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Vitamins
Shahd AlAli
Water soluble vitamins Fat soluble vitamins
Absorbed directly from the gut to
the bloodstream
Dissolved in dietary fats to
lymphatic system and then
bloodstream and bind to protein
carrier
Less likely to be toxic = excreted
in urine
Stored in adipose tissues *can be
toxic
Vitamin B, Biotin, Folic acid,
Vitamin C
K A D E
Organic component required as cofactor or anabolism or catabolism
Vitamin B1 Thiamine
 Fount in grains, meats
 It’s a coenzyme for CHO metabolism
 The active form is thiamine pyrophosphate TPP (ATP transfer to thiamine)
TTP is used as a coenzyme for
 Transketolation reactions in PPP )
 Conversion of pyruvate to acetyl-CoA (PDH)
Thaimine deficiney is most commonly caused due to chronic alcoholism
What if thiamine levels were low?
1. Decrease the amounts of acetyl-CoA to enter TCA cycle and increase amounts of
pyruvate available for anaerobic oxidation so more lactic acid
Paresthesias
Beriberi (wet/dry)
 Wet: involves the cardiovascular system & neuropathy
 Dry beriberi: affect both peripheral nerves (motor and sensory neuropathies)
 Wernicke-Korsakoff syndrome occurs in chronic alcoholics with B1 deficiency triad
 Wernicke’s encephalopathy:
1. Ophthalmoplegia
2. Truncal ataxia
3. Confusion
Untreated encephalopathy progress to Korsakoff’s syndrome impaired short memory
Vitamin B6- Pyridoxine
 A pyridine derivative
 Found in wheat, egg yolk and meats
 Its responsible for the conversion transamination, deamination and creating the
enzymes of liver AST and ALT
 Deficiency of vitamin B6 can result in convulsion and hyperirritability
 Decreased concentration of vitamin B6 may occur after the used of
Oral contraceptives, isoniazid, penicillamine
Vitamin B6 excess causes sensory neuropathy
Vitamin B12- Cobalamin
 Animal products are the only source of vitamin B12
 Can be stored in the body for up to 3 years
 Required IF for absorption in the distal 3rd of ileum
 Vitamin B12 dependent enzymes
Methionine synthase , Methylmalonyl-CoA mutase (TCA)
Causes of deficiency:
 pernicious anemia
 Gastroectomy
 Infections H.pylori
 Pancreatic insufficiency
 Folate circulates as methyl-THF removal of methyl group allows
the participation in synthesis of DNA precursors
1. Methyl group is transferred to vitamin B12
2. Vitamin B12 then transfer it to homocysteine > methionine
Increased serum homocysteine (increased risk of thrombosis)
Vitamin B12 is a cofactor for the conversion of methylmalonic
acid to succinyl CoA (imp for FA metabolism)
Deficiency of vitamin B12 results in increased levels of
methylmalonic acid which impairs spinal cord myelination.
Methylmalonyl
-CoA mutase
Methionine synthase
Clinical Signs of Vitamin B12 deficiency
 Neuropathy charactirized by defective myelin formation and subacute
degeneration of dorsal and lateral spinal columns. Poor proprioception and
vibratory sensation (posterior column) and spastic paresis (lateral)
Vitamin A
 i. Retinoids of animal origin
 ii. Carotenoids, found in plants
 Vit. A deficiency cause: blindness, increased susceptibility to
infectious diseases
 Vit. A excess causes: tissue damage, toxicity of CNS (headache,
nausea, ataxia, and anorexia, increased CSF pressure), also affects
the liver, bones and skin
Summary
Vitamin Deficiency Excess
Vitamin B1 Wet beriberi : cardiovascular
Dry beriberi:
Wernicke’s encaphylopathy
1. Ophthalmoplegia
2. Truncal ataxia
3. Confusion
Korsakoff’s syndrome:
impaired short memory
-
Vitamin B6 Convulsion and
hyperirritability
Sensory neuropathy
Vitamin B12 Subacute combined
degeneration of spinal cord
(poor proprioception and
vibratory sensation)
-
Vitamin A Blindness tissue damage, toxicity of CNS
(headache, nausea, ataxia, and
anorexia, increased CSF pressure

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Vitamins and Neuropathy

  • 2. Water soluble vitamins Fat soluble vitamins Absorbed directly from the gut to the bloodstream Dissolved in dietary fats to lymphatic system and then bloodstream and bind to protein carrier Less likely to be toxic = excreted in urine Stored in adipose tissues *can be toxic Vitamin B, Biotin, Folic acid, Vitamin C K A D E Organic component required as cofactor or anabolism or catabolism
  • 3. Vitamin B1 Thiamine  Fount in grains, meats  It’s a coenzyme for CHO metabolism  The active form is thiamine pyrophosphate TPP (ATP transfer to thiamine) TTP is used as a coenzyme for  Transketolation reactions in PPP )  Conversion of pyruvate to acetyl-CoA (PDH) Thaimine deficiney is most commonly caused due to chronic alcoholism What if thiamine levels were low? 1. Decrease the amounts of acetyl-CoA to enter TCA cycle and increase amounts of pyruvate available for anaerobic oxidation so more lactic acid Paresthesias
  • 4. Beriberi (wet/dry)  Wet: involves the cardiovascular system & neuropathy  Dry beriberi: affect both peripheral nerves (motor and sensory neuropathies)  Wernicke-Korsakoff syndrome occurs in chronic alcoholics with B1 deficiency triad  Wernicke’s encephalopathy: 1. Ophthalmoplegia 2. Truncal ataxia 3. Confusion Untreated encephalopathy progress to Korsakoff’s syndrome impaired short memory
  • 5. Vitamin B6- Pyridoxine  A pyridine derivative  Found in wheat, egg yolk and meats  Its responsible for the conversion transamination, deamination and creating the enzymes of liver AST and ALT  Deficiency of vitamin B6 can result in convulsion and hyperirritability  Decreased concentration of vitamin B6 may occur after the used of Oral contraceptives, isoniazid, penicillamine Vitamin B6 excess causes sensory neuropathy
  • 6. Vitamin B12- Cobalamin  Animal products are the only source of vitamin B12  Can be stored in the body for up to 3 years  Required IF for absorption in the distal 3rd of ileum  Vitamin B12 dependent enzymes Methionine synthase , Methylmalonyl-CoA mutase (TCA) Causes of deficiency:  pernicious anemia  Gastroectomy  Infections H.pylori  Pancreatic insufficiency
  • 7.  Folate circulates as methyl-THF removal of methyl group allows the participation in synthesis of DNA precursors 1. Methyl group is transferred to vitamin B12 2. Vitamin B12 then transfer it to homocysteine > methionine Increased serum homocysteine (increased risk of thrombosis) Vitamin B12 is a cofactor for the conversion of methylmalonic acid to succinyl CoA (imp for FA metabolism) Deficiency of vitamin B12 results in increased levels of methylmalonic acid which impairs spinal cord myelination. Methylmalonyl -CoA mutase Methionine synthase
  • 8. Clinical Signs of Vitamin B12 deficiency  Neuropathy charactirized by defective myelin formation and subacute degeneration of dorsal and lateral spinal columns. Poor proprioception and vibratory sensation (posterior column) and spastic paresis (lateral)
  • 9. Vitamin A  i. Retinoids of animal origin  ii. Carotenoids, found in plants  Vit. A deficiency cause: blindness, increased susceptibility to infectious diseases  Vit. A excess causes: tissue damage, toxicity of CNS (headache, nausea, ataxia, and anorexia, increased CSF pressure), also affects the liver, bones and skin
  • 10. Summary Vitamin Deficiency Excess Vitamin B1 Wet beriberi : cardiovascular Dry beriberi: Wernicke’s encaphylopathy 1. Ophthalmoplegia 2. Truncal ataxia 3. Confusion Korsakoff’s syndrome: impaired short memory - Vitamin B6 Convulsion and hyperirritability Sensory neuropathy Vitamin B12 Subacute combined degeneration of spinal cord (poor proprioception and vibratory sensation) - Vitamin A Blindness tissue damage, toxicity of CNS (headache, nausea, ataxia, and anorexia, increased CSF pressure

Editor's Notes

  1. Proximal tubule compete with lactic acid wins and beta-hydroxydase and uric acid buits up