Dr. Basim Al-Ka'abi
Blood Physiology
Fifth Lecture
1
Lecture Name: Anemia: Classification and Types
Lecturer Name: Dr. Basim A. Al-Ka'abi
Department: Medical Physiology
Stage: First Stage Medical Students
Lecture Objectives:
By the end of this lecture the students should be able to know the following:
Definition and main classifications of anemia.
Pathological classification of anemia and its subtypes.
An idea to some types of anemias.
References:
Barrett, K et al. (2018). Ganong's Review of Medical Physiology. Twenty-
sixth edition. USA.
Guyton, A and Hall, J (2015). Text Book of Medical Physiology.
Thirteenth edition. Philadelphia, USA.
Dr. Basim Al-Ka'abi
Blood Physiology
Fifth Lecture
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Anemia
-Anemia is a functional inability of the blood to supply the tissue with
adequate oxygen for proper metabolic functions, caused by reduction in the
number of RBCs, quantity of Hb and volume of packed red cells/100 ml of
blood.
There are two main classifications of anemia
1. The pathogenic and etiological classification.
2. Morphological classification.
Pathogenic and etiological classification
-The main pathogenic and etiological factors responsible for causing
anemia are:
(1) Impaired RBC’s production:
A- Iron deficiency anemia
-Iron deficiency is a state in which body iron stores are depleted. The
causes of iron deficiency are related to poor dietary supplementation,
diminished absorption, increased requirements and excessive blood loss.
-Myeloperoxidase is an iron-containing enzyme that is essential to
neutrophil phagocytosis and bacterial killing, both functions may be
diminished with iron depletion, so cell-mediated immunity (T cell
function) can be impaired, but antibody production (B cell function) is
normal.
-Iron deficiency anemia is associated with a deficiency of Hb in the red
cells (hypochromic anemia) and cells that are smaller than normal
(microcytic anemia).
Dr. Basim Al-Ka'abi
Blood Physiology
Fifth Lecture
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B- Megaloblastic anemia
-It occurs due to deficiency of vitamin B
12
or folic acid. As described
previously, impaired DNA synthesis can be caused by vitamin B
12
and folic
acid deficiency. This anemia is associated with a deficiency of red cells,
but the cells that are present will be larger than normal (megaloblasts) and
will contain an adequate amount of Hb, so, the type of anemia produced in
both of these condition is called macrocytic normochromic anemia.
(2) Excessive loss of blood:
A- Acute blood loss
-After rapid hemorrhage the body replaces the plasma within 1-3 days, but
this leaves a low concentration of RBCs. If a second hemorrhage does not
occur, the RBCs concentration returns to normal within 3-4 weeks.
B- Chronic blood loss
-The person frequently cannot absorb enough iron from the intestine to
form Hb as rapidly as it is lost, therefore, RBCs are then produced with too
little Hb inside them, giving rise to microcytic hypochromic anemia.
(3) Excessive destruction of RBCs:
Hemolytic anemias
-A hemolytic state exists when the survival of the red cell inside the body
is shortened.
-The presence of anemia in an individual patient is, however, dependent on
the degree of hemolysis and the compensatory response of the erythroid
elements of the bone marrow.
-Normal bone marrow is able to increase its output about 6-8 folds, so that
anemia is not manifest until this capacity is exceeded, corresponding to
a red cell lifespan of about 15-20 days or less.
Dr. Basim Al-Ka'abi
Blood Physiology
Fifth Lecture
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Hemolytic anemias may be classified as follows:
(1) Intracorpuscular defects
-Which are hereditary defects as follows:
1. Defects in the red cell membrane.
2. Enzyme defects.
3. Hemoglobinopathies.
(2) Extracorpuscular defects
-Any external factor that is able to destroy red cells, such as:
1. Immune hemolytic anemia.
2. Chemicals and toxins.
3. Physical agents.
4. Infections.
Intracorpuscular defects
(A) Red cell membrane defects
Hereditary spherocytosis (HS)
-In which the RBCs are very small in size and they are spherical in shape
rather than being biconcave discs.
-In HS, there is a loss of surface area of the red cell resulting in
a decreased surface-to-volume ratio, therefore these cells are less
deformable than normal.
-Therefore, on passing through the splenic pulp they are easily ruptured by
even slight compression.
(B) Enzyme defects
Glucose-6-phosphate dehydrogenase (G6PD) deficiency
-Glucose-6-phosphate dehydrogenase deficiency is a genetic abnormality
that results in an inadequate amount of G6PD enzyme in the blood. This is
Dr. Basim Al-Ka'abi
Blood Physiology
Fifth Lecture
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a very important enzyme that regulates various biochemical reactions in
the body.
-This enzyme is also responsible for keeping RBCs healthy so they can
function properly and live a normal life span. Without enough of it,
hemolysis of RBCs occurs.
-In people with G6PD deficiency, hemolytic anemia can occur after eating
fava beans or certain legumes. It may also be triggered by infections or by
certain drugs, such as:
a. Antimalarials, a type of medication used to prevent and treat malaria.
b. Sulfonamides, a medication used for treating various infections.
c. Aspirin, a drug used for relieving fever, pain, and swelling.
d. Some nonsteroidal anti-inflammatory medications (NSAIDs).
-Most people with G6PD deficiency usually don't experience any
symptoms. However, some may develop symptoms when they’re exposed
to the medication, food, or infection that triggers the early destruction of
red blood cells. Once the underlying cause is treated or resolved, symptoms
of G6PD deficiency usually disappear within few weeks.
(C) Hemoglobinopathy syndromes
1. Sickle cell anemia
-The RBCs contain an abnormal type of Hb called HbS, in which the α
chains are normal but the β chains are abnormal, due to replacement of one
glutamic acid residue by a valine residue.
-This abnormal Hb is insoluble at low O
2
tensions, so when it is exposed to
low concentration of O
2
, it precipitates into long crystals inside RBCs.
-These crystals elongate the cell and give it a sickle-like appearance rather
than being a biconcave disc. The precipitated Hb also damages the cell
membrane, so that the cells become highly fragile.
Dr. Basim Al-Ka'abi
Blood Physiology
Fifth Lecture
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2. Thalassemia
-Is another hereditary type of anemia in which the RBCs are unable to
synthesize adequate amounts of either the alpha or beta polypeptide chains
required to form the Hb.
-There are two major types of thalassemia: Alpha thalassemia that is caused
by a defect in the rate of synthesis of α chains, and beta thalassemia that is
caused by a defect in the rate of synthesis of β chains.
-Both types are hypochromic microcytic anemias.