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Dr.K. R. Prabhakar,
Asst.Proffessor
Pathophysiology
 This is due to vitamin B₁₂ and folic acid deficiency
 Impairment of DNA synthesis and cell proliferation
in precursor cells of RBCs.
 Cytosolic growth is not impaired ,cytosole ↑
 Hence primitive RBCs become big(megaloblast)
 Mature RBCs diminish(anemia),
 Prone to hemolysis-hemolytic anemia.
 Mammals can not synthesise vit B₁₂ .
 Sources of vit B₁₂ are- fish, meat, liver, eggs, yeast &
milk.
 Commercial source- from streptomyces griseus.
Deficiency causes:
 Insufficient dietary intake (RDA-2µg)
 ↓absorption or utilisation
 Prolonged chemotherapy (interfers with purine
metabolism).
 Fish tape worm infestation
 Pernicious anemia:
• Important cause of vit B₁₂ deficiency
• Hereditary autoimmune disease in which antibodies
develop against intrinsic factor(IF)
• ABs either bind to IF or IF-B₁₂ complex and prevents
binding to IF receptors in ileum.
 Availability of IF decreases in
• Post gastrectomy patients, diseases of ileum &
surgical removal of ileum.
Chemistry:
 Vit B₁₂ is a generic term for cyanocobalamin &
hydroxocobalamin.
 Only cobalt containing amino compounds known to
occur in nature.
 Methylcobalamin & 5deoxoadenosyl cobalamin act
as coenzymes and are active forms of vit B₁₂ though
unstable.
Pharmacokinetics
 Absorption from GIT depends on various transfer
mechanisms.
 After liberation from food interacts with R-proteins
in stomach protect it from acid degradation.
 In the duodenum the pancreatic proteases degrade
the complex to free cobalamin.
 Vit B₁₂ is now absorbed on to the IF .
 IF- cobalamin complex is transported across ileum
cell membrane through IF specific receptors
 In enterocytes IF liberates cobalamin which is
converted to methylcobalamin
 Transcobalamin II transports it to portal circulation.
 Vit B₁₂ is taken up by cells by endocytosis.
 Excess vit B₁₂ is stored as 5-deoxoadenosylcobalamin
in hepatocytes.
 Liver can store up to 4-6 mg of vit B₁₂ .
 Stores can last for 5 yrs even if intake is stopped.
Metabolic functions
 Cobalamins- cofactors for 2 main enzymatic process
 1. Cofactor for methionine synthase –converts
homocysteine to methionine &
 5-methyl tetrahydrofolate to tetrahydrofolic acid.
In vitB₁₂ deficiency
 5-methyl-tertrahydrofollic acid gets trapped.
 Defective DNA synthesis & ultimately megaloblastic
bone marrow.
 2. Deoxyadenosyl cobalamin activates
methylmalonyl-coA mutase
In vitB₁₂ deficiency
 methylmalonyl coA accumulate results in faulty fatty
acid synthesis.
 Incorporates in to cell membranes of CNS leads to
neurological symptoms due to inadequate myelin
synthesis-
 Peripheral neuropathy,
 Dementia,
 Loss of motor and sensory reflexes.
Therapeutic uses
 Most commonly used preparations are
 cyanocobalamin
 hydroxycobalamin
 methylcobalamin
 Given orally or deep intramuscularly never given i.v.
 Hydroxycobalamin is longer acting but development
of Abs to transcobalamin II –vit B₁₂ complex made its
use lesser.
 Methylcobalamin is used to treat neurological
deficits in vit B₁₂ deficiency.
 Dose: cyanocobalamin or hydroxycobalamin 100-
1000 µg/day i.m on alternative days for 2 weeks
followed by once a month.
 Methylcobalamin 1000-1500 µg/day orally.
 I.M therapy brings changes in bone marrow with in
2-3 mts with improvement in neurological symptoms
 Also called polyglutamate as each folic acid molecule
may have 2-8 molecules of glutamic acid.
 Humans can not synthesise folic acid
Dietary sources:
 Green leafy vegetables, fruits, mushrooms, liver,
meat, kidney, eggs, milk & yeast.
 One of the B group vitamin.
Pharmacokinetics
 Absorption occurs primarily in proximal jejunum.
 Carboxypeptidases in jejunum hydrolyse dietary
polyglutamates to folic acid.
 Dihydrofolate reductase converts folic acid to
tetrahydrofolic acid(THFA) in mucosa & methylated
to (5-MeTHFA)
 Converted to THFA by methionine synthase in
tissues.
 About 5-20 mg is stored in liver.
 Undergoes enterohepatic circulation similar to vitB₁₂.
 Trace amounts are excreted in urine & faeces.
 Stores last for about only 3 months.
Metabolic functions:
 THFA is transformed to folate cofactors – folinic acid,
10-formyl THFA, 5,10-methylene-THFA etc. donates
one carbon units in oxidation.
 THFA through 1-C transfer reactions is involved in
synthesis of purines and pyrimidines which are
essential for DNA synthesis.
Deficiecy causes
 Dietary lack.
 Malabsorption syndrome (coeliac disease or crohns
disease).
 Excessive demand as in pregnancy & anemia.
 Liver diseases and renal dialysis.
 Drug induced- methotrexate, phenytoin,
phenobarbitone.
 Deficiecy leads to megaloblast anemia and
teratogenic effects.
Therapeutic use
 RDA of folic acid is 50 µg,
 During pregnancy & lactation up to 200-300 µg/day.
 Therapeutic doses are 1-5 mg/day.
Uses-
 Folinic acid for prophylaxis or treatment of
methotrexate toxicity.
 Folate deficiency by phenobarbitone & phenytoin.
 Prophylactically during pregnancy, lactation.
 Folic acid is always given with vit B₁₂ to treat
megaloblastic anemia.
 In the presence of vitB₁₂ deficiency if only folic acid is
used it will improve only anemia but worsen
neurological deficit as it does not convert
methylmalonyl CoA to succinyl CoA.
 Adverse effects :rare for both vit B₁₂ &folic acid.
 Cytokine produced in juxtatubular cell in kidney &
also macrophages.
 Essential for normal erythropoiesis.
 Anaemia and hypoxia are sensed by kidney cells.
 Induce rapid secretion of EPO→ acts on erythroid
marrow.
 EPO receptor is a JAK-STAT-binding receptor.
 Recombinant human erythropoietin are Epoetin α, β.
 Administered by i.v. or s.c. injection.
 Plasma t½ of 6–10 hr, but action lasts several days.
 Darbepoetin – longer acting glycosylated form of
epoetin, injected weekly.
Uses
 Primary use- anaemia of chronic renal failure.
 Anaemia in AIDS patients treated with zidovudine.
 Cancer chemotherapy induced anaemia.
 Preoperative increased blood production for
autologous transfusion during surgery.
 Anemia in premature infants.
 Supplemented with iron & folic acid.
 Preferable for smptomatic patients with Hb ≤ 8 g/dl.
 Epoetin 25–100 U/kg s.c. or i.v. 3 times a week (max.
600 U/kg/week).
 Reduces need for transfusions
 It is prudent to start with a low dose and titrate
upwards to keep haematocrit between 30–36%, and
Hb 10–11 g (max 12 g) per dl.
Thank you

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Glomerular Filtration and determinants of glomerular filtration .pptx
 

Treatment of other anemias

  • 2. Pathophysiology  This is due to vitamin B₁₂ and folic acid deficiency  Impairment of DNA synthesis and cell proliferation in precursor cells of RBCs.  Cytosolic growth is not impaired ,cytosole ↑  Hence primitive RBCs become big(megaloblast)  Mature RBCs diminish(anemia),  Prone to hemolysis-hemolytic anemia.
  • 3.  Mammals can not synthesise vit B₁₂ .  Sources of vit B₁₂ are- fish, meat, liver, eggs, yeast & milk.  Commercial source- from streptomyces griseus. Deficiency causes:  Insufficient dietary intake (RDA-2µg)  ↓absorption or utilisation  Prolonged chemotherapy (interfers with purine metabolism).  Fish tape worm infestation
  • 4.  Pernicious anemia: • Important cause of vit B₁₂ deficiency • Hereditary autoimmune disease in which antibodies develop against intrinsic factor(IF) • ABs either bind to IF or IF-B₁₂ complex and prevents binding to IF receptors in ileum.  Availability of IF decreases in • Post gastrectomy patients, diseases of ileum & surgical removal of ileum.
  • 5. Chemistry:  Vit B₁₂ is a generic term for cyanocobalamin & hydroxocobalamin.  Only cobalt containing amino compounds known to occur in nature.  Methylcobalamin & 5deoxoadenosyl cobalamin act as coenzymes and are active forms of vit B₁₂ though unstable.
  • 6. Pharmacokinetics  Absorption from GIT depends on various transfer mechanisms.  After liberation from food interacts with R-proteins in stomach protect it from acid degradation.  In the duodenum the pancreatic proteases degrade the complex to free cobalamin.  Vit B₁₂ is now absorbed on to the IF .  IF- cobalamin complex is transported across ileum cell membrane through IF specific receptors
  • 7.  In enterocytes IF liberates cobalamin which is converted to methylcobalamin  Transcobalamin II transports it to portal circulation.  Vit B₁₂ is taken up by cells by endocytosis.  Excess vit B₁₂ is stored as 5-deoxoadenosylcobalamin in hepatocytes.  Liver can store up to 4-6 mg of vit B₁₂ .  Stores can last for 5 yrs even if intake is stopped.
  • 8. Metabolic functions  Cobalamins- cofactors for 2 main enzymatic process  1. Cofactor for methionine synthase –converts homocysteine to methionine &  5-methyl tetrahydrofolate to tetrahydrofolic acid.
  • 9.
  • 10. In vitB₁₂ deficiency  5-methyl-tertrahydrofollic acid gets trapped.  Defective DNA synthesis & ultimately megaloblastic bone marrow.  2. Deoxyadenosyl cobalamin activates methylmalonyl-coA mutase
  • 11. In vitB₁₂ deficiency  methylmalonyl coA accumulate results in faulty fatty acid synthesis.  Incorporates in to cell membranes of CNS leads to neurological symptoms due to inadequate myelin synthesis-  Peripheral neuropathy,  Dementia,  Loss of motor and sensory reflexes.
  • 12. Therapeutic uses  Most commonly used preparations are  cyanocobalamin  hydroxycobalamin  methylcobalamin  Given orally or deep intramuscularly never given i.v.  Hydroxycobalamin is longer acting but development of Abs to transcobalamin II –vit B₁₂ complex made its use lesser.
  • 13.  Methylcobalamin is used to treat neurological deficits in vit B₁₂ deficiency.  Dose: cyanocobalamin or hydroxycobalamin 100- 1000 µg/day i.m on alternative days for 2 weeks followed by once a month.  Methylcobalamin 1000-1500 µg/day orally.  I.M therapy brings changes in bone marrow with in 2-3 mts with improvement in neurological symptoms
  • 14.  Also called polyglutamate as each folic acid molecule may have 2-8 molecules of glutamic acid.  Humans can not synthesise folic acid Dietary sources:  Green leafy vegetables, fruits, mushrooms, liver, meat, kidney, eggs, milk & yeast.  One of the B group vitamin.
  • 15. Pharmacokinetics  Absorption occurs primarily in proximal jejunum.  Carboxypeptidases in jejunum hydrolyse dietary polyglutamates to folic acid.  Dihydrofolate reductase converts folic acid to tetrahydrofolic acid(THFA) in mucosa & methylated to (5-MeTHFA)  Converted to THFA by methionine synthase in tissues.  About 5-20 mg is stored in liver.
  • 16.  Undergoes enterohepatic circulation similar to vitB₁₂.  Trace amounts are excreted in urine & faeces.  Stores last for about only 3 months. Metabolic functions:  THFA is transformed to folate cofactors – folinic acid, 10-formyl THFA, 5,10-methylene-THFA etc. donates one carbon units in oxidation.  THFA through 1-C transfer reactions is involved in synthesis of purines and pyrimidines which are essential for DNA synthesis.
  • 17. Deficiecy causes  Dietary lack.  Malabsorption syndrome (coeliac disease or crohns disease).  Excessive demand as in pregnancy & anemia.  Liver diseases and renal dialysis.  Drug induced- methotrexate, phenytoin, phenobarbitone.  Deficiecy leads to megaloblast anemia and teratogenic effects.
  • 18. Therapeutic use  RDA of folic acid is 50 µg,  During pregnancy & lactation up to 200-300 µg/day.  Therapeutic doses are 1-5 mg/day. Uses-  Folinic acid for prophylaxis or treatment of methotrexate toxicity.  Folate deficiency by phenobarbitone & phenytoin.  Prophylactically during pregnancy, lactation.
  • 19.  Folic acid is always given with vit B₁₂ to treat megaloblastic anemia.  In the presence of vitB₁₂ deficiency if only folic acid is used it will improve only anemia but worsen neurological deficit as it does not convert methylmalonyl CoA to succinyl CoA.  Adverse effects :rare for both vit B₁₂ &folic acid.
  • 20.  Cytokine produced in juxtatubular cell in kidney & also macrophages.  Essential for normal erythropoiesis.  Anaemia and hypoxia are sensed by kidney cells.  Induce rapid secretion of EPO→ acts on erythroid marrow.  EPO receptor is a JAK-STAT-binding receptor.
  • 21.  Recombinant human erythropoietin are Epoetin α, β.  Administered by i.v. or s.c. injection.  Plasma t½ of 6–10 hr, but action lasts several days.  Darbepoetin – longer acting glycosylated form of epoetin, injected weekly.
  • 22. Uses  Primary use- anaemia of chronic renal failure.  Anaemia in AIDS patients treated with zidovudine.  Cancer chemotherapy induced anaemia.  Preoperative increased blood production for autologous transfusion during surgery.  Anemia in premature infants.  Supplemented with iron & folic acid.
  • 23.  Preferable for smptomatic patients with Hb ≤ 8 g/dl.  Epoetin 25–100 U/kg s.c. or i.v. 3 times a week (max. 600 U/kg/week).  Reduces need for transfusions  It is prudent to start with a low dose and titrate upwards to keep haematocrit between 30–36%, and Hb 10–11 g (max 12 g) per dl.