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Management of GI and Endocrine Conditions > Lecture 14 - Absorption and What Goes Wrong > Flashcards

Lecture 14 - Absorption and What Goes Wrong Flashcards

1
Q

What are vitamins?

A

organic compounds that are required in small quantities for a variety of biochemical functions

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2
Q

water soluble vitamins?

A

B complexes (B12 & B9)

c or ascorbic acid

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3
Q

Fat soluble vitamins?

A

A or retinol

D or cholecalciferol

E or tocopherol

K

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4
Q

What is B12 known as?

A

cobalamin

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5
Q

where is B12 synthesised?

A

solely by microorganisms

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6
Q

Where do ruminants obtain B12 from?

A

the foregut

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7
Q

Human source of B12?

A

animal origin e.g. meat, fish, diary products

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8
Q

What are free from B12?

A

vegetables, fruits and other non-animal foods unless contaminated by bacteria

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9
Q

Who are more at risk of developing B12 deficiency?

A

vegetarians and vegans

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10
Q

RDA of B12?

A

1.-2.5 mcg/day

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11
Q

How much B12 does a western diet contain?

A

5-30 mcg

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12
Q

what are the body stores of B12?

A

2-5 mg

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13
Q

how much B12 a day does an adult lose?

A

1-3mcg (~0.1% of body stored)

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14
Q

how is B12 lost from the body?

A

in urine and faeces

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15
Q

How much B12 is stored if the supply is cut off?

A

enough for 2-5 years

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16
Q

two mechanisms for B12 absorption?

A

passive absorption and active transport

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17
Q

Passive absorption of B12?

A

through buccal, duodenal and ileal mucosa

rapid but insufficient

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18
Q

How much of an oral dose of B12 is passively absorbed?

A

<1%

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19
Q

active transport of B12?

A

normal physiological mechanism

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20
Q

Where does active transport of B12 occur?

A

through the ileum

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21
Q

What mediates active transport of B12?

A

gastric intrinsic factor

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22
Q

How much B12 is absorbed by active transport?

A

~70% of ingested amount

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23
Q

where is haptocorrin produced?

A

salivary glands

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24
Q

where is intrinsic factor produced?

A

secreted by parietal cells, secretion parallels that of gastric acid

it is a glycoprotein

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25
Q

how is B12 transported in the plasma?

A

bound to transcobalamin I, II, III

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26
Q

What is B12 mainly bound to in the plasma?

A

transcobalamin II

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27
Q

Where is vitamin B12 stored?

A

in the liver

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28
Q

What % of the transcobalamin is II?

A

~10%

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29
Q

What is a cellular role of B12?

A

it is an essential co-enzyme for 2 enzymes in the body

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30
Q

What is B12 an essential co-enzyme for?

A

the conversion of homocysteine to methionine

the conversion of methylmalonyl-coA to succinyl-CoA

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31
Q

What happens in the absence of intrinsic factor?

A

inadequate amounts of B12 are absorbed

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32
Q

what does inadequate absorption of B12 result in?

A

megaloblastic anaemia

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33
Q

What is pernicious anaemia classed as?

A

when megaloblastic anaemia is due to the absense of intrinsic factor

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34
Q

What is B12 essential for?

A

normal formation of red blood cells

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35
Q

What is megaloblastic anaemia characterised by?

A

insufficient/usually large and irregular shaped RBC due to the defective erythrocyte production due to lack of B12

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36
Q

What causes the unusually shaped RBC?

A

The inhibition of DNA synthesis during RBC production, the cell cycle cannot progress and this leads continuing cell growth without division resulting in macrocytosis

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37
Q

What is pernicious anaemia?

A

autoimmune atrophic gastritis - main cause severe vitamin B12 deficiency

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38
Q

What causes pernicious anaemia?

A

destruction of gastric parietal cells and the associated lack of intrinsic factor

immune response is directed against H+/K+ATPase

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39
Q

What does pernicious anaemia cause?

A

achlorhydria (production of gastric acid is low or absent)

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40
Q

What else can cause pernicious anaemia?

A

antibodies directed against intrinsic factor itself

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41
Q

Aetiology of B12 deficiency?

A

inadequate dietary intake (rare)

loss of gastric parietal cells or intrinsic factor

functionally abnormal intrinsic factor

bacterial overgrowth in intestine

disorders of ileal mucosa

disorders of plasma transport

dysfunctional uptake and use of B12 by cells

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42
Q

bacteria overgrowth causing B12 deficiency?

A

stagnant loop syndrome

bacteria that are present will compete with the body for the vitamin

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43
Q

Disorders of ileal mucosa causing B12 deficiency?

A

resection, absence of cubam receptor on ileal cells

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44
Q

Disorders of plasma transport causing B12 deficiency?

A

transcobalamin II deficiency

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45
Q

Drug induced B12 deficiency?

A

PPI and H2 antagonists

oral contraceptives and hormone replacement therapy

metformin

cholchicine

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46
Q

PPI and H2 antagonist B12 deficiency?

A

reduction in stomach acid reduces separation of B12 from food

can cause gastric hypochlorhydria (reduced acid)

oral replacement therapy may be used

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47
Q

Oral contraceptives and hormone replacement B12 deficiency?

A

thought to be due to a reduction in B12 carrier transcobalamin

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48
Q

Metformin B12 deficiency?

A

reduces B12 absorption

mechanism unknown

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49
Q

Cholchicine B12 deficiency?

A

used to treat gout

impairs or inhibits receptors on terminal ileum (cubam receptors)

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50
Q

What is the normal serum B12 levels?

A

115-1000pmol/L

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51
Q

What is the hallmark of symptomatic B12 deficiency?

A

megaloblastic anaemia

52
Q

What happens in advanced, severe cases?

A

anaemia may be severe, with haematocrit as low as 10-15%

53
Q

what are normal haematocrit values?

A

40% for women and 45% for men

54
Q

What might megaloblastic anaemia be accompanied by?

A

leucopaenia, thrombocytopaenua and hypersegmented neutrophils

55
Q

What are hypersegmented neutrophils?

A

normally the nucleus of neutrophils have 1-2 segments but these have 5 or 6

56
Q

What is the haematocrit?

A

pack cell volume, % volume of RBC in blood

57
Q

What do RBC look like in megaloblastic anaemia?

A

erythrocytes are not uniform biconcave disc shape, they are large and have unusual shape

58
Q

What are the neurological symptoms of B12 deficiency?

A

paresthesia (pins and needles) in hands and feet

sensory loss

gait ataxia

weakness in legs

subacute combined degeneration of the spinal cord

59
Q

What is B12 necessary for in the CNS?

A

development and initial myelination of the CNS and maintenance of its normal function

60
Q

What can occur in the CNS with B12 deficiency?

A

demyelination of the spinal cord and peripheral nerves

at first the covering of the myelin sheath is damaged but then the entire nerve cel is affected

61
Q

What is subacute combined degeneration of the spinal cord?

A

mentioned previously

affects the brain and peripheral nerves

serious condition and recovery is more likely is treated early

62
Q

Digestive consequences of B12 deficiency?

A

hunters glossitis - tongue is smooth, red and shiny

can be sore

63
Q

CV consequences of B12 deficiency?

A

angina

venous thromboembolic disease

64
Q

Gynaecological consequences of B12 deficiency?

A

infertility

65
Q

% of cyanocobalamin in human serum?

A

0-10%

66
Q

% of hydroxocobalamin in human serum?

A

8-15%

67
Q

% of deoxyadenosylcobalamin in human serum?

A

22-39%

68
Q

% of methylcobalamin in human serum?

A

36-62%

69
Q

What is cyanocobalamin?

A

synthetic vitamin B12

70
Q

What are the active forms of vitamin B12?

A

deoxyadenosylcobalamin and methylcobalamin

71
Q

Treatment of vitamin B12 deficiency?

A

oral (cyanocobalamin)

parenteral (hydroxocobalamin)

72
Q

When must treatment be parenteral?

A

in the case of gastric intrinsic factor deficiency (pernicious anaemia) or total gastrectomy

73
Q

How long is treatment for B12 deficiency?

A

lifelong for patients with permanently decreases ability to absorb B12

74
Q

Why is hydroxocobalamin given?

A

it has a longer half life than cyanocobalamin

75
Q

Dose of parenteral hydroxocobalamin?

A

1mg three times per week for 2 weeks, then 1mg every 3 months thereafter

intramuscularly

76
Q

What is vitamin B9 known as?

A

folate, folic acid

77
Q

Sources of B9?

A

dark green leafy veg (broccoli, lettuce, brussel sprouts and spinach) and dried legumes (beans, lentils, chickpeas)

fruits and fruit juices

meat, seafood, poultry and eggs

fortified cereals and breas

78
Q

RDA of B9?

A

200mcg/day

79
Q

RDA of B9 in pregnancy?

A

400mcg/day supplement

80
Q

How is folate destroyed?

A

Easily by heating, particularly in large volumes of water - leaching into cooking water when boiling

81
Q

Why do we need folic acid from diet everyday?

A

it cannot be stored in the body

82
Q

When is supplement needed in pregnancy?

A

From before conception till 12th week

83
Q

What are natural folates conjugated to?

A

polyglutamyl chain - containing a different number of glutamic acids (1-7)

84
Q

How are folates absorbed?

A

in the monoglutamate form

85
Q

What is folic acid composed of?

A

pteridine ring
paramino benzoic acid

glutamic acid

86
Q

What is glutamic acid?

A

an amino acid that can synthesise itself

87
Q

What are the polyglutamates hydrolysed by?

A

folypoly-gamma-glutamate carboxypeptidase (folate conjugase)

88
Q

What is the number of glutamic acid residues dependent on?

A

the type of food, can range from 1-7

89
Q

Where is the polyglutamate chain removed?

A

in the apical brush borders of the mucosal cells (folate conjugase)

90
Q

Where is folate conjugase found?

A

widely distributed in the mucosa of the small intestine

91
Q

what does loss of activity of folate conjugase cause?

A

impaired folate absorption

92
Q

What is the main dietary folate?

A

N5-methyltetrahydrofolate (5-MTHF)

93
Q

Where are folates absorbed?

A

duodenum or jejunum

94
Q

What is the proton-coupled folate transporter?

A

transport by this is pH dependent and uses energy generated by downhill movement of protons

95
Q

What is the reduced folate carrier?

A

an anionic exchanger, mediating the cellular uptake of folate in exchange for anions

96
Q

What does the reduced folate carrier have affinity for?

A

for the reduced folates e.g. 5methyltetrafolate and 5-tetrahydrofolate but not folic acid

97
Q

What do enterocytes have?

A

folate receptors which bind folate and internalise it by receptor mediated endocytosis

98
Q

How is folate exported from enterocyte?

A

by an organic anion transporter (OAT)

99
Q

How is most folate transported?

A

as mono-glutamyl dertivative

100
Q

How does folate circulate?

A

free in the blood, some (~1/3) is bound to albumin

101
Q

What is normal folate plasma concentration?

A

10-30nmol/L

102
Q

How is folate taken up into cells?

A

same as into enterocytes (PCFT, RFC, folate receptor)

103
Q

How do folates exist inside cells?

A

as poly-glutamate conjugates (75%)

104
Q

What happens to monoglutamates in a cell?

A

they leak out at a fairly rapid rate

105
Q

What are the cell requirements for folate?

A

folate is crucial for the transfer of one-carbon units to amino acids, nucleotides and other biomolecules

106
Q

What is dietary folic acid the starting material for?

A

the fundamental molecule, tetrahydrofolate

107
Q

What reduces folate and what is it reduced to?

A

Dihydrofolate reductase

reduced partially to dihydrofolate or completely to tetrahydrofolate

108
Q

Aetiology of folate deficiency?

A

inadequate dietary intake

congenital defects in the uptake system (PCFT)

intestinal disease (coeliac disease, IBD, tropical sprue)

drug interactions

chronic alcohol use

increased cellular requirement (pregnancy)

109
Q

What drugs can affect folate deficiency?

A

cholestyramine, sulfasalazine, trimethoprim, methotrexate, metformin

110
Q

How does alcohol affect folate?

A

accelerates folate breakdown

111
Q

When do mutations in PCFT occur?

A

in patients with hereditary folate malabsorption syndrome

112
Q

How does cholestyramine affect folate?

A

binds to folate in the GI tract and prevents its absorption

113
Q

Why is more folate needed during pregnancy?

A

deficiency can impair foetal development

114
Q

Symptoms of folate deficiency?

A

sore tongue and pain swallowing

GI symptoms (especially after meals)

neurologic (cognitive impairment, dementia, depression)

115
Q

What can severe folate deficiency result in?

A

megaloblastic anaemia

116
Q

What else should be looked for when considering folate deficiency?

A

marked weight loss

117
Q

What are consequences of folate deficiency?

A

neural tube defects such as spina bifida and anencephaly

118
Q

When do neural tube defects occur?

A

first month of pregnancy

119
Q

What is the neural tube?

A

the embryonic precursor of the brain and spinal cord

120
Q

What is spina bifida?

A

the spinal column does not close completely

121
Q

What is anencephaly?

A

most of the brain and skull do not develop

122
Q

How can oral folic acid prevent neural tube defects?

A

When taken before and during pregnancy it can prevent about 75%

123
Q

Treatment of folate deficiency?

A

Oral folic acid for 1-4 months, 5mg daily

oral route is sufficient even when there is malabsorption

124
Q

When is folate deficiency treated until?

A

Until haematological recovery occurs

125
Q

What must be excluded before giving folic acid?

A

Vitamin B12 deficiency - symptoms are similar but folic acid may worsen the neurological complications

Management of GI and Endocrine Conditions (24 decks)

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