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Digestion And Metabolism > Water Soluble Vitamins > Flashcards

Water Soluble Vitamins Flashcards

1
Q

What are vitamins?

A
  • Organic compounds that cannot be synthesized by humans and must be supplied by diet
  • Required for functions like co-enzymes or as hormones
  • Thirteen vitamins
  • Classified based on solubilit
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2
Q

What are fat soluble vitamins?

A

• Absorption depends on normal fat digestion and absorption
• Maldigestion and malabsorption of dietary fats results in secondary
deficiency (bile duct obstruction, cystic fibrosis).
• Stored in liver (Vitamin K stored in least amounts)

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3
Q

What are the functions of fat soluble vitamins?

A

Vitamin A : Vision, epithelial tissue, growth
Vitamin D : Bone mineralization, blood calcium regulation
Vitamin E : Lipid soluble anti-oxidant
Vitamin K : Clotting factor synthesis; Coenzyme

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4
Q

What are the consequences of primary deficiency?

A

Primary deficiency
• Dietary deficiency
• Starvation
• Malnutrition

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5
Q

Explain secondary vitamin deficiency

A

Secondary deficiency
• Reduced intake
• Dental problems, chronic disease, morning sickness

  • Malabsorption
    • Diarrhea, genetic defects
    • Post-bariatric surgery
  • Increased requirements
    • Pregnancy, post-operative, periods of rapid growth
  • Increased loss
    • Lactation
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6
Q

Whaat are the characteristics of water soluble vitamins?

A
  • Daily supplements (not stored, except vitamin B12)
  • Do not require bile salts and chylomicrons for absorption (Absorption easier than fat soluble vitamins)
  • Toxicity not common (excess excreted in urine)
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7
Q

What is the significance of ascorbic acid (vitamin C)?

A

• Water soluble vitamin
• Connective tissue (collagen synthesis) and wound healing
– Prolyl and lysyl hydroxylase coenzyme – Hydrogen bond formation →
Collagen stability

• Absorption of iron
– Ferrous state
– Low dietary vitamin C → Microcytic anemia (reduced iron absorption) • Water soluble anti-oxidant: Free radical scavenger

– Antioxidant vitamins C, E and beta-carotene (provitamin A)
• Reduce chronic disease

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8
Q

What is scurvy?

A
  • Perifollicular hemorrhages (Fragile blood vessels)
  • Sore, spongy gums: Bleeding gums
  • Loose teeth
  • Bleeding into joints
  • Frequent bruising
  • Impaired/ delayed wound healing

Connective tissue defects (decreased hydroxyl groups): fewer H-bonds in collagen

Similar to vitamin K deficiency – Molecular mechanism for increased bleeding tendency is very different!!!!

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9
Q

What is the earliest sign of scurvy?

A

Perifollicular hemorrhages

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10
Q

What are the parts of the vitamin B complex?

A
  • Thiamine (B1)
  • Riboflavin (B2)
  • Niacin (B3)
  • Pantothenic acid (Coenzyme A) (B5)
  • Pyridoxine (B6)
  • Biotin (B7)
  • Folic acid (B9)
  • Cobalamin (B12)

Water soluble vitamins NOT stored – daily supplements essential (Vitamin B12 stored in liver)

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11
Q

What is the coenzyme of vitamin B1? What is the function?

A

• Coenzyme: TPP (Thiamine pyrophosphate)

• Coenzyme
– Oxidative decarboxylation of alpha-keto acids – maintains nerve
tissue (PDH complex, α-ketoglutarate dehydrogenase, branched chain
α-keto acid dehydrogenase)
– Transketolase in pentose phosphate pathway (HMP shunt)
– B1 supplementation Maple syrup urine disease (MSUD)***

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12
Q

What are the dietary sources of vitamin B1/thiamine?

A

• Dietary Sources:
– Widely available in diet BUT
– Deficient in Refined foods like polished rice, white flour, white sugar

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13
Q

What reactions require TPP?

A

Branched chain amino acid —>Branched chain keto acid

MSUD —>
Branched chain keto acid dehydrogenase
TPP
Branched chain metabolites

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14
Q

What are the consequences of thiamine deficiency?

A

Beriberi

• Polished rice is staple
• Affects aerobic tissues (Brain and cardiac muscle)
• Polyneuropathy: Disruption of motor, sensory and reflex
arcs; progress to paralysis (Dry beri beri)
• Cardiovascular:Cardiacfailure(Wetberiberi)
• Laboratorytests
– Low erythrocyte transketolase activity
– Serum thiamine levels

Pedal edema in wet beriberi

Wernicke-Korsakoff syndrome

Wernicke - Korsakoff syndrome:
• Devastating neurologic complication in chronic alcoholics
• Ophthalmoplegia and nystagmus (to and fro eyeball movement)
• Ataxia, confusion, disorientation and loss of memory
• Confabulation

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15
Q

What are the coenzyme forms of vitamin B2?

A

Riboflavin

• Coenzyme forms
– Flavin mononucleotide (FMN)
– Flavin adenine dinucleotide (FAD)
• Oxidation-reduction reactions of TCA cycle, beta oxidation (Succinate dehydrogenase, PDH, Acyl CoA DH…..)

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16
Q

Describe riboflavin deficiency (vitamin B2)

A

• Nutritional
Signs and symptoms

  • Cheilosis – areas of pallor, cracks and fissures at angles of mouth
  • Glossitis – inflammation and atrophy of tongue
  • Facial dermatitis
17
Q

What are the coenzyme forms of vitamin B3 (niacin)?

A

• Coenzyme forms
– NAD+
– NADP+

VITAMIN B3 (NIACIN)
• Coenzymes in oxidation-reduction reactions
– NAD+ – Dehydrogenases (PDH, alpha-ketoglutarate dehydrogenase, malate
dehydrogenase, …..)
– NADP+ – HMP shunt and fatty acid and cholesterol synthesis (G6PD, HMG
CoA reductase, …)

• Therapeutic uses:
– Inhibits adipose tissue lipolysis and reduces free fatty acids: Type IIb
hyperlipoproteinemi

18
Q

Describe niacin deficiency

A

Pellagra (rough skin): 3Ds
• Dermatitis (skin)
– Exposed areas of body
– Redness, thickening and roughening of skin

• Diarrhea (GIT)

• Dementia (CNS)
– Neuron degeneration in brain and spinal tracts
– Loss of memory

• Death

19
Q

Describe pellagra dermatitis

A

‘Necklace like’ and hands and legs

20
Q

Describe the significance of tryptophan as a precursor of NAD+

A

• Tryptophan forms NAD+ and NADP+ (refer amino acid metabolism)

• Risk factors for Niacin deficiency (Pellagra)
– Corn based diets (Niacin and tryptophan deficient)
– Hartnup disease (Neutral amino acid transporter defect)* -
Dietary niacin supplements
– Carcinoid syndrome* (excessive tryptophan to serotonin
conversion; less tryptophan for NAD formation)

21
Q

What is the significance of biotin?

A
  • Carboxylation reactions
  • Multiple carboxylase deficiency***: Defect in incorporating biotin
  • Coenzyme for:
    • Pyruvate carboxylase (gluconeogenesis) – Impaired gluconeogenesis
    • Acetyl-CoA carboxylase (fatty acid synthesis) – Hair loss and dermatitis
    • Propionyl-CoA carboxylase (Conversion of propionyl CoA to methylmalonyl

CoA) – High serum propionate levels
• Avidin (raw egg white), inhibits biotin absorption

22
Q

Discuss isoniazid therapy as a risk of pyridoxine deficiency

A

• Isoniazid (anti-tuberculosis drug)

– Inactivates pyridoxine

– Pyridoxine supplements given with INH

– Peripheral neuropathy: Adverse effect if B6 supplements not administered

23
Q

What are the manifestations of pyridoxine deficiency?

A
  • Microcytic anemia (Reduced heme synthesis due to low ALA synthase activity)
  • Peripheral neuropathy (Reduced neurotransmitter formation)

• Increased cardiovascular disease risk (high plasma homocysteine
levels)

• Seizures in infants (Reduced neurotransmitter formation)

24
Q

Explain the two reactions of vitamin B12 is used for

A
  1. Methionine synthase
    – Converts methyl tetrahydrofolate to tetrahydrofolate: Required for DNA synthesis
    – In B12 deficiency, methyltetrahydrofolate trap (folate trap): Macrocytic anemia
  2. Methylmalonyl CoA mutase
    • Amino acids and odd-chain fatty acid metabolism forms propionyl CoA
    • Elevated serum methylmalonate
    • Methylmalonate results in neurological
    manifestations: Interferes with myelin formation • Vit B12 supplements in inherited methylmalonic
    aciduria**
25
Q

Describe the ansorption of vitamin B12

A
  • Animal products; Vegans risk of deficiency
  • Intrinsic factor (IF) by gastric parietal cells for Vit B12 absorption; Achlorhydria (risk factor)
  • Parietal cell destruction due to autoantibodies - Lack of IF – Poor B12 absorption - Pernicious anemia
  • IF-B12 complex absorbed in terminal ileum
26
Q

What are the risk factors of vitamin B12 deficiency?

A

– Lack of intrinsic factor (IF): Pernicious anemia, After Bariatric surgery

– Ileal mucosal disease

26
Q

What are the risk factors of vitamin B12 deficiency?

A

– Lack of intrinsic factor (IF): Pernicious anemia, After Bariatric surgery

– Ileal mucosal disease

27
Q

What are the clinical features of deficiency of vitamin B12?

A

Clinical features:
• Macrocytic megaloblastic anemia
– Macrocytes in peripheral blood film
– Megaloblasts in bone marrow (megaloblastic anemia) – Secondary to folate deficiency (folate trap)

• Neuropsychiatric symptoms
– Tingling and numbness in extremities; Psychiatric manifestations
– Myelin degeneration in motor and sensory pathways due to
methylmalonate

28
Q

What is the significance of folic acid?

A

• FH4 receives 1-carbon groups from amino acids
• Uses 1-C groups for purine and pyrimidine synthesis (thymidylate
synthesis) (DNA synthesis)
• Methyl THF → THF requires Vitamin B12 (Methionine synthase

29
Q

What are the symptoms of folic acid deficiency?

A
  • Dietary lack of green leafy vegetables
  • Impaired absorption (Intestinal mucosal disease)
  • Increased requirement as in pregnancy
  • Folate antagonists: Methotrexate (inhibitor of dihydrofolate reductase)
  • Folate trapping due to B12 deficiency
• Macrocytic megaloblastic anemia
• Macrocytes in peripheral blood smear
• Megaloblasts in bone marrow
• NO neurological features
– Methylmalonate levels are normal
30
Q

Compare maacrocytic anemias in vitamin B12 and folate deficiency

A

Vitamin B12 deficiency
• Clinical features: Anemia with associated neurological features
• Anemia – Macrocytic (MCV increased) and megaloblastic bone marrow
• Serum homocysteine and serum methylmalonate levels are elevated
• Anemia is due to folate trap
• Neurological features due to accumulation
of methylmalonate (affects myelination)
• Risk factors: Parietal cell destruction (pernicious anemia); ileal mucosal disease or resection; vegan diet
• Serum vitamin B12 levels are low

Folate deficiency
• Clinical features: Macrocytic anemia
• Anemia – Macrocytic (MCV increased)
and megaloblastic bone marrow
• Serum homocysteine levels are elevated; Serum methylmalonate levels are normal
• Anemia is due to folate deficiency
• NO neurological features
• Risk factors: pregnancy, malabsorption syndrome, folate antagonist treatment
• Serum folate levels are low
31
Q

How is megaloblastic anemia treated?

A

Treatment of megaloblastic anemia:
Combination of folic acid and cobalamin

Refer: Vit B12 and folic acid lecture for differences between Folic acid and vit B12 deficiency

32
Q

What is the significance of folic acid during pregnancy?

A
  • Folate requirement increases during pregnancy
  • Rapidly dividing fetal cells vulnerable to folate deficiency
  • High incidence of fetal neural tube defects (Spina bifida and anencephaly)
  • Supplements at time of conception and during first trimester

Digestion And Metabolism (57 decks)

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