Peripheral blood smear for megaloblastic anemia (blood)

Macrocytes – defective erythrocytes, oval macrocytes (Fig. 3).

Anisopoikilocytosis (various shapes and sizes of erythrocytes, Fig. 3)

Low reticulocyte count

The appearance of a certain number of nuclear erythrocytes

Hypersegmented neutrophils (Fig. 3)

Giant platelets (Fig. 3)

Pancytopenia (anemia, leukopenia, thrombocytopenia).

An increase in MCV, MCH with normal MCHC is observed in megaloblastic anemia, since the content of hemoglobin in cells is increased in proportion to the increase in the size of red blood cells.

In the bone marrow with megaloblastic anemia, the myeloid / erythroid ratio is changed (from 2:1 to 1:2) due to the large number of erythroid precursors.

Biochemical changes in megaloblastic anemia: indirect bilirubin is increased, lactate dehydrogenase activity is increased in ~ 1000, homocysteine content is increased, vitamin B12 content is reduced.

Clinical manifestations of msegaloblastic (pernicious anemia) – anemia, in which vitamin B12 deficiency is caused by autoimmune destruction of the parietal cells of the stomach that produce the intrinsic factor: all symptoms of anemia + • weight loss, gastrointestinal tract disorders, pain in the tongue or mouth, glossitis; pallor and yellowness of lemon color, early gray hair, vetiligo. Neurological changes (may be irreversible): dementia, depression, behavioral changes (megaloblastic madness); difficulty walking.

Pathogenesis of pernicious anemia (megaloblastic anemia)

Vitamin B12 is usually absorbed in the ileum. For the absorption of vitamin B12 in the ileum, an internal factor (specific protein) is required – enterocytes (cells of the intestinal mucosa) of the ileum have receptors not for B12, but for the internal factor. The binding of the vitamin B12-intrinsic factor complex to the receptor is accompanied by endocytosis (the complex “falls” into the enterocyte).

Intrinsic factor is secreted by the parietal cells of the fundus of the gastric mucosa . Pernicious anemia is the result of autoimmune destruction of cells in the gastric mucosa, leading to intrinsic factor deficiency and malabsorption of vitamin B12.

Manifestation of pernicious anemia (megaloblastic anemia)

Defective DNA synthesis is carried out in all proliferating cells, including the gastrointestinal tract, which is manifested by glossitis (Fig.)

The most characteristic changes in the gastric mucosa in pernicious anemia are the absence of parietal cells in the fundic glands of the stomach and a decrease in the number of chief cells – glandular cells. The glandular epithelium of the gastric mucosa is replaced by goblet cells that secrete mucus. These cells are similar to those found in the colonic mucosa. The pathological phenomenon of replacement of the glandular cells of the stomach by cells that secrete mucus is known as intestinalization of the stomach (the transformation of the gastric mucosa into the intestinal mucosa) (Fig.) – characteristic of megaloblastic anemia.

The main changes in vitamin B12 deficiency involve the brain and spinal cord. Damage to the nervous system is caused by degeneration of myelin due to the accumulation of methylmalonate and propionate due to impaired conversion of methylmalonyl CoA in the absence of vitamin B12

All these changes are also observed in folic acid deficiency, with the exception of neurological changes, since methyl malonate does not accumulate in folic acid deficiency.

Be First to Comment

Leave a Reply

Your email address will not be published.