2. Introduction
Anemia is one of the most under diagnosed
conditions and, if left untreated, can have many
serious implications such as cardiovascular disease
and compromised immune functions
3. Definition
Anaemia ( from Greek word anaimia, meaning lack
of blood)
is a decrease in number of red blood cells (RBCs) or
less than the normal quantity of hemoglobin in the
blood.
6. Red blood cell
cytoplasm is rich in Hb
mature red blood cells are flexible biconcave disks
that lack a cell nucleus
2.4 million new erythrocytes are produced per
second.
develop in the bone marrow and circulate for about
100–120 days in the body before their components
are recycled by macrophages.
7. RBC
women have about 4 to 5 million erythrocytes per
microliter (cubic millimeter) of blood and
men about 5 to 6 million;
people living at high altitudes with low oxygen
tension will have more
Each RBC contains approx. 270 million of Hb
biomolecules, each carrying 4 heme groups.
RBCs of an average adult human male store
collectively about 2.5 grams of iron, representing
about 65% of the total iron contained in the body
12. Mean corpuscular hemoglobin concentration
(MCHC)
measure of the concentration of Hb in a given
volume of packed RBCs.
32 to 36 g/dl
MCHC
Hb
────
HCT
14. Anemia is actually a sign of
a disease process rather
than a disease itself
15. Causes
• Iron deficiency
anemia
• Anemia of chronic
disease
• Anemia from active
bleeding
Anemia related to
pregnancy
Anemia related to poor
nutrition
Pernicious Anemia
Sickle cell anemia:
Thalassemia
Alcoholism
Bone marrow-related
anemia
Aplastic anemia
Hemolytic anemia
Anemia related to
medications
17. Classification
If the cells are smaller than normal (under 80 fl), the
anemia is said to be microcytic;
if they are normal size (80–100 fl), normocytic;
if they are larger than normal (over 100 fl), the
anemia is classified as macrocytic.
19. Iron deficiency anemia
Iron is an essential part of Hb
low iron levels result in decreased incorporation of
hemoglobin into red blood cells
hypochromic (paler than usual) and microcytic
(smaller than usual)
Causes
insufficient dietary intake
absorption of Iron
losses due to diseases.
bleeding lesions of the gastrointestinal tract
parasitic infestation
20.
21. Anemia of chronic diseases
Any long-term medical condition .
The exact mechanism of this process in unknown,
chronic infection or a cancer
people with chronic (long-standing) kidney disease.
22. Anemia of chronic diseases
crohn’s
disease
SLE
rheumatoid
arthritis,
ulcerative
colitis
Cancer Long-term
infections,
Liver
cirrhosis
CKD
25. Macrocytic anemia
Megaloblastic anemia, the most common cause of
macrocytic anemia
due to a deficiency of either vitamin B12, folic acid (or
both).
Causes
gastric bypass surgery
Hypothyroidism
Alcoholism
Drugs that affect DNA
Leukemia
The anticonvulsant drug dilantin
26. Normocytic anemia
overall hemoglobin levels are decreased,
but the red blood cell size(MCV) remains normal.
Causes
Acute blood loss
Anemia of chronic disease
Hemolytic anemia
Aplastic anemia
27. Aplastic anemia
decrease in or damage to marrow stem cells, damage to
the microenvironment within the marrow, and
replacement of the marrow with fat.
It results in bone marrow aplasia (markedly reduced
hematopoiesis)
CAUSES
congenital or acquired
Idiopathic
Infections and pregnancy
certain medications, chemicals,
or radiation damage
29. Sickle cell anemia
autosomal recessive
RBC that assume an abnormal, rigid, sickle shape
Sickling decreases the cells' flexibility and results in a
risk of various complications.
The sickling occurs because of a mutation in the
hemoglobin gene
32. the signs that may indicate anemia
Change in stool color
rapid heart rate
low blood pressure
rapid breathing
pale or cold skin
yellow skin called jaundice if anemia is due to red blood
cell breakdown
heart murmur
enlargement of the spleen with certain causes of anemia
37. Anemia Prevention
eating a healthy diet and limiting alcohol use.
seeing a doctor regularly and when problems arise
routine blood work
38. Anemia Prognosis
cause of the anemia and how severe it is
age
makes almost any medical problem worse
Editor's Notes
Blood is comprised of two parts; a liquid part called the plasma and a cellular part. The cellular part contains several different cell types. One of the most important and most numerous types and the most numerous cell type are red blood cells. The other cell types are the white blood cells and platelets. Only red blood cells are discussed in this article. The purpose of the red blood cell is to deliver oxygen from the lungs to other parts of the body.
Red blood cells are produced through a series of complex and specific steps. They are made in the bone marrow (inner part of some bones that make most of the cells in the blood), and when all the proper steps in their maturation are complete, they are released into the blood stream. The hemoglobin molecule is the functional unit of the red blood cells and is a complex protein structure that is inside the red blood cells. Contrary to most cells in the human body, red blood cells do not have a nucleus (metabolic center of a cell).
Even though the red blood cells (or RBCs) are made within the bone marrow, many other factors are involved in their production. For example, iron is a very important component of the hemoglobin molecule; erythropoietin, a molecule secreted by the kidneys, promotes the formation of red blood cells in the bone marrow.
However, it can include decreased oxygen-binding ability of each hemoglobin molecule due to deformity or lack in numerical development as in some other types of hemoglobin deficiency
The blood's red color is due to the spectral properties of the hemic iron ions in hemoglobin. Each human red blood cell contains approximately 270 million of these hemoglobin biomolecules, each carrying four heme groups; hemoglobin comprises about a third of the total cell volume. This protein is responsible for the transport of more than 98% of the oxygen (the remaining oxygen is carried dissolved in the blood plasma). The red blood cells of an average adult human male store collectively about 2.5 grams of iron, representing about 65% of the total iron contained in the body
The normal RBC is a biconcave disk that resembles a soft ball
compressed between two fingers (Fig. 33-2). It has a diameter of
about 8 ìm and is so flexible that it can pass easily through capillaries
that may be as small as 2.8 ìm in diameter. The RBC membrane
is so thin that gases, such as oxygen and carbon dioxide, can
easily diffuse across it; the disk shape provides a large surface area
that facilitates the absorption and release of oxygen molecules.
measure of the average red blood cell size that is reported as part of a standard complete blood count. allows classification as either a microcytic anemia (MCV below normal range), normocytic anemia (MCV within normal range) or macrocytic anemia (MCV above normal range). To calculate the MCV, expressed in femtoliters (fL, or 10-15L), the following formula is used:10 x hematocrit (%) divided by RBC count (millions/mm3). The normal range for MCV is: 80-99 fL.
Red blood cell size
In the morphological approach, anemia is classified by the size of red blood cells; this is either done automatically or on microscopic examination of a peripheral blood smear. The size is reflected in the mean corpuscular volume (MCV).
The normal RBC is a biconcave disk that resembles a soft ball
compressed between two fingers (Fig. 33-2). It has a diameter of
about 8 ìm and is so flexible that it can pass easily through capillaries
that may be as small as 2.8 ìm in diameter. The RBC membrane
is so thin that gases, such as oxygen and carbon dioxide, can
easily diffuse across it; the disk shape provides a large surface area
that facilitates the absorption and release of oxygen molecules.
Hb E is an inherited autosomal recessive variation of Hb A that
occur in the beta (â)-globin protein chain of Hb A. The formation
of Hb E occurs by substitution lysine for glutamic acid at condon 26
of the â-chain. Hemoglobin E disease (Hb EE) occurs when an
infant inherits two copies of the Hb E variant gene, one from each
parent. If both parents have the E trait, there is a 25 percent chance
with each pregnancy that the child will inherit homozygous Hb EE.
. Hb E is a mildly unstable hemoglobin that denatures easilyHemoglobin E is believed to be the most common â-chain
hemoglobin variant in the world. Prevalence is very high among persons from Southeast Asia, especially
in Cambodia, Laos and Thailand. The borders of these countries are considered the “Hb E Triangle”.
Hb E is also found in Vietnam, Malaysia, northeastern India, Bangladesh, Pakistan, Nepal and Sri Lanka.
It is estimated that 30 million Southeast Asians are heterozygous for Hb E and 1 million are homozygous
Hb EE. This variation began as a response to the selective pressure of malaria.
Hemoglobin C (abbreviated as Hb C or HbC) is an abnormal hemoglobin with substitution of a glutamic acid residue for a lysine residue at the 6th position of the β-globin chain. This mutated form reduces the normal plasticity of host erythrocytes causing a hemoglobinopathy. In those who are heterozygous for the mutation, about 28–44% of total hemoglobin (Hb) is HbC, and no anemia develops.
Sideroblasts are atypical, abnormal nucleated erythroblasts (precursors to mature red blood cells) with granules of iron accumulated in perinuclear mitochondria.[3] Sideroblasts are seen in aspirates of bone marrow. Sideroblastic anemia or sideroachrestic anemia is a disease in which the bone marrow produces ringed sideroblasts rather than healthy red blood cells (erythrocytes).[1] It may be caused either by a genetic disorder or indirectly as part of myelodysplastic syndrome,[2] which can evolve into hematological malignancies (especially acute myelogenous leukemia). In sideroblastic anemia, the body has iron available but cannot incorporate it into hemoglobin, which red blood cells need to transport oxygen efficiently. Acquired Myelodysplasia mtDNA point mutations, and unknown Drugs Ethanol, INH, chloramphenicol, cycloserine Toxins Lead, zinc Nutritional Pyridoxine deficiency, copper deficiency
Iron is an essential part of hemoglobin, and low iron levels result in decreased incorporation of hemoglobin into red blood cells
. Iron is an essential part of hemoglobin, and low iron levels result in decreased incorporation of hemoglobin into red blood cellsis caused by insufficient dietary intake or absorption of iron to replace losses from menstruation or losses due to diseases.
Anemia related to kidney disease: The kidneys release a hormone called the erythropoietin that helps the bone marrow make red blood cells. In people with chronic (long-standing) kidney disease, the production of this hormone is diminished, and this in turn diminishes the production of red blood cells, causing anemia. This is called anemia related to chronic kidney disease
Causes Of Anemia Of Chronic Disease:
Although the exact cause of anemia of chronic disease is not known, it is related to the effects of chronic diseases on the red blood cells. These conditions cause a number of changes in the body’s red blood cells. The lifespan of red blood cells becomes shorter, production of new red blood cells in the bone marrow slows down, and iron is “withheld” so that it cannot be used to make new red blood cells. Normally the body recycles iron from “old” red blood cells and uses it to make new ones
In anemia of chronicdisease, the body does not recycle iron as easily, so it is “held up” in the old red blood cells.Anemia is a lower-than-normal number of red blood cells in the blood. Certain chronic infections, inflammatory diseases, and other illnesses can affect the body’s ability to produce red blood cells.Conditions that can lead to anemia of chronic disease include:* Autoimmune disorders, such as crohn’s disease, systemic lupus erythematosus, rheumatoid arthritis, ulcerative colitis* Cancer, particularly lymphoma and Hodgkin’s disease* Chronic kidney disease* Liver cirrhosis* Long-term infections, such as bacterial endocarditis, osteomyelitis (bone infection), HIV/AIDS, hepatitis B or hepatitis C.
Normal hemoglobin is composed of four protein chains, two α and two β globin chains arranged into a heterotetramer. Thalassemia patients produce a deficiency of either α or β globin, unlike sickle-cell disease, which produces a specific mutant form of β globin.
Three main forms have been described: thalassemia major, thalassemia intermedia and thalassemia minor. Individuals with beta thalassemia major usually present within the first two years of life with severe anemia, poor growth, and skeletal abnormalities during infancy. Affected children will require regular lifelong blood transfusions. Beta thalassemia intermedia is less severe than beta thalassemia major and may require episodic blood transfusions. Transfusion-dependent patients will develop iron overload and require chelation therapy to remove the excess iron. Bone marrow transplants can be curative for some children with beta thalassemia major.[1] Transmission is autosomal recessive; however, dominant mutations have also been reported. Genetic counseling is recommended and prenatal diagnosis may be offered
Three main forms have been described: thalassemia major, thalassemia intermedia and thalassemia minor. Individuals with beta thalassemia major usually present within the first two years of life with severe anemia, poor growth, and skeletal abnormalities during infancy. Affected children will require regular lifelong blood transfusions. Beta thalassemia intermedia is less severe than beta thalassemia major and may require episodic blood transfusions. Transfusion-dependent patients will develop iron overload and require chelation therapy to remove the excess iron. Bone marrow transplants can be curative for some children with beta thalassemia major.[1] Transmission is autosomal recessive; however, dominant mutations have also been reported. Genetic counseling is recommended and prenatal diagnosis may be offered
Megaloblastic anemia, the most common cause of macrocytic anemia, is due to a deficiency of either vitamin B12, folic acid (or both).
Aplastic anemia
radiation therapy
chemotherapy
toxic chemicals
some medications
bone marrow infections
The loss of red blood cell elasticity is central to the pathophysiology of sickle-cell disease. Normal red blood cells are quite elastic, which allows the cells to deform to pass through capillaries. In sickle-cell disease, low-oxygen tension promotes red blood cell sickling and repeated episodes of sickling damage the cell membrane and decrease the cell's elasticity. These cells fail to return to normal shape when normal oxygen tension is restored. As a consequence, these rigid blood cells are unable to deform as they pass through narrow capillaries, leading to vessel occlusion and ischaemia.
The actual anaemia of the illness is caused by haemolysis, the destruction of the red cells, because of their misshape. Although the bone marrow attempts to compensate by creating new red cells, it does not match the rate of destruction.[24] Healthy red blood cells typically live 90–120 days, but sickle cells only survive 10–20 days.[25]
Normally, humans have Haemoglobin A, which consists of two alpha and two beta chains, Haemoglobin A2, which consists of two alpha and two delta chains and Haemoglobin F, consisting of two alpha and two gamma chains in their bodies. Of these, Haemoglobin A makes up around 96-97% of the normal haemoglobin in humans.
Sickle-cell anaemia is caused by a point mutation in the β-globin chain of haemoglobin, causing the hydrophilic amino acid glutamic acid to be replaced with the hydrophobic amino acid valine at the sixth position. The β-globin gene is found on chromosome 11. The association of two wild-type α-globin subunits with two mutant β-globin subunits forms haemoglobin S (HbS). Under low-oxygen conditions (being at high altitude, for example), the absence of a polar amino acid at position six of the β-globin chain promotes the non-covalent polymerisation (aggregation) of haemoglobin, which distorts red blood cells into a sickle shape and decreases their elasticity.
The loss of red blood cell elasticity is central to the pathophysiology of sickle-cell disease. Normal red blood cells are quite elastic, which allows the cells to deform to pass through capillaries. In sickle-cell disease, low-oxygen tension promotes red blood cell sickling and repeated episodes of sickling damage the cell membrane and decrease the cell's elasticity. These cells fail to return to normal shape when normal oxygen tension is restored. As a consequence, these rigid blood cells are unable to deform as they pass through narrow capillaries, leading to vessel occlusion and ischaemia.
The actual anaemia of the illness is caused by haemolysis, the destruction of the red cells, because of their misshape. Although the bone marrow attempts to compensate by creating new red cells, it does not match the rate of destruction.[24] Healthy red blood cells typically live 90–120 days, but sickle cells only survive 10–20 days.[25]
Normally, humans have Haemoglobin A, which consists of two alpha and two beta chains, Haemoglobin A2, which consists of two alpha and two delta chains and Haemoglobin F, consisting of two alpha and two gamma chains in their bodies. Of these, Haemoglobin A makes up around 96-97% of the normal haemoglobin in humans.
Change in stool color, including black and tarry stools (sticky and foul smelling), maroon-colored, or visibly bloody stools if the anemia is due to blood loss through the gastrointestinal tract.
