Lecture 8- Thiamin Flashcards

1
Q

food sources of thiamin

A

wholegrains,

pork (also other meats)

potatoes and their skin

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2
Q

what is enrichment

A

when you add in the nutrient to make up for some kind of processing that removed the nutrient

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3
Q

what is fortification

A

adding the nutrient to food that lots of people eat

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4
Q

3 examples of food related thiamin losses

A

1- refining grains
2- thiamin antagonists
3- thiaminases = enzymes that act on thiamin

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5
Q

how does refining grains result in thiamin losses

A

going from something like wholegrain down to brown down to white flour or bread etc

this removes thiamin, but improves shelf life as the embryo germ is removed

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6
Q

what are 3 thiamin antagonists and what are they found in

A

sulfites (preserve the colour of meat)

cyanogenic glycosides (in cassava)

tannins (tea, coffee, betel nuts)

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7
Q

how do tannins make thiamin less bioavailable

A

they will oxidise thiamin, making it less easy for your body to absorb

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8
Q

what are thiaminases

A

enzymes that act on thiamin

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9
Q

how can thiaminases cause thiamin losses

A

plants such as bracken fern

some kaimoana such as carp, mussels

some insects including African silk worm larvae

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10
Q

where is betel nut chewing an important practice

A

in South and South-East Asia, Asia Pacific

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11
Q

what is betel nut chewing considered

A

a stimulant drug, addictive

(one portion has the effect of about 6 cups of coffee)

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12
Q

what are the long term impacts of betel nut chewing

A

discolouration of teeth and gums, mouth ulcers and oral cancers

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13
Q

what is the chemical structure of thiamin

A

colourless organosulfur compound

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14
Q

is thiamin water soluble or water insoluble

A

water soluble

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15
Q

when is thiamin stable

A

when in acid solution and when frozen

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16
Q

when is thiamin unstable

A

unstable to heat, UV light and alkali

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17
Q

what are 3 of the 5 phosphorylated forms of thiamin (one of them has two names)

A

thiamin monophosphate (TMP)

thiamin diphosphate also known as thamin pyrophosphate (TPP)

thiamin triphosphate (TTP)

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18
Q

all forms of thiamin can be interconverted in tissues but what is the distribution of these usually

A

80% is TPP

5-10% is TTP

remainder TMP, free thiamin

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19
Q

how is thiamin converted to thiamin pyrophosphate

A

thiamin diphosphotransferase converted thiamin to its active form (TPP) via TMP

so converts it to thiamin monophosphate first and then thiamin pyrophosphate

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20
Q

where is thiamin absorbed

A

mainly in the jejunum and ileum

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21
Q

what are the two forms of thiamin absorption and when do they usually happen

A

active carried mediated process at low concentrations

passive diffusion at high concentrations (more at supplement level)

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22
Q

what is the bioavailability of thiamin

A

little information

absorption can be inhibited by alcohol consumption

absorption will increase when intakes are low

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23
Q

where is ~90% of the thiamin in your blood and why

A

in erythrocytes (red blood cells) in blood

because there is a TPP dependent enzyme that is on your red blood cells

24
Q

where is thiamin found in the plasma

A

majority bound to proteins, mainly albumin

25
Q

what is the average human storage of thiamin and how long does it take for this to be depleted

A

~25-30mg

can be depleted within 2-3 weeks

26
Q

what are the highest tissue concentrations of thiamin

A

skeletal muscle

heart

brain

liver

kidneys

27
Q

where is thiamin also present in the body

A

plasma / serum, milk, cerebrospinal fluid

28
Q

what does thiamin have a critical role in

A

energy metabolism (key role in carbohydrate metabolism)

29
Q

what enzymes is thiamin required for (4)

A

transketolase

a-ketoglutarate
dehydrogenase

pyruvate dehydrogenase

branched chain a-keto acid dehydrogenase

30
Q

what is a good measure of thiamin status

A

transketolase

31
Q

what kind of diets are risk factors for thiamin deficiency

A

monotonous diet with low thiamin staple

regular consumption of thiamin antagonists (e.g betel nut)

regular consumption of thiaminases (e,g raw fish)

32
Q

what are other factors that are risk factors for thiamin deficiency

A

breastfed infants from thiamin deficient mothers

co-morbidities such as severe acute malnutrition with fever and shock, use of dextrose-based IV fluid

disease states with low thiamin intakes, absorption, thiamin utilisation (e.g alcohol dependancy, bariatric surgery)

33
Q

what was the historical approach to Beriberi diagnosis

A

“wet” if it predominantly affects the cardiovascular system accompanied by oedema

“dry” is predominantly affects the peripheral nervous system

34
Q

what was the historical symptoms that people then thought was Wernicke-Korsakoff encephalopathy

A

presents with neurological signs

35
Q

classic syndrome of thiamin deficiency is Beriberi, what is it characterised by

A

oedema and cardiac enlargement due to intense vasodilation from

accumulation of pyruvate and lactate in tissues

bradycardia (bounding pulse)

cardiac failure

36
Q

what is the response of Beriberi to thiamin treatment

A

prompt response to thiamin treatment > recovery could be 1-3 days

37
Q

what does chronic Beriberi affect rather than the cardiovascular system

A

the peripheral nerves

38
Q

what are symptoms of chronic Beriberi

A

foot drop

loss of sensation in feet

absent ankle reflexes

39
Q

what are the non specific signs associated with infantile beriberi

A

irritability

refusal to breastfeed

vomiting

incessant “piercing” cry that may become a “silent” cry

40
Q

what are the later signs of infantile beriberi

A

chronic heart failure

41
Q

in low income countries what often happens with infantile beriberi

A

death before diagnosis

42
Q

what is infantile beriberi often misdiagnosed as

A

viral infection, malaria, pneumonia

43
Q

in older infants and children what is beriberi often misiagnosed as

A

meningitis

44
Q

what are the more neurological symptoms associated with beriberi in older infants and children

A

loss of appetite, bulging frontanelle, loss of consciousness

45
Q

what is the most common form of thiamin deficiency in older children and adults

A

Wernikes encephalopathy

46
Q

what does Wernike’s encephalopathy affect in the brain and therefore what does this impact

A

cerebellum and brain stem = abnormal eye movement, gait ataxia, cognitive impairment

47
Q

what is the most severe form of Wernike-Korsakoff encephalopathy and what does this cause

A

Korsakoffs psychosis = amnesia, confusion, confabulation , little or no working memory

48
Q

who is Wernike-Korsakoff encephalopathy most common in and why

A

most common in people with alcohol dependancy

because decreased intestinal thiamin absorption and increased thiamin requirements for metabolism

49
Q

what is possible if thiamin deficiency is corrected before development of significant brain damage in Wernike-Korsakoff encephalopathy

A

the neurological symptoms may be reversed

50
Q

mild thiamin deficiency is non specific and easily overlooked, especially in older adults, what are the symptoms

A

sleeplessness, depression, weight loss, malaise, anorexia, fatigue

51
Q

possible causes of mild thiamin deficiency

A

low intakes
lowered absorption
multiple medications

52
Q

what is thiamin deficiency disorders an umbrella term for

A

describe the spectrum of overlap of clinical presentations attributable to thiamin deficiency across the life course

53
Q

what are the 5 categories to the spectrum of thiamin deficiency disorders by the WHO

A

acute cardiologic form
aphonic form
pseudo meningitic form
encephalopathy
peripheral neuropathies

54
Q

what is the acute cardiologic form of thiamin deficiency associated with

A

heart

55
Q

what is the aphonic form of thiamin deficiency associated with

A

lack of sound - peak prevalence in 4-6 month old infants

initially hoarse cry until no sound is produced while crying

56
Q

strategies to improve thiamin status

A

rice and wheat flour fortification programmes that include thiamin

57
Q

what is the upper level for intake of thiamin

A

no upper level, just pee it all out