient's
particular genetic defect, there may be a ton of spherocytes (which look smaller
than normal red cells, and lack central pallor) or just a few.

HS: moderate amount of 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).

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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 enough G6PD around, 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.

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).

G6PD deficiency: bite cell

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

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Sickle-Cell Anemia
Pathogenesis
Sickle cell anemia is a type of hemoglobinopathy (a group of diseases of
hemoglobin characterized by point mutations in a globin chain gene). The
abnormal hemoglobin in sickle cell anemia changes shape when it releases oxygen,
causing it to polymerize, which distorts the red cell into a sickle shape.
Sickle cells are fragile, and they stick together in small vessels, leading to ischemia.
Tiny, repeated infarcts in the spleen lead to fibrosis and eventual "autosplenectomy"
(the spleen becomes a small, fibrotic lump that doesn't work well at all).

Morphology
During times of decreased oxygenation ("crises"), sickle cells are present in the
blood. Also, after autosplenectomy occurs, you can see a "post-splenectomy blood
picture," which includes things the spleen normally removes, like nucleated red
blood cells, Howell-Jolly bodies, and Pappenheimer bodies.

Sickle cell anemia: lots of sickle cells

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.

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

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.

Moderate thalassemia: target cells, 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.

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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). Splenic macrophages think these
antibody-coated red cells are yummy, and they nibble on them (or gobble them up
entirely).
In cold autoimmune hemolytic anemia (CAIHA), the patient makes IgM anti-redcell 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).

CAIHA: red cell agglutinates

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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), the anti-human globulin will
attach to those antibodies, bridging the red cells and making them clump together.
So if you see red cell clumping, that means the patient's red cells are coated with
antibodies, and the patient's 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.

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Microangiopathic Hemolytic Anemia

Pathogenesis
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, malignancies (especially adenocarcinoma), sepsis,
trauma, and artificial heart valves.

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

MAHA: schistocyte

Treatment
The important thing is to figure out whats causing the MAHA and then treat that.
Schistocytes are never normal - so if you see them, you have to seek out an
underlying cause!

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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.

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.

Anemia of chronic disease: pretty normal-looking blood smear

Iron studies
serum iron
TIBC
ferritin (ferritin is an acute phase reactant - so 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.

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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 potential causes are numerous (like drugs, viruses, or hereditary
conditions), but in many cases, no specific cause can be identified.

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".

Aplastic anemia: "empty" bone marrow

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.

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Preview: The Complete

Hematopathology Guide
Everything you need to know about hematopathology,
illustrated with tons of nice photos and easy ways to
remember what you learn.
The only reason I did well in hemepath in medical
school is because of you."
Richard, Medical Student

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 mature-appearing
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!

Pathophysiology
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.

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One of the major causes of mortality in these patients is infection. As 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.

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

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.

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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 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.

!
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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%.

CML, blood: leukocytosis with left shift

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).

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Bone marrow
The bone marrow is hypercellular, with a pan-myeloid hyperplasia (all the myeloid
cells are increased neutrophils and precursors, red cell precursors, and
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.

CML, bone marrow: hypercellular

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 is a
super-powerful tyrosine kinase that drives the cells to grow like crazy.

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Heres a weird fact: the Philadelphia chromosome is found not only in the myeloid
cells in CML, but also in some B lymphocytes! Thats weird, considering that this is
a myeloid lesion with no morphologic changes in the lymphoid cells. This probably
means that the initial bad cell (the one that became malignant) was a very early stem
cell, one that hadnt even committed itself to myeloid or lymphoid lineage yet - so
the Philadelphia chromosome is present in all the descendants of that cell. Further
supporting this idea is the fact that when patients enter blast crisis, the blasts are
sometimes 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.
Not long ago, a new drug called imatinib (or Gleevec) was developed. This drug
targets the bcr-abl gene product, preventing it from exerting its massive tyrosinekinase-mediated growth stimulation. 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.

This marks the end of this preview. You can read more about the book here.

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