Vitamins and Minerals Flashcards

1
Q

Vitamin A

A

Retinoids

  • 11-cis retinal required for vision
  • Retinoic Acid required for mucus secreting cells (specialized epithelium), and growth
  • Retinol required for reproduction

Transported in blood via retinol binding protein (Alpha 1 plasma protein)

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2
Q

Mechanism of action of Retinol in vision

A
  1. Retinol transported in to retinal pigment cell
  2. Retinol converted to 11-cis retinal and enters photoreceptor (rod) cell
  3. 11-cis retinal combines with Opsin to form Rhodopsin
  4. Absorption of photon catalyzes isomerization of 11-cis retinal to all-trans-retinol leading to an electrical signal
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3
Q

Mechanism of action of Retinoic acid in epithelial cells

A

Retinol enters epithelial cells and is oxidized to Retinoic Acid

Retinoic Acid moved from cytosol to nucleus and binds with receptor

Retinoic acid-receptor complex binds to chromatin activating the transcription of specific genes (keratin)

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4
Q

Vitamin A Deficiency

A

Due to deficiency in diet or malabsorption

Causes:

  • Night blindness
  • Xeropthalmia- dryness of conjunctiva and cornea
  • Bitot’s Spots - build up of keratin in the conjuntiva
  • Keratomalacia - corneal erosion and ulceration
  • Increased pulmonary infections- epithelium not maintained
  • Immune Deficiency
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5
Q

Vitamin A Toxicity

A
  • Hypervitaminosis A –raised intracranial pressure –headaches –may mimic brain tumors
  • Dry and pruritic skin
  • Enlarged liver
  • Pregnancy –spontaneous abortions and congenital malformations in the fetus.
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6
Q

7-dehydrocholesterol

A

Intermediate in cholesterol synthesis

Forms Cholecalciferol (D3) in the skin

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7
Q

1,25-dihydroxycholecalciferol

A

Active form of Vitamin D. formed by two rounds of hydroxylation of vitamin D precursors

Round 1 in Liver
Round 2 in Kidney

Has a similar method of action as that of Vitamin A

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8
Q

Vitamin D Deficiency

A

Due to malabsorption, inadequate sunlight, chronic liver or renal disease

Causes:

  • Rickets in children
  • Overgrowth of costochondral junction - rachitic rosary
  • Pigeon chest
  • Osteomalacia in adults
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9
Q

Alpha tocopherol

A

Most active form of Vitamin E

Most important role is as an antioxidant

Deficiency:

  • Hemolytic Anemia- abnormal cell membranes
  • Reduced deep tendon reflexs and gait problems due to axonal degradation
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10
Q

Vitamin K

A

Cofactor in gamma-carboxylase in formation of clotting factors II, VII, IX, X as well as protein C and S

In humans it is synthesized by bacterial flora or obtained in the diet.

–Phylloquinone(plants) –dietary source
–Menaquinone(bacteria) -intestine

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11
Q

Vitamin K Deficiency

A

Neonates:
Hemorrhagic Disease - Bleeding at various sites of the body

Adults:
Hematuria
Melena - black tarry stools
Eccymoses - bruises
Bleeding from the gums
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12
Q

Vitamin C

A

Ascorbic Acid

Required for maintenance of normal connective tissue (collagen synthesis (Pro hydroxylation)) and wound healing

Required for the absorption of Iron - reduces Iron in the stomach

Antioxidant

Deficiency causes scurvy

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13
Q

Thiamine

A

Vitamin B1

Required Cofactor for:

  • pyruvate dehydrogenase (pyruvate to Acetyl CoA)
  • Alpha-ketoglutarate dehydrogenase (TCA Cycle)
  • Branched chain Alpha-ketoacid dehydrogenase (metabolism of BCAA)
  • Acts as a coenzyme for transketolase in the pentose phosphate shunt
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14
Q

TTP Deficieny

A

Dry BeriBeri: polyneuropathy that can lead to paralysis

Wet BeriBeri: Cardiac failure

Wernicke-Korsakoff Syndrome:
Associated with chronic alcoholism
•Ophthalmoplegiaand nystagmus(to and fro movement of eyeballs)
•Ataxia, confusion, disorientation and loss of memory
•Confabulation

(Diagnosis –increase in erythrocyte transketolaseactivity on addition of TPP)

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15
Q

Riboflavin

A

VItamin B2

Coenzyme forms: FAD/FADH2 and FMN

Participates in oxidation –reduction reactions of TCA cycle, beta oxidation (Succinate dehydrogenase, PDH, Acyl CoA DH…..)

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16
Q

FAD Deficiency

A

Nutritional deficiency

Signs and symptoms
•Cheilosis–areas of pallor, cracks and fissures at the angles of the mouth
•Glossitis–inflammation and atrophy of the tongue
•Facial dermatitis

17
Q

Niacin

A

Vitamin B3

Act as coenzymes in oxidation-reduction reactions
–NAD+ –Dehydrogenases
–NADP+ –Reactions in the HMP shunt and fatty acid synthesis

Therapeutic uses:
–Niacin inhibits lipolysis in the adipose tissue and greatly reduces production of free fatty acids –treatment of type IIb hyperlipoproteinemia

Tryptophan can be used to synthesize NAD+ and NADP+

18
Q

Vitamin B3 Deficiency

A

Pallagra

Characterized by dermatitis, dementia, Diarrhea, and can lead to death

Patients with Hartnup’sdisease can have pellagra-like symptoms*** -Need supplementation of dietary niacin

•Patients with carcinoid syndrome may also have pellagra

19
Q

Biotin

A

Vitamin B7

Prosthetic group for most carboxylation reactions

  • Pyruvate carboxylase
  • Acetyl-CoA carboxylase (FA Synthesis)
  • Propionyl-CoA carboxylase (Odd chain FA oxidation)
20
Q

Pyridoxine

A

Vitamin B6

Precursor for pyridoxyl phosphate (PLP) which is a coenzyme for:
–Transamination (amino acid metabolism)
–Amino acid decarboxylation (synthesis of neurotransmitters)
–Condensation (ALA synthase in heme synthesis)
–Conversion of homocysteine to cysteine

21
Q

Vitamin B6 Deficiency

A

Caused by Izoniazide administration for TB

Signs and symptoms:
•Microcytic anemia (ALA synthase in Heme)
•Peripheral neuropathy (reduced neurotransmitters)
•Increased risk of cardiovascular disease (high levels of plasma homocysteine)
•Seizures may occur

22
Q

Cobalamin

A

Vitamin B12

Intrinsic Factor required for absorption

  • Synthesis of Met from homocysteine.
  • Converts methyl tetrahydrofolate to tetrahydrofolate (THF) required for DNA synthesis
  • Conversion of FA, BCAA and Met to Succynyl CoA (a methylmalonyl CoA mutase cofactor)
23
Q

Vitamin B12 Deficiency

A

Macrocytic anemia - trapped THF in methyl form (

Neurological manifestations - accumulation of methylmalonate in the body. (Methylmalonyl aciduria)

Pernicious anemia - Lack of Intrinsic Factor for Vitamin B12 absorption from animal foods

24
Q

Folic Acid

A

Vitamin B9

Active form is Tetrahydrofolate (THF) produced by dihydrofolate reductase (requires 2 NADPH)

  • Key role in one carbon metabolism
    THF receives one-carbon fragments from donors and transfers them to intermediates in purine and pyrimidine synthesis
  • Synthesis of Met to homocystine
  • Degradation of Histidine (FlGlu to glutamate)
  • Conversion of Serine to Glycine
25
Q

Vitamin B9 Deficiency

A

Folate dediciency due to lack of dietary intake (fruits and veg), impaired absorption &/or reabsorption, Methotrexate administration, trapping due to Vit B12 deficiency

  • Megaloblastic anemia
  • inability for cells to synthesize DNA due to lack of purines and pyrimidines
  • Homocystinuria

High FlGlu in urine used as a test for folate deficiency

(Never treat with Folic acid alone!! always pair with Vit B12 till definite cause is established)

Most common vitamin deficiency

26
Q

Copper Reactions

A

Cytochrome C - Part of complex IV of the Electron transport chain

Superoxide Dismutase

Lysyl and prolyl Oxidase - Synthesis of Collagen

Tyrosinase - Sythesis of Melanin

Dopamine Beta-hydroxylase - Neurotransmitter synthesis

Ceruloplasm formation in the liver

27
Q

Copper Deficiency

A

Microcytic Anemia - Ceruloplasm needed for Iron metabolism in Heme formation

Vascular tissue degradation/aneurysm formation due to decreased lysyl and Pro oxidase activity

Menke’s syndrome

28
Q

Menke’s Syndrome

A

Inherited defect in absorption of copper from the GI tract.

Hair is twisty, grayish and “kinky”

•Copper deficiency can lead to aneurysms and cerebral dysfunction

X-linked

29
Q

Wilson’s Disease

A

Accumulation of toxic levels of copper in vital organs including liver, brain and eye

Defect is found in the copper transporting ATPase in the liver needed to attach copper to ceruloplasmin and also to excrete copper into the bile

30
Q

Iron

A

Required for Heme synthesis and in redox reations

Heme from meat better absorbed. Veg need to be transferred to Ferric Iron (Fe+++) by low pH and vit C for absorption

Ceruloplasmin (ferroxidase) participates in the release of ferrous iron (Fe++) from intestinal cells and forms ferric iron which is needed for transport in the blood

31
Q

Iron Deficency

A

Hypochromic microcytc anemia

Chronic bleeding

Fatigue
brittle nails
Pica (appetite for dirt)

32
Q

Hereditary Hemochromatosis

A

Excessive absorption of Iron

Autosomal recessive

Excess iron damages tissues by:
•Lipid peroxidationthrough free radicals
•DNA damage

Clinical Features:
•More common in males; presenting age 40
•Liver damage –cirrhosis; hepatocellular carcinoma
•Diabetes –destruction of pancreas
•Cardiac dysfunction
•Acute synovitis
•Brownish skin pigmentation (Bronze color of skin)

33
Q

Nutritional Anemias

A
MICROCYTIC - reduced synthesis of heme
Seen in Deficiency of:
Iron
Copper
Vit B6 (PLP) - ALA synthase cofactor

MACROCYTIC - reduced cell division
Seen in Deficiency of Vitamin B12 and Folic Acid

34
Q

Zinc

A

wound healling

35
Q

Cystein

A

An AA formed from homocystein. requires Vit B6.

  • Forms Taurine via cystein deoxygenase
  • A precursor of PAPS for sulfination reactions.
36
Q

Methotrexate

A

Competitively inhibits Dihydrofolate Reductase in THF synthesis from folate

Used to treat psoriasis, arthritis and neoplastic diseases.

Sulfonamides do the same in microorganisms. (block dihydropterate synthetase)