TUTORIAL REPORT

HEMATOIMMUNOLOGY
1ST SCENARIO
Pale and Weak

Composed by
1. Atika Threenesia 1318011025
2. Ayang Tria Putri B. 1318011028
3. Farras Cahya Puspitha 1318011068
4. Fauziah Lubis 1318011070
5. Indira Malahayati 1318011083
6. Indrani Nur Winarno P. 1318011084
7. Lisa Ayu Pratiwi 1318011094
8. Marco Manza Adiputra 1318011101
9. Noviyanti Choirunnisa H. 1318011122
10. Rika Partika 1318011143
11. Salsabila Septira 1318011147
12. Samintola Dolok Saribu 1318011148

MEDICAL FACULTY
LAMPUNG UNIVERSITY
2015
 PREFACE

Thank God we pray for the presence of the Almighty God because of His
blessings, His grace and His guidance we can finished this report. This report
contains of the result from our discussion in tutorial. This report was made in
order to meet the duty of this blok of Hematoimmunology.

We recognize, in this report there are many mistakes and shortcomings. These are
due to the limited ability, knowledge and experience that we have. However, there
are many people who have helped us by providing documents or resources,
provide thought input. Therefore we expect criticism and suggestions for the
improvement and perfection of this report in the future. Hopefully, this report can
be useful for us and the readers.
Case 1
Pale and Weak

Ms. Kinara, 23 years old, came to the doctor because of fatigue and headache. 2
months earlier, she felt weak, fatigue and headache. She rarely eats meat. Four
months ago, she got menometrorhagia and the illness has recovered about 3 weeks
ago. Physical examination showed her conjungtiva is pale. There is atropy of
tongues papilla. Laboratory examination result showed Hb 10g/dl, MCV 73 fl,
MCH 24 pg, peripheral blood film showed microcytic hypocrome anemia,
leucocyte and trombocyte are normal.
STEP 1

1. What is Menometrorhagia?
Menometrorrhagia is the name of a condition characterized by excessive
or prolonged uterine bleeding that occurs very frequently. There are
numerous factors that can lead to this disorder.
Menometrorrhagia is a condition in which prolonged or excessive uterine
bleeding occurs irregularly and more frequently than normal.

2. What is MCV and MCH?

MCV (Mean Corpuscular Volume)
The size or volume of the average eritroit. MCV increases when red cells
are larger than normal (macrocytic), for example in anemia due to vitamin
B12 deficiency. MCV decreased when erythrocytes is smaller than normal
(microcytic) as in anemia due to iron deficiency.
Mean corpuscular hemoglobin (MCH).
The average amount of hemoglobin in erythrocytes. Erythrocytes are
larger (macrocytic) tend to have a higher MCH. Conversely, the smaller
erythrocytes (microcytic) will have a lower value of MCH.

3. What is microcytic hypocromic anemia?

Microcytic anemia is any of several types of anemia characterized by
small red blood cells (called microcytes). The MCV is the average red
blood cell size.
In microcytic anemia, the red blood cells (erythrocytes) are usually also
hypochromic, meaning that the red blood cells appear paler than usual.
This is reflected by a lower-than-normal mean corpuscular haemoglobin
concentration(MCHC), a measure representing the amount of haemoglobin
per unit volume of fluid inside the cell.
 STEP 2

1. How is the process of the hematopoiesis especially erythropoiesis?

2. What is the definition and the types of the anemia?
3. What is the diagnosis and the differential diagnosis of this case?
4. Is there any correlation of the Ms. Kinaras symptom with the habbit of
menometrorrhagia and the rarely-eats-meat habbit?
5. What are the pathophysiology of the sign and symptom of the patient?
6. What are the laboratory tests needed to diagnose anemia?
7. What are the therapy for anemia?
STEP 3
1. Hematopoiesis
Hematopoiesis is a process of blood cell production and maturation in the
bone marrow. The process begins with the pluripotent stem cell.
The stem cell is capable to proliferate, differentiate and replicate.The
differentiation into a myeloid or lymphoid stem cell takes place in
response of growth factors (cytokines).
The lymphoid stem cell differentiates into a pre-B or pre-T stem cell.
The myeloid stem cell produces an intermediate stem cell which
differentiates into erythroid, megakarycytic, myeloid, monocytic,
eosinophilic or basophilic lineage.

Erythropoiesis
Erythropoiesis is the development process in which new erythrocytes are
produced, through which each cell matures in about seven days. Through
this process, erythrocytes are continuously produced in the red bone
marrow of large bones, at a rate of about 2 million cells per second in a
healthy adult. (In the embryo, the liver is the main site of red blood
cell production). The production can be stimulated by the hormone
erythropoietin (EPO), which is synthesized by the kidney.

2. Anemia may be defined as any condition resulting from a significant decrease

in the total body erythrocyte mass. Anaemia is usually defined clinically as a
reduction of the haemoglobin concentration to less than 130 g/l (males) or less
than 120 g/l (females). It is a common problem
The main causes of anaemia can be usefully classified according to the associated
red cell changes:
(a) Hypochromic, Microcytic
Including: iron deficiency (the commonest cause of anaemia)
caused of chronic disease
sideroblastic
thalassaemia (common in some populations)
(b) Normochromic, Macrocytic
Including: vitamin B12 or folate deficiency
alcohol
myelodysplasia
(c) Polychromatophilic, Macrocytic
Including: haemolysis
(d) Normochromic, Normocytic
Including: chronic disorders
renal failure
diseases of the bone marrow
(e) Leucoerythroblastic
Including: myelofibrosis
leukaemia
metastatic carcinoma.

3. The diagnosis of this case is iron-deficiency anemia.

The differential diagnosis are : - anemia caused of a chronic disease
- sideroblastic anemia

4. There is a correlation between the habbitual of the patient with the symptom.
Patient tend to rarely eats meat. Meat is included in a high-iron-source food. We
can get iron from protein, especially animals protein. So, patient will not have so
many irons storage on her bones. And also, patient have a menometrorrhagia,
which is the condition where the body will lose much blood. With the iron-
deficiency condition, it can caused anemia and will caused patient suffering these
symptom, like feeling weak and have a headache.

5. Anemia will caused these situation in humans body.

a. Decreased hemoglobin oxygen affinity
b. Redistribution of blood flow
c. Increased cardiac output
 These condition will caused the symptom appear. When symptoms do
develop, they are pretty much what you would expect given the precarious state of
oxygen delivery to the tissues: dyspnea on exertion, easy fatigability, fainting,
lightheadedness, tinnitus, and headache.
Clinical signs of a slowly developed anemia are pallor, tachycardia, and a
systolic ejection murmur. In rapidly developing anemia (as from hemorrhage and
certain catastrophic hemolytic anemias), additional symptoms and signs are noted:
syncope on rising from bed, orthostatic hypotension (i.e., the blood pressure falls
when the patient is raised from the supine to the sitting or standing positions) and
orthostatic tachycardia.

6. Laboratory tests to diagnose anemia

Screening test : - Hemoglobin level
- Erytrocytes index : MCV, MCH, MCHC
- Peripheral blood film

Routine test : - Erytrocytes sedimentation rate (ESR)

- Differential count
- Reticulocytes level
- Trombocytes level
Bone marrow examination test
Test based indication : - Serum iron, TIBC, Transferrin saturation, ferritin serum.
- B12 and folat acid level
- Reticulocytes count, Coombs test.
Etc.

7. The treatment for anemia :

Oral Iron
Injectable iron
Blood transfusions
Hyperbaric oxygen
Erythrpoiesis-stimulating agent
Nutrition treatment
STEP 4

1. Hematopoiesis
In humans, hematopoiesis begins in the yolk sac and transitions into the liver
temporarily before finally establishing definitive hematopoiesis in the bone
marrow and thymus. Experiments with human embryos confirm observations
in the hemangioblast, a common precursor for endothelial and hematopoietic
cells. In humans, HSCs are present in close proximity to endothelial cells
(Tavian et al., 2010), and flow cytometry-sorted vascular endothelial cells from
fetal and embryonic human blood-forming tissues cultured over a layer of MS-
5 stromal cells underwent hematopoiesis (Tavian et al., 2010). These
endothelial cells were sorted from the human embryonic aorta between day 27
and day 40 of development, which is when HSCs are present in this region.
Studies using transplantation of HSCs from human embryos into immune-
deficient mice have confirmed that the first definitive human HSCs are born in
the AGM.

Hematopoiesis begins with the most basic blood cell, the stem cell or
pluripotent hematopoietic stem cell (PHSC). The end products of this
process are mature white blood cells (which provide our bodies with protection
from infection), mature red blood cells (which carry oxygen to the cells and
tissues in our bodies), and platelets (which help control bleeding after injury).

PHSCs have the ability to either divide and create other PHSCs, or to commit
into one of several differentiation pathways. These pathways eventually
result in the production of a type of blood cell.

If a PHSC commits to producing mature blood cells, they will undergo several
(usually five or more) cell divisions before becoming that cell. Every time the
cell divides, it takes on more and more of the characteristics of the adult cell it
will become. In other words, it becomes more differentiated or specialized. The
term hematopoiesis describes the process of blood cell development, from
PHSC, through differentiation, to a mature blood cell.

Colony-forming units
There are various kinds of colony-forming units:
Colony-forming unit lymphocyte (CFU-L)

Colony-forming unit erythrocyte (CFU-E)

Colony-forming unit granulo-monocyte (CFU-GM)

Colony-forming unit megakaryocyte (CFU-Me)

Colony-forming unit Basophil (CFU-B)

Colony-forming unit Eosinophil (CFU-Eo)

Erythropoiesis
All blood cells are formed in the bone marrow. This is the erythrocyte factory,
which is soft, highly cellar tissue that fills the internal cavities of bones.

HUMAN BONE MARROW

During intrauterine development, the early stages of life, erythrocytes are

produced first by the yolk sac and then by the developing spleen during the
third month of gestation, until the bone marrow is formed in the seventh month
and takes over erythrocyte production exclusively.

Erythrocyte differentiation
Erythrocyte differentiation takes place in 8 stages. It is the pathway through
which an erythrocyte matures from ahemocytoblast into a full-blown
erythrocyte. The first seven all take place within the bone marrow. After stage
7 the cell is then released into the bloodstream as a reticulocyte, where it then
matures 1-2 days later into an erythrocyte.

The stages are as follows:

1. Hemocytoblast, which is a pluripotent hematopoietic stem cell
2. Common myeloid progenitor, a multipotent stem cell
3. Unipotent stem cell
4. Pronormoblast
5. Basophilic normoblast also called an erythroblast.
6. Polychromatophilic normoblast
7. Orthochromatic normoblast
8. Reticulocyte
There are 4 major steps in erythropoiesis. Erythrocytes are derived in the red
bone marrow from pluripotent stem cells that give rise to all types of blood
cells. Myeloid stem cells are partially differentiated cells that give rise to
erythrocytes and several other types of blood cells.

Nucleated erythroblasts are committed to becoming mature erythrocytes. These

cells extrude their nucleus and organelles, making more room for hemoglobin.
Reticulocytes are immature red blood cells that contain organelle remnants.
Mature erythrocytes are released into the capillaries. The pictures in
this link and here show the steps of differentiation.

Distinct Characteristics of Erythrocytes during Erythropoiesis

These characteristics can be seen during the course of erythrocyte maturation:
The size of the cell decreases
The cytoplasm volume increases
Initially there is a nucleus and as the cell matures the size of the nucleus
decreases until it vanishes with the condensation of the chromatin material.

Regulation of Erythropoiesis
Thinking logically, we might suspect that because the primary function of
erythrocytes is to transport O2 in the blood, the primary stimulus for
erythrocyte production is low O2 levels. We would be correct, but low O2
levels do not stimulate erythropoiesis by acting directly on the bone marrow.
Instead, it stimulates the kidneys to secrete the hormone erythropoietin into the
blood, and this hormone in a domino effect stimulates the bone marrow to
produce erythrocytes.
 Erythropoietin acts on derivatives of undifferentiated cells that have already
been committed to becoming red blood cells (RBCs), stimulating the
proliferation and maturation of these cells into mature RBCs. This increase in
erythropoietic activity elevates the number of circulating RBCs, thereby raising
the O2 carrying capacity of the blood and restoring the delivery of O2 to the
body tissues to normal. Once the O2 level in the tissues of the kidneys is
brought back to normal, erythropoietin secretions is turned down until it is
needed again. This is an example of a negative feedback mechanism.

2.
Classification of Anemia by Cause
Mechanism Examples
Blood loss

Acute GI bleeding
Injuries
Childbirth
Surgery

Chronic Bladder tumors

Cancer or polyps in GI tract
Heavy menstrual bleeding
Kidney tumors
Ulcers in the stomach or small intestine

Deficient erythropoiesis*

Microcytic Iron deficiency

Iron-transport deficiency
Iron utilization defect
Iron reutilization defect
Thalassemias (also classified under excessive
hemolysis due to intrinsic RBC defects)

Normochromic-normocytic Aplastic anemia

 Hypoproliferation
In kidney disease
In endocrine failure (thyroid, pituitary)
In protein depletion
Myelodysplasia
Myelophthisis

Macrocytic Copper deficiency

Folate deficiency
Vitamin B12 deficiency
Vitamin C deficiency

Excessive hemolysis due to extrinsic RBC defects

Reticuloendothelial hyperactivity Hypersplenism

with splenomegaly

Immunologic abnormalities Autoimmune hemolysis

Cold antibody hemolysis (paroxysmal cold
hemoglobinuria)
Warm antibody hemolysis
Isoimmune (isoagglutinin) hemolysis

Mechanical injury Infection

Trauma

Excessive hemolysis due to intrinsic RBC defects

Membrane alterations, acquired Hypophosphatemia

Paroxysmal nocturnal hemoglobinuria
Stomatocytosis

Membrane alterations, congenital Hereditary elliptocytosis

Hereditary spherocytosis

Metabolic disorders (inherited Embden-Meyerhof pathway defects

enzyme deficiencies) G6PD deficiency
Hemoglobinopathies Hb C disease
Hb E disease
Hb S-C disease
Hb S-thalassemia disease
Sickle cell disease (Hb S)
Thalassemias (, -, and )

*Classified according to RBC indices.

Iron Deficiency Anaemia

The most common form of anaemia is iron deficiency anaemia which is usually
due to chronic blood loss caused by excessive menstruation. Increased
demands for iron, such as foetal growth in pregnancy, and children undergoing
rapid growth spurts in infancy and adolescence, can also cause iron deficiency
anaemia.

Causes
Iron deficiency occurs when the rate of loss or use of iron is more than its rate
of absorption and use. The reasons for this are
Chronic blood loss: Most commonly due to excessive menstruation or
bleeding into or from the gut as a result of a peptic ulcer, gastritis,
haemorrhoids or in children, worm infestation.
Increased use of iron: In pregnancy, due to the growth of the foetus or
children undergoing rapid growth spurts in infancy and adolescence.
Decreased absorption of iron after a partial or total removal of the
stomach, lack of stomach acid, chronic diarrhoea, or malabsorption.

Signs and symptoms

The most common symptoms of chronic anaemia include tiredness, weakness,
shortness of breath and sometimes, a fast heartbeat. The tongue may also
become smooth, shiny and inflamed - this is called glossitis. Angular stomatitis
(erosion, tenderness and swelling at the corners of the mouth) may also occur.
In some instances, the patient also suffers from pica, a craving for strange
foods such as starch, ice and clay. The symptoms of the underlying cause of the
iron deficiency may be present such as heavy menstrual bleeding or abdominal
pain due to peptic ulceration.

Risk
Infants and young children, women, and adults who have internal bleeding are
at highest risk for iron-deficiency anaemia.

Aplastic Anaemia
Overview
Aplastic anaemia is a blood disorder in which the body's bone marrow doesn't
make enough new blood cells. This may result in a number of health problems
including arrhythmias, an enlarged heart, heart failure, infections and bleeding.
Aplastic anaemia is a rare but serious condition. It can develop suddenly or
slowly and tends to worsen with time, unless the cause is found and treated.

Causes
Damage to the bone marrow's stem cells causes aplastic anaemia. In more than
half of people who have aplastic anaemia, the cause of the disorder is
unknown. A number of acquired diseases, conditions, and factors can cause
aplastic anaemia including
Toxins, such as pesticides, arsenic, and benzene
Radiation and chemotherapy
Medicines such as chloramphenicol
Infectious diseases such as hepatitis, Epstein-Barr virus, cytomegalovirus,
parvovirus B19, and HIV
Autoimmune disorders such as lupus and rheumatoid arthritis
Inherited conditions, such as Fanconi anaemia, Shwachman-Diamond
syndrome, dyskeratosis congenital and Diamond-Blackfan anaemia may
also cause aplastic anaemia.
Signs and symptoms
The most common symptoms of aplastic anaemia are
Fatigue
Shortness of breath
Dizziness
Headache
Coldness in your hands or feet
Pale skin, gums and nail beds
Chest pains

Treatment
Treatment for aplastic anaemia includes blood transfusions, blood and marrow
stem cell transplants, and medication. These treatments can prevent or limit
complications, relieve symptoms, and improve quality of life.

In some cases, a cure may be possible. Blood and marrow stem cell transplants
may cure the disorder. Removing a known cause of aplastic anaemia, such as
exposure to a toxin, may also cure the condition.

Risk
People of all ages can get aplastic anaemia. However, it is most common in
adolescents, young adults and the elderly. Men and women are equally likely to
have it. A person's risk for aplastic anaemia is higher if you have
Been exposed to toxins
Taken certain medicines or had radiation or chemotherapy treatment
Certain infectious diseases, autoimmune disorders, or inherited conditions

Pernicious Anaemia
Overview
Pernicious anaemia is a condition in which the body can't make enough healthy
red blood cells because it doesn't have enough vitamin B12 (a nutrient found in
certain foods). People who have pernicious anaemia can't absorb enough
vitamin B12 due to a lack of intrinsic factor (a protein made in the stomach).
However, other conditions and factors can also cause vitamin B12 deficiency.

Causes
A lack of intrinsic factor is a common cause of pernicious anaemia as the body
can't absorb enough vitamin B12. Some pernicious anaemia occurs because the
body's small intestine can't properly absorb vitamin B12 which may be due to
the wrong bacteria in the small intestines; certain diseases that interfere with
vitamin B12 absorption; certain medicines; surgical removal of part of the
small intestine; and tapeworm infection. Sometimes people develop pernicious
anaemia because they don't get enough vitamin B12 in their diets.

Signs and symptoms

Apart from the symptoms of anaemia (fatigue, dizziness, etc.), the vitamin B12
deficiency may also have some serious symptoms such as
Nerve damage
Neurological problems such as confusion, dementia, depression, and
memory loss.
Symptoms in the digestive tract include nausea and vomiting, heartburn,
abdominal bloating and gas, constipation or diarrhoea, loss of appetite, and
weight loss.
An enlarged liver
A smooth, beefy red tongue
Infants who have vitamin B12 deficiency may have poor reflexes or
unusual movements, such as face tremors.

Treatment
Pernicious anaemia is treated by replacing the missing vitamin B12 in the
body. People who have this disease may need lifelong treatment.
 Risk
You are at higher risk for pernicious anaemia if you
Have a family history of the condition.
Have had part or all of your stomach removed.
Have certain autoimmune disorders that involve the endocrine glands, such
as Addison's disease, type 1 diabetes, Graves' disease, and vitiligo.
Have had part or all of your small intestine removed.
Have certain intestinal diseases or disorders that prevent your body from
properly absorbing vitamin B12.
Take medicines that prevent your body from properly absorbing vitamin
B12.
Are a strict vegetarian who doesn't eat any animal or diary products and
doesnt take a vitamin B12 supplement, or if you eat poorly overall.

3. The diagnosis of this case is iron deficiency anemia.

Iron Deficiency Anemia
Anemia is a condition where the number of healthy red blood cells (RBCs) in
the blood is lower than normal. RBCs transport oxygen throughout the body, so
a shortage of these cells can be serious.

Iron-deficiency anemia is the most common type of anemia. It commonly

affects children and women of all ages - especially women who are
menstruating. It's estimated that at least 1 in 5 women in North America does
not have enough iron in her blood. It can also seriously affect men when it is
caused by colon polyps, colon cancer, or other gastrointestinal (GI)
malignancies (cancers). Iron-deficiency anemia is often one of the first warning
signals that a person may have a GI malignancy.

Symptoms and Complications

The symptoms of anemia vary, depending on the degree of RBC loss or
shortage. Menstrual bleeding or iron deficiency tends to cause mild chronic
anemia with symptoms of fatigue, pallor (pale skin color), and weakness.
 If anemia is due to major blood loss, such as in cases of severe GI bleeding
caused by ulcers, you may feel dizzy and very weak, especially if you stand up
suddenly. Severe anemia can cause tissues and organs to be completely starved
of blood and oxygen. When this happens, cells rapidly die in a process called
ischemia.

Making the Diagnosis

Your doctor will ask for a blood sample that will be sent to the laboratory for a
hemoglobin level. This measures the number of grams of hemoglobin per liter
of your blood. Your blood will also be checked for levels of white blood cells,
platelets, and various other blood components. The laboratory will also look at
the size and shape of your RBCs.

The different levels and how the blood cells look can tell the doctor a lot about
what's causing the anemia. For instance, low red and white cells suggest a
condition involving the bone marrow or spleen. The doctor will then test for
other conditions, depending on the results of your initial blood test.

5. The pathophysiology sign and simptom of anemia

a. Decreased hemoglobin oxygen affinity
Increased oxygen extraction of anemic blood by the tissues produces
increased concentration of deoxyhemoglobin in the rbc, which stimulates
the production of 2,3-diphosphoglycerate (2,3-DPG). 2,3-DPG shifts the
hemoglobin-oxygen dissociation curve to the right, thus allowing the tissues
to more easily strip the hemoglobin of its precious electron-accepting cargo:
b. Redistribution of blood flow
In anemia selective vasoconstriction of blood vessels subserving certain
nonvital areas allows more blood to flow into critical areas. The main donor
sites who sacrifice their aerobic lifestyle are the skin and kidneys. Shunting
of blood away from cutaneous sites is the mechanism behind the clinical
finding of pallor, a cardinal sign of anemia. Although the kidney can hardly
be thought of as a nonvital area, it receives (in the normal state) much more
blood flow than is needed to meet its metabolic requirements. Although (by
definition) total body red cell mass is decreased in anemia, in the
chronically anemic patient the total blood volume paradoxically is
increased, due to increased plasma volume. It is as if the body were trying to
make up in blood quantity what it lacks in quality.

c. Increased cardiac output

The heart can respond to tissue hypoxia by increased cardiac output. The
increased output is matched by decreased peripheral vascular resistance and
decreased blood viscosity (thinner blood flows more freely than thick
blood), so that cardiac output can rise without an increase in blood pressure.
Generally, anemia must be fairly severe (hemoglobin < 7 g/dL) before
cardiac output rises.

When the above mechanisms are overwhelmed by the increasing magnitude of

the anemia, or when the demands of physical activity or intercurrent illness
overwhelm them, a clinical disease state becomes apparent to the physician and
to the patient. The severity of clinical symptoms bears less relationship to the
severity of the anemia than to the length of time over which the condition
develops. An acute hemorrhagic condition may produce symptoms with loss of
as little as 20% of the total blood volume (or 20% of the total red cell mass).
Conversely, anemias developing over periods long enough to allow
compensatory mechanisms to operate will allow much greater loss of rbc mass
before producing symptoms. It is not terribly uncommon to see a patient with a
hemoglobin of 4 g/dL (hematocrit 12 cL/L), representing a loss of 70% of the
 rbc mass, being reluctantly dragged into a clinic by relatives concerned that he
or she is looking a bit washed out.

When symptoms do develop, they are pretty much what you would expect
given the precarious state of oxygen delivery to the tissues: dyspnea on
exertion, easy fatigability, fainting, lightheadedness, tinnitus, and headache. In
addition, the hyperdynamic state of the circulatory system can produce
palpitations and roaring in the ears. Pre-existing cardiovascular pathologic
conditions are, as you would expect, exacerbated by the anemia. Angina
pectoris, intermittent claudication, and night muscle cramps speak to the effect
of anemia on already compromised perfusion.

Clinical signs of a slowly developed anemia are pallor, tachycardia, and a

systolic ejection murmur. In rapidly developing anemia (as from hemorrhage
and certain catastrophic hemolytic anemias), additional symptoms and signs
are noted: syncope on rising from bed, orthostatic hypotension (i.e., the blood
pressure falls when the patient is raised from the supine to the sitting or
standing positions) and orthostatic tachycardia. Keep in mind that if anemia
develops through rapid enough bleeding, the hematocrit and hemoglobin will
be normal (since in hemorrhage the rbc's and plasma are lost in proportion).
Because of this, your appreciation of these clinical signs will serve you better
in diagnosing this type of anemia than will the laboratory.

6. Laboratory examination to diagnose anemia

a. Screening test : - Hemoglobin level
- Erytrocytes index : MCV, MCH, MCHC
- Peripheral blood film

b. Routine test : - Erytrocytes sedimentation rate (ESR)

- Differential count
- Reticulocytes level
- Trombocytes level
c. Bone marrow examination test

d. Test based indication

- Iron deficiency anemia : Serum iron, TIBC, Transferrin saturation, ferritin
serum.
- Megaloblastic anemia : B12 and folat acid level
- Hemolityc anemia : Reticulocytes count, Coombs test.
- Acute leukemia : cytochemistry

e. Non-hematologic laboratory examination

- Liver physiology
- Kidney physiology
- Endocrine physiology
- Uric acid level

f. The other laboratory examination

- Tissues biopsy
- Radiology
- Molecular biology

7. Treatment for Anemia

The treatment for anemia depends on the underlying illness causing it.
Severe bleeding is usually treated with blood transfusions. You may also
need regular transfusions of blood if you have a serious chronic type of
anemia (e.g., Fanconi's anemia or sickle cell anemia). There has been a great
improvement in lifespan for people with sickle cell anemia. In the past,
those with the disease often did not survive to adulthood.

Iron supplements are used to treat iron-deficiency anemia. Infants who have
this problem tend to be bottle-fed. A baby is able to absorb more iron from
breast milk than from cow's milk. You may want to take iron supplements
for yourself when breast-feeding your child. Iron supplements will also help
in cases of mild anemia that's due to GI or menstrual bleeding.
Vitamin B12, vitamin C, and folic acid are all crucial to RBC production;
therefore, a deficiency in any one of these vitamins puts you at risk for
anemia. Good sources of vitamin B12 include beef and fish. Vegetables
don't contain this vitamin, so if you don't eat meat, fish, or dairy products,
you'll need to take vitamin B12 supplements. Sources of folic acid include
spinach, green peas, oranges, and cantaloupe. Iron in vegetables is not as
well absorbed by the body as iron from meat sources, so you may also need
to take iron supplements.

When anemia is caused by decreased production of RBCs, such as in cancer

or severe kidney disease, medications such as epoetin alfa and darbepoetin
alfa can be used. These medications mimic the action of erythropoietin, the
natural hormone that causes the bone marrow to produce more RBCs.

All medications have both common (generic) and brand names. The brand
name is what a specific manufacturer calls the product (e.g., Tylenol). The
common name is the medical name for the medication (e.g.,
acetaminophen). A medication may have many brand names, but only one
common name. This article lists medications by their common names. For
more information on brand names, speak with your doctor or pharmacist.