GIT physiology 5 Flashcards

1
Q

transcriptional regulators

A

vitamins A and D binds to receptors that form a transcriptional regulatory complex that changes gene expression

  • vitamin D receptor is a transcription factor
  • Retinoic X receptor is a transcription factor (vit A)
  • vit K modifies existing proteins by adding carboxyl groups to increase activity
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2
Q

action of Vit K on transcription

A

modifies structure of existing proteins to increase their activity via glutamate residue carboxylation

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3
Q

ROS

A

reactive oxygen species

  • proteins and sugars - glycation
  • DNA - mutations
  • membranes - lipid peroxidation
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4
Q

reactive oxygen species examples

A

OH, H2O2, O2

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5
Q

effects of ROS

A
  • proteins and sugars - glycation
  • DNA - mutations
  • membranes - lipid per oxidation
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6
Q

vitamin classification

A

lipid soluble - A, D, E, K

water soluble - all others

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7
Q

lipid soluble vitamins

A

hydrophobic, absorbed with lipids using bile
- transported in blood in lipoproteins or attached to specific binding proteins
more likely to accumulate in the body and lead to toxicity hypervitaminosis

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8
Q

water soluble vitamins

A

8x B vitamins and vit C

  • hydrophilic and dissolve in water
  • not readily stored, excreted from the body
  • does not cross plasma membranes, need carrier proteins
  • consistent daily intake is needed and deficiency problems are common
  • many types of water soluble vitamins are synthesised by bacteria and fungi, small amounts synthesised in GI tract
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9
Q

vit B1

A

thiamin

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10
Q

vit B2

A

riboflavin

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11
Q

vit B3

A

niacin

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12
Q

vit B4

A

pantothenic acid

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13
Q

vit B6

A

pyridoxine and pyridoxamine

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14
Q

vit B 7

A

biotin

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15
Q

vit B9

A

folic acid

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16
Q

vit B12

A

cobalamin

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17
Q

Vit C

A

ascorbic acid

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18
Q

thiamin

A
B1
used to form thiamin pyrophosphate coenzyme used in:
- CHO and AA metabolism
- DNA/RNA/neurotransmitter synthesis
- TCA cycle
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19
Q

thiamin deficiency

A

problems with energy and neurotransmitter production

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20
Q

beriberi

A

deficiency of thiamin

  • CNS problems: memory loss, confusion, ataxia (gait coordination)
  • peripheral neuropathy - muscle weakness, muscle wasting
  • wernickle-korsakoff syndrome - alcohol induced dementia
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21
Q

deficiency of thiamin is called

A

beriberi

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22
Q

toxicity symptoms of thiamin

A

no toxicity symptoms due to water solubility

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23
Q

wernickle-korsakoff syndrome

A

chronic alcohol use interferes with absorption of Vit B1
alcohol induced dementia
B1 chronic deficiency

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24
Q

riboflavin used to make

A

forms coenzyme flavin-mononucleotide (FMN) and flavin adenine dunucleotid (FAD)

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25
Q

FMN and FAD

A
coenzymes formed from riboflavin 
prosthetic groups for many redox enzymes 
- coenzymes in proton transformation 
- TCA cycle 
- beta oxidation of fatty acids
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26
Q

riboflavin is

A

B2

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27
Q

riboflavin deficiency occurs in

A

B2 deficiency is rare

- only occurs with proliferation in high cell turnover tissues

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28
Q

symptoms of riboflavin deficiency

A
  • problems with proliferation in high cell runner tissues
  • inflammation in the lining of the mouth and tongue
  • dry and scaling skin keratitis, dermatitis and iron deficiency anaemia
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29
Q

riboflavin toxicity

A

no toxicity

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30
Q

niacin is

A

B3

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31
Q

niacin comes in

A

2 forms

- nicoinic acid and nicotinamide

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32
Q

niacin in used to make

A

NAD and NADP

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33
Q

NAD and NADP are used in

A

coenzymes in CHP, lipids, AA metabolism (TCA cycle)

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34
Q

biosynthesis of niacin

A

liver can slowly synthesise niacin from tryptophan (essential AA)

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35
Q

deficiency of niacin

A

effects tissue with high energy requirements of cellular turnover

  • pellagra - a serious deificiency of niacin
  • four D’s - diarrhoea, dermatitis, dementia and death
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36
Q

pellagra

A

serious deficiency of niacin

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37
Q

symptoms of pellagra

A

four D’s - diarrhoea, dermatitis, dementia, and death

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38
Q

pellagra occurs in

A

alcoholics, strict vegetarians, those with poor nutrition

- very rare - common in food

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39
Q

toxicity of niacin B3

A

no toxicity

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40
Q

pantothenic acid is

A

B5

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41
Q

pantothenic acid forms

A

acetyl Co-A

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42
Q

acetyl Co-A is made of

A

pantoic acid and beta-alanine

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43
Q

Co-A is essential for

A

TCA cycle
metabolism of fatty acids
formation of sterols
- acetylcholine production

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44
Q

deficiency of pantothenic acid

A

EXTREMELY rare because its is very ubiquitous

- hypothetically it would cause general metabolic deficiencies and neurological problems

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45
Q

toxicity of pantothenic acid

A

no toxicity

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46
Q

pyrodoxine is

A

B6

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47
Q

pyridoxine does

A

group of 3 related compounds
precursor of active coenzyme pyridoxal phosphate - PLP
- coenzyme in amino acid synthesis and gluconeogenesis

48
Q

PLP is essential for

A
  • RBC metabolic, haemoglobin formation

- neurotransmitter biosynthesis

49
Q

deficiency is pyridoxine

A

anaemia
neurological problems
inflammation of the GI tract - stomatitis, glossitis and dermatitis

50
Q

B6 toxicity

A

toxicity above 200mg/day

51
Q

biotin is

A

B7

52
Q

biotin is used for

A

prothetic group of several ATP-dependant carboxylase enzymes
coenzyme for FA synthesis, gluconeogenesis, CHO, fat and protein metabolism

53
Q

defificency of biotin

A

very rare
inflammation of the GI tract and skin
consumption of raw eggs
produced by gut bacteria

54
Q

toxicity of biotin

A

no toxicity

55
Q

folic acid is

A

B9

56
Q

folate

A

pteroglutamic acid

once de-glutamated to be folic acid, then hydrated is becomes tetrathydrofolate

57
Q

tetrahydrofolate

A

coenzyme of many tranferases

- essential in purine and pyrimidine synthesis

58
Q

deficiency of folic acid

A

very rare

  • effects high turnover/RNA synthesis)
  • suppression of nervous system
59
Q

folic acid deficiency in pregnant women

A

leads to major birth defects

neural tube defects - span bifida

60
Q

cobalamin

A

vitamin B12

61
Q

cobalamin catalyses which reactions

A

catalyses reactions of two enzymes

  • methionine synthase - DNA synthesis
  • methylmalonyl-CoA mutase - energy metabolism
62
Q

cobalamin is essential for

A

energy metabolism ‘
purine and pyrimidine synthesis
RBC maturation, cell growth, nervous system maturation

63
Q

deficiency of B12 is common in

A

vegetarians and vegans

64
Q

deficiency of B12 causes

A

effects high turnover/RNA synthesis

- microcytic anaemia and nervous system problems

65
Q

2 antioxidant vitamins

A

E - lipid soluble

C - water soluble

66
Q

lipid soluble antioxidant

A

E

67
Q

water soluble anti oxidant

A

C

68
Q

vit E protects from

A

lipid peroxidation, membranes, membrane bound proteins

69
Q

vit E protects from

A

free radicals in solution (DNA< non-membrane bound proteins

70
Q

what do vit E and C do

A

get rid of free radicals

71
Q

ascorbic acid is

A

vit C

the principle water soluble antioxidant and free radical scavenger

72
Q

ascorbic acid is involved in

A
  • cofactor in the synthesis of noradrenaline
  • leukocyte motility
  • synthesis of collagen
73
Q

deficiency of vit C is called

A

scurvy

74
Q

scurvy

A

occurs over 3-5 months
neuronal problems - fatigue, decline in psychomotor performance and motivation, dyspnoea
- collagen problems - spongy gums, and bleeding from all mucus membranes and loss of teeth

75
Q

tocopherol is

A

vit E
a family of 4 tocopherols
most common is a-tocopherol

76
Q

tocopherol does

A

antioxidant

  • prevents lipid peroxidation
  • stops free radical reactions
77
Q

deficiency of tocopherol

A

impairment in fertility in men
peripheral neuropathy
- anaemia, diminished RBC lifespan
- virtually never occurs

78
Q

toxicity of tocopherol

A

rare, increased bleeding

79
Q

retiniocs acid is

A

vit A

80
Q

precursors of vit A

A

carotenoids (plants) and retinol esters (animal)

81
Q

functions of retinoic acid

A

transcriptional regulation - retinioc X receptor is a TF

visual pigment - forms rhodopsin in retinal photoreceptors

82
Q

toxicity of retinoic acid

A

acute - headache, vimiting, impaired consciousness

chronic - weight loss, vomiting, joint pain, blurred vision, hair loss, excessive bone growth

83
Q

retiniocs acid in pregnancy

A

both excess and deficiency are teratogenic

84
Q

retiniocs acid in chemotherapy

A

is chemotherapeutic

used to kill rapidly proliferating cells

85
Q

vit D

A

not a vitamin

synthesised in the skin

86
Q

vit D3 made from

A

7-dehydrocholesterol + UVB

87
Q

vit D2 from

A

vitamin supplements

88
Q

transformations of D3

A

cholecalciferol
calcidiol
calcitriol

89
Q

calcitriol

A

transported in the blood on a carrier - VDBP - vitamin D binding protein
binds vitamin D receptor - transcription receptor
regulates Ca2+ levels
- increase Ca2+ absorption
- switches on genes of Ca2+ transporters and Ca2+ binding proteins

90
Q

deficiency of calcitriol

A

causes Ca2+ deficiency

91
Q

deficiency of calcitriol happens due to

A

malabsorption or lack of UVB

92
Q

calcitriol is

A

vit D

93
Q

Ca2+ deficiency in developing child is called

A

rickets

94
Q

symptoms of Ca2+ deficiency

A

soft and pliable bones = impaired ossification

osteomalacia in adults - after closure of epiphyseal plates

95
Q

vitamin DD is used to make

A

TRPV6 - calcium transporter
and calbindin which binds free calcium inside cell to lower concentration of free calcium allowing calcium to flow into the cell along its concentration gradient

96
Q

koagulationsvitamin is

A

vit K

97
Q

2 forms of koagulationsvitamin

A

K1 - phylloquinon - plants

K2 - menaquinon -animals/bacteria

98
Q

koagulationsvitmain does

A

coenzyme for y-glutamyl carboxylase

99
Q

y-glutamyl carboxylase

A

carboxylates glutamate residues in specific proteins to activate function

100
Q

vit K dependant proteins

A

blood coagulation - prothrombin (Factor 2), factors 7, 9, 10, and proteins C, S, Z
bone metabolism - osteocalcin, matriculates Gla protein (MGP), periostatin

101
Q

deficiency of vit K

A

rare because vit K is abundant in the diet
causes fat malabsorption and liver failure
blood clotting disorders - may be dangerous in newborns
osteoporosis due to decreased activity of osteoblasts

102
Q

toxicity of vit K

A

no toxicity

103
Q

absorption of lipophilic vitamins

A

co-absorption with digested fat in bile salt micelles

104
Q

absorption of water soluble micelles

A

specific transporters

except B12

105
Q

how does B9 get into the cell

A

B9 has lots of glutamate residues
all except 1 glutamate must be removed
folate conjugase removes glutamate residues
enters through folate transporter
dihydrofolate reductase sticks on a methyl group and 4 hydroxyl groups
transported into plasma
carried around as methyl tetrahydrofolate

106
Q

how does vit B12 enter the cell

A

via receptor mediated endocytosis
receptor binds to intrinsic factor and intrinsic factor binds to B12 - receptor cannot bind directly to B12
intrinsic factor secreted in the stomach but the pH is too low to bind intrinsic factor to vit B12 in the stomach
haptocorrin binds B12 in the stomach
proteases digest haptocorrin in the duodenum but do not ingest intrinsic factor because it is covered in sugars
intrinsic factor binds B12 and there is receptors for intrinsic factor in the ileum
endoscope forms and enzymes liberate intrinsic factor
Vit B12 binds transcobalamin 2 and enters plasma
cells have a receptor for transcobalamin 2

107
Q

what liberates Vit B12 from food

A

pepsin liberates Vit B 12

108
Q

haptocorrin

A

binds vit B 12 in he acidic stomach

109
Q

why can’t intrinsic factor binds vit B12 in the stomach

A

too acidic

110
Q

where is cobalamin taken up

A

in the ileum binded to intrinsic factor

111
Q

what happens to haptocorrin in the duodenum

A

proteases digest haptocorrin to liberate the cobalamin and the cobalamin binds the intrinsic factor

112
Q

why isn’t intrinsic factor digested in the duodenum

A

covered in sugars so the proteases can’t reach it

113
Q

how it cobalamin transported through plasma

A

bound to transcobalamin 2

114
Q

how is cobalamin taken up into cells from plasma

A

receptor mediated endocytosis by binding transcobalamin 2

115
Q

having toxic effects due to too much of a vitamin is called

A

hypervitaminosis