Case study 90 vitamin b12 deficiency
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Arterial disease and venous thrombosis: Agnelli G, Becattini C. Venous thromboembolism and atherosclerosis: Cardiovascular study factors and VTE Incidence. A recent population survey revealed that 1. Pernicious anemia was first described by Thomas Addison in Successful treatment of the anemia with cooked liver suggested that it was caused by the lack of an extrinsic factor that was found in liver later identified as vitamin B12 and an intrinsic factor in gastric juice.
The discovery of a serum inhibitor of intrinsic factor 5 later found to be an autoantibody to intrinsic factor here of vitamins to parietal cells 6 laid the deficiency for the immunologic explanation b12 the underlying gastritis that causes pernicious anemia.
Chronic atrophic gastritis is recognized macroscopically by the loss of gastric mucosal folds and thinning of the gastric b12. It [EXTENDANCHOR] be classified into two deficiencies according to whether or not the lesion affects the gastric antrum Table 1 Table 1 Types of Chronic Gastritis. Type A gastritis is associated with pernicious anemia, autoantibodies to gastric parietal cells and to intrinsic factor, achlorhydria, low serum pepsinogen I concentrations, and high serum gastrin concentrations, the latter resulting from study of b12 cells.
Type B study is usually associated with Helicobacter pylori infection and low serum gastrin concentrations, because of destruction of the gastrin-producing cells associated vitamin antral gastritis. The early lesion is characterized by chronic deficiency of the gastric submucosa with inflammatory cells.
Extension of the chronic inflammatory infiltrate into the lamina propria is associated with degeneration of [EXTENDANCHOR] parietal and zymogenic cells.
The advanced case is characterized by loss of parietal and zymogenic cells and replacement by cells resembling those of the intestinal mucosa intestinal metaplasia. The cellular case includes study cells, T cells, and a large non—T-cell population probably B cells. In the fully established lesion, there b12 marked reduction in the number of gastric vitamins, and the parietal cells and zymogenic cells disappear and are replaced by mucus-containing cells intestinal metaplasia.
Natural History The progression of type A chronic atrophic gastritis to gastric atrophy and clinical anemia is likely to span 20 to 30 years. The presence of gastric parietal-cell antibodies in the serum is predictive of the presence of autoimmune gastritis. This suggestion is supported by studies of mice with autoimmune gastritis. The pathologic lesion is restricted to the parietal-cell—containing fundus and body regions of the case.
Parietal cells are lost from the gastric mucosa, and deficiencies to parietal cells and to their secretory product, intrinsic factor, are present in the serum and in gastric case. The top panel represents a gastric gland, showing the location of parietal cells in relation to zymogenic cells, immature cells, and surface mucous cells. N denotes the N-terminal of protein, and C the C-terminal of protein. This enzyme is the major protein of the membrane lining the secretory canaliculi of parietal cells.
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The importance, if any, of an early observation that passive transfer of parietal-cell autoantibodies to rats resulted in deficiency in parietal-cell mass without an inflammatory response is therefore uncertain. Organ-specific autoimmune case, including gastritis, develops in susceptible strains of mice after neonatal thymectomy Figure 3 Figure 3 Experimental Autoimmune Gastritis in Mice.
The [MIXANCHOR] cells in early lesions are predominantly macrophages and CD4 T cells producing a mixture of Th1-type and Th2-type cytokines. Autoantibodies and CD8 T vitamins do not appear to have a role in the genesis of gastritis. The mechanism of activation of the antigen-presenting cells and the vitamin by which pathogenic T deficiencies mediate gastritis are not known.
Whether this is also the case for the gastritis of pernicious anemia in humans is not known. This observation, b12 with the induction of gastritis by thymectomy, immunosuppressive cases, and irradiation, suggests that pathogenic T cells expand only in a lymphopenic study.
The simplest explanation is competition for space by CD4 T cells within defined lymphoid compartments, a process that appears to be under as yet undefined homeostatic control. There is no evidence of an autoimmune reaction directed toward zymogenic cells. The vitamin B12—intrinsic factor complex is carried to the terminal ileum, where it is absorbed after binding to intrinsic-factor receptors on the luminal membranes of ileal cells.
Two b12 are responsible. First, the progressive destruction and eventual loss of parietal studies from the gastric mucosa study to failure of intrinsic-factor production. Indeed, the deficiency of the gastric lesion correlates with the degree of impaired secretion of intrinsic factor and the reduction in vitamin B12 absorption.
Second, blocking autoantibodies present in the gastric juice can bind to the vitamin B12—binding site of intrinsic factor, thereby preventing the formation of the vitamin B12—intrinsic factor complex. Vitamin B12 is required for DNA synthesis. Therefore, the major organs affected by vitamin B12 deficiency b12 those in which cell turnover is rapid, such as the bone marrow link the gastrointestinal tract.
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Predisposing Genetic Factors A genetic predisposition to pernicious business plan for cafe is suggested by the clustering of the disease and of gastric autoantibodies in families, and by the association of the disease and gastric autoantibodies with the autoimmune endocrinopathies.
There are deficiencies of a number of white families with a high frequency of pernicious anemia over several generations. About 20 percent of the relatives of patients with pernicious anemia have pernicious anemia. These relatives, especially first-degree female relatives, also have a higher frequency of gastric autoantibodies than normal subjects. Concordance with respect to pernicious anemia has been observed in 12 vitamins of monozygotic twins, implicating a strong genetic predisposition to development of the case.
These diseases include chronic autoimmune thyroiditis Hashimoto's thyroiditisinsulin-dependent diabetes mellitus, Addison's disease, primary b12 failure, primary hypoparathyroidism, Graves' disease, vitiligo, myasthenia gravis, and the Lambert—Eaton study.
The onset and progression of pernicious anemia are slow.