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Vitamin B12 deficiency anemia
(B12-DA)
ПоПпрмтрмрморммм
Prepared by the assistant
of the Department of
Propedeutics of Childhood
Diseases Koishybaeva
K.Zh.
Vitamin B12 deficiency anemia (B12-DA)
a disease caused by a
deficiency of vitamin
B12 in the body
B12 metabolism
Vitamin B12 food
STOMACH
"R-protein + vitamin B12"
Internal factor
R-protein
salivary glands
INTESTINES
ILEUM
рН=7, Са2+
Pancreatic lipase
Release of vitamin B12
from the connection with the R-
protein
Complex formation
"Vitamin B12 + intrinsic factor"
Dimerization of the complex
"Vitamin B12 + intrinsic factor"
Vitamin B12 Internal factor
Vitamin B12
+
transcobalamin II
Vitamin B12
+
transcobalamin I and III
BONE MARROW Escrow
in the liver
Synthesis
nucleic acids
BLOOD
I
II
III
ETIOLOGY
B12-DA can be a consequence of vitamin
deficiency in the diet (strict vegetarianism)
hereditary disorders (congenital absorption
deficiencies - Castle's internal factor, transport
and metabolism of vitamin B12),
acquired defects in vitamin absorption in the
terminal ileum with celiac disease, kwashiorkor,
marasmus, regional ileitis, multiple diverticulosis
of the small intestine, diphyllobothriasis,
resections of the stomach and ileum, autoimmune
atrophic gastritis.
Введите текст
Causes of congenital (hereditary) forms of vitamin B12-
deficiency anemia (Lanzkowsky R., 2000)
II. Impaired absorption of vitamin B12:
1. Insufficient secretion of Castle's intrinsic factor (IF) 1:
- congenital IF deficiency (quantitative or qualitative);
- juvenile autoimmune pernicious anemia;
- juvenile pernicious anemia with autoimmune polyendocrine
pathology and autoimmune gastritis;
- juvenile pernicious anemia with IgA deficiency.
2. Insufficient absorption in the small intestine (selective
malabsorption of vitamin B12):
- abnormal IF;
- violation of the transport of cobalamin to enterocytes
(Imerslund-Gresbeck syndrome).
Введите текст
Causes of congenital (hereditary) forms of vitamin B12-
deficiency anemia (Lanzkowsky R., 2000)
II. Disruption of vitamin B12 transport:
- congenital deficiency of transcobalamin II;
- transient deficiency of transcobalamin II;
- partial deficiency of transcobalamin I.
III. Vitamin B12 metabolism disorders:
- deficiency of adenosylcobalamin - diseases of cobalamin A and
B;
- deficiency of methylmalonyl-CoA mutase;
- combined deficiency of adenosylcobalamin and methylmalo-
nil-CoA mutases - diseases of cobalamin C, D, F;
- methylcobalamin deficiency - cobalamin E, G.
Pathogenesis of megaloblastic anemias
Lack of tetrahydrofolate
Disruption of thymidine synthesis
Impaired DNA synthesis (but RNA synthesis persists)
S-stage lengthening of the cell cycle
Delay of mitosis and accumulation of cytoplasm volume
Megaloblastic type of hematopoiesis
Defectiveness of megalocytes,
megaloblasts
Weak deformability of
megalocytes
Inside bone marrow cell
death
Hemolysis of megalocytes
in capillaries
Anemia
Methylcobalamin deficiency Folic acid deficiency
Введите текст
Clinic
 B12-DA can appear in children already in the second half of life with
congenital absence of Castle's intrinsic factor or transcobalamin deficiency.
 Schoolchildren and adults are characterized, in addition to signs of
megaloblastic anemia (pallor, icterus of the sclera and skin, dry skin, brittle
nails and hair, weakness, malaise, poor appetite with a particular aversion
to meat, etc.), glossitis with papillary atrophy (lacquered tongue) , soreness
of the tongue and aphthae
 changes in the nervous system are known as funicular myelosis (ataxia,
paresthesia, hyporeflexia, clonuses, the appearance of pathological reflexes,
for example, Babinsky, feeling of cotton feet, hallucinations, delirium)
 moderate signs of heart failure (energetic-dynamic myocardial
insufficiency), diarrhea, moderate enlargement of the spleen and liver.
Laboratory signs of B12-deficiency anemia
Blood.
• Megalocytes - hyperchromic erythrocytes with a diameter
of more than 9.5 microns with a low life expectancy (30-
40 days), anisocytosis;
• Poikilocytosis (pear-shaped, oval erythrocytes);
• Red blood cells with Jolly bodies and Cape rings;
• Giant hypersegmented neutrophils, aneosinophilia and
abasophilia.
• Reticulocytopenia
• Thrombocytopenia (ugly platelets
• Bone marrow.
• Hypercellular (due to erythrokaryocytes)
• Megaloblasts, megalocytes
• Absence of oxyphilic forms of cells - "blue" bone marrow
(due to the abundance of basophilic megaloblasts).
Hyperbilirubinemia
Hypersideremia
Due to the breakdown of defective
megalocytes
Additional research
• Decreased serum vitamin B12 (<200 ng / L)
• Decreased serum folate (<4 μg / L) and
erythrocytes (<140 μg / L)
• In the urine, increased excretion of
methylmalonic acid (differential diagnostic
sign with PDA).
Treatment
1. Eliminate the cause that led
to this pathology.
2. Diet: table number 5
according to Pevzner for
children of early and preschool
age - proper balanced nutrition
with the inclusion in the diet of
foods rich in vitamins B12, folic
acid, iron (vegetable purees,
meat, fruit and vegetable juices,
yolk, etc.).
3. Daily regimen with sufficient
stay in the fresh air, therapeutic
massage, exercise therapy,
hydromassage.
Treatment
• Parenteral administration of
vitamin B12 at a dose of 200-500
mcg daily. For neurological
manifestations, the dose is
increased to 1 mg. It must be
remembered that in children of
the first months of life, vitamin
B12 in doses of more than 10
mcg / kg is not absorbed and
inhibits the function of the
thyroid gland. With hereditary
forms of B12-DA, after the relief
of acute phenomena, it is
recommended
• 1 mg of cyanocobalamin should
be injected every 3 months.
Criteria for the
effectiveness of
therapy
• Against the background of
the introduction of vitamin
B12, after 48-72 hours, the
change of megaloblastic
hematopoiesis to
normoblastic begins, a
decrease in serum levels of
bilirubin and LDH activity;
maximum reticulocytosis is
noted at the beginning of
the 2nd week of treatment.
LITERATURE
1. В.Г. Майданник Педиатрия 2-ое издание, исправленное и
дополненное 2002г., 770 стр.
2. Детские болезни/2012-2013гг. : т.1 / ред. И.Ю. Мельникова.
- М. : ГЭОТАР-медиа, 2009г.,319 стр.
3. Клинические рекомендации. Детская гематология, под ред.
А.Г. Румянцева, А.А. Масчана, Е.В. Жуковской. - М. :
ГЭОТАР-Медиа, 2015 .
4. Anoop Verma, Vijay P Makhija. - Электрон. текстовые дан.
- New Delhi; Panama City; London: JAYPEE BROTHERS
MEDICAL PUBLISHERS(P) LTD, 2012.
5. Google/другие интернет ресурсы.

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Vitamin B12 deficiency anemia (B12-DA),PPT. eng.pptx

  • 1. Vitamin B12 deficiency anemia (B12-DA) ПоПпрмтрмрморммм Prepared by the assistant of the Department of Propedeutics of Childhood Diseases Koishybaeva K.Zh.
  • 2. Vitamin B12 deficiency anemia (B12-DA) a disease caused by a deficiency of vitamin B12 in the body
  • 3. B12 metabolism Vitamin B12 food STOMACH "R-protein + vitamin B12" Internal factor R-protein salivary glands INTESTINES ILEUM рН=7, Са2+ Pancreatic lipase Release of vitamin B12 from the connection with the R- protein Complex formation "Vitamin B12 + intrinsic factor" Dimerization of the complex "Vitamin B12 + intrinsic factor" Vitamin B12 Internal factor Vitamin B12 + transcobalamin II Vitamin B12 + transcobalamin I and III BONE MARROW Escrow in the liver Synthesis nucleic acids BLOOD I II III
  • 4. ETIOLOGY B12-DA can be a consequence of vitamin deficiency in the diet (strict vegetarianism) hereditary disorders (congenital absorption deficiencies - Castle's internal factor, transport and metabolism of vitamin B12), acquired defects in vitamin absorption in the terminal ileum with celiac disease, kwashiorkor, marasmus, regional ileitis, multiple diverticulosis of the small intestine, diphyllobothriasis, resections of the stomach and ileum, autoimmune atrophic gastritis.
  • 5. Введите текст Causes of congenital (hereditary) forms of vitamin B12- deficiency anemia (Lanzkowsky R., 2000) II. Impaired absorption of vitamin B12: 1. Insufficient secretion of Castle's intrinsic factor (IF) 1: - congenital IF deficiency (quantitative or qualitative); - juvenile autoimmune pernicious anemia; - juvenile pernicious anemia with autoimmune polyendocrine pathology and autoimmune gastritis; - juvenile pernicious anemia with IgA deficiency. 2. Insufficient absorption in the small intestine (selective malabsorption of vitamin B12): - abnormal IF; - violation of the transport of cobalamin to enterocytes (Imerslund-Gresbeck syndrome).
  • 6. Введите текст Causes of congenital (hereditary) forms of vitamin B12- deficiency anemia (Lanzkowsky R., 2000) II. Disruption of vitamin B12 transport: - congenital deficiency of transcobalamin II; - transient deficiency of transcobalamin II; - partial deficiency of transcobalamin I. III. Vitamin B12 metabolism disorders: - deficiency of adenosylcobalamin - diseases of cobalamin A and B; - deficiency of methylmalonyl-CoA mutase; - combined deficiency of adenosylcobalamin and methylmalo- nil-CoA mutases - diseases of cobalamin C, D, F; - methylcobalamin deficiency - cobalamin E, G.
  • 7. Pathogenesis of megaloblastic anemias Lack of tetrahydrofolate Disruption of thymidine synthesis Impaired DNA synthesis (but RNA synthesis persists) S-stage lengthening of the cell cycle Delay of mitosis and accumulation of cytoplasm volume Megaloblastic type of hematopoiesis Defectiveness of megalocytes, megaloblasts Weak deformability of megalocytes Inside bone marrow cell death Hemolysis of megalocytes in capillaries Anemia Methylcobalamin deficiency Folic acid deficiency
  • 9. Clinic  B12-DA can appear in children already in the second half of life with congenital absence of Castle's intrinsic factor or transcobalamin deficiency.  Schoolchildren and adults are characterized, in addition to signs of megaloblastic anemia (pallor, icterus of the sclera and skin, dry skin, brittle nails and hair, weakness, malaise, poor appetite with a particular aversion to meat, etc.), glossitis with papillary atrophy (lacquered tongue) , soreness of the tongue and aphthae  changes in the nervous system are known as funicular myelosis (ataxia, paresthesia, hyporeflexia, clonuses, the appearance of pathological reflexes, for example, Babinsky, feeling of cotton feet, hallucinations, delirium)  moderate signs of heart failure (energetic-dynamic myocardial insufficiency), diarrhea, moderate enlargement of the spleen and liver.
  • 10. Laboratory signs of B12-deficiency anemia Blood. • Megalocytes - hyperchromic erythrocytes with a diameter of more than 9.5 microns with a low life expectancy (30- 40 days), anisocytosis; • Poikilocytosis (pear-shaped, oval erythrocytes); • Red blood cells with Jolly bodies and Cape rings; • Giant hypersegmented neutrophils, aneosinophilia and abasophilia. • Reticulocytopenia • Thrombocytopenia (ugly platelets • Bone marrow. • Hypercellular (due to erythrokaryocytes) • Megaloblasts, megalocytes • Absence of oxyphilic forms of cells - "blue" bone marrow (due to the abundance of basophilic megaloblasts). Hyperbilirubinemia Hypersideremia Due to the breakdown of defective megalocytes
  • 11. Additional research • Decreased serum vitamin B12 (<200 ng / L) • Decreased serum folate (<4 μg / L) and erythrocytes (<140 μg / L) • In the urine, increased excretion of methylmalonic acid (differential diagnostic sign with PDA).
  • 12. Treatment 1. Eliminate the cause that led to this pathology. 2. Diet: table number 5 according to Pevzner for children of early and preschool age - proper balanced nutrition with the inclusion in the diet of foods rich in vitamins B12, folic acid, iron (vegetable purees, meat, fruit and vegetable juices, yolk, etc.). 3. Daily regimen with sufficient stay in the fresh air, therapeutic massage, exercise therapy, hydromassage.
  • 13. Treatment • Parenteral administration of vitamin B12 at a dose of 200-500 mcg daily. For neurological manifestations, the dose is increased to 1 mg. It must be remembered that in children of the first months of life, vitamin B12 in doses of more than 10 mcg / kg is not absorbed and inhibits the function of the thyroid gland. With hereditary forms of B12-DA, after the relief of acute phenomena, it is recommended • 1 mg of cyanocobalamin should be injected every 3 months.
  • 14. Criteria for the effectiveness of therapy • Against the background of the introduction of vitamin B12, after 48-72 hours, the change of megaloblastic hematopoiesis to normoblastic begins, a decrease in serum levels of bilirubin and LDH activity; maximum reticulocytosis is noted at the beginning of the 2nd week of treatment.
  • 15. LITERATURE 1. В.Г. Майданник Педиатрия 2-ое издание, исправленное и дополненное 2002г., 770 стр. 2. Детские болезни/2012-2013гг. : т.1 / ред. И.Ю. Мельникова. - М. : ГЭОТАР-медиа, 2009г.,319 стр. 3. Клинические рекомендации. Детская гематология, под ред. А.Г. Румянцева, А.А. Масчана, Е.В. Жуковской. - М. : ГЭОТАР-Медиа, 2015 . 4. Anoop Verma, Vijay P Makhija. - Электрон. текстовые дан. - New Delhi; Panama City; London: JAYPEE BROTHERS MEDICAL PUBLISHERS(P) LTD, 2012. 5. Google/другие интернет ресурсы.