Vitamin B12 deficiency pathophysiology: Difference between revisions
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__NOTOC__ | __NOTOC__ | ||
{{Vitamin B12 deficiency}} | {{Vitamin B12 deficiency}} | ||
{{CMG}} | {{CMG}} {{AE }}{{NA}} | ||
{{SI}} | |||
==Overview== | ==Overview== | ||
==Pathophysiology== | == Pathophysiology == | ||
* Dietary Vitamin B12 binds to salivary R factor then the complex arrives at small intestine.<ref name="pmid28722952">{{cite journal |vauthors=Ankar A, Bhimji SS |title= |journal= |volume= |issue= |pages= |date= |pmid=28722952 |doi= |url=}}</ref> | |||
* In duodenum Vitamin B12 is detach from R- factor by pancreatic proteases. | |||
* Now free B12 binds to intrinsic factor which is secreted by gastric parietal cell. | |||
* The intrinsic factor - B12 complex is absorbed in the ileum. | |||
* Absorbed vitamin B12 is use in metabolic pathways which is important for neurologic and hematologic function if vitamin B12 is deficit regardless of the cause many impairments may occur . | |||
* Vitamin B12 is a cofactor for the enzyme methionine synthase which convert homocysteine to methionine as a result methyl- THF is converted to THF which is use in synthesis of pyrimidine base of DNA. | |||
* In B 12 deficiency homocysteine accumulate which cause megaloblastic anemia and hypersegmented neutrophils. | |||
* Vitamin B 12 is a cofactor for enzyme methylmalonyl-COA mutase , which converts methylmalonic-COA to succinyl-COA. In B 12 deficiency methylmalonic acid (MMA ) will accumulate. MMA and elevated level of homocysteine cause damage of myelin as a result subacute combined degeneration of spinal cord ( SCDSC ) occur . This affects dorsal columns, lateral corticospinal tracts and spinocerebellar tract as result loss of proprioception , ataxia , peripheral neuropathy and dementia. | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
{{WH}} | |||
{{WS}} | |||
[[Category:Hematology]] | [[Category:Hematology]] | ||
[[Category:Gastroenterology]] | [[Category:Gastroenterology]] | ||
Latest revision as of 00:42, 30 July 2020
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Nabeel Ahmed, M.B.B.S
Overview
Pathophysiology
- Dietary Vitamin B12 binds to salivary R factor then the complex arrives at small intestine.[1]
- In duodenum Vitamin B12 is detach from R- factor by pancreatic proteases.
- Now free B12 binds to intrinsic factor which is secreted by gastric parietal cell.
- The intrinsic factor - B12 complex is absorbed in the ileum.
- Absorbed vitamin B12 is use in metabolic pathways which is important for neurologic and hematologic function if vitamin B12 is deficit regardless of the cause many impairments may occur .
- Vitamin B12 is a cofactor for the enzyme methionine synthase which convert homocysteine to methionine as a result methyl- THF is converted to THF which is use in synthesis of pyrimidine base of DNA.
- In B 12 deficiency homocysteine accumulate which cause megaloblastic anemia and hypersegmented neutrophils.
- Vitamin B 12 is a cofactor for enzyme methylmalonyl-COA mutase , which converts methylmalonic-COA to succinyl-COA. In B 12 deficiency methylmalonic acid (MMA ) will accumulate. MMA and elevated level of homocysteine cause damage of myelin as a result subacute combined degeneration of spinal cord ( SCDSC ) occur . This affects dorsal columns, lateral corticospinal tracts and spinocerebellar tract as result loss of proprioception , ataxia , peripheral neuropathy and dementia.