AceMed Universities MU Plovdiv Medicine Year 4 Internal Diseases – Part 1 (Rheumatology, Pulmonology, Phthisiatrics, Cardiology, Haematology) Topic 51 Internal Diseases – Part 1 (Rheumatology, Pulmonology, Phthisiatrics, Cardiology, Haematology) · MU Plovdiv
2. Megaloblastic anemia - classification. Pernicious anemia
Inside: 5 sections · 4 labelled pictures · 6 tables · 15 flashcards · 10 min
Topic 51 of 68 in the MU Plovdiv syllabus for Internal Diseases – Part 1 (Rheumatology, Pulmonology, Phthisiatrics, Cardiology, Haematology) (Medicine, Year 4). The free AceMed note covers it in 5 sections, about 1,483 words (10 min of reading), with 15 flashcards .
In this note Essay 2- Megaloblastic anemia - classification. Pernicious anemia Vitamin B12 deficiency anemia Vitamin B9 deficiency anemia Pernicious anemia Macrocytic and megaloblastic anemias Essay 2- Megaloblastic anemia - classification. Pernicious anemia What are megaloblastic anemias? Group of anemias in which the erythroblasts in the bone marrow show a characteristic abnormality - maturation of the nucleus being delayed relative to that of the cytoplasm Classification Megaloblastic anemia can be classified into two types dependant on the etiology: Vitamin B12 deficiency anemia Vitamin B9 deficiency anemia Clinical features of megaloblastic anemias Insidious onset with gradually progressive symptoms! Mild jaundice Glossitis Angular cheilosis Mild symptoms of malabsorption with weight loss Purpura as a result of thrombocytopenia Vitamin B12 deficiency anemia Etiology Inadequate intake Absorption defects (blind loop syndrome)Intrinsic factor deficiency Chronic atrophic gastritis Drugs (DHF reductase inhibitors, purine antagonists, pyrimidine antagonists)Inherited metabolic diseases (Lesh-Nyhan syndrome, homocysteinuria)Pathogenesis B12 is a cofactor for two important reactions in body (synthesis of DNA anvention of abnormal FA from being incorporated into neuronal lipidsNeeded to convert Uridine to thymidine and also to produce myelin B12 is found in foods of animal origin only B12 binds to intrinsic factor and travels to the ileum where it binds to cubillin which recognises Castle’s factor So if Castle’s factor is missing, B12 cannot be reabsorbed Defects in transport pathway can also cause deficiency When B12 is deficient, red cells are large due to excess RNA production, immature nuclei and show cellular destruction Purine and thymidylate synthesis is inhibited Erythroblast apoptosis is seen Decreased intrinsic factor is caused by:Atrophic gastritis Gastrectomy Autoimmune antibodies against parietal cells or B12-factor complex B12 deficiency is also called pernicious anemia (resulting from hereditary atrophic gastritis) Symptoms Clinical presentation consists of:Anemic syndrome - presents with jaundice, since large RBC are stuck in spleen, patients are well adaptedGI syndrome - prolonged DNA maturation results in impaired regeneration (leads to inflammation), hunters glossitis, loss of papillaeNeurological syndrome - due to demyelination, loss of proprioception, psychiatric problems,Weakness Cardiopulmonary involvement Lemon-colour complexion Loss of appetite Weight loss Nausea Constipation Sore throat Canker sores Change in personality, psychosis Sterility Decreased osteoblast activity NTD in fetus Diagnosis Lab findings - macrocytic cells, leukopenia and thrombocytopeniaElevated LDH Reticulocytopenia Increased indirect Br B12 deficiency can be confirmed with elevated MMA and homocysteine levels and low B12 levels Treatment Usually, treatment consists of supplying the vitamin that is deficient! B12 can ONLY be given via IM! Sublingual, nasal spray and gel forms are available
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