Anemia Is A Major Public Health Problem Biology Essay


Anemia is a major public health problem in the world. Anemia reduces the volume of red blood cells and the conditions for reducing the blood concentration of hemoglobin (Hb) in the blood, characterized in that the. RBC in blood volume decreases the amount of oxygen to reduce the body's tissues and organs reached, resulting in a series of adverse symptoms. Anemia often looked pale and weak, can feel out of breath or weakness. He may know a beating heart. For women, anemia and reduce the efficiency of their work, and their risk of anemia, causes of poverty, including inadequate intake of iron, folic acid, vitamin B12 and other nutrients. In thalassemia, sickle cell disease, malaria, intestinal parasites such as hook worm infection can also lead to anemia. The anemia associated with an increased incidence of infectious diseases can appear diseases. Anemia challenges children, pregnant adult men or women pregnant. Iron deficiency is the most common form of nutritional deficiency. The size and the number of RBC are reduced. Spectrum iron deficiency is the depletion of iron, which will result in a physiological damage, the iron-deficiency anemia, the impact of the operation of several organ systems. I often use the terms anemia, iron deficiency anemia, iron deficiency anemia convertible car, but not equivalent. It can only be diagnosed with anemia, iron deficiency anemia; there is more evidence of iron deficiency anemia.


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achlorhydric anemia

achrestic anemia

acquired hemolytic anemia

addisonian anemia

Addison's anemia

anemia gravis

anemia neonatorum

angiopathic hemolytic anemia

aplastic anemia

asiderotic anemia

autoimmune hemolytic anemia

Bartonella anemia

Belgian Congo anemia

Biermer's anemia

brickmaker's anemia

cameloid anemia

chlorotic anemia

congenital anemia

congenital aplastic anemia

congenital dyserythropoietic anemia

congenital hemolytic anemia

congenital hypoplastic anemia

congenital non regenerative anemia

Cooley's anemia

cow milk anemia

crescent cell anemia

deficiency anemia

Diamond-Blackfan anemia

dilution anemia

dimorphic anemia

diphyllobothrium anemia

drepanocytic anemia

dyshemopoietic anemia

Ehrlich's anemia

elliptocytary anemia

elliptocytic anemia

elliptocytotic anemia

equine infectious anemia

erythroblastic anemia

erythronormoblastic anemia

essential anemia

Faber's anemia

false anemia

familial erythroblastic anemia

familial hypoplastic anemia

familial microcytic anemia

familial pyridoxine-responsive anemia

familial splenic anemia

Fanconi's anemia

feline infectious anemia

fish tapeworm anemia

folic acid deficiency anemia

globe cell anemia

goat's milk anemia

ground itch anemia

Heinz body anemia

hemolytic anemia

hemolytic anemia of newborn

hemorrhagic anemia

hookworm anemia

hyperchromic anemia

hypochromic anemia

hypochromic microcytic anemia

hypoferric anemia

hypoplastic anemia

icterohemolytic anemia

infectious anemia

intertropical anemia

iron deficiency anemia

isochromic anemia

lead anemia

Lederer's anemia

leukoerythroblastic anemia

local anemia

macrocytic achylic anemia

macrocytic anemia

macrocytic anemia of pregnancy

macrocytic anemia tropical

malignant anemia

Marchiafava-Micheli anemia

megaloblastic anemia

megalocytic anemia

metaplastic anemia

microangiopathic hemolytic anemia

microcytic anemia

microdrepanocytic anemia

milk anemia

mountain anemia

myelophthisic anemia

neonatal anemia

normochromic anemia

normocytic anemia

nutritional anemia

nutritional macrocytic anemia

osteosclerotic anemia

ovalocytic anemia

pernicious anemia

physiologic anemia

polar anemia

posthemorrhagic anemia

primary erythroblastic anemia

primary refractory anemia

pure red cell anemia

radiation anemia

refractory anemia

scorbutic anemia

secondary refractory anemia

sickle cell anemia

sideroblastic anemia

slaty anemia

spastic anemia

spherocytic anemia

splenic anemia

target cell anemia

toxic anemia

traumatic anemia

tropical anemia

unstable hemoglobin hemolytic anemia



Anaemia in pregnancy is defined as a haemoglobin concentration < 11.0 g/dl or <10.5 g/dl in the second half of pregnancy( or haematocrit <32% )

Anaemia can be classified as mild, moderate or severe based on haemoglobin concentration in the blood, according to the classification developed by the World Health Organization(WHO).


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Mild anaemia Hb 9 -10.9 gm /dl

Moderate anaemia Hb 7-8.9 gm /dl

Sever anaemia Hb < 7gm /dl

Very sever anaemia Hb < 4gm/dl


There are 3 main causes:

1. Erythrocyte production: (hypo proliferative anemia )

. Fe deficiency

. Folic acid

. Vitamin B12

2- RBC destruction:

3- RBC loss:

90% anemia in pregnancy is due to Fe deficiency

But important Anaemia which can be presented during pregnancy are categorize below.


Nutritional deficiency anaemias

Iron deficiency

Folate deficiency

Vit. B12 deficiency



Sickele cell disease (SCD)

3. Physiological anaemia

Hydraemic state of pregnancy would cause too. A disproportionate increase in the volume of plasma, red blood cells, hemoglobin and haematocreit significantly reduced during pregnancy. Also a corresponding reduction in hemoglobin, in so far as avarying occasionally as low as 80%. Images are and normocytic pigmented dilution. This is so called physiological anemia.



Autoimmune hemolytic

Hodgkin's disease


Paroxysmal nocturnal haemoglobinurea



Iron deficiency anemia occurs when there is not enough iron for hemoglobin synthesis gemoglobina.Normalny retained for as long as possible after iron stores are depleted, latent iron deficiency is said to have been present during this period.

Iron deficiency is the most common nutrient deficiency veschestv.Razmer and number of red blood cells is reduced. There is a state of iron deficiency, from the consumption of iron that does not cause physiological disorders, to iron deficiency anemia, which affects the functioning of several organs and sistem.Usloviya anemia, iron deficiency and iron deficiency anemia are always used interchangeably, but are not equivalent. Anemia can only be diagnosed as iron deficiency anemia, when there is more evidence of iron deficiency

Iron requirement

Iron required for fetus and placenta 500mg.

Iron required for red cell increment 500mg

Post-partum loss 180mg.

Lactation for 6 months - 180mg.

Total requirement 1360mg

subtracted (saved as a result of amenorrhea) 350mg

So actual extra demand 1000mg

Full iron stores 1000mg

Etiology of iron deficiency Anaemia

Depleted iron stores; dietary lack, chronic renal failure, worm infestation, chronic menorrhagia

Chronic infections; like malaria

Repeated pregnancies ;

With interval < 1 year

Blood loss at time of delivery

Multiple pregnancies.

More iron deficiency due to loss of blood, usually from the uterus or gastrointestinal tract (GIT). Premenopausal women in a state of uncertainty due to the balance of the menstrual function. Iron deficiency drive more than a quarter of the population, but one iron nutritional deficiency is rare in developed countries. The most common cause of iron deficiency in the world is the loss of blood from the gastrointestinal tract as a result of infection nematody.Nizkoe quality diet that contains mostly vegetables, and finds to the high prevalence of iron deficiency in developing countries. Even in developed countries, iron deficiency is not uncommon in infancy, where iron supply is insufficient for the needs of growth. It is more common in babies born prematurely or with the introduction of mixed feeding is delayed

Clinical features

Clinical features occur as a result of tissue iron deficiency. These are mainly epithelial changes induced by the effect of inadequate iron in the cells. Symptoms of the anaemia,

angular stomatitis-

inflammation and fissuring radiating from the commissures of the mouth secondary to predisposing factors such as lost vertical dimension in denture wearers, nutritional

atrophy of the papillae of the tongue

brittle hair

brittle nails

spoon-shaped nails (koilonychia)

A malformation of the nails in which the outer surface is concave; often associated with iron deficiency or softening by occupational contact with oils.

a syndrome of dysphagia and glossitis


The diagnosis of iron deficiency anemia depends on good clinical history with questions about dietary intake, regular self-medication with non-steroidal anti-inflammatory drugs (which can cause gastro-intestinal bleeding), as well as the presence of blood in the stool (which may be a sign of hemorrhoids, or cancer of the lower intestine). In women, a careful study of the duration of the period, the occurrence of blood clots and the number of sanitary pads or tampons (normal 3-5/day), used to be done.

Effects of anaemia in pregnancy

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High output Cardiac failure (more likely if precelampsia present. inadequate tissue oxygenation increase requirments for excessive blood flow )

Post pregnancy hypertension(PPH)

Predisposes to infection

Risk of thrombo-embolism

Delayed general physical recovery especially after caesarian section


Intra uterine life (IUGR)

Preterm birth

Low body weight (LBW)

Depleted Fe store

Delayed Cognitive function


Blood count and film

The red cells are microcytic (MCV < 80 FL) and hypochromic (MCH < 27 pg). There is poikilocytosis and anisocytosis. Target cells are seen.

Serum iron and iron-binding capacity

The serum iron falls and the total iron-binding capacity (TIBC) rises in iron deficiency compared with normal. Iron deficiency is regularly present when the transferrin saturation (i.e. serum iron divided by TIBC) falls below 19%.

Serum ferritin

The levels of serum ferritin contemplate the amount of stored iron. The normal values for serum ferritin are 30-300 μg/L (11.6-144 nmol/L) in males and 15-200 μg/L (5.8-96 nmol/L) in females. In simple iron deficiency, a low serum ferritin confirms the diagnosis. However, ferritin is an acute-phase reactant, and levels increase in the presence of inflammatory or malignant diseases. In these cases, measurement of serum iron/TIBC, serum ferritin and soluble transferrin receptors is used.

Serum soluble transferrin receptors

The number of transferrin receptors increases in iron deficiency. The results of this immune assay compares well with results from bone marrow aspiration at estimating iron stores. This assay can help to distinguish between iron deficiency and anaemia of chronic disease , and may avoid the need for bone marrow examination even in complex cases.

Bone marrow

Erythroid hyperplasia with ragged normoblasts is seen in the marrow in iron deficiency. Staining using Perls' reaction (acid ferrocyanide) does not show the characteristic Prussian-blue granules of stainable iron in the bone marrow fragments or in the erythroblasts. Examination of the bone marrow is not essential for the diagnosis of iron deficiency but it may be helpful in the investigation of complicated cases of anaemia, e.g. to determine if iron deficiency is present in a patient with anaemia of chronic disease.

Urine for haemturia.

Stool examination for ova ,cyst and occult blood.

Treatment & Management


To achieve a normal Hb by end of pregnancy.

To replenish iron stores.

Two ways to correct anaemia,

Iron supplementation - ( Oral Fe, Parenteral Fe)

Blood transfusion.

may be required to treat severe anaemia near term or when some other complication such as placenta praevia present.

Gross anaemia-

Packed red cells transfusion (Under cover of loop diuretic)

Exchange transfusion (Under cover of loop diuretic)

Choice of method: It depends on three main factors,

1.Severity of the anaemia

(Hb < 8gm/dl)- preferably parenteral theraphy in the form of intra muscular (I/M) or intravenous (I/V) iron

I/M : ( Iron sorbitol) with "Z" technique

I/V : (iron sucrose)

2.Gestational Age.

3.Presence of additional risk factor

The correct management of iron deficiency is find and treat the relevent cause, and to give iron to cure the anaemia and replace iron stores. The responce to iron therapy can monitored using the reticulocyte count and Hb level, with an expected rise in haemoglobin of 1 g/dL per week.

Oral iron is all that is required in most cases. The better preparation is ferrous sulphate (200 mg three times per day , a total of 180 mg ferrous ) which are absorbed when the patient is fasting. If the patient has side-effects like nausea, diarrhoea or constipation, taking the tablets with food or reducing the dose using a preparation with minimum iron such as ferrous gluconate (300 mg twice a day, only 70 mg ferrous) is all that is normally required to reduce the symptoms. The use of expensive iron compounds especially, the slow release ones which release iron further away its main sites of absorption, is dispensable.

In developing countries, issue of iron tablets is the main approach for the consolation of iron deficiency. but, iron supplementation programmes have been impassive,presumably mainly because of poor compliance.

Oral iron must be given for long enough to compensate the Hb level and to replenish the iron stores. This can take 6 months. The commonest causes of failure of compliancy to oral iron are:

• lack of compliance

• continuing haemorrhage

• incorrect diagnosis, e.g. thalassemia trait.

These possibilities should be considered before parenteral iron is used. However, parenteral iron is required by uncertain patients, including those who have general impatience of oral preparations even at low dose, those with severe malabsorption, and those who have chronic gastrointestinal diseases like ulcerative colitis or Crohn's disease. Iron stores are replaced much faster with parenteral iron than with oral iron, but the haematological response is no quicker. Parenteral iron can be supplied as repeated deep intramuscular injections of iron-sorbitol (1.5 mg of iron per kg bodyweight) or by slow intravenous infusion of iron-sucrose.

Side effect of Fe Oral therapy

Gastrointestinal(G.I) upset.



Skin discolouration

Local abscess

Allergic reaction

Fe over load.



The second common during pregnancy. The main cause is insufficient consumption, which may occur alone or in combination with excessive use or malabsorption of folate. At the cellular level, folic acid is reduced to dihydrofolate a tetrahydro-folic acid (THF) is required for cell growth and division .. Body reserves of folic acid, in contrast to vitamin B12 is very low (about 10 mg). At deficient diet, folic acid deficiency develops in about 4 months, but a deficiency of folic acid may develop more rapidly in patients who have a poor intake and excessive use of folic acid. Thus, more active reproduction and growth of tissues is more dependent on food folate acid.So bone marrow and epithelial lining so much risk

Folate requirement

Non pregnant women 50 -100 microgram per day

Pregnant woman 300-400 microgram per day

Usually folic acid present in diets like fresh fruits and vegetables and destroyed by cooking.

Etiology of folate deficiency anaemia(causes)

Nutritional (major cause)

Poor intake

Alcohol excess (also causes impaired utilization)

Old age

Poor social conditions


Poor intake due to anorexia


Gastrointestinal disease, e.g. partial gastrectomy, coeliac disease, Crohn's disease

Antifolate drugs







Excess utilization






Haematological disease with excess red cell production, e.g. haemolysis

Haemodialysis or peritoneal dialysis

Inflammatory disease

Malignant disease with increased cell turnover

Metabolic disease, e.g. homocystinuria


Occurs in small bowel disease, but the effect is minor compared with that of anorexia

Clinical features & effects during pregnancy

Patients with folate deficiency may be asymptomatic or symptoms of anemia or underlying cause. Glossitis may occur. Unlike B12 deficiency, neuropathy occurs.

1.Maternal risk:

Megaloblastic anemia

2.Fetal risk:

Pre-conception deficiency cause neural tube defect and cleft palate etc.


Haematological values

MCV is characterized by> 96 FZ, if not cause concomitant microcytosis when it can be dimorphic picture with normal / low average MCV.Perifericheskoy blood film shows macrocytes with hypersegmented polymorphs with six or more lobes in the nucleus If severe, it may be leukopenia, and thrombocytopenia.

Blood measurements

Serum and red cell folate were analyzed by radioisotope dilution or immunological methods. Normal levels of serum folate is 4-18 mg / L (5-63 nmol / L). Number of folate in red blood cells is the best measure of tissue folic acid, a normal range of 160-640 mg / ml.

Investigation of further

In many cases, the cause of folic acid deficiency is not evident from clinical or dietary history. Occult gastrointestinal disease should then be suspected and related studies, such as a biopsy of the small intestine should be performed.

Treatment & management

Folic acid deficiency can be corrected by giving 5 mg of folic acid daily, the same thing happens hematologic response, as seen after treatment of vitamin B12. Treatment should be for about 4 months to replace the body stores. Any major cause, such as celiac disease, should be treated. Prophylactic folic acid (400 micrograms per day) is recommended for all women planning a pregnancy to reduce neural tube defects. Many experts also recommend prophylactic administration of folic acid during pregnancy. Can this be achieved by increasing the consumption of foods high in folic acid, or women should take folic acid supplements is under discussion. Women who have had a child with a neural tube defect should take 5 mg of folic acid daily before and during a subsequent pregnancy. Prophylactic folic acid is also found in chronic hematological disorders, where there is a rapid turnover yacheyki.Doze 5 mg every week would be sufficient.



It is rare. Vitamin B12 is synthesized by certain microorganisms, and humans are ultimately dependent on animal sources. It is found in meat, fish, eggs and milk, but not in plants. Vitamin B12 is not usually destroyed by cooking. The average daily diet contains 5-30 μg of vitamin B12, of which 2-3 μg is absorbed. The average adult stores some 2-3 mg, mainly in the liver, and it may take 2 years or more after absorptive failure before B12 deficiency develops, as the daily losses are small (1-2 μg). The main function of B12 is the methylation of homocysteine to methionine with the demethylation of methyl THF polyglutamate to THF. THF is a substrate for folate polyglutamate synthesis.

Deoxyadenosylcobalamin is a coenzyme for the conversion of methylmalonyl CoA to succinyl CoA. Measurement of methylmalonic acid in urine was used as a test for vitamin B12 deficiency but it is no longer carried out routinely.

Etiology of folate deficiency anaemia(causes)

The most common cause of vitamin B12 deficiency in adults is pernicious anaemia. Malabsorption of vitamin B12 because of pancreatitis, coeliac disease or treatment with metformin is mild and does not usually result in significant vitamin B12 deficiency.

Low dietary intake


Impaired absorption;


Pernicious anaemia


Congenital deficiency of intrinsic factor

Small bowel

ileal disease or resection

Bacterial overgrowth

Tropical sprue

Fish tapeworm (Diphyllobothrium latum)

Abnormal utilization

Congenital transcobalamin II deficiency

Nitrous oxide (inactivates B12)

Pernicious anaemia

Pernicious anaemia (PA) is an autoimmune disorder in which there is atrophic gastritis with loss of parietal cells in the gastric mucosa with consequent failure of intrinsic factor production and vitamin B12 malabsorption.


This disease is common in the elderly. It can be seen in all races, but occurs more frequently in fair-haired and blue-eyed individuals, and those who have the blood group A. It is more common in females than males. There is an association with other autoimmune diseases , particularly thyroid disease, Addison's disease and vitiligo. Approximately one-half of all patients with PA have thyroid antibodies. There is a higher incidence of gastric carcinoma with PA than in the general population. Two types of intrinsic factor antibodies are found: a blocking antibody, which inhibits binding of intrinsic factor to B12, and a precipitating antibody, which inhibits the binding of the B12-intrinsic factor complex to its receptor site in the ileum.

Clinical features & effects during pregnancy

The onset of PA is insidious, with progressively increasing symptoms of anaemia. Patients are sometimes said to have a lemon-yellow colour owing to a combination of pallor and mild jaundice caused by excess breakdown of haemoglobin. A red sore tongue (glossitis) and angular stomatitis are sometimes present. The neurological changes, if left untreated for a long time, can be irreversible. These neurological abnormalities occur only with very low levels of serum B12 (less than 60 ng/L) and occasionally occur in patients who are not clinically anaemic.


Haematological tests.

Bone marrow test

Serum bilirubin.

Serum vitamin B12 is

Serum folate level

Gastrointestinal investigations

Schilling test.

Absorption tests


 shoud be give Vit B12 1mg I/M weekly for 6 weeks.


Inherited disorders of haemoglobin. Hb abnormalities may be,

Homozygous - inherited from both parents. (Sufferer of disease)

Hetrozygous - inherited from one parent. (Carrier/trait of disease)

Two types in pregnancy,


Defect may be in Globin chain synthesis.

Sickle cell disease (SCD)

Defect may be in Structure of globin chains.


The synthesis of globin chain is partially or completely suppressed resulting in reduced Hb. content in red cells, which then have shortened life span.


Alpha thalassaemia.

Beta thalassaemia:



Beta thallassemia minor

Beta Thallassemia trait

It is heterozygous inheritance from one parent & Most frequent encountered variety.

Partial suppression of the Hb synthesis.

It is a mild anaemia.


Hb around 10 g/dl.

Red cell indices: low MCV.

Low MCH.

Normal MCHC.

Diagnostic test: Hb Electrophoresis


Same as normal woman in pregnancy.

Frequent testing of Hb level.

Iron & folate supplements in usual dose.

(Parenteral iron should be avoided because of iron overload.)

If those not responded I/M folic acid.

Blood transfusion close to time of delivery.

Beta Thallassaemia Major

Homozygous inheritance from both parents.

Sever anaemia.

Diagnosed is wanted in paediatric season.

Treatment is blood transfusion.

Alpha thalassemia

Both heterozygous & homozygous forms exist.

Alpha thallassaemia trait.

Alpha thallassaemia major

Sickle Cell Disease (SCD)

Sickling crises frequently occurs in pregnancy, puerperium & in state of hypoxia.

Increased incidence of abortion and still birth growth restriction, premature birth and intrapartum fetal distress with increased perinatal mortality.Sickle cell trait does not pose any significance clinical problems. It is autosomally inherited.Hb precipitates and makes the RBCs rigid & sickle shaped.Also this is a syndrome.


Hb Electrophoresis

Sickledext test is screening test


(No curative Treatment. It is only symptomatic)

Well hydration

effective analgesia

prophylactic antibiotics

O2 inhalation,

Folic acid

Oral iron supplement (I/V iron is contra indication)

Blood transfusion