As an outcome of loss of any one of the following vitamin B12, folic acid and inherent factor can lead to slow imitation of the erythroblasts in the bone marrow. As an outcome, these raise too large, with odd shapes, and are known as magaloblasts . Thus, atrophy of the stomach mucosa, as occur in pernicious anemia or loss of the complete stomach as the outcome of gastrectomy can guide to megaloblastic anemia. Also, patients who have intestinal sprue, in which folic acid, B12, and other vitamin B compounds are poorly absorbed, often develop megaloblastic anemia .

Because the erythroblasts cannot proliferate quickly enough to form normal numbers of red blood cells, the cells that are formed are more often than not oversized, of bizarre shapes, and have fragile membranes. These cells rupture with no trouble, leaving the person in dire require of an adequate number of red cells.

In this form of anemia the blood cells are superior to normal, but fewer in number. In its place of 5,000,000 red cells per cubic millimeter, the count may drop to 1,000,000. Trouble arise because the "intrinsic factor" normally created by the stomach is not present to encourage the absorption of vitamin B12 from the intestine. This disease was once extremely serious but not these days.

People with megaloblastic anemia may undergo from atrophic gastritis due to loss of the intrinsic issue usually present in the gastric juice. Patients with megaloblastic anemia might also undergo from neuritis linking the nerves of the spine. There might not be any pain, but such people may have complexity walking in the dark. All cases of neuritis should be methodically investigated to be sure the patient does not have diabetes or a number of other underlying diseases.

Causes of Megaloblastic anemia

In every case of Megaloblastic anemia there is inadequate secretion of intrinsic issue by the stomach. This is necessary for the absorption of the extrinsic factor, vitamin B12 or cyanocoblamin, which is accountable for the maturation of red blood corpuscles: the deficiency causes Megaloblastic degeneration of the bone marrow and of the poster lateral column of the spinal cord and peripheral nerves. Due to inadequacy of vitamin B12 erythropoietin takes the abnormal Megaloblastic path, producing pathological erythrocytes, which get into the general circulation and are willingly destroyed by the reticuloendothelial cells. The outcome is progressive Megaloblastic anemia.

Folic acid has also been found to result maturation of the red blood corpuscles. Achlorhydria is forever present. Any trouble of fat metabolism are not so comprehensible even in higher cases, fat loss is not marked. But blood cholesterol may be to a number of extents lowered.

Signs and Symptoms of Megaloblastic anemia

The skin is lemon yellow in color, the body is found quite well nourish with yellowish fat and reddish brown muscles. The serous membranes and retina have petechial hemorrhages. The interior organs come into sight anemic.

Heart is flabby, pale yellow, dilate and the myocardium and particularly the subendocardial tissues show fatty degeneration.

Mucous membranes of the tongue, stomach and from time to time of intestines are frequently distended. In the stomach, the changes are more noticeable in the fundus with atrophy of the glands and vanishing of the peptic and oxyntic cells.

In a small number of cases, the spinal cord shows degeneration of the posterior and side columns.

Liver is slightly enlarged and shows fatty degeneration. In liver, in the kidneys and in other tissues, iron is deposited. Spleen is to some extent enlarged and more so during exacerbations viewing marked reticulo-endothelial cellular activity.

Achlorhydria is always present and this is often associated with loss of appetite, flatulence, nausea, vomiting and diarrhoea; severe paroxysmal epigastric pain is present in some cases and also glossitis causing smooth glazed tongue in an advanced case.

Complexion becomes progressively pale and in an advanced case, lemon yellow and waxy. The skin, conjunctiva and the mucous membrane of the mouth and tongue appear noticeably bloodless.

Later on, the ankles become oedematous; occasionally anasarca and hydrothorax may appear.

Moderate degrees of fever of unequal type are more often than not present particularly during relapses.

Weakness increasingly increase afterwards even slight effort causes marked dsypnoea, palpitation, giddiness and faintness.

Gastric contents show absence of hydrochloric acid and pepsin. The urine and stool include a surplus of bile pigments.

Complications

Complications are comparatively few. Carcinoma of the stomach, gall bladder diseases, gout, venous thrombosis, rarely retinal hemorrhages and many undercurrent diseases are occasionally associated.

Treatment

The specific treatment is to supply the haemopoietic principle in adequate doses. Vitamin B12 is so effective that it has nearly replaced liver extract injections. It must be remembered that given alone it may precipitate or aggravate spinal lesion.

Oral administration of dilute hydrochloric acid later than food is helpful in a number of cases.