Denise Marie Gonzaga Ongteco

MT- 3A

Hematology Lecture

Laboratory
Types of Anemia Etiology Physiology Morphology
Diagnosis
Aplastic anemia An inciting event, The blood is Normally, red blood
develops when such as a virus or pancytopenic, cell, white blood cell
damage occurs to medical drug, meaning that the and platelet levels
your bone marrow, provokes an red cells, white cells, stay within a certain
slowing or shutting aberrant immune and platelets are all range. Your doctor
down the production response, triggering decreased. may suspect aplastic
of new blood cells. oligoclonal The bone marrow is anemia when all three
Bone marrow is a expansion of markedly of these blood cell
red, spongy material cytotoxic T cells hypocellular, or levels are very low.
inside your bones that destroy "empty". Bone marrow biopsy.
Aplastic Anemia
that produces stem hematopoietic stem To confirm a
cells, which give rise cells (left panel, diagnosis, you'll need
to other cells. Stem Onset). Bone to undergo a bone
cells in the bone marrow marrow biopsy.
marrow produce transplantation or
blood cells — red immunosuppressive
cells, white cells and therapy leads to
platelets. In aplastic complete response
anemia, the bone (CR) or partial
marrow is described response (PR) by
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in medical terms as eradicating or
aplastic or suppressing
hypoplastic — pathogenic T-cell
meaning that it's clones (middle
empty (aplastic) or panel, Recovery).
contains very few Relapse occurs with
blood cells recurrence of the
(hypoplastic). immune response,
and the
immunologically
stressed and
depleted stem-cell
compartment also
allows selection of
abnormal
hematopoietic
clones that manifest
as paroxysmal
nocturnal
hemoglobinuria,
myelodysplasia
(MDS), and
occasionally acute
myelogenous
leukemia (AML)
(right panel, Late
Disease).

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  Blood loss. Iron is required for  Hypochromic,  Red blood cell
Blood contains the formation of the microcytic anemia size and color.
iron within heme moiety in • Increased With iron
red blood hemoglobin, anisocytosis deficiency
cells. So if you myoglobin, and • Increased anemia, red
lose blood, haem enzymes, also poikilocytosis blood cells are
you lose some known as • Decreased smaller and
iron. Women cytochromes. Adults reticulocyte number paler in color
with heavy lose approximately 1 (because there’s not than normal.
periods are at mg (men) to 1.5 mg enough iron around)  Hematocrit.
risk of iron (premenopausal This is the
deficiency women) a day in percentage of
anemia faeces and your blood
because they desquamated volume made
Iron-deficiency mucosal and skin
lose blood up by red blood
Anemia cells. The heme
during cells. Normal
menstruation. from destroyed or levels are
Slow, chronic senescent red blood generally
blood loss cells is recycled back between 34.9
within the into new RBCs. [6] and 44.5
body — such Iron, which is percent for
as from a absorbed mostly in adult women
peptic ulcer, a the jejunum, is and 38.8 to 50
hiatal hernia, a transported by percent for
colon polyp or transferrin and adult men.
colorectal stored in either These values
cancer — can ferritin or may change
cause iron hemosiderin forms. depending on
deficiency [14] If more iron is your age.

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 anemia. lost or needed than  Hemoglobin.
Gastrointestin can be absorbed, Lower than
al bleeding iron stores are used normal
can result up, and the patient hemoglobin
from regular becomes iron levels indicate
use of some deficient. Poor iron anemia. The
over-the- stores result in normal
counter pain impaired hemoglobin
relievers, haemoglobin range is
especially synthesis and a generally
aspirin. hypochromic, defined as 13.5
 A lack of iron microcytic anaemia. to 17.5 grams
in your diet. Anaemia then (g) of
Your body results in decreased hemoglobin per
regularly gets oxygen-carrying deciliter (dL) of
iron from the capacity and the blood for men
foods you eat. resultant symptoms and 12.0 to 15.5
If you of fatigue, low g/dL for
consume too energy level, and women. The
little iron, dyspnoea on normal ranges
over time your exertion. for children
body can vary depending
become iron on the child's
deficient. age and sex.
Examples of  Ferritin. This
iron-rich foods protein helps
include meat, store iron in
eggs, leafy your body, and
green a low level of

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 vegetables and ferritin usually
iron-fortified indicates a low
foods. For level of stored
proper growth iron..
and
development,
infants and
children need
iron from
their diets,
too.
 An inability to
absorb
iron. Iron from
food is
absorbed into
your
bloodstream in
your small
intestine. An
intestinal
disorder, such
as celiac
disease, which
affects your
intestine's
ability to absorb
nutrients from

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 digested food,
can lead to iron
deficiency
anemia. If part
of your small
intestine has
been bypassed
or removed
surgically, that
may affect your
ability to absorb
iron and other
nutrients.

 An inability to
absorb iron.
Iron from food
is absorbed
into your
bloodstream
in your small
intestine. An
intestinal
disorder, such
as celiac
disease, which
affects your
intestine's
ability to
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 absorb
nutrients from
digested food,
can lead to
iron deficiency
anemia. If part
of your small
intestine has
been bypassed
or removed
surgically,
that may affect
your ability to
absorb iron
and other
nutrients.
 Pregnancy.
Without iron
supplementati
on, iron
deficiency
anemia occurs
in many
pregnant
women
because their
iron stores
need to serve
their own

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 increased
blood volume
as well as be a
source of
hemoglobin
for the
growing fetus.

G6PD deficiency is a The pentose Without exposure The diagnosis of

common, X-linked monophosphate to offending agents, G6PD deficiency is
reduction in the shunt is the only most patients have made by a
activity of glucose-6- means of NADPH no anemia. After quantitative
phosphate generation in red exposure, though, spectrophotometric
Glucose-6-
dehydrogenase blood cells and patients get an analysis or, more
phosphate-
(G6PD), which therefore crucial in acute hemolytic commonly, by a rapid
dehydrogenase
makes erythrocytes protecting red cells episode, with cell fluorescent spot test
deficiency
susceptible to against oxidative fragments, detecting the
oxidative stress and damage. In a G6PD microspherocytes, generation of
usually causes acute deficient patient, and bite cells NADPH from NADP.
hemolytic anemia in oxidative stresses (caused by recent The test is positive if
response to a can denature pitting of Heinz the blood spot fails to

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 “trigger.” G6PD hemoglobin and bodies). Supravital fluoresce under
enzyme deficiency is cause intravascular staining reveals ultraviolet light.8 In
the most common hemolysis Heinz bodies (these field research, where
enzyme defect. decrease quick screening of a
in number as Hgb large number of
bottoms out, patients is needed,
because younger other tests have been
cells have greater used; however, they
G6PD activity). require definitive
testing to confirm an
abnormal result.9,10
Tests based on
polymerase chain
reaction detect
specific mutations and
are used for
population screening,
family studies, or
prenatal diagnosis.
Sickle cell disease is Sickle cell disease In the blood, A blood test can check
caused by a genetic (SCD) and its particularly during for hemoglobin S —
abnormality in the variants are genetic crises, sickle cells the defective form of
gene for disorders resulting are present. After hemoglobin that
hemoglobin, which from the presence of autosplenectomy underlies sickle cell
Sickle cell Anemia
results in the a mutated form of occurs, there anemia. In the United
production of sickle hemoglobin, is what’s called a States, this blood test
hemoglobin. When hemoglobin S (HbS). "post-splenectomy is part of routine
oxygen is released ... Approximately blood picture": newborn screening
from sickle half the individuals nucleated red blood done at the hospital.

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 hemoglobin, it sticks with homozygous cells, targets, But older children
together and forms HbS disease HowellJolly and adults can be
long rods, which experience vaso- bodies, tested, too. In adults,
damage and change occlusive crises. ThePappenheimer a blood sample is
the shape of the red frequency of crises is
bodies, and a drawn from a vein in
blood cell. extremely variable. slightly increased the arm
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).
HS is caused by a Spectrin deficiency  Mild The principal
variety of mutations Ankyrin defects normochromi laboratory studies
that lead to defects Band 3 deficiency c, normocytic used in the diagnosis
in red blood cell Protein 4.2 (pallidin) anemia. of hereditary
(RBC) membrane deficiency  Numerous spherocytosis (HS)
proteins. HS usually Aquaporin-1 spherocytes. include the following:
Hereditary is transmitted as an Red blood cell Complete blood cell
spherocytosis autosomal antibodies count. Reticulocyte
dominant trait, and count. Mean
the identification of corpuscular
the disorder in hemoglobin
multiple concentration
generations of (MCHC).
affected families is

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the rule.
Homozygosity for
this dominantly
transmitted HS
gene has not been
identified, which
suggests that the
homozygous state
is incompatible with
life.

Twenty-five percent
of all newly
diagnosed patients
do not demonstrate
a dominant
inheritance pattern.
Parents of these
patients do not
have clinical or
hematologic
abnormalities.
Some of these
sporadic cases may
result from new
mutations.

An autosomal
recessive mode of
inheritance also
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 occurs, as indicated
by descriptions of
families in which
apparently healthy
parents have had
more than one
affected child.
Recessive
inheritance may
account for 20-25%
of all HS cases. It
manifests only in
individuals who are
homozygous or
compound
heterozygous and
often is associated
with severe
hemolytic anemia.

If you're missing two In the severe forms, In mild thalassemia, Doctors diagnose
genes, you have such as β patients have a mild thalassemia’s using
alpha thalassemia thalassemia major or microcytic, blood tests, including
trait (also called Cooley anemia, the hypochromic a complete blood
Thalassemia alpha thalassemia same anemia. Sometimes count (CBC) and
minor). You may pathophysiology there are special hemoglobin
have mild anemia. If applies with target cells, or cells tests. A CBC
you're missing three substantial with basophilic measures the amount
genes, you likely exaggeration. The stippling. Patients of hemoglobin and the

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 have hemoglobin H significant excess of with severe different kinds of
disease (which a free α chains caused thalassemia have a blood cells, such as
blood test can by the deficiency of whopping red blood cells, in a
detect). This form of β chains causes anemia marked sample of blood.
thalassemia causes destruction of the anisocytosis and
moderate to severe RBC precursors in poikilocytosis.
anemia the bone marrow (ie,
ineffective
erythropoiesis).
Autoimmune Autoimmune In WAIHA, the Direct antiglobulin
hemolytic anemia hemolytic anemia blood smear shows test (DAT)
(AIHA) is a group of and hereditary prominent Also called the
rare but serious spherocytosis are spherocytosis. In Coombs test. Mix
blood disorders. examples of CAIHA, if you make patient's red cells
They occur when extravascular the blood with anti-human
the body destroys hemolysis because smear at a cool globulin (an antibody
red blood cells more the red blood cells temperature, you against
rapidly than it are destroyed in the can see nice big red human
Autoimmune produces them. A spleen and other blood cell immunoglobulins). If
hemolytic anemia condition is reticuloendothelial agglutinates the red cells are
considered idiopathic tissues. (clumps) coated with antibodies
when its cause is Intravascular (as they are in some
unknown. hemolysis occurs in immune
hemolytic anemia processes, see later),
due to the following: the anti-human
... Transfusion of globulin will attach to
ABO incompatible those antibodies,
blood. bridging the red cells
and making them

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 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.
MAHAs can be In medicine The blood smear The term "thrombotic
caused by a variety (hematology) shows schistocytes, microangiopathy
of inherited and microangiopathic which are small, (TMA)" is also used
acquired etiological hemolytic anemia pointy red cell to describe syndromes
insults; however, (MAHA) is a fragments. characterized by
their final common microangiopathic MAHA,
pathway appears to subgroup of thrombocytopenia,
be inappropriate hemolytic anemia and thrombotic
systemic platelet (loss of red blood lesions in small blood
plugging within cells through vessels. The most
Microangiopathic
small vessels, destruction) caused prominent diagnoses
hemolytic anemia
resulting in by factors in the associated with TMA
generation of small blood vessels. are thrombotic
microthrombi in the It is identified by the thrombocytopenic
microcirculation of a finding of anemia purpura (TTP) and
number of organs. In and schistocytes on hemolytic uremic
the classic case of microscopy of the syndrome (HUS).
HUS caused by blood film.
Shiga Toxin E. coli
(STEC) strain
0157:H7, the shiga

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 toxin damages
endothelial cells,
resulting in platelet
aggregation and
thus deposition of
microthrombi.
However, other
causes for MAHAs
have been
recognized including
other bacteria,
inherited defects,
drugs, malignancies,
and in some cases
idiopathic triggers.
 Vitamin B-12 Megaloblastic Blood One test used to
Deficiency anemia is caused by • Macrocytic anemia diagnose many forms
Vitamin B-12 is a various DNA (MCV >100) of anemia is the
nutrient found in synthesis defects. In • Oval macrocytes. complete blood count
some foods like Folate deficiency, • Hypersegmented (CBC). This test
meat, fish, eggs, and purine biosynthesis (more than 4 lobes) measures the different
Megaloblastic milk. Some people is affected because neutrophils. parts of your blood.
Anemia can’t absorb enough folic acid is essential Bone marrow The red blood cells
vitamin B-12 from in this process. • “Megaloblastic” will appear larger and
their food, leading to Folic acid is cells: giant red cell underdeveloped if you
Megaloblastic essential for purine or neutrophil have megaloblastic
anemia. biosynthesis. Folic precursors with anemia.
Megaloblastic acid absorbed from nuclear-cytoplasmic
anemia caused by the diet must be asynchrony (mature

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vitamin B-12 activated to produce cytoplasm,
deficiency is referred active immature nucleus).
to as pernicious tetrahydrofolic acid
anemia. (THF). THF is
necessary for single
Vitamin B-12 carbon transfers in
deficiency is most the synthesis of
often caused by the pyrimidine
lack of a protein in nucleotides.
the stomach called Without adequate
“intrinsic factor.” levels of biologically
Without intrinsic active THF, the
factor, vitamin B-12 ability to repair and
can’t be absorbed, replicate DNA is
regardless of how decreased. Vitamin
much you eat. It’s B-12 is a cofactor
also possible to for the activation of
develop pernicious folic acid in a step
anemia because there that also converts
isn’t enough vitamin homocysteine to
B-12 in your diet. methionine.
 Folate In the case of
Deficiency inadequate folic acid
Folate is intake, THF
another production is
nutrient that’s depleted, and DNA
important for synthesis is slowed.
the The effect on
development hematopoiesis is to

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of healthy red reduce the rate of
blood cells. cell production,
Folate is resulting in
found in foods pancytopenia. In the
like beef liver, cells that are
spinach, and produced, the effect
Brussels created is an arrest
sprouts. You of nuclear
can also find it maturation. In other
in fortified words, the cells that
cereals. Folate are produced have
is often mixed immature nuclei
up with folic compared with the
acid — degree of
technically, maturation of the
folic acid is the cytoplasm.
artificial form
of Folate,
found in
supplements.

Your diet is an
important
factor in
making sure
you have
enough
Folate. Folate
deficiency can

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 also be caused
by chronic
alcohol abuse,
since alcohol
interferes with
the body’s
ability to
absorb folic
acid. Pregnant
women are
more likely to
have Folate
deficiency,
because of the
high amounts
of Folate
needed by the
developing
fetus.
Anemia of chronic In anemia of chronic The blood shows a In anemia of chronic
disease is a condition inflammation normochromic, inflammation without
that can be without iron normocytic anemia iron deficiency,
associated with deficiency, ferritin is with minimal ferritin is normal or
Anemia of chronic many different normal or high, anisocytosis and high, reflecting the
disease underlying disorders reflecting the fact poikilocytosis fact that iron is
including chronic that iron is (it’s a “bland- sequestered within
illnesses such as sequestered within looking” anemia). cells, and ferritin is
cancer, certain cells, and ferritin is Some cases (about being produced as an
infections, and being produced as 25%) are microcytic, acute phase reactant.

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autoimmune and an acute phase but the MCV rarely In iron deficiency
inflammatory reactant. gets anemia ferritin is low.
diseases such as below 72 fL. Total iron-binding
rheumatoid arthritis capacity (TIBC) is
or lupus. ... Anemia high in iron
of chronic disease is deficiency, reflecting
usually a mild or production of more
moderate condition. transferrin to increase
iron binding; TIBC is
low or normal in
anemia of chronic
inflammation.

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