Hematology

Step to PG-MD/MS/DNB - Dr.Akif A.B
- Dr.Akif A.B

Explaining full hematology in pdf is not possible
So I will just try to help u with the peripheral smear pictures of Various conditions
Rest u can follow in whichever book u r reading………….

The red blood cells here are
normal RBC's.
They have a zone of central
pallor about 1/3 the size of the
RBC.
The RBC's demonstrate minimal
variation in size (anisocytosis) and
shape (poikilocytosis).
A few small fuzzy
blue platelets are seen.
Segmented
neutrophil
Band
neutrophil

A normal mature
lymphocyte with a
single large nucleus
Segmented
neutrophil

Here is a monocyte.
It is slightly larger than a lymphocyte and
has a folded nucleus.

In the center of the field is an eosinophil with a bilobed nucleus and
numerous bright red cytoplasmic granules.
Just underneath it is a small lymphocyte.
Eosinophil
small
lymphocyte

There is a basophil in the center of the field that has a multi-lobed nucleus (like
PMN's) and numerous coarse, dark blue granules in the cytoplasm, just like tissue
mast cells.
A band neutrophil is seen on the left, and a large, activated lymphocyte on the
right.
basophil
band
neutrophil

The RBC's here have stacked together in long chains.
This is known as "rouleaux formation" and it happens with increased
serum proteins, particularly fibrinogen and globulins.
Such long chains of RBC's sediment more readily.
This is the mechanism for the sedimentation rate, which increases non-
specifically with inflammation and increased "acute phase" serum proteins.
Seen in Multiple Myeloma

The RBC's here appear smaller than normal and have an increased zone of central
pallor.
This is indicative of a hypochromic (less hemoglobin in each RBC) and
microcytic (smaller size of each RBC) anemia. There is also increased
anisocytosis (variation in RBC size) and poikilocytosis (variation in RBC
shape).
Seen in
Iron deficiency
Anemia

larger zones of central pallor in these small RBCs, along with
poikilocytosis.
The most common cause for a hypochromic microcytic anemia
is iron deficiency.
Central
Pallor

Microcytosis is indicated by the low MCV
(mean corpuscular volume).
Hypochromia correlates here with the low
MCH (mean corpuscular hemoglobin).

The peripheral blood smear shown here appears normal, because it is.
A normal neutrophil and lymphocyte are present. Only a CBC will
demonstrate anemia.
This is a normochromic, normocytic anemia.

There is impaired utilization of iron, without either an absolute deficiency or
an excess of iron.
There is cytokine-mediated blockage in transfer of iron from the storage pool
to the erythroid precursors in the bone marrow.
The defect is either inability to free the iron from macrophages or to load it onto
transferrin.
Inflammatory cytokines also depress erythropoiesis
Inflammatory conditions release cytokines such as interleukins 1 and 6 (IL1,
IL6) that stimulate hepatic production of hepcidin, which reduces iron
absorption and decreases release of iron from stores in macrophages.
Anemia of chronic disease is addressed by treating the underlying
condition.

Here is a hypersegmented neutrophil that is present with megaloblastic
anemias.
There are 8 lobes instead of the usual 3 or 4.
Such anemias can be due to folate or to B12 deficiency.
The size of the RBC's is also increased (macrocytosis, which is hard to appreciate
in a blood smear)

The macro-ovalocytes in a
case of pernicious anemia are
larger than the normal
small lymphocyte.
Note that these large RBCs lack
a zone of central pallor.
There is no polychromasia, and if
a reticulocyte count were
done, it would be low.
The serum homocysteine and methylmalonic acid levels are increased,
often before macrocytosis and a decrease in cobalamin (B12) occurs.
As the disease progresses cobalamin (vitamin B12) levels will be consistently
decreased as well.
Only homocysteine will be increased with folate deficiency.

There are numerous fragmented RBC's seen here.
Some of the irregular shapes appear as "helmet" cells.
Such fragmented RBC's are known as "schistocytes" and
they are indicative of a microangiopathic hemolytic anemia (MAHA) or
other cause for intravascular hemolysis.
This finding is typical for disseminated intravascular coagulopathy (DIC).

The CBC of a patient with microangiopathic hemolytic
anemia (MAHA) demonstrates a markedly increased
RDW (red cell distribution width) due to the marked
variation in size and shape of the RBC population.

The RBC in the center of the field contains several Howell-Jolly bodies, or
inclusions of nuclear chromatin remnants.
There is also a nucleated RBC just beneath this RBC. Abnormal and aged RBC's
are typically removed by the spleen.
The appearance of increased poikilocytosis, anisocytosis, and RBC inclusions
suggests that a spleen is not present.(Asplenia)
Nucleated
RBC
Howell-Jolly
bodies

The size of many of these RBC's is
quite small, with lack of the central
zone of pallor.
These RBC's are spherocytes.
In hereditary spherocytosis,
there is a lack of spectrin, a key
RBC cytoskeletal membrane
protein.
This produces membrane
instability that forces the cell to the
smallest volume--a sphere.
In the laboratory, this is shown by
increased osmotic fragility.
The spherocytes do not survive
as long as normal RBC's.

The sinusoids are packed with
RBC's in this case of hereditary
spherocytosis.
The osmotic fragility of spherocytes
is increased, because the RBC's
have decreased surface area per
unit volume.
The major clinical features are
anemia, splenomegaly, and
jaundice.
An aplastic crisis may occur with
parvovirus infection.

increased central pallor,
consistent with hypochromic
microcytic anemia. The most
common cause is iron deficiency.
RBC's are large and lack central pallor,
consistent with macro-ovalocytes.
The most common cause is
megaloblastic anemia, from vitamin
B12 or folate deficiency.
RBC's are small and lack central pallor,
consistent with spherocytes lacking
central pallor. Hereditary
spherocytosis.

The nucleated RBCs contain basophilic stippling of the cytoplasm.
This suggests a toxic injury to the bone marrow, such as lead poisoning.
Such stippling may also appear with severe anemia, such as a megaloblastic
anemia.

Atypical lymphocytes are shown here.
These WBC's are "atypical" because they are larger (more cytoplasm) and have
nucleoli in their nuclei.
Such atypical lymphocytes are often associated with infectious mononucleosis
from Epstein-Barr virus (EBV) infection.

Bilobed neutrophils
this is indicative of an uncommon condition known as Pelger-Huet
anomaly, an inherited condition.
associated with abnormal neutrophil function.
Just be aware of this condition when you get back a manual differential
count with mostly "bands", but the WBC count is normal or the patient
shows no signs of infection or inflammation.

This is sickle cell anemia
- Autosomal Recessive Disease

Though in early childhood the spleen may be enlarged with sickle cell anemia,
continual stasis and trapping of abnormal RBC's leads to infarctions that eventually
reduce the size of the spleen tremendously by adolescence.
This is sometimes called "autosplenectomy".
Seen here is the small remnant of spleen in a patient with sickle cell anemia.
Autosplenectomy

Severe, chronic anemias (such as thalassemias and sickle cell
anemia) can increase the bone marrow response to form RBC's.
This drive for erythropoiesis may increase the mass of marrow and
lead to increase in marrow in places, such as the skull seen here, that is
not normally found.
Such an increase in marrow in skull may lead to "frontal bossing" or
forehead prominence because of the skull shape change.

This patient has hemoglobin SC disease, with hemoglobin S and
hemoglobin C both present.
With SC disease, the RBC's may sickle, but not as commonly as with
Hemoglobin SS disease.
The hemoglobin C leads to the formation of "target" cells--RBC's that
have a central reddish dot. In the center of the field is a rectangular RBC
that is indicative of a hemoglobin C crystal, which is also characteristic
for
Hemoglobin C
Disease.
Hemoglobin C
Crystal

Hematopoietic elements in this bone marrow biopsy are markedly
reduced.
This is a case of aplastic anemia.
Aplastic Anemia

In contrast to aplastic anemia, leukemia results in a highly cellular marrow.
The marrow between the pink bone trabeculae seen here is nearly 100% cellular,
and it consists of leukemic cells of acute lymphocytic leukemia (ALL) that have
virtually replaced or suppressed normal hematopoiesis.
Thus, though the marrow is quite cellular, there can be peripheral cytopenias.

The WBC's seen here are lymphocytes, but they are blasts--very immature cells
with scant cytoplasm and large nuclei that contain nucleoli.
Such abnormal lymphocytes are indicative of acute lymphoblastic
leukemia (ALL).
ALL is more common in children than adults.
Blast Cells

These mature lymphocytes are
increased markedly in number.
They are indicative of
chronic lymphocytic
leukemia
most often seen in older
adults.
This disease responds poorly
to treatment
CLL is defined by more than 5000/microliter B lymphocytes in peripheral blood
marking with CD23 and CD5.
Though CLL is a B cell proliferation, marking with CD19 and CD20, it is characterized
by the presence of a T cell marker, CD5, as shown by flow cytometry here.
This is a systemic disease, and organ involement outside of marrow, such as spleen and
liver, is known as small lymphocytic lymphoma (SLL).

-very large, immature myeloblasts with many nucleoli.
- "Auer rod" composed of crystallized granules.
-These findings are typical for acute myelogenous leukemia (AML)
- most prevalent in young adults.
Acute Myelogenous
Leukemia (AML)
Auer rod

There are numerous granulocytic forms seen here, including immature myeloid
cells and bands. This condition is one of the myeloproliferative states and is
known as chronic myelogenous leukemia (CML) that is most prevalent in
middle-aged adults.
A useful test to help distinguish this disease is the leukocyte alkaline
phosphatase (LAP) score, which should be low with CML and high with a
leukemoid reaction.
Chronic Myelogenous
Leukemia (CML)

Myeloid cells of CML are also characterized by the Philadelphia
chromosome (Ph1) on karyotyping.
This is a translocation of a portion of the q arm of chromosome 22 to
the q arm of chromosome 9, designated t(9:22).

Here is another view of a peripheral blood smear in a patient with CML.
Often, the numbers of basophils and eosinophils, as well as bands and more
immature myeloid cells (metamyelocytes and myelocytes) are increased.
Unlike AML, there are not many blasts with CML.

The structure of a lymph node is
diagrammed above:
A - Afferent lymphatic channels
B - Subcapsular sinus
C - Follicle
D - Sinuses
E - Paracortical region
F - Medullary cords
G - Efferent lymphatic channel

Here is the normal appearance of a benign reactive lymph node.
Lymphatics that drain tissues peripheral to the node enter the subcapsular sinus
and lymph percolates around and into lymphoid follicles of variable size and
having a surrounding mantle zone that is surrounding a pale germinal
center in which the immune responses are often generated with a predominance
of B cells..
Mantle Zone
Germinal Center

Mantle Zone
Germinal Center

Hematology

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