Types of Anemia

John Adel Samuel

Student ID: 20417
Level 2

Computer Science
Medical Informatics Program
Contents
1 Abstract 2

2 Introduction 2

3 Anemia Classification 3
3.1 Based on Severity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
3.2 Based on Morphology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
3.3 Based on Etiology(Cause) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3

4 Types of Anemia 3
4.1 Iron-deficiency Anemia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
4.2 Pernicious Anemia (Vitamin B12 /Folic acid Deficiency Anemia) . . . . . . . . . 4
4.3 Hereditary Spherocytosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
4.4 Sickle Cell Anemia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6
4.5 Aplastic Anemia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7
4.6 Thalassemia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8
4.7 G6PDH deficiency . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8
4.8 Hemorrhagic Anemia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9

5 Resources 10

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1 Abstract
This research paper aims to explore and classify the major types of anemia, with a focus on their
underlying causes, affected populations, clinical symptoms, diagnostic criteria, and available
treatments. The study delves into the pathophysiology of iron-deficiency anemia, pernicious
anemia, hereditary spherocytosis, sickle cell anemia, aplastic anemia, and thalassemia. By
examining each type individually, the paper provides a comprehensive understanding of how
different anemias manifest, how they are diagnosed through both clinical presentation and
laboratory tests, and how they are managed in medical practice.

2 Introduction
Anemia can be defined as a low oxygen-carrying capacity or, in other words, a decrease in the
number of red blood cells or hemoglobin, whether due to a deformity in the red blood cell or a
deficiency of a substance needed in hemoglobin synthesis.
For a more specific definition, Anemia is a condition in which hemoglobin levels are lower than
normal, specifically < 120 g/l in females and < 140 g/l in males.

Common symptoms may include: tiredness, weakness, shortness of breath, pale or yellowish
skin, irregular heartbeat, dizziness, chest pain, cold limbs, and headache.
It’s worth noting that if a person has any of these symptoms, that doesn’t necessarily mean
he/she has anemia. Consider seeing a doctor before making any assumptions.

According to the World Health Organization ,or WHO for short, 40% of children 6–59
months of age, 37% of pregnant women, and 30% of women 15–49 years of age worldwide are
anaemic. for more information click here.

According to a statistical paper that was published in (10-Jul-2024) by John Elflein, in 2021,
it was estimated that around 24 percent of the population worldwide had anemia, a decrease
from a prevalence of 28 percent in the year 1990. That means in 2021, around 1.92 billion
people across the world had anemia. However, the majority of cases are mild, with less than
one percent of people suffering from severe anemia. for more information click here

This research paper aims to classify and describe the major types of anemia highlight their
causes, symptoms, and treatments.

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3 Anemia Classification
Anemia can be classified in number of different ways and here are some of these classifications:

3.1 Based on Severity

ˆ Mild Anemia: Hb 10 to 12 g/dL in women and to 13.5 g/dL in men.

ˆ Moderate Anemia: Hbhemoglobin 8 to 9.9 g/dL.

ˆ Severe Anemia: Hb 6.5 to 7.9 g/dL.

ˆ Life-Threatening Anemia: Hb < 6.5 g/dL.

3.2 Based on Morphology

ˆ Microcytic anemia: MCV < 80 fL

ˆ Normocytic anemia: MCV ≈ 80 − 100 fL

ˆ Macrocytic anemia: MCV > 100 fL

Note: MCV stands for Mean Corpuscle Volume and it is the average size of RBCs. It’s calcu-
PCV
lated by this equation: RBCs count
× 10
Where PCV stands for hematocrit value which the volume of RBCs to the total blood volume
and it is usually 42 ± 6% for females and 46 ± 6% for males.

3.3 Based on Etiology(Cause)

ˆ Decreased red blood cell (RBC) production

ˆ Increased RBC destruction

ˆ Blood loss

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4 Types of Anemia
There are a huge number of anemia types, in this paper I will cover the most important ones:

4.1 Iron-deficiency Anemia

1. Definition:
in the RBC, there is a pigment called protoporphyrin 9 which reacts with the iron through
a process called ferrochelatase. In this process, the iron and the protoporphyrin are con-
verted into heme which is essential for hemoglobin synthesis. It is considered a microcytic
anemia
2. Causes:
ˆ blood loss (maybe ulcer)
ˆ heavy menstruation
ˆ low iron diet
3. Risk Groups:
ˆ Women who menstruate, particularly if menstrual periods are heavy.
ˆ Women who are pregnant or breastfeeding or those who have recently given birth.
ˆ People who have undergone major surgery or physical trauma.
ˆ People with gastrointestinal diseases such as celiac disease (sprue), inflammatory
bowel diseases such as ulcerative colitis, or Crohn disease.
ˆ People with peptic ulcer disease.
ˆ People who have undergone bariatric procedures, especially gastric bypass opera-
tions.
ˆ Vegetarians, vegans, and other people whose diets do not include iron-rich foods
(Iron from vegetables, even those that are iron-rich, is not absorbed as well as iron
from meat, poultry, and fish.).
ˆ Children who drink more than 16 to 24 ounces a day of cow’s milk (Cow’s milk not
only contains little iron, but it can also decrease absorption of iron and irritate the
intestinal lining causing chronic blood loss.).
4. Symptoms:
ˆ Shortness of breath(dyspnea)
ˆ fatigue
ˆ increased workload on heart
ˆ tachycardia
ˆ dizziness
5. Diagnosis: IDA can be determined by low MCV, high Red Blood Cell Distribution
Width (RDW), mentzer’s index (MI) > 13%, iron studies specifically low ferritin and
transferrin.
6. Treatment options:
ˆ prescribe more iron
ˆ if severe, could resort to blood transfusion

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4.2 Pernicious Anemia (Vitamin B12 /Folic acid Deficiency Anemia)
1. Definition: Normally, the stomach has a type of cells called parietal cells that secrete a
glycoprotein which is called intrinsic factor. Usually, B12 binds to the intrinsic factor. The
anemia arise due to the blockage of B12 from binding to the intrinsic factor as the immune
cells produce antibodies that bind to the intrinsic factor and in response, B12 wouldn’t
be absorbed thus not getting to the blood stream where it can bind to transcobalamin 1
or 2.
B12 is needed for the DNA of the RBCs during erythropoiesis process at the basophillic,
polychromatic and orthochromatic erythroplasts where the DNA matures and condenses
till it gets expelled out of the cell. So, if B12 isn’t present the RBCs will be huge and
that’s why it is considered a macrocytic anemia, specifically megaloblastic anemia

2. Causes: autoimmune condition

3. Risk Groups: Pernicious anemia is more common in people of Northern European and
African descent than in other ethnic groups. Older people also are at higher risk for the
condition.

4. Symptoms: the RBCs are so big that they can get stuck inside the capillaries and
undergo hemolysis which can lead to its loss

5. Diagnosis: a test for methylmalonic acid and homocysteine levels can be made if the
first is high and the second is high then it’s a B12 deficiency but if it was normal for the
first one and high for the second one then it’s a B9 deficiency.
Also, medical history plays a great factor in detecting this type of anemia.

6. Treatment options: intramuscular injections of B12 .

4.3 Hereditary Spherocytosis

1. Definition: RBCs have many different proteins, some of which are: spectrin,ankryin,
band 3, protein 4.1, glycophorins.
For this type, the most important ones are spectrin and ankryin. These two maintain
the shape of the cell, if a problem or a deficiency occur, the RBCs wouldn’t hold its
bioconcave shape and takes a spherical form, hence the name spherocytosis.

2. Causes: Genetic condition

3. Risk Groups: affects people who have Northern Europe or North American ancestry.
(Northern Europe is the northern part or region of the European continent.) Data vary
on how many people have hereditary spherocytosis. Healthcare providers estimate that 1
person in 2,000 to 5,000 people worldwide may have hereditary spherocytosis. (The 2021
global population was 7.9 billion.)
for more information click here

4. Symptoms:

ˆ MCV is usually microcytic but hyperchromic.

ˆ usually caught within the sinusoidal capillaries within the spleen or liver or bone
marrow.
ˆ if the spherocytes enter the spleen, phagocytosis takes place resulting in splenomegaly
(enlargement of the spleen).

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 ˆ causes hemolytic anemia.

5. Diagnosis: it can be detected by evaluating symptoms, asking questions about the

patient’s medical history and his/her biological family medical history, and by doing
several tests. This test may include:
(For more information, click here)

ˆ Complete blood count (CBC)

ˆ Peripheral blood smear
ˆ Reticulocyte count
ˆ Direct antiglobulin (Coombs) test
ˆ Bilirubin level
ˆ Red cell osmotic fragilit
ˆ Plasma membrane electrophoresis

6. Treatment options:
(for more information, click here)

ˆ phototherapy
ˆ blood transfusion
ˆ splenectomy
ˆ gallbladder removal (cholecystectomy)

4.4 Sickle Cell Anemia

1. Definition: it is a point mutation (a mutation due to insertion, change, or deletion of
a certain nucleotide in the DNA sequence) specifically, a missense mutation (a mutation
due to change in the nucleotide).
On the beta chain, the 6th amino acid is normally glutamic acid but when the mutation
happens the Glu gets converted to Valine(Val) and these amino acids are different in their
physical properties and their pka ’s, for instance, Val is a hydrophobic amino acid while
Glu is a hydrophilic or polar amino acid.
Normally, the hemoglobin start polymerizing and start connecting to one another and
when they do so, they take on this weird structure which takes on this sickle shape.
when there is no oxygen the cell takes the sickle form but when oxygen is present it binds
to it making the cell in a normal form.
This process of changing back and forth from sickle shape to normal one is called sickling.

2. Causes: a missense mutation

3. Risk Groups: For a baby to have sickle cell anemia, both parents must carry a sickle cell
gene. In the United States, sickle cell anemia most commonly affects people of African,
Mediterranean and Middle Eastern descent.
For more information click here

4. Symptoms:

ˆ they can get stuck easily in capillaries.

ˆ vaso-occlusive crisis

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 ˆ penile arterioles
ˆ priapism
ˆ splenomegaly

5. Diagnosis: genetic screening

6. Treatment options:

ˆ supplying oxygen
ˆ opioids
ˆ fluids
ˆ Hydroxyurea

4.5 Aplastic Anemia

1. Definition: it is a type of anemia where the bone marrow has a problem which in this
case doesn’t affect the RBCs only but also WBCs and platelets.
In this type the erythropoiesis process is affected resulting in anemia.
But since this type affects the other cells it’s not anemia only but it’s: anemia, leukopenia
and thrombocytopenia which can be called all together pancytopenia.

2. Causes:

ˆ 65% of aplastic anemia is idiopathic or in other words it can be caused by drugs like:
chloramphenicol, benzenes, streptomycin, and a lot of other different drugs.
ˆ it could be due to viruses like cytomegaly virus, epstein barr virus, radiation , fanconi
syndrome

3. Risk Groups:
(for more information, click here)
Aplastic anemia is rare. Factors that can increase risk include:

ˆ Treatment with high-dose radiation or chemotherapy for cancer.

ˆ Exposure to toxic chemicals.
ˆ The use of some prescription drugs — such as chloramphenicol, which is used to
treat bacterial infections, and gold compounds used to treat rheumatoid arthritis.
ˆ Certain blood diseases, autoimmune disorders and serious infections.
ˆ Pregnancy, rarely.

4. Symptoms:

ˆ increased infection rate

ˆ increased bruising or bleeding

5. Diagnosis:
(for more information, click here)

ˆ bone marrow biopsy

ˆ CBC

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 6. Treatment options:
(for more information, click here)

ˆ blood transfusions
ˆ stem cell transplant
ˆ immunosuppressants
ˆ bone marrow stimulants
ˆ antibiotics, antivirals

4.6 Thalassemia
1. Definition: the hemoglobin consists of 2α chains and 2β chains. Thalassemia is a mi-
crocytic anemia where one of these 4 chains is missing.
There are two types:
α + 2β = α− thalassemia
2α + β = β− thalassemia

2. Causes: genetic condition

3. Risk Groups: more common within the Mediterranean ancestry

4. Symptoms: symptoms of severe thalassemia can includ:

(for more information, click here)

ˆ Tiredness, also called fatigue.

ˆ Weakness.
ˆ A change in skin color or a yellowing of skin and eyes.
ˆ Changes or problems with facial bones.
ˆ Slow growth.
ˆ Swelling of the stomach area, also called the abdomen.
ˆ Dark urine.
ˆ Poor appetite.

5. Diagnosis:
(for more information, click here)

ˆ medical history, since thalassemia is highly dependent on genetic factor

ˆ Complete Blood Count (CBC)
ˆ special hemoglobin test
ˆ genetic testing

6. Treatment options: giving blood transfusions, taking iron supplements, and bone stem
cell transplant

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4.7 G6PDH deficiency
1. Definition:
It stands for Glucose 6-phosphate dehydrogenase.
Here is how the story goes:
Normally, we have free radicals that our body produces all the time like O− −
2 , OH , HOCl,
H2 O2 which is called reactive oxygen species or ROS for short.
If the ROS weren’t treated they will damage the hemoglobin where the hemoglobin will
start percipitating and goes and binds to the inner cell membrane (Heinz bodies), that
causes the red blood cell membrane to become less flexible, less pliable, less able to bend
and squeeze through capillaries and that can cause hemolytic anemia where the RBCs
will be destroyed resulting in RBCs count drop.
Fortunately, there is a molecule called glutathione and it has thiol groups, these glu-
tathiones will take some of the ROS to make them less toxic, it will donate hydrogen to
oxygen so we can have water.
After losing the hydrogen atoms they form a disulfide bond and in order to go back to
their reduced form, they depend upon a molecule called Nicotinamide adenine dinucleotide
phosphate or NADPH for short which drops those hydride ions and those electrons to
make NADP+, enzymes that drive this step include glutathione peroxidase and redu-
catase enzymes.
Here comes the G6PDH into play where it is used to make NADPH.

2. Causes: G6PD deficiency is inherited. It is caused by changes (mutations) to the G6PD

gene. The gene is located on the X chromosome and is passed from parents to their
children.
(for more information, click here)

3. Risk Groups: Things that increase your chances of inheriting G6PD deficiency include
your:
(for more information, click here)

ˆ sex (specially, males)

ˆ geographic locations
ˆ race

4. Symptoms:
(for more information, click here)

ˆ Fatigue
ˆ Rapid heart rate (tachycardia)
ˆ Shortness of breath (dyspnea)
ˆ Yellowing in your skin or the whites of your eyes (signs of jaundice)
ˆ Skin that’s paler than usual (also pale lips and tongue)
ˆ Dark, yellow-orange or tea-colored pee
ˆ An enlarged spleen(splenomegaly)

5. Diagnosis: Tests to diagnose G6PD deficiency include:

(for more information, click here)

ˆ A complete blood count (CBC)

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 ˆ A peripheral blood smear
ˆ A bilirubin test
ˆ A G6PD test

6. Treatment options: it depends on the severity of the case but usually, it can be treated
by:
(for more information, click here)

ˆ blood transfusion
ˆ phototherapy

4.8 Hemorrhagic Anemia

It is an anemia due to blood loss like an accident, peptic ulcer and others.

5 Resources
This research was highly inspired by a video on types of anemia from Ninja Nerd on YouTube.
Click here to watch the video.
Other than that, here are the other resources:

ˆ For symptoms of anemia:

https://www.mayoclinic.org/diseases-conditions/anemia/symptoms-causes/syc-20351360

ˆ For anemia classification based on severity:

https://empendium.com/mcmtextbook/chapter/B31.II.15.1.#:~:text=Classification%
20based%20on%20the%20severity,6.5%20to%207.9%20g%2FdL.

ˆ For anemia classification based on morphology:

https://www.labce.com/spg2114726_morphologic_classification_of_anemias.aspx?
srsltid=AfmBOopUfZDiQcqw8UjC9N2DdXkjQ_X7yFc2p8LnZNpQbIAgeU8h4CSg

ˆ For anemia classification based on etiology:

https://emedicine.medscape.com/article/780176-overview?form=fpf

ˆ IDA risk groups:

https://www.hematology.org/education/patients/anemia/iron-deficiency

ˆ B12 deficiency risk groups:

https://www.hoacny.com/patient-resources/blood-disorders/what-pernicious-anemia/
what-are-risk-factors-pernicious-anemia#:~:text=Pernicious%20anemia%20is%20more%
20common,higher%20risk%20for%20the%20condition.

The other resources are in-line references.

I also used an AI agent (ChatGPT) to be specific, it only helped me in research, orientation
and formatting of the LATEXmarkup language (this document was written using LATEXnot word)
and writing the Abstract.

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