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SEMINAR ON,
ANEMIA.
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INTRODUCTION.
Anaemia is a common nutritional deficiency disorder and global public health problem
which affects both developing and developed countries with major consequences for
human health and their social and economic development (WHO 2005). According to
WHO (2004) reports, one third of the global populations (over 2 billion) are anaemic
due to imbalance in their nutritious food intake.
Anemia is a condition that develops when your blood lacks enough healthy red blood
cells or hemoglobin. Hemoglobin is a main part of red blood cells and binds oxygen. If
you have too few or abnormal red blood cells, or your hemoglobin is abnormal or low,
the cells in your body will not get enough oxygen which will result in anemia.
WHO estimates that even among the South Asian countries, India has the highest
prevalence of anaemia. What is even more important is the fact that about half of the
global maternal deaths due to anaemia occur in South Asian countries; India
contributes to about 80 per cent of the maternal deaths due to anaemia in South Asia
(Ezzati et al., 2002)
MEANING.
DEFINITION OF ANEMIA
Anemia is a clinical condition that results from an insufficient supply of healthy red
blood cells, the volume of packed RBSs and quantity of haemoglobin.
ETIOLOGY.
Red blood cells can be lost through bleeding, which often can occur slowly over a
long period of time, and can go undetected. This kind of chronic bleeding commonly
results from the following:
With this type of anemia, the body may produce too few blood cells or the blood cells
may not function correctly. In either case, anemia can result. Red blood cells may be
faulty or decreased due to abnormal red blood cells or a lack of minerals
and vitamins needed for red blood cells to work properly. Conditions associated with
these causes of anemia include the following:
Iron-deficiency anemia
Vitamin deficiency
When red blood cells are fragile and cannot withstand the routine stress of the
circulatory system, they may rupture prematurely, causing hemolytic anemia.
Hemolytic anemia can be present at birth or develop later. Sometimes there is no
known cause. Known causes of hemolytic anemia may include:
CLASSIFICATION OF ANEMIAS
Anemias can be classified by cytometric schemes (i.e., those that depend on cell size
and hemoglobin-content parameters, such as MCV and MCHC), erythrokinetic
schemes (those that take into account the rates of rbc production and destruction), and
biochemical/molecular schemes (those that consider the etiology of the anemia at the
molecular level.
A. Cytometric classification
Because cytometric parameters are more easily and less expensively measured than
are erythrokinetic and biochemical ones, it is most practical to work from the
cytometric classification, to the erythrokinetic, and then (hopefully) to the
biochemical. Your first job in working up a patient with anemia is to place the case in
one of three major cytometric categories:
These include:
These include:
2. thalassemias
These include:
2. folate deficiency
B. Erythrokinetic classification
You would now want to proceed with classifying your case based on the rate of rbc
turnover. If this is high, a normoregenerative anemia exists. Such anemias are seen in
hemolysis (excess destruction of rbc's) or hemorrhage (loss of rbc's from the vascular
compartment. In these cases, the marrow responds appropriately to anemia by briskly
stepping up the production of rbc's and releasing them into the bloodstream
prematurely. There are several lab tests that allow you to determine if increased rbc
turnover exists:
1. Reticulocyte count
For instance: A normal person with an rbc count of 5,000,000 /microliter and an
absolute reticulocyte count of 50,000 /microliter would have a relative retic count of
1.0%. An anemic person with 2,000,000 rbc's/microliter and the same 50,000
retics/microliter would have an apparently "abnormal" relative retic count of 2.5 %
and could be misdiagnosed as having high turnover.
Clearly, one needs to find some way to correct the raw retic count so as to avoid this
problem. One can easily calculate the absolute retic count (in cells/microliter) by
multiplying the rbc count by the relative retic count. The normal range for the absolute
retic count is 50,000-90,000 /microliter.
When red cells, at the end of their 120-day life-span, go to the great spleen in the sky,
they are systematically dismantled. Through a series of biochemical steps too boring
to go into even here, the heme is changed into bilirubin. The bilirubin is greedily
scarfed up by the liver, conjugated with glucuronide, squirted into the alimentary tract
in the bile, and converted to urobilinogen by evangelical colonic bacteria. The
urobilinogen is excreted in the stool (most of it) or reabsorbed and excreted in the
urine (very little of it). This is summarized in the next diagram.
In cases of accelerated rbc destruction, the capacity of the liver to capture bilirubin is
saturated, and the concentration of unconjugated bilirubin in serum increases,
occasionally to the point of producing clinical jaundice. Moreover, the increased
production of urobilinogen that results is reflected by increased urobilinogen
concentration in the urine. Unconjugated bilirubin is not water soluble and therefore
will not be excreted in the urine, despite its elevation in the serum.
When an rbc is destroyed, the liberated hemoglobin binds mole-for-mole with a serum
protein, haptoglobin. The "purpose" of this reaction is to keep the kidneys from
squandering iron (free hemoglobin is freely filtered by the glomerulus, but
hemoglobin-haptoglobin complexes are too big to muscle their way through, so that
they are safe to bumble their way back to the reticuloendothelial system where they
can be properly disassembled). The serum haptoglobin concentration then decreases.
Laboratory measurement of haptoglobin is fairly easy and yields useful information to
assist in documenting decreased rbc life span.
In the case of hemolysis which takes place in the bloodstream (rather than in the RES),
so-called intravascular hemolysis, additional biochemical phenomena are observed
(see diagram, below). Free hemoglobin in excess of that which binds haptoglobin is
rapidly filtered into the urine. What remains in the plasma spontaneously degrades into
metheme and globin. A portion of metheme binds albumin to produce a measurable
compound, methemalbumin, while the remainder binds to a measurable serum
protein, hemopexin, which then decreases in serum concentration. All of the
substances whose names are boxed in the diagram are those whose laboratory
measurement is feasible and helpful in documenting hemolysis.
Bone marrow biopsy
This can be used to directly observe any accelerated production of rbc's. The ratio of
the number of myeloid to erythroid precursors (the M:E ratio) tends to decrease in
high-production states, and the marrow becomes hypercellular. Marrow biopsy is not
usually performed just to measure the M:E ratio, but to answer other hematologic
questions that have been raised.
C. Biochemical classification
Finally, one should attempt to determine the etiology of the anemia as specifically as
possible. In some cases (e.g., iron deficiency), etiologic classification is easily
attained; in others (e.g.. aplastic anemia) the biochemical mechanism of disease may
be hopelessly elusive. Generally, biochemical tests are aimed at identifying a depleted
cofactor necessary for normal hematopoiesis (iron, ferritin, folate, B 12), an abnormally
functioning enzyme (glucose-6-phosphate dehydrogenase, pyruvate kinase), or
abnormal function of the immune system (the direct antiglobulin [Coombs'] test).
TYPES OF ANAEMIA
There are several types and classifications of anaemia. The occurrence of anaemia is
due to the various red cell defects such as production defect (aplastic anaemia),
maturation defect (megaloblastic anaemia), defects in haemoglobin synthesis (iron
deficiency anaemia), genetic defects of haemoglobin maturation (thalassaemia) or due
to the synthesis of abnormal haemoglobin (haemoglobinopathies, sickle cell anaemia
and thalassaemia) and physical loss of red cells (haemolytic anaemias) (Mukherjee
and Ghosh, 2012).
This is a condition in which the body lacks the amount of red blood cells to keep up
with the body’s demand for oxygen. Understanding the different classifications can
help to recognize the symptoms and also to avoid anaemia in the first place.
Iron is essential for the various activities of the human body especially in the
haemoglobin synthesis. The following figure shows the distribution and storage of
iron (Fe) in the various parts of the human body. Iron deficiency anaemia is a
condition in which the body has too little iron in the bloodstream. This form of
anaemia is more common in adolescents and in women before menopause. Blood loss
from heavy periods, internal bleeding from the gastrointestinal tract, or donating too
much blood can all contribute to this disease.
A low level of iron, leading to anaemia, can result from various causes. The causes of
irondeficiency anaemia are pregnancy or childhood growth spurts, Heavy menstrual
periods, Poor absorption of iron, Bleeding from the gut (intestines), dietary factors
(iron poor or restricted diet), medication (aspirin ibuprofen, naproxen and diclofenac),
Lack of certain vitamins (folic acid and vitamin B12), Bleeding from the kidney,
Hookworm infection, Red blood cell problems, Bone marrow problems (Harper et al.,
2015).
Symptoms
Tiredness, lethargy, feeling faint and becoming breathless easily, headaches, irregular
heartbeats (palpitations), altered taste, sore mouth and ringing in the ears (tinnitus).
Anaemia in pregnancy increases the risk of complications in both mother and baby
such as low birth weight baby, preterm (premature) delivery and postnatal depression.
Low iron reserves in the baby may also lead to anaemia in the newborn baby (Pasricha
et al., 2010).
Symptoms
Haemolytic anaemia is a condition in which red blood cells are destroyed and removed
from the bloodstream before their normal lifespan is up. Haemolytic anaemia can
affect people of all ages, races and sexes. Haemolytic anaemia can lead to various
health problems such as fatigue, pain, arrhythmias, an enlarged heart and heart failure.
Inherited haemolytic anaemias include Sickle cell anaemia, Thalassaemias, hereditary
spherocytosis, hereditary elliptocytosis, Glucose-6-phosphate dehydrogenase (G6PD)
deficiency, Pyruvate kinase deficiency. Acquired haemolytic anaemias include
Immune haemolytic anaemia, Autoimmune haemolytic anaemia, Alloimmune
haemolytic anaemia, Drug-induced haemolytic anaemia, Mechanical haemolytic
anaemias, Paroxysmal nocturnal haemoglobinuria, Certain infections and substances
can also damage red blood cells and lead to haemolytic anaemia.
Symptoms
The most common symptom of anaemia is fatigue. A low red blood cell count can also
cause shortness of breath, dizziness, headache, coldness in your hands or feet, pale
skin, gums and nail beds, as well as chest pain. Symptoms of haemolytic anaemia
include Jaundice, Pain in the upper abdomen, Leg ulcers and pain, A severe reaction to
a blood transfusion. Treatments for haemolytic anaemia include blood transfusions,
medicines, plasmapheresis, surgery, blood and marrow stem cell transplants and
lifestyle changes (Natasha and Yasmin 2010).
Anaemia in which the body makes sickle-shaped ("C"-shaped) red blood cells is called
Sickle Cell anaemia. It contain abnormal haemoglobin which causes sickle shape and
can’t move easily through the blood vessels. The clumps of sickle cells block blood
flow that lead to the limbs and organs. Blocked blood vessels causes pain, serious
infections, and organ damage. Sickle cells usually die after about 10 to 20 days and the
body can’t reproduce red blood cells fast enough to replace the dying ones, which
causes anaemia.
Symptoms
Sickle cell anaemia is an inherited, lifelong disease and most common in Africa,
South or Central America, Caribbean islands, Mediterranean countries, India and
Saudi Arabia. symptoms include Fatigue, Shortness of breath, Dizziness, Headache,
Coldness in the hands and feet, Pale skin, Chest pain.
2.5. Thalassaemia
Thalassaemia is an inherited blood disorder which cause the body to make fewer
healthy red blood cells and less haemoglobin. The two major types of thalassaemia are
alpha- and beta thalassaemia. The most severe form of alpha thalassaemia is known as
alpha thalassaemia major or hydrops fetalis, while the severe form of beta
thalassaemia is known as thalassaemia major or Cooley’s anaemia. Thalassaemias
affect both males and females and occur most often in people of Italian, Greek, Middle
Eastern, Asian, and African descent.
Haemoglobin in red blood cells has two kinds of protein chains: alpha globin and beta
globin. If your body doesn’t make enough of these protein chains, red blood cells
don’t form properly and can’t carry enough oxygen. Genes control how the body
makes haemoglobin protein chains. When these genes are missing or altered,
thalassaemias occur. Thalassaemias are passed on from parents to their children
through genes.
Symptoms
Symptoms of thalassaemias are caused by a lack of oxygen in the blood stream. The
severity of symptoms depends on the severity of the disorder. People who have alpha
or beta thalassaemia can have mild anaemia, People with beta thalassaemia intermedia
have mild to moderate anaemia. They may also have other health problems including
slowed growth and delayed puberty, bone problems and an enlarged spleen.
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. Damage to the
bone marrow’s stem cells causes aplastic anaemia (Scheinberg and Young, 2012).
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 and
Diamond-Blackfan anaemia may also cause aplastic anaemia (Brodsky and Jones,
2005).
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 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. Blood and marrow stem
cell transplants may cure the disorder.
PATHOPHYSIOLOGY.
Anemia is the lack of enough healthy red blood cells (RBC) or hemoglobin (HGB),
which is the part of the red blood cell that binds oxygen to the blood. This lack of
HGB restricts the amount of oxygen available to create energy within the cells (ATP).
This decrease in oxygenation (hypoxia) results in altered pH and can lead to damage
of organ systems including cardiac, respiratory and renal disease.
CLINICAL MANIFESTATIONS.
The symptoms of anemia vary according to the type of anemia, the underlying cause,
the severity and any underlying health problems, such as hemorrhaging, ulcers,
menstrual problems, or cancer. Specific symptoms of those problems may be noticed
first.
The body also has a remarkable ability to compensate for early anemia. If your
anemia is mild or has developed over a long period of time, you may not notice any
symptoms.
Dizziness
Pale skin
Leg cramps
Insomnia
People whose anemia is caused by a deficiency of Vitamin B12 may have these
symptoms:
Dementia
Constipation
Vomiting
Anemia caused by chronic red blood cell destruction may include these symptoms:
Leg ulcers
Symptoms of gallstones
Fatigue
Susceptibility to infection
Symptoms of anemia caused by sudden red blood cell destruction may include:
Abdominal pain
Seizures
DIAGNOSIS.
MANAGEMENT.
MEDICAL MANAGEMENT.
TREATMENT.
If you suddenly lose a large volume of blood, you may be treated with fluids, a
blood transfusion, oxygen, and possibly iron to help your body build new red blood
cells. Chronic blood loss is treated by identifying the source of bleeding, stopping
the bleeding, and, if necessary, providing treatment for iron-deficiency anemia.
The type of treatment you receive depends on the cause of decreased red blood cell
production.
With iron deficiency anemia, recommend iron supplements that contain the ferrous
form of iron, which your body can absorb easily. Timed-release iron supplements
are not a good choice for most people, because iron is primarily absorbed in the
upper part of the digestive tract. If you use iron supplements, remember the
following cautions:
Always consult with your doctor before taking iron supplements. Excess iron
intake can be harmful. Symptoms of iron overload
include fatigue, vomiting, diarrhea, headache, irritability, heart disease, and
joint problems.
Iron supplements -- like all supplements and any medication -- should be kept
out of the reach of children. Iron poisoning is one of the most common causes
of accidental poisoning in young children. It can prove fatal in a matter of
hours. Symptoms of poisoning in a child include dizziness, confusion,
nausea, vomiting, and diarrhea. Seek medical help immediately.
Watch for side effects. You may need to continue taking iron supplements for
up to one year. Taking iron supplements with food can help prevent common
side effects, which may include nausea, diarrhea, constipation, and stomach
pain. Let your doctor know if you continue to have side effects. Different
formulations are available.
Watch for drug interactions. Tell your doctor if you are being treated for another
condition. For example, calcium supplements interfere with iron absorption, so
it is best to take them at different times of the day.
The body absorbs iron best when taken in a mildly acidic medium, so your
doctor may suggest taking iron with a half-glass of orange juice or with vitamin
C.
Treatment depends on the cause of the deficiency. If your body stores are depleted
of vitamin B12, your doctor will most likely prescribe vitamin B12 injections.
Vitamin B12 can also be given by mouth, but very high doses are needed. Vitamin
B12 can also been given under the tongue or in a nasal spray, but these
preparations are expensive and have not been adequately studied to be
recommended. There is a good chance that many of the symptoms of deficiency
will improve once the body is provided with the needed B12.
Some people with vitamin B12 deficiency have a permanent inability to absorb
vitamin B12 and will need injections every one to three months or pills daily for
the rest of their lives.
Good dietary sources of folate include fresh fruits, green leafy vegetables, and
cruciferous vegetables (cauliflower, broccoli, and Brussels sprouts); dairy products;
and whole grain cereals. Vegetables should be eaten raw or lightly cooked.
This anemia tends to be more persistent and difficult to treat. The treatments for
hereditary anemias, such as thalassemia or sickle cell disease, vary widely and
depend on the specific condition and the severity of symptoms. Some anemias will
not require any treatment, while others may require repeated transfusions and other
aggressive measures. Although aplastic anemia will occasionally go into
spontaneous remission, some people with this disorder require bone marrow
transplantation.
Supportive treatment -- like intravenous fluids and pain medication -- will often be
given. A blood transfusion may be necessary in some cases. Steroids can halt the
body's immune attack on its own red blood cells. Certain damaging factors can be
removed from the blood by a treatment called plasmapheresis.
Longstanding hemolytic anemia can cause gallstones to develop from the by-
products of red blood cell destruction. Gallbladder surgery may be necessary for
symptomatic gallstones. A type of hemolytic anemia that occurs more commonly
in children is associated with kidney damage, and dialysis may be necessary. In
extremely rare cases, bone marrow transplantation may be the only solution for
certain types of hemolytic anemia.
Occasionally, children with sickle cell disease who have an appropriate donor may
be cured by a bone marrow transplant. Alternatively, a drug called hydroxyurea
(Droxia, Hydrea, Silkos) appears to stimulate the formation of an alternate form of
hemoglobin that isn't susceptible to the sickling, and may be used to reduce the
frequency of bone pain. The bone pain can usually be eased with pain medications
and the anemia may require transfusions. Hydroxyurea may also decrease the need
for blood transfusions.
Low levels of vitamin B12 can lead to pernicious anemia. This type of anemia
often is treated with vitamin B12 supplements. Food sources of vitamin B12
include Breakfast cereals with added vitamin B12, Meats such as beef, liver,
poultry, and fish, Eggs and dairy products (such as milk, yogurt, and cheese),
Foods fortified with vitamin B12, such as soy-based beverages and vegetarian
burgers.
Folic acid (folate) is a form of vitamin B that’s found in foods. Your body needs
folic acid to make and maintain new cells. Folic acid also is very important for
pregnant women. It helps them avoid anemia and promotes healthy growth of the
fetus.Good sources of folic acid include Bread, pasta, and rice with added folic
acid, Spinach and other dark green leafy vegetables, Black-eyed peas and dried
beans, Beef liver, Eggs, Bananas, oranges, orange juice, and some other , fruits and
juices.
4.3 Vitamin C
Vitamin C helps the body absorb iron. Good sources of vitamin C are vegetables
and fruits, especially citrus fruits. Citrus fruits include oranges, grapefruits,
tangerines, and similar fruits. Fresh and frozen fruits, vegetables, and juices usually
have more vitamin C than canned ones. Other fruits rich in vitamin C include kiwi
fruit, strawberries, and cantaloupes. Vegetables rich in vitamin C include broccoli,
peppers, Brussels sprouts, tomatoes, cabbage, potatoes, and leafy green vegetables
like turnip greens and spinach.
5.1 Fruits
Fruits such as iron-rich apples and tomatoes are great to eat when treating anemia.
Other fruits that effectively treat anemia are plums, bananas, lemons, grapes,
raisins, oranges, figs, carrots and raisins when eaten in large quantities.
5.2 Honey
Honey is a potent source of iron, copper and manganese. When these elements are
combined they aid in hemoglobin synthesis. Honey is therefore a powerful weapon
against anemia.
5.3 Meats
Red meats such as kidney, heart and liver are effective at treating anemia. Also
poultry, fish and oyster are effective against anemia.
5.4 Vegetables
Vegetables such as spinach, lettuce, beet, broccoli, fenugreek, celery and kale are
iron-rich, energy-filled vegetables that treat anemia effectively. These vegetables
are not only rich in iron but also Vitamin B-12 and folic acid, energy-boosting
nutrients that the body needs to heal from anemia. Beetroot juice is an iron-rich
vegetable juice that those suffering from anemia can drink as a tonic against fatigue
and lethargy.
Legumes and nuts such as pulses, almonds, whole grain cereals, dry dates, peanuts
and walnuts are effective against the symptoms and causes of anemia.
NURSING MANAGEMENT
NURSING ASSESSMENT
HISTORY PHYSICAL LAB FINDINGS
EXAMINATION
Positive family history of • Pallor, icterus, petechiae WBC and platelet count
anaemia • Temperature • Lymph (aplastic
• Ethnic origin nodes • Enlarged spleen • anaemia)
• Acuteness of onset of Tachycardia, hypotension • Reticulocyte count (red
anaemia cell
• Bleeding: stool, urine, aplasia)
lungs, • MCV (iron or vitamin
menses deficiency,
• Infection: Parvovirus thalassaemias)
B19, • RBC morphology:
Hepatitis, HIV - double RBC population
• Phlebotomy (transfusion, sideroblastic
• Jaundice, dark urine anaemia, high HbF)
• Petechiae - RBC agglutination (cold
• Symptoms from other agglutinins)
organs (CNS, - schizocytes
gastritis) (microangiopathy)
• Masses, nodes - spherocytes (immune
• Alcohol consumption haemolysis)
• Diet: low fruit, no meat • Bilirubin, LDH,
• Pica (abnormal food haptoglobin,
habits) Coombs test (haemolysis)
• Drugs • Kidney function (Epo
• Previous transfusion deficiency)
• Occult blood in the
stools
(chronic blood loss)
• C-reactive protein
(inflammation)
• Iron studies + vitamins
(serum
iron, TIBC, ferritin, B12,
folates)
depending on MCV
NURSING DIAGNOSIS.
CONCLUSION
Anaemia is the important global health risk factor faced by the teenagers and
pregnant women nowadays. Anaemia should be diagnosed earlier and treated to get
a healthy generation. Anemia is strictly defined as a decrease in red blood cell
(RBC) mass. The function of the RBC is to deliver oxygen from the lungs to the
tissues and carbon dioxide from the tissues to the lungs. This is accomplished by
using hemoglobin (Hb), a tetramer protein composed of heme and globin. In
anemia, a decrease in the number of RBCs transporting oxygen and carbon dioxide
impairs the body’s ability for gas exchange. [1] The decrease may result from blood
loss, increased destruction of RBCs (hemolysis), or decreased production of RBCs.
BIBLIOGRAPHY.