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Nutrition and Drug Monitoring > Vitamin and Trace Elements > Flashcards

Vitamin and Trace Elements Flashcards

1
Q

What are vitamins?

A
  • Vitamin is general term for a number of unrelated organic substances that occur in food and are required in trace amounts (μg to mg quantities per day)
  • Essential micronutrients with diverse biochemical functions which cannot be synthesised in the organism, or are not made in sufficient quantity
  • Humans require 13 vitamins: 4 fat soluble (A, D, E, K) and 9 water soluble (C and 8 B vitamins)
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2
Q

What are examples of Nutritional Deficiency?

A
  • Deficiency of vitamins and trace elements relatively uncommon in developed world
  • Worldwide vitamin A, iodine and iron deficiencies are a major health problem
  • Deficiency may be due to poor diet e.g. alcoholism, malabsorption, Inborn error of metabolism, food fads
  • When deficient or inadequately absorbed, characteristic clinical disorders arise
  • For most micronutrients, a recommended dietary allowance (RDA) has been agreed
  • Where evidence is lacking, an adequate intake (AI), based on observation, is use
  • Micronutrients generally function as gene activators, free-radical scavengers, or coenzymes or cofactors in metabolic reactions
  • Excessive intakes of micronutrients can result in toxicity
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3
Q

How are Vitamin Absorbed?

A

Water-Soluble Vitamins (Vitamin B and C)

  • Enter the villi from lumen of intestine via simple diffusion
  • Travel through the body via blood vessels

Fat-Soluble Vitamins (Vitamins A, D, E, K)

  • Solubilised by Micelles. Move from lumen to intestine through epithelial cells together with long fatty acids and monoglycerides via simple diffusion
  • Store in body for long period of times which known as lipocytes
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4
Q

What are forms of Vitamin A?

A
  • Alcohols (retinols)
  • Aldehydes (retinals)
  • Retinoic acid
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5
Q

How do Retinols get formed and how is it used?

A
  • The body can convert β-carotene and other carotenoids to retinol
  • Retinol is the principal circulating form
  • Retinoic acid binds to retinoic acid receptors (RAR) and to retinoid X receptors (RXR)
  • RAR/RXR heterodimers function as ligand-dependent transcription factors and account for many of the pleiotrophic effects of retinoids
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6
Q

How is Vitamin A stored?

A
  • Stored in liver, requires transport proteins to be mobilised. Plasma vitamin A does not fall until hepatic stores are severely depleted
  • Adequate vitamin A does not necessarily reflect adequate liver stores
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7
Q

How is Vitamin A transported in the body?

A
  • Bound to retinol binding protein (RBP) and pre-albumin. RBP is a negative acute phase reactant so may result in apparent low vitamin A
  • Evidence vitamin A can decrease by as much as 50%
  • Renal failure may increase RBP and therefore vitamin A
  • Zinc is required for RBP synthesis
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8
Q

What are sources of Vitamin A?

A
  • Spinach
  • Tomato
  • Potation
  • Carrots
  • Eggs
  • Dairy
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9
Q

What are functions of Vitamin A?

A
  • Vision: 11-cis-retinal binds to opsin to form rhodopsin, the visual pigment in rod cells in the retina
  • Reproduction: Spermatogenesis in male
  • Growth: Required for bone growth to keep pace with CNS growth
  • Differentiation: Normal differentiation of epithelial cells
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10
Q

What results from Vitamin A deficiency?

A

Deficiency – concentrations of less than 0.5 μmol/L causes

  • Night blindness
  • Xerophthalmia (Xerophthalmia is a medical condition in which the eye fails to produce tears)
  • Blindness

Rare in affluent countries due to liver stores. May be leading cause of preventable blindeness in children. Plasma levels may not be indicative of total body deficiency. May not decrease until liver depleted

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11
Q

What are the worries with excess viramin A?

A
  • Hypervitaminosis A
  • Acute (short term) toxicity may lead to nausea, vomiting, severe headaches, dizziness, fatigue, irritability, dry skin and cerebral oedema
  • Chronic (long term) toxicity from moderately high doses may lead to dry skin, joint and bone pain, dry lips, anorexia, psychiatric changes and cerebral oedema
  • Severe toxicity can lead to eye and liver damage
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12
Q

What should be done with Vitamin A during pregnancy?

A

Limit Vitamin A when pregnant as it is a teratogen

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13
Q

What is Carotinaemia?

A
  • Reversible yellowing of skin
  • Does not cause toxicity as its metabolic conversion is regulated by vitamin A status
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14
Q

How is Vitamin A investigated?

A
  • Assessed by measuring serum/plasma retinol
  • HPLC with UV, electrochemical or mass spectrometry detection
  • Reference method: Gas chromatography-isotope dilution mass spectrometry
  • Protect sample from light to prevent false increase in concentration
  • Retinol binding protein and transthyretin may also be measured
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15
Q

What are forms of Vitamin D?

A
  • Vitamins D2 (ergocalciferol)
  • Vitamin D3 (cholecalciferol)
  • Active form is 1,25 (OH)2 Vitamin D which binds to nuclear vitamin D
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16
Q

What are sources of Vitamin D?

A
  • Fish
  • Eggs
  • Milk
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17
Q

What are the functions of Vitamin D?

A

Regulation of Calcium and Phosphate:

  • Increases intestinal absorption of Calcium
  • Resorption and formation of bone, via PTH
  • Reduces renal excretion of Calcium
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18
Q

How does Vitamin D increase the intestinal absoprtion of calcium and phosphate?

A
  • Small intestine absorbs 10-15% dietary calcium in low vitamin D state. Rises to 30-40% with adequate vitamin D
  • Low calcium absorption can lead to increased PTH (surrogate marker)
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19
Q

What are the effects of deficeincy of Vitamin D?

A
  • Rickets in Children
  • Osteomalacia in Adults. Characterised by incomplete mineralisation of the underlying mature organic bone matrix (osteoid)
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20
Q

What are the effects of excess in Vitamin D?

A
  • Early symptoms are GI related: anorexia, diarrhoea, nausea, vomiting
  • Bone pain, headaches, muscle and joint pain, excessive thirst, weakness, nervousness, itching, kidney stones. Hypercalcaemia is responsible for most symptoms seen with vitamin D toxicity

Toxicity defined by institute of medicine as >500 nmol/L 25(OH)vitamin D in the short term.

Long term optimal level of 50 – 100 nmol/L

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21
Q

What are investigations for Vitamin D?

A

Reference method:

  • Isotope dilution liquid chromatography tandem mass spectrometry

Routine methods:

  1. Immunoassay
    • Cheap, quick and automated
    • Must measure total vitamin D (i.e. vitamin D2 and vitamin D3)
  2. Liquid chromatography-mass spectrometry (LCMS)
    • Allows separation of vitamin D2 and D3
    • More expensive and labour intensive
    • Used for 1,25(OH)2 Vitamin D
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22
Q

Which forms of Vitamin D are looked at in the investigations?

A
  • Status is assessed by measuring the major storage forms 25-hydroxyvitamin D3 and D2.
  • Bound to vitamin D binding protein and albumin in plasma. Also, C-3 epimer in infants. Requires extraction step for measurement.
  • 1,25(OH)2 Vitamin D can also be measured but this is rarely required in practice (pmol/L quantities)
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23
Q

What are deatures of Vitamin E?

A
  • 8 compounds - α-tocopherol is the main form
  • ​Liver takes up vitamin E after the various compounds have been absorbed in small intestine
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24
Q

How do Lipids in Serum affect the Vitamin E?

A
  • Vitamin E is bound to low density β-lipoproteins and pre-albumin in plasma.
  • If concentration of lipid in serum rises, vitamin E will move from cell membrane to bind to lipoproteins in serum.
  • May result in an elevated vitamin E and can mask deficiency. May determine vitamin E expressed in relation to lipids
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25
Q

What are functions of Vitamin E?

A
  • Anti-oxidant protecting cells from free radicals
  • Protects unsaturated fatty acids against free radical mediated oxidation
  • Protects cell membranes
  • Involved in immune function
  • May protect against cardiovascular disease
  • Inhibits activity of PKC which is involved in cell proliferation and differentiation in smooth muscle cells, platelets and monocytes
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26
Q

What are 3 groups that could become deficient in Vitamin E?

A
  • Fat malabsorption e.g. Cystic Fibrosis
  • Premature, very low birth weight infants (poor placental transport)
  • Rare congenital disorders of fat metabolism e.g. Abetalipoproteinemia
27
Q

What are signs of Vitamin E deficiency?

A
  • Haemolytic anaemia due to the shortened lifespan of erythrocytes with fragile membranes which not respond to iron therapy
  • Myopathy
  • Retinopathy
  • Ataxia
  • Neuropathy
28
Q

What are consequences of excess in Vitamin E?

A
  • Low toxicity
  • High intakes may impair absorption of other fat-soluble vitamins
  • Can therefore result in vitamin K deficiency and consequently bleeding problems
  • Taking large doses in conjunction with anticoagulant or antiplatelet medication such as warfarin can increase risk of bleeding
29
Q

What are forms of Vitamin K?

A
  • Vitamin K1 (phylloquinone): Synthesized by plants and present in food. Carried in Chylomicrons
  • Vitamin K2 (menaquinone): Synthesized in humans by intestinal bacteria
  • Synthetic vitamin K’s: K3 (menadione) & K4 (menadiol)
30
Q

What are the functions of Vitamin K?

A
  • Promotes blood clotting and is required for the conversion of several clotting factors and prothrombin
  • Necessary for liver synthesis of plasma clotting factors II, VII, IX and X.
31
Q

What happens with Vitamin K deficiency?

A
  • Rare in adults, unless on warfarin. Can also occur with fat malabsorption
  • Haemorrhagic disease of the newborn develops readily. Intestinal flora isn’t become established within the first week of birth
  • Early breast milk is low in vitamin K
32
Q

What are consequences of Vitamin K excess?

A

Vitamin K1 is relatively safe and up to 1mg/day unlikely to result in adverse effects

Synthetic forms, particularly water-soluble Vitamin K3 are more toxic

  • High doses result in oxidative damage, red cell fragility, formation of methaemoglobin
  • In premature infants, this has caused liver problems and brain damage
33
Q

What are investigations for Vitamin K

A
  • Vitamin K concentration is influenced by plasma triglyceride concentration due to association with VLDL
  • May be reported as a ratio. Can be measured directly using HPLC with fluorimetric detection
  • Can be measured indirectly by prothrombin time (INR)
34
Q

What are features of Vitamin C?

A
  • Humans are unable to synthesise vitamin C endogenously
  • There are higher requirements in diets devoid of fresh fruits & vegetables and in smokers, Pregnancy, post-operative patients
  • Circulates bound to albumin
35
Q

What are fucntions of Vitamin C?

A

Collagen Synthesis

  • Cofactor for hydroxylation of proline & lysine residues during synthesis of collagen.
  • Without hydroxylation, collagen cannot form a triple helix and lacks tensile strength.

Antioxidant

  • Regenerates other antioxidants e.g. vitamin E

Iron absorption

  • Facilitates intestinal absorption of dietary non-haem Fe by keeping it in the Fe2+ state
36
Q

What does Vitamin C deficiency cause?

A

Leads to Scurvy

  • Easy bruising and bleeding, teeth and gum disease, hair loss
  • Scurvy is treated with vitamin C supplements. It quickly improves symptoms.
  • Some symptoms, such as joint pain, will usually resolve within 48 hours. Most people will make a full recovery within two weeks.
37
Q

What odes Vitamin C excess lead to?

A
  • Doses >1g/day can cause GI side effects
  • Possible increase in oxalate excretion and increased risk of renal stones
  • Promotes iron overload in patients with thalassemia or hemochromatosis
  • No evidence that increased vitamin C reduces the incidence or duration of colds
38
Q

What is the Rebound effect in Vitamin C excess?

A
  • Prolonged high intakes of vitamin C increases rate of turnover so sudden cessation can result in rebound deficiency.
  • People who take Vitamin C supplements at high doses should be advised not to take them for prolonged periods, and then to reduce the level of intake gradually
39
Q

What are investigations for Vitamin C?

A
  • Can be measured in plasma but unreliable in the acute phase response
  • Affected by recent intake
  • Measured by HPLC with fluorimetric detection
  • Samples very unstable, must be treated with metaphosphoric acid and frozen
40
Q

What are the B vitamins?

A
  • Thiamine (vitamin B1)
  • Riboflavin (vitamin B2)
  • Niacin (vitamin B3)
  • Pantothenic acid (vitamin B5)
  • Vitamin B6
  • Biotin (vitamin B7)
  • Folic acid (vitamin B9)
  • Vitamin B12
41
Q

What are features of Vitamin B1?

A
  • Active form is (TPP).
  • Main circulating form of vitamin B1 is thiamin diphosphate (TDP).
  • It is mainly found in red blood cells (>90%)
  • Coenzyme for small number of enzymes which are critical in the catabolism of amino acids and carbohydrates e.g. Transketolase, Pyruvate dehydrogenase
  • Required for ATP production
42
Q

What are causes of Vitamin B1 deficiency?

A
  • Primary: Found in areas where polished rice or refined carbohydrates is the major part of diet
  • Secondary: Alcoholics (decreased intake), pregnancy, lactation, hyperthyroidism, fever (increased demand)
43
Q

How is Subclinical Thiamine Deficiency detected?

A
  • Subclinical thiamine deficiency can be unmasked in malnourished patients given IV glucose due to increased metabolic requirements for the vitamin.
  • Alcoholic and others at risk must receive IV thiamine 100mg before receiving IV glucose solutions
44
Q

What are the effects of deficiency in Vitamin B1?

A

Beriberi

  • Neuropathy, burning feet, decreased sensation, muscle pain, muscle weakness, epileptic fits
  • Cardiac symptoms (wet beriberi) - heart failure

Wernicke’s encephalopathy & Korsakoff’s Psychosis

  • Cerebral - most sufferers are alcoholics
45
Q

What are investigations for Vitamin B1?

A
  • Can be measured directly from whole blood sample using HPLC with fluorimetric detection
  • Transketolase activation assay as an indirect measurement of status
46
Q

What are the functions of Vitamin B2?

A
  • Usually found as part of FAD (flavine adenine dinucleotide) and FMN (flavine adenine mononucleotide)
  • Involved with many enzymes which catalyse redox reactions. FAD is part of the electron transfer chain
  • Also involved with enzymes which work with cytochrome P450, a system which metabolises many drugs and toxins
47
Q

What are the effets in Vitamin B2 deficiency?

A
  • Rarely seen in isolation
  • Symptoms include sore throat, sore tongue, sore mouth, sore corners of lips
  • Alcoholics are at risk, as are lactose-intolerant people, who avoid dairy products
48
Q

How does vitamin B2 found in plasma and how is it investigated?

A
  • Vitamin B2 is bound to albumin in plasma. Albumin is a negative acute phase reactant so concentrations of Vitamin B2 therefore fall in acute phase
  • Measured in whole blood/packed red cells
  • HPLC with fluorimetric detection
49
Q

What are functions of Vitamin B3?

A
  • Used to make NAD (nicotinamide adenine dinucleotide) and NADP (nicotinamide adenine dinucleotide phosphate)
  • Coenzymes to more than 200 enzymes which are involved in redox reactions
  • In high doses, has been used to treat CVD risk: ↓ Lp(a), ↑ HDL-cholesterol, ↓ triglycerides
50
Q

What odes deficiency of Vitamin B3 cause?

A

Pellagra -3 Ds

  • Diarrhoea
  • Dementia
  • Dermatitis

Tryptophan can be used by the liver to synthesise niacin,

  • Conditions such as Hartnup disease (deficient tryptophan absorption), carcinoid (↑ need for tryptophan to make 5HT) and isoniazid (used to treat TB) can result in pellagra
51
Q

What are functions of Vitamin B5?

A
  • Required to synthesise coenzyme A along with metabolism and synthesis of fats, proteins and glucose
52
Q

What does deficiency of Vitamin B5 lead to?

A
  • Very rare in isolation, but can lead to lack of energy
  • Tingling feet
  • Parasthesia
  • Muscle cramps
53
Q

What are forms for Vitamin B6?

A
  • Main forms are Pyridoxal (PL) and pyridoxal 5’ phosphate (PLP)
  • PLP is the functional form
  • Bound to albumin in plasma and albumin is a negative acute phase reactant so PLP concentrations can therefore fall in acute phase
54
Q

What are functions of Vitamin B6?

A

Co-enzyme in many enzymatic reactions in metabolism:

  • PLP co-factor for amino acid metabolism: transamination, deamination, and decarboxylation
  • Conversion of tryptophan to niacin
  • Release of glucose from glycogen, haem synthesis
  • Synthesis of neurotransmitters e.g. serotonin
55
Q

What are the effects of Vitamin B6 deficiency?

A
  • Pellagra-like syndrome, with seborrheic dermatitis, glossitis, and cheilosis
  • Depression, confusion, EEG abnormalities, and seizures. Seizures, particularly in infants, may be refractory to treatment with anticonvulsants
  • Normocytic, microcytic, or sideroblastic anemia can also develop.
56
Q

What are causes of Vitamin B6 deficiency?

A
  • Inadequate intake (alcoholics)
  • Pyridoxine-inactivating drugs (e.g. anticonvulsants, isoniazid)
  • Isoniazid can induce B6 deficiency by forming an inactive derivative with pyridoxal phosphate
  • B6 supplement is thus an adjunct to isoniazid treatment
57
Q

What are investigations for Vitamin B6 deficeincy?

A

Generally, measure PLP only, but can also measure pyridoxic acid and pyridoxal. This is especially useful in the diagnosis of hypophosphatasia

  • Low levels of Akaline phosphatase
  • Elevated PLP
  • Low plasma PA

Measured in whole blood/red cells by HPLC with fluorimetric detection

58
Q

What is the fucnion of Viamin B7?

A
  • Required for cell growth, fat and amino acid metabolism
  • Cofactor for carbon dioxide transfer in several carboxylase enzymes
59
Q

What leads to Vitamin B7 deficiency?

A
  • Rare as gut flora produce biotin in excess of daily requirements
  • Number of metabolic disorders where problems with biotin use
60
Q

What are functions of Vitamin B9?

A
  • Coenzyme in methylation reactions, DNA synthesis, synthesis of methionine from homocysteine.
  • Higher requirements in pregnancy.
61
Q

What are causes of Vitamin B9 deficiency?

A
  • Malabsorption
  • Use of drugs that interfere with folic acid metabolism (anticonvulsants, methotrexate)
  • Disease states which increase cell turnover (e.g. leukaemia, haemolytic anaemias, psoriasis)
62
Q

What are symptoms of Vitamin B9 deficiency?

A
  • ↑ Homocysteine levels (a correlate with ↑ cardiovascular disease risk) seen
  • Macrocytic anaemia which can lead to lethargy and weakness
  • Foetal developmental abnormities: neural tube defects (anencephaly, spina bifida)
63
Q

What are functions of Viitamin B12?

A
  • Important role in metabolism of carbohydrates, proteins and lipids
  • Essential role in blood cell production in bone marrow
  • Unlike most water-soluble vitamins, B12 can be stored in liver
64
Q

What are causes of Vitamin B12 deficiency?

A
  • Pernicious anaemia: autoimmune destruction of IF-producing cells in stomach. Needs intrinsic factor produced by stomach for absorption. IF-B12 complex absorbed in terminal ileum
  • Malabsorption: lack of stomach acid (atrophic gastritis, drugs which inhibit acid-production), pancreatic disease, small bowel disease
  • ↓ methionine synthase activity traps folate in an inactive form, leading to symptoms of folic acid deficiency: macrocytic anaemia.
  • Vegan diet

Nutrition and Drug Monitoring (17 decks)

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