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MDENT210 > Nutrition > Flashcards

Nutrition Flashcards

1
Q

Where are vitamins supplied from?

A

Diet, some can be synthesised (D - sun. B&K -gut bacteria)

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2
Q

What type of compounds are vitamins?

A

Organic

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3
Q

What type of functions do they have?

A

Co-enzymes, hormones, cell signalling, antioxidants, regulators of growth & differentiation

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4
Q

What can affect absorption of vitamins?

A

Properties of the food e.g. low in fat
pre-existing disease e.g. ceiliac - impaired fat absorption and gastritis (low acid- b12)
Drugs may compete for absorption and kill bacteria

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5
Q

What is RDA?

A

recommended daily allowance - an intake that is adequate to ensure the requirements of all health people are met

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6
Q

Which vitamins are fat soluble and which are water soluble?

A 
Fat soluble:
Vitamin A
Vitamin D
Vitamin E
Vitamin K

Water soluble:
B vitamins
Vitamin C

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7
Q

What type of vitamins can be stored?

A

Fat soluble stored. water soluble not stored

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8
Q

What is the active form of vitamin A?

A

Retinoids

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9
Q

What pigments give retinoids?

A

Carotenoid pigments (e.g. B carotene)

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10
Q

What is the function of vitamin A?

A

binds to proteins (opsin) in the cells of the retina to form visual pigments

Nuclear modulator of gene expression:

Cell proliferation

Differentiation
(especially epithelia)

Development

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11
Q

What are the symptoms of a vitamin A deficiency?

A

Major cause of blindness in children under 5 in developing countries

impaired resistance to infection - differentiation and function of lymphocytes and neutrophils affected

mild deficiency = night blindness

severe deficiency = metaplasia and keratinisation of the conjuctiva epithelial cells and thickening of the cornea (xerophthalmia)

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12
Q

What process produces vitamin D endogenously?

A

(D3 -photolysis of 7-dehydrocholesterol)

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13
Q

What are the functions of vitamin D?

A

Maintenance of plasma Calcium concentration (along with parathyroid hormone and calcitonin)

Steroid hormone activating nuclear receptors and influencing > 50 genes

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14
Q

What is cholecalciferol?

A

Vitamin D3 which is made by the skin when exposed to sunlight

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15
Q

What is egocalciferol?

A

also known as vitamin D2 and calciferol, is a type of fat soluble vitamin D found in food and used as a dietary supplement

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16
Q

What is the role of vitamin D in bone metabolism?

A
  • Vit D stimulates intestinal Calcium and phosphate absorption and renal Ca reabsorption - mineralisation of bone is controlled by the availabiliy of Ca and PO4

Osteoblasts have receptors for calcitriol (active metabolite of vitamin D)

Osteoclast activity/number (paradoxically) increased

= Promotes formation and mineralisation of bone

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17
Q

What condition is caused by Vit D deficiency?

A

Rickets and osteomalacia (the softening of the bones caused by impaired bone metabolism primarily due to inadequate levels of available phosphate, calcium, and vitamin D)

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18
Q

What is vitamin E?

A

Lipid soluble antioxidant - very active free radical trapping

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19
Q

What does vitamin E do?

A

Free radical trapping

Cell signalling (inactivates protein kinase C)

deficiency not normally a problem

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20
Q

What does vitamin K do?

A

Co-enzyme in postranslational carboxylation of glutamate to γ carboxy glutamate (gla)

Permits binding of proteins to membrane phospholipids

Klotting: vitamin K dependent proteins involved in blood coagulation (thrombin factors VII, IX and X, protein C, S, Z)

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21
Q

What are vitamin K antagonists?

A

Anticoagulants e.g. warfarin

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22
Q

What can vitamin K deficiency lead to?

A

Haemorrhagic disease

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23
Q

Name some of the B vitamins

A 
Thiamin (B1), 
ribofavin (B2), 
Niacin (B3), 
B6, 
Folic acid (B9), 
B12, 
pantothenic acid (B5)
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24
Q

What are all B vitamins?

A

Co-enzymes (co-factors)

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25
Q

What does Thiamin (b1) do?

A

Co-enzyme in central energy yielding pathways (pyruvate & keto-glutarate dehydrogenase)

Co-enzyme in pentose phosphate pathway (transketolase: NADPH for biosynthesis & ribose for nucleotides)

Co-enzyme in catabolism of leu, isoleu & val

Regulates nerve chloride channels

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26
Q

What does defiency of Thiamin lead to?

A

Berberi-peripheral neuritis: weakness, stiffness

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27
Q

What does Riboflavin (b2) do?

A

Electron carriers in a variety of oxidation & reduction reactions central to metabolism (mitochondrial electron transport chain)

B2 remain bound to enzyme

FAD (flavin adenine dinuceotide), FMN (flavin mononucleotide) oxidising coenzymes which accept two H atoms

Deficiency common but rarely a problem - bacterial synthesis, conservation and re-utilisation

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28
Q

What does Niacin (B3) do?

A

Precursor of co-enzymes NAD (nicotinamide adenine dinucleotide) & NADP (phosphate)

Electron carriers in metabolic redox reactions

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29
Q

Where is B3 synthesised from?

A

Dietary tryptophan

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30
Q

What deficiency is Niacin B3?

A

Pellegra - demention, diarrhea and dermatitis

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31
Q

What does vitamin B6 do?

A

Amino acid metabolism (transamination)

deficiency virtually unkown

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32
Q

What does vitamin B12 and folate (b9) do?

A

Co enzymes

DNA and myelin synthesis

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33
Q

What does deficiency of vitamin B12 and folate b9 lead to?

A

Anaemia and neurological damage

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34
Q

What role does vitamin C play?

A

Specific role in two enzyme classes:
Dopamine β-hydroxylase: synthesis of adrenaline and noradrenaline (Cu + dependent)

Lysine and proline hydrolyases: maturation of connective tissue (collagen)

Iron uptake: keeps iron as Fe2+, chelates it which increases absorbtion

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35
Q

Why may dentists be the first to spot a vitamin deficiency?

A

Rapid turnover of epithelium makes it sensitive to nutritional deficiencies

Vitamins involved with: wound healing, bleeding, resistance to infection, bone/tooth Ca2+

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36
Q

What facial manefestations of vitamin deficiencies are there?

A

Malar pigmentation (niacin, B vitamins), nasiolabiial seborrhea (niacin, riboflavin, b6 iron), lack of colour (malnutrition)

Lips - angular fissues (niacin, b6, riboflavin, iron), cheilosis (niacin, b6, riboflavin)

Gingiva - Spongy, bleeding, abnormal redness - vitamin C

Tongue - glossitis (folate, niacin, iron, b6, b12)
pale, atrophic, smooth/slick filiform papillary atrophy (iron, folate)
Magenta colour - riboflavin

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37
Q

What are triacylglycerols used for?

A

Fuel

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38
Q

What are glycerophospholipids used for?

A

Membranes

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39
Q

What is cholesterol used for?

A

Membranes

Bile salts: lipid digestions
steroid hormones: communication

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40
Q

What are triacylglycerols composed of?

A

3 fatty acids and glycerol joined by ester bonds

fatty acids have variable length and can be saturated or unsaturated (c=c)

efficient form to store energy

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41
Q

What are the sources of lipids?

A

Diet

make fat from carbohydrates (in liver)

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42
Q

Which type of lipid is a main dietary lipid?

A

Triacylglycerols

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43
Q

What do bile salts do?

A

Emulsify lipids into smaller droplets

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44
Q

What do lipases do?

A

Break down fatty acids from triacylglycerols and then form micelles, absorbed by epithelial cells

These are packaged as chylomicrons in the cells by the RER and golgi complex

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45
Q

What is the fate of chylomicrons?

A

Packaged back into triacylglycerols
The triacylglycerols in them get digested by lipoprotein lipase (LPL)

The fatty acids are absorbed by cells and the other remnants are absorbed by liver

LPL is produced by adipose, muscle and lactating mammary gland cells which is regulated by insulin

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46
Q

Why are chylomicrons packaged with an outer layer of phospholipids?

A

Hydrophobic so keeps the water out

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47
Q

What is an apoprotein?

A

a protein which together with a prosthetic group forms a particular biochemical molecule such as a hormone or enzyme.

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48
Q

What can LPL recognise?

A

The apoproteins so grab the circulating chylomicrons

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49
Q

What is predominantly the remnants of chylomicrons?

A

cholesterol and glycerol

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50
Q

Where are fatty acids synthesised mainly?

A

Liver - reactions in the cytoplasm

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51
Q

What can endodogenous lipids be packaged with to form VLDL (very low density lipoprotein)?

A

Proteins

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52
Q

What is the fate of VLDL?

A

The triacylglycerols in it are digested by LPL regulated by insulin

fatty acids absorbed by the cells

vldl remnant remains - mainly cholesterol

same fate as chylomicrons (dietary fat)

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53
Q

What becomes the main energy source during fasting?

A

fatty acids

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54
Q

Where are long chain fatty acids released from and what is it stimulated by?

A

Long chain fatty acids released from adipose tissue, stimulated by reduced insulin and increased glucagon

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55
Q

What is the main fatty acid oxidation pathway?

A

B-oxidation

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56
Q

How do fatty acids enter tissues?

A

Diffusion

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57
Q

What are the fatty acids activated to using ATP?

A

fatty acyl coA (INTERMEDIATE)

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58
Q

Where is the fatty acyl coA transported to?

A

Mitochondrial matrix

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59
Q

What is the fatty acyl coA converted to in mitochondria

A

Acetyl coA producing NADH AND FAD2H

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60
Q

What does the acetyle coA enter then?

A

TCA cycle

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61
Q

Why do fatty acids produce a lot of energy?

A

2 carbons used each time the process happens and chains have many carbons so lot of energy produced continously

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62
Q

What can fatty acyl coA’s be used to produce?

A

Convert bacj to triacyglycerols for storage
energy - b oxidation ketogenesis
membrane lipids - phospholipids, sphingolipids

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63
Q

Fed state

A

Packaged chylomicrons produced
lots of glucose coming in - VLDL produced
insulin increased
fatty acids taken to tissues intrinsically and extrinsically

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64
Q

Fasting state

A

Release of fatty acids
put through b oxidation to produce energy and ketone bodies - more energy
generate glucose in the liver

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65
Q

Where does cholesterol come from?

A

synthesised or from diet

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66
Q

Why is cholesterol important?

A

Component of cell membranes
precursor of bile salts
precursor of steroid hormones
precursor of vitamin D

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67
Q

What is cholesterol a major component of?

A

Blood lipoproteins

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68
Q

How is cholesterol taken up

A

Mainly by diffusion in gut enterocytes- not good for you

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69
Q

Why does cholesterol entry have to be regulated?

A

cannot be fully metabolised

but excess can be transported back into gut to be excreted

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70
Q

Where is cholesterol synthesised?

A

cytosol in liver

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71
Q

What molecule is mainly used to start cholesterol synthesis?

A

Acetyl coA

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72
Q

Which enzyme is a good drug target for cholesterol reduction?

A

HMG- coA reductase

statin - lowers cholesterol in blood, comeptitively inhibits the enzyme so this can be designed to look like its substrate - higher affinity for the enzyme

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73
Q

What are the 4 steps for cholesterol synthesis?

A

Acetyl coA - mevalonate

mevalonate - isoprenes

isoprenes (5c) - squalene (30c)

squalene - cholesterol

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74
Q

What happens to leftover cholesterol?

A

Converted to bile salts - stored in gallblader, secreted into gut

converted to biliary cholesterol into gut and can be reabsorbed

can be converted to cholesterol esters and packaged into VLDL to go to tissues

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75
Q

Why are bile salts effective as detergents?

A

Because they carry charge - electrons around them

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76
Q

What affects the recycling of cholesterol to the liver?

A

interact with bacteria that chemically alter them which deconjugate and dehydroxylate slightly so less able to reabsorb the cholesterol

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77
Q

What are cholesterolr and cholesterol esters transported in?

A

Lipoproteins (cholesterol helps stabilise them)

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78
Q

how does cholesterol enter the cell?

A

VLDL remnant left behind

these are converted to IDL (intermediate) and LDL (low)

LDL contain a lot of cholesterol and cholesterol esters

this can be returned to liver to make more VLDL or taken up by other cells needing cholesterol

		- e.g. membrane synthesis
		- e.g steroid hormone synthesis
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79
Q

How are LDL endocytosed?

A

Recognised by the apoproteins on their surface by the LDL receptors

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80
Q

What happens to excess LDL?

A

Endocytosed by macrophages (scavenger receptors - recognise some apoproteins)

the ldl causes some of the macrophages to change into foamy cells - cause bumps in the vessels, blood rushes by and causes small thrombus to form, blood clot gets bigger etc which can cause inflammation and contribute to atherosclerosis

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81
Q

Why is maintenance of blood glucose levels essential?

A

Blood glucose too high = causes release of water from tissues - dehydration and death

Blood glucose too low - lack of fuel to produce ATP
brain depends on glucose as fuel - coma
red blood cells low on ATP, can’t provide oxygen to tissues - death

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82
Q

What happens to insulin and glucagon levels when glucose increases after eating a meal?

A

Insulin increases and glucagon decreases

Insulin allows uptake of glucose

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83
Q

What does glucagon do?

A

Increase in glucagon causes release of glucose

decrease in glucagon causes uptake and storage of glucose

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84
Q

Where do the three main sources of glucose come from?

A

Diet
Glycogen degradation
gluconeogenesis

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85
Q

Which sources of glucose are critical during fasting?

A

Glycogen degradation

Gluconeogenesis

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86
Q

What is glycogen?

A

Major storage form of glucose in humans in liver and muscle

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87
Q

What is the structure of glycogen?

A

Branched chains of glucose joined by alpha 1-4 linkages with branching by alpha 1-6 linkages

one carbon is joined to protein - glycogenin (reducing end)

forms huge polymers

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88
Q

What are the differences in processes in muscle and liver of glycogen?

A

Muscle - glycogen undergoes glycolysis mainly so that ATP is produced for energy

Liver - glycogen undergoes gluconeogenesis mainly to produce glucose which is released into the blood to raise blood glucose

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89
Q

What does glycogen synthesis require?

A

Energy in the form of UTP (uridine triphosphate)

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90
Q

What are the steps of glycogen synthesis?

A
  1. Glucose is transerred from UDP glucose to glycogenin (enzyme that polymerises first few molecules)
  2. Glycogen synthase transfers glucose from UDP glucose to growing chain
  3. This forms a 1-4 linkages
  4. When 11 residues are reached, 6-8 cleaved off and rejoined by alpha 1-6 linkages by branching enzyme.
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91
Q

Which two enzymes is glycogen degradation carried out by? and what do they do?

A

Glycogen phosphorylase - removes glucose molecules at end of chains

Debranching enzyme - acts as transferase, removing glucose molecules near branch point
- also cleaves branch point

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92
Q

What hormones regulate glycogen degradation in the liver and what are their effects?

A
  • insulin decreases degradation
  • glucagon increases degradation
  • adrenaline increases degradation
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93
Q

What stimulates glycogen degradation in the muscles?

A

Low ATP (high AMP)

Calcium and adrenaline

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94
Q

What process happens when glycogen stores are exhausted?

A

Gluconeogenesis

95
Q

How long after a meal does it take for glycogen to start degrading?

A

3 hours

96
Q

How long after a meal does it take for gluconeogenesis to start?

A

30 hours

97
Q

What is gluconeogenesis?

A

Process that produces glucose from non-carbohydrate sources

only occurs in liver except in extreme starvation

98
Q

Why is gluconeogenesis important?

A

Maintains availability of glucose during fasting/starvation or intense exercise

99
Q

What are the 4 main enzymes in gluconeogenesis?

A

Glucose 6 phosphate
fructose 1,6 bisphosphate
phosphoenolpyruvate carboxykinase
pyruvate carboxylase

100
Q

What are the non-carbohydrate sources of glucose?

A

Amino acids - mainly alanine but others
Lactate - produce during intense exercise
Glycerol - derived from triacylglycerols
Propionate - from fermentation of fibre

101
Q

What can lactate, alanine and amino acids be fed in to produce? (gluconeogenesis)

A

Pyruvate

Amino acids - also in TCA cycle

102
Q

What can glycerol be used to produce in gluconeogenesis?

A

Glycerol 3 phosphate

103
Q

What are the two main regulatory factors in gluconeogenesis?

A
  1. Substrate availability (more substrate more gluconeogenesis)
    1. Activity of key enzymes
104
Q

How does subtrate availability affect gluconeogenesis?

A
  • when blood glucose low, low insulin stimulates release of:
    glycerol from adipose tissue
    amino acids from muscle
    • intense exercise releases lactate from muscle

These increase the non carbohydrate sources for gluconeogenesis

105
Q

How does enzyme activity affect gluconeogenesis?

A

Three key regulatory steps:

Pyruvate —-> phosphoenolpyruvate
Fructose 1,6-bisphosphate —->Fructose 6-phosphate
Glucose 6-phosphate —->Glucose

Can be allosteric or at level of gene expression

106
Q

What is the energy provided by for gluconeogenesis?

A

Fatty acid oxidation

107
Q

What are the uses of blood glucose?

A

muscle storage for later use - glycogen
energy source for muscle and other tissues
storage as fat (triglycerides)
excretion in urine with high blood sugar - diabetes
energy for CNS and brain
liver storage for later use - glycogen

108
Q

What happens when there is high blood sugar?

A

Beta cells in the islets of langerhans (pancrease) secrete insulin which stimulates muscles and fat cells to take up glucose from the blood for storage - normal blood glucose achieved

109
Q

What happens when there is low blood sugar?

A

The alpha cells in the islets of langerhans in the pancreas secrete glucagon which stimulates the liver to break down glycogen and release glucose into the blood - normal blood glucose achieved

110
Q

What are is the blood glucose level in normal fasting conditions?

A

3-5 mmol/l

111
Q

What are the blood glucose levels in diabetic fasting conditions?

A

4-7 mmol/l

112
Q

What are the normal blood glucose levels after a meal?

A

less than 10 mmol/l 90 min post food

113
Q

What are the normal blood glucose levels in a diabetic after a meal?

A

greater than 20 mmol/l

114
Q

What is Diabetes Mellitus?

A

Metabolic disorder of carbohydrate metabolism

characteristic - hyperglycemia (increase in blood glucose over prolonged period of time)

115
Q

What are some of the complications/ co-morbidities of diabetes?

A

Stroke
Heart disease
hypertension
peripheral vascular disease

Retinopathy
nephropathy - renal damage
peripheral neuropathy - nerve damage
food problems

periodontal disease

116
Q

What are the symptoms of diabetes?

A 
Blurry vision
increased thirst and need to urinate
Feeling tired or ill
Recurring skin, gum, bladder infections
Dry, itchy skin
Unexpected weight loss
Slow healing cuts & bruises
Loss of feeling or tingling feeling in the feet
117
Q

What are the types of diabetes?

A

Type I (insulin dependent)
Type II
Gestational diabetes
Impaired glucose tolerance (IGT) and impaired fasting glycaemia (IFG)

118
Q

What is type 1 diabetes?

A

Chronic (generally) childhood disease
Affects 18-20 per 100 000 children in UK
Sometimes associated with thyroid disease
Genetic susceptibility shown
Linked to viral infection (e.g. congenital rubella syndrome)

Affects islets of Langerhans
Beta cells are killed by antibodies
Therefore, lack of insulin production

119
Q

What is type 2 diabetes?

A

Non-insulin dependent or adult-onset diabetes

can have genetic predisposition - primary beta cells defect - damaged/inadequate insulin

or environmental cause - obesity - peripheral insulin resistance - inadequate glucose uptake

genetics can cause peripheral insulin resistance

hyperglycaemia and free fatty acids leading to type 2 diabetes

120
Q

What is insulin resistance?

A

when cells in your muscles, body fat and liver start resisting or ignoring the signal that the hormone insulin is trying to send out—which is to grab glucose out of the bloodstream and put it into our cells

121
Q

What happens in the liver, muscle and fatty tissue in insulin resistance?

A

Liver - becomes slow to replenish glycogen as glucose not taken up by cells,so blood glucose increases

muscle - glycogen storage decreases and glucose not taken up by cells so blood glucose decreases

fatty tissue - fat is broken down instead and used as an energy store as cells not taking up glucose

122
Q

What are the main syptoms of type 2 diabetes? (3 p’s)

A

Polyuria (frequent urination due to osmotic diuresis)

Polydisia (Increased thirst & increased fluid intake due to polyuria)

Polyphagia (Increased appetite)

Other symptoms:
Dry mouth, itchiniess, increased incidence of thrush, cramps, skin infections

123
Q

When does gestational diabetes come on?

A

Onset in late 2nd trimester (20-28 weeks)

2-5 % of all pregnancies

124
Q

What are the predisposing factors to gestational diabeetes?

A

age (>35 although can occur in younger mums)

6X more common in South Asian decent
3X more common in African-Caribbean people

obesity

125
Q

What are the symptoms of gestational diabetes?

A

No obvious external symptoms

On occasions, classic diabetes symptoms are observed
excessive thirst
frequent urination
increased appetite

126
Q

Why does gestational diabetes occur?

A

Hormonal changes  cells less responsive to insulin

Increase resistance to insulin

127
Q

What is the long term effect of gestational diabetes?

A

Larger babies

Mum at risk of Type 2 diabetes

128
Q

How are diabetes and pre-diabetes diagnosed?

A

Fasting plasma glucose (FPG)
Measures blood glucose when the person has not eaten for at least 8h (detect diabetes & pre-diabetes)

Oral glucose tolerance test (OGTT)
Measures glucose after an individual has fasted for at least 8h and 2h after consuming a glucose containing drink (detect diabetes & pre-diabetes)

Random plasma glucose test
Casual plasma glucose test; i.e. measures glucose irrespective of whether the person has eaten or not (diagnose diabetic only)

129
Q

What is the glycated haemoglobin test?

A

It measures the amount of glucose attaching to haemoglobin in the blood (irreversible)

Hb1Ac gives an indication of average glucose level for 8-12 weeks

Normal: 3.5-5.5%
Diabetes: ~6.5%

130
Q

What is the fructosamine test?

A

Formed from serum proteins such as albumin
(reaction between fructose & amine). When glucose levels in the blood are elevated over a period of time, glucose molecules permanently combine with proteins in the blood in a process called glycation

Used in cases of
blood loss
haemolytic anaemia
sickle cell anaemia

Gives an average results for the last 2-3 weeks

Tends to be basis of over-the-counter tests

A high fructosamine level means that the average blood glucose over the previous 2 to 3 weeks has been elevated. In general, the higher the fructosamine level, the higher the average blood glucose level.

131
Q

What other factors can cause hyperglycaemia?

A

Steroids
Antipsychotics
Diuretics
Antihypertensive

132
Q

What other factors can cause hypoglycaemia?

A

Alcohol
Hormone deficiencies
Prolonged starvation

133
Q

What is the management of type 1 diabetes?

A

Insulin (Essential)
Exercise
Diet (low in fat, cholesterol & simple sugar)

134
Q

What is the management of type 2 diabetes?

A 
Weight reduction
Diet
Exercise
If above not successful then,
Oral hypoglycaemic medications & then insulin
135
Q

What do oral hypoglycaemic agents do?

A

Biguanides (Metformin)- Type 2 diabetes & Type 1 with insulin therapy

Inhibits glucose production by the liver (gluconeogenesis)

Useful in patients who are obese

Sulphonylureas ( Tolbutamide, gliclazide, glimepiride)

increase amount of insulin made in pancreas (requires functional islets of Langerhans)

Long lasting effect

Problem: hypoglycaemia in elderly patients or those with kidney problems

Unwanted effects:
Appetite stimulants (weight gain)
Hypoglycaemia 
GI upsets (3% of patients)
Potentially teratogenic (do not use in pregnancy or planning one)
136
Q

What are the unwanted effects of oral hypoglycaemic agents?

A 
GI disturbance
Lactic acidosis (contraindicated for those with renal, severe pulmonary or cardiac conditions)
137
Q

What drugs augment the effects of sulfonylureas?

A

NSAIDs
Alcohol
Antibacterial (Sulphonamides, trimethoprim, chloramphenicol)
Antifungal (Miconazole, fluconazole)

138
Q

What drugs decrease the effects of sulfonylureas?

A

Diuretics

Corticosteroids

139
Q

What dental problems are linked to diabetes?

A 
red swollen gums
bleeding on brushing
more plaque
tooth decay
periodontitis
ulcers
decreased saliva
bacteria can enter blood stream - endocarditis 
longer healing time
140
Q

What is nutrition?

A

sum of processes for living organism to
receive and use materials from environment to
promote its own vital activities

141
Q

What are nutrients?

A

• substances digested, absorbed, promote

body function

142
Q

What is an essential nutrient?

A

substance necessary for life,

cannot be synthesised by body, must be in diet

143
Q

What is a diet?

A

foods selected

144
Q

What is malnutrition?

A

incorrect amount of one or more nutrients in diet (not just lack)

145
Q

What is anabolism?

A

Simple molecules —> complex, requires energy

results in growth

146
Q

What is catabolism?

A

Complex molecules —> simple, releases energy

occurs during starvation+illness, energy intake↓

147
Q

What are the basic roles of carbohydrates, fats, proteins, vitamins and minerals and water?

A 
• Carbohydrate heat and energy
• Fats heat and energy
incorporated into body tissue
• Protein tissue formation and repair
broken down to produce energy
• Vitamins and Minerals
for regulation of body processes
incorporated into tissue (minerals)
• Water fluid medium essential for metabolism
temperature regulation
waste product excretion
148
Q

What is a calorie?

A

(kCal), unit of heat

149
Q

What is a joule?

A

unit of heat/muscular/electrical energy

• measured by oxidation of food

150
Q

What are the advantages of non-starch polysaccharides?

A

bulky and take longer to eat
• prolonged feeling of fullness as stay in stomach longer
• prevent constipation, colonic cancer

151
Q

What is the link of NSP’s to colon cancer?

A

NSP’s bind and dilute by increase faecal bulk, so deceasing transit time which decreases exposure to the body

152
Q

What are the disadvantages of non-starch polysaccharides?

A

• bind to minerals (Ca, Fe) —> deficiencies
• wind from metabolism of NSP in caecum and colon:
methane, CO2
, H2
depending on type of NSP and bacterial flora
• insufficient energy intake:
bulky
take longer to eat

153
Q

What enzymes are carbohydrates first broken down by?

A

Salivary amylase –> monosaccharides

154
Q

What is the glycaemic index?

A

• rate at which carbohydrate reaches bloodstream as glucose

155
Q

What happens with a decrease in carbohydrate intake to protein and fat metabolism?

A

More fat metabolised - ketoacidosis

more protein broken down - depletion of muscle

156
Q

Give some examples of monounsaturated fats

A

Olives, nuts avocado

157
Q

Give some examples of polyunsaturated fats

A
  • omega 3 oily fish, soya bean

* omega 6 sunflower seeds, wheat germ, corn

158
Q

What are essential fatty acids used for?

A
  • for structure and function of cell membranes
  • to regulate cholesterol metabolism
  • vegetable and marine oils
159
Q

Where are fats digested?

A

Stomach and small intestine

160
Q

What are the functions of fat?

A

• energy for tissue activity and body temperature maintenance
• incorporated into body structure
e.g. brain + nervous tissue
• hold position and protection of vital organs
• insulation (subcutaneous heat loss)
• satiety – presence in duodenum delays stomach emptying
• provide fat-soluble vitamins and assist absorption

161
Q

Which nutrient is the mainconstituent of every living cell?

A

Protein

162
Q

What process can turn proteins/peptides into amino acids?

A

Transamination in the liver

163
Q

What are the functions of proteins?

A

• replacement during metabolism and wear and tear
e.g. hair, nails, skin, digestive secretions, bone, dentine, epithelium, antibodies
• new tissue production
e.g. growth, recovery from injury, pregnancy, lactation
• forming enzymes, hormones
• energy source

164
Q

What is the fat of proteins?

A

structural proteins, converted into other aas, oxidised for energy

165
Q

Which vitamins can be made by intestinal bacteria?

A

• vitamin K and some of B group vitamins

166
Q

How much of the body is minerals?

A

3%

167
Q

What is the function of minerals?

A

Essential constituents of soft tissues, fluids, skeleton, teeth
• Incorporated into enzymes, proteins and soluble salts

168
Q

How much of the body is water?

A

65-70%

169
Q

What is the function of water?

A
  • fluid medium for almost all body processes
  • intra- and extra-cellular fluids
  • body secretions, excretions
  • sufficient urine flow, prevention of constipation
  • joint lubrication
  • temperature control (lung and skin evaporation)
170
Q

How is water lost from the body?

A

lost: urine, faeces, sweat (lose salt), exhaling,
vomiting, diarrhoea, haemorrhage,
exudate from burns

171
Q

What is water intake balanced by?

A

thirst, kidney regulation

172
Q

What happens if there’s too much water?

A

kidneys can`t keep up excretion
blood diluted, lower salt concentrations
water moves from blood to cells and organs
brain swells and prevents vital functions

173
Q

What is energy required for in the body?

A

growth and maintenance of body tissues
• maintenance of body temperature
• voluntary and involuntary muscle movement

174
Q

What are the calories and energy given from 1g of carbohydrate, protein, fat and alcohol?

A

• 1g carbo  16kJ (4kCal), most efficient source
• 1g fat  37kJ (9kCal)
• 1g protein  17kJ (4kCal), takes time to turn into energy, needs
energy
• 1g alcohol  29kJ (7kCal)

175
Q

What is your basal metabolism?

A

amount of energy required for basic life

processes e.g. heartbeat, respiration, cellular activity

176
Q

What is a healthy balanced diet?

A

• Lots of fruit and vegetables (40%)
• Starchy staple foods (wholemeal bread, wholegrain cereals; 40%,
incl B vits and fibre)
• Protein rich foods (lean meat, fish, eggs, lentils)
• Some dairy foods (pref. lower fat variety)

177
Q

What are the food standards agency guidelines for a healthy diet?

A

Base meals on starchy foods
• 5 (7) portions of different fruit and vegetables per day
• 2 portions of fish per week (incl. 1 portion oily fish)
• Cut down on saturated fat and sugar
• Eat less salt (no more than 6g day)
• Get active and try to be a healthy weight
• Drink plenty of water
• Limit alcohol intake

178
Q

What are the key findings from the WCRF report?

A 
Things that decrease risk of cancer:
Physical activity (colorectum,
breast, endometrium)
• Wholegrain, foods containing
dietary fibre (colorectum)
• Non-starchy vegetables (mouth,
pharynx, larynx)
• Fruit (as above, lung)
Things that increase risk of cancer:
Body fatness (11 cancers)
• Adult weight gain (breast)
• Processed foods high in fat,
starches, sugars (through
weight gain and obesity)
• Red meat (colorectum)
• Processed meat (stomach,
colorectum)
• Alcoholic drinks (7 cancers)
179
Q

What are the key lifestyle recommendations for the prevention of cancer?

A

Be a healthy weight and avoid weight gain in adult life - greater fatness causes many cancers and overweight in childhood often leads into adulthood

Be physically active - protects against weight gain/obesity and several cancers

Limit consumption of ‘fast foods’ and
other processed foods high in fat,
starches or sugars - cause of weight gain, Glycaemic load is a cause of endometrial cancer

Limit consumption of sugar-sweetened
drinks - weight fain/obesity

Eat a diet rich in wholegrains, vegetables,
fruits and beans/pulses/legumes - whole grains protect against colorectal cancer, non starchy veg and fruit protect against aerodigestive cancers, decreases likelihood of obesity

Limit consumption of red and
processed meat - causes colorectal cancer, processed meat can cause stomach cancer

Limit alcohol - causes many cancer

Do not use supplements for cancer prevention - High-dose beta-carotene supplements are a cause of lung cancer in current and former smokers.

For mothers; breastfeed your baby, if you can -Breastfeeding protects the mother against breast cancer
 Having been breastfed helps protects children against excessive
weight gain, overweight and obesity

180
Q

How can policy be used to improve adherence to lifestyle recommendations?

A

Nourishing framework:
NOURIS:
- nutrition label standards
- offer healthy foods
- use economic tools to address food affordability
- restrict food advertising and other promotions
- Improve nutritional quality of whole food supply
- set incentives and rules to create a healthy retail and food service environment

H - harness food supply chain and actions across sectors to ensure coherence with health
I - inform people about food and nutrition through public awareness
N- Nutrition advice and counselling in health care settings
- G - give nutrition education and kills

New policy framework:

  • healthy enhancing environments
  • systems change
  • behaviour change communication (check powerpoint for picture)

obstacles:
social. economic, built environment, food environment

181
Q

What is the relationship between lifestyle and cancer?

A

Food, nutrition, obesity and physical activity all affect DNA repair, proliferation, hormonal regulation, differentiation, inflammation and immunity, apoptosis, cell cycle, carcinogen metabolism which all can lead to cancer

182
Q

What are the causes of cancer?

A

Mututations - passed onto subsequent cells which accumulate

loss of genes

risk increases with age

chemical carcinogens

radiation

viruses

hromones

diet

gender

metabolic state

smoking/alcohol

15% inherited, 85% environmental

183
Q

What was the approach fine-tuned since the 2007 report?

A

 Greater focus on cohort studies
 More pooled analyses of cohort studies
 Greater opportunities to analyse by cancer subtype
 More stratified analyses (eg smoking status)
 More evidence about dietary patterns
 Greater use of non-linear analysis; permits
identification of thresholds of association

184
Q

What is the most convincing lifestyle factor that increases the risk of a lot of different types of cancers?

A

Adult body fatness

185
Q

What were the limitations of the WCRF report?

A

Poorly characterised exposures
Inconsistencies in definition of disease
endpoint
Residual confounding
Evidence comes mainly from Europe and US
Lack of understanding of nutrition impact on
biological mechanisms

186
Q

What are the lifestyle risk factors for cancer of the mouth, pharynx or larynx?

A

– Smoking
– Drinking alcohol
– Being overweight/obese

limited evidence for non-starchy veg, healthy dietary patterns and coffee decreasing risk

  • only alcohol, smoking, and body fatness have strong evidence for increasing risk
187
Q

What are the other risk factors for cancers of the mouth, pharynx and larynx?

A

• Other risk factors:
– Age – risk increases as you get older
– Gender – mouth and throat cancer is three times more common in men than
in women (may in part be related to higher rates of smoking in men)
– Infection with human papilloma virus (HPV) increases the risk of mouth and
throat cancer
– Exposure to asbestos may increase the risk of laryngeal cancer

188
Q

What are some examples of implemented policies that have helped to change lifestyle behaviour? (health enhancing, systems change and behaviour change communication)

A

Health-enhancing environments
• Restriction of alcohol consumption in public places
(Costa Rica)
• Sugar sweetened beverage tax (Mexico)
• Tax incentives to promote physical activity (Finland)

Systems change
• Co-ordinated multisectorial approach (Tanzania)

Behaviour change communication
• Breastfeeding media campaign (Bangladesh)
• Livelighter campaign (Australia)

189
Q

What is an eating disorder?

A

Complex mental illness
Behaviours are often a way of coping with an underlying issue
can affect anybody

190
Q

What are the predisposing factors to an eating disorder?

A

No specific cause / multifactorial

Can be predisposed:
high achievers/goal oriented families
previous bullying/teasing relating to appearance
broken families
peer/family/social pressures
genetic (esp. in Anorexia)
hormonal/neurotransmitters
hobbies/sports
physical/sexual abuse
191
Q

What is the clinical presentation and medical management of orthorexia?

A

Not clinically recognised as a separate eating disorder
Obsession with eating ‘pure’ or ‘clean’ foods
Feelings of extreme guilt if eat something unhealthy
Judging others
Behaviour is used to:
cope with negative thoughts or feelings
feel in control

Fatigue
Poor immune responses
Malnutrition:
angular chelitis 
recurrent apthous ulceration
Management:
therapies to tackle underlying mental health disorder (e.g. CBT, counselling)
192
Q

What is the clinical presentation and medical management of anorexia nervosa?

A

Body image disorder
Sufferers often believe they are fat, even when they are severely underweight
Disproportionate concerns about weight gain (e.g. from OCP)
Rapid weight loss
Secretive behaviours and social withdrawal

hair loss, muscle wastage, fine downy hair, weak bones

consequences:
Faltering growth
Delayed puberty
amennorrhea
infertility
Dehydration
kidney failure
Cardiac
heart failure/death
management:
Multidisciplinary and long term
Psychoeducation about anorexia
Mental health
family therapy for children
CBT/Group therapy
Monitoring physical health 
‘no blame’ approach
weight gain key for recovery
meal planning and vitamin supplements
Pharmacological interventions
TCA/SSRI
Counselling for family
Inpatient care
Not force-fed unless lack mental capacity
Dental considerations:
Halitosis - ‘pear-drops’ (ketosis)
Dry mouth – TCAs
Drug dosages 
Reduced immune response
periodontal disease
angular chelitis (malnutrition)
Medical emergencies
vasovagal syncope (faint)
cardiac arrest
193
Q

What is the clinical presentation and medical management of bulimia nervosa?

A 
Serious mental illness
Cyclical binge-eating and purging behaviours
self-induced vomiting
obsessive exercising
use of laxatives/enemas/diuretics
Binges are often distressing:
sufferers are not in control 
eat until painfully full
Often have a history of anorexia or obesity

bloating, inflammation of gut, back of throat, acid burns on knuckles

Normal/slightly overweight
Laxative abuse
Lazy colon/increased risk of colon cancer
Dehydration/electrolyte imbalance
Vomiting
Barrett’s oesophagus
Diabulimia (hyperglycaemia)
Cardiac
arrhythmias
heart failure/death
management:
Multidisciplinary and long term
Educate re. harmful effects of purging
Mental health
family therapy for children
CBT
Monitoring physical health inc. risk factors
‘no blame’ approach
meal planning and vitamin supplements
Support for family
dental considerations:
Regular dental reviews needed (NICE, 2017)
Orofacial features:
parotid enlargement
acne
oral ulceration
Medical emergencies:
vasovagal syncope
cardiac event
Dental features
Erosion
vomit pH ~3.8
palatal surfaces of incisors
perimylolysis (molars)
Caries
Dental management 
Specialist shared care
Prevention
education
2800ppm/5000ppm  fluoride toothpaste
fluoride varnish 4 x per year
fissure sealants
mouthwash after vomiting
no brushing for > 1 hour
CPP-ACP (tooth mousse)
Saliva substitutes
Monitor:
Smith and Knight/BEWE
Study models/clinical photos
Restore
ideally once stable
minimally invasive
adhesive restorations (direct/indirect)
Multidisciplinary input
Oral med - ulceration
Radiology - sialography
194
Q

What is the clinical presentation and medical management of binge eating disorder?

A

Binges similar to bulimia, but without purging
Buying lots of food and hoarding it
Secretive eating – rapidly and until over-full
Social withdrawal
More common in adults
May have had another ED previously or go on to develop one

Weight gain
Bad skin
Bloating and constipation
Stomach rupture
Longer term:
obesity
type II diabetes
sleep apnoea
heart disease

BED medical management:
Mental health
CBT/group CBT
outpatient care unless self harm/suicide risk
Monitoring physical health inc. risk factors
daily food intake plan – avoid dieting
weight monitoring

dental considerations
Caries
Weight
dental chair max. 127kg
GA airway risks
Medical emergencies
hypoglycaemia
MI
cardiac arrest
195
Q

What is the clinical presentation and medical management of Obesity?

A

BMI 30 and above
Not classified as an eating disorder, though there may be some overlapping features
Can be many reasons why a person is obese
may or may not be related to underlying mental health
Clinical features and dental considerations similar to BED
Management tailored to the underlying cause:
exercise on prescription
healthy living classes
CBT/Counselling

196
Q

What are some of the factors that decide choice of food?

A

age, gender, mood

cost, availability, preference, advertising, income, environment, transport, social status, location, culture, religion

197
Q

What happens to the energy and nutrient requirement of an adults diet?

A

Nutrient requirements stay the same but energy requirements fall - less calories needed

198
Q

What are the nutrient and food recommendations?

A

Fat total intake ~35% dietary energy- Reduced fat spreads and low-fat dairy

Saturated Fat total intake <11% dietary energy
Replace sat. fats and oils with those low in sat., rich in polyunsaturates

Complex Carbohydrates increase by 50%
Increase consumption of fruit, vegetables, bread, potatoes

199
Q

What are the alcohol guidelines?

A

Men and women less or equal to 14 unites a week, spread out over more than 3 days
none in pregnancy

200
Q

What are the salt recommendations?

A

6g, 2.4g sodium (Na x2.5= salt)

201
Q

What happens when cholesterol oxidises?

A

Forms atheromas, narrowing the arteries

202
Q

What is the reference and suggested range for total, LDL and HDL cholesterol?

A

Total 3.5-7.8 <5.2 LDL cholesterol 2.3-6.1 <4.0 HDL cholesterol 0.8-1.7 >1.15

203
Q

What are the guidelines for a healthy diet on a budget?

A
  • plan >1 day ahead, shopping list; buy in quantities you will use; supermarket brands
  • try small amounts of new foods
  • buy fruit and veg regularly (markets) and store carefully
  • include generous helpings of starchy foods per meal (cheap, filling, healthy) • buy the leanest meat you can afford (mix with veg/pulses to casseroles to go further); tinned/frozen fish and meat cheaper
  • careful cooking re: fuel use e.g. water in kettle, toaster cf grill, multiple dishes in oven, lids on saucepans, share (+shopping)
  • beware processed foods (contents and cost)
204
Q

Why may the nutrient requirements of older people be more difficult to achieve?

A

Poor appetite
in pain
have a disability

205
Q

What are the causes of older mal/undernourishment?

A

Extreme age • increasing frailty increases the risk

Social isolation and loneliness
• ~14%+ live alone; social contact aids well-being

Loss of appetite
• food enjoyment depends on visual appearance, taste, smell
• smoking, poor OH, drugs
• salivary secretion - taste, chewing and swallowing (salivary gland dysfunction: Sjögren`s syndrome; xerostomia [drugs]; chemotherapy: mucositis, candidiasis)

Mental disturbances
• e.g. dementia – forget, lack of motivation

Physical disability

Dental problems
• 200-300kcal less intake due to poor-fitting dentures
• due to discomfort
• results in soft, bland diet; indigestion

Dysphagia: swallowing difficult or painful
• MS, MND, CV attack/stroke, radiotherapy, surgery, confusion
• IV fluids, fluid thickeners, gastrostomy feeding
• speech-, occupational-, physio-therapists, dietitian

Foods difficult to chew or swallow:
hard (toast, crackers, raw vegetables); chewy (meat); sticky (mashed potato); crumbly (fruit cake)

Constipation/bowel problems: due to reduced gut motility and inactivity (fibre and fluids

206
Q

How can you prevent older mal/undernourishment?

A

Dehydration
• 6-8 glasses, account for spills
• headache, constipation (disorders of GIT), UTIs, confusion

Home care assistants
• buy and prepare

Meals on wheels
• portability, loss of nutrients, punctuality

Lunch clubs
• ideal, less nutrient deterioration, social contact

Institutions
• puréed food unappetising, taste similar if taste and smell
• sip feeds (Fortisip)
• Percutaneous Endoscopic Gastrostomy (PEG) feeding

207
Q

What did the national diet and nutritional survey look at?

A

Food consumption, nutrient intakes and nutritional status 1.5yrs+ living in private UK households

interviews, diet-diary, main food provider (purchase, prepare), nurse visits, blood, urine • different data, but can compare previously • continuous, cross-sectional data • blood indices of nutritional status and 24hr urinary sodium in children and older adults (from ‘11/’12) • new in ’15/’16 – free sugars and fibre (as AOAC=total dietary fibre=NSPs and cellulose, etc. following SACN 2015 carbs report)

208
Q

What did the national diet and nutrition survey find?

A
  • Adults was 19-64yrs & 65+ (now 65-74 and 75+ ‘older old’ i.e. 3 grps) • High quality, nationally representative data • Overall diet and nutrient intakes similar to previous assessments
  • Takeaways/eating out Fridays and Saturdays* • High meat and vegetable intake on Sundays* *but still some bias on weekends days even though sample days changed • Vegetarian, smoking, obesity, blood pressure, alcohol

• 31, 32 and 19% (3 age grps) meet 5-a-day target • Oily fish: below and no change over time • Processed meat: mean consumption reduced (and women meeting <70g/dy recommendation) • Saturated fat: above recommendations and no change over time • Mean total fat: met recommendation <35% total food energy, except in older old • Free Sugars signif reduced: in men cf yrs 1 and 2, tho’ above recommendations; BUT is 11.1, 11.2 and 11.3% in all 3 adult age groups • Fibre: 15-20g/dy (below recommendation 30g/dy) • Vitamins and minerals: less than RNI, esp. iron. • Salt: above

209
Q

What developmental defects of teeth are associated with nutrition?

A

deficiencies - calcium, vitamin A and D (hypoplastic enamel), manlnutrition

excesses - fluoride, tetracycline - if given during enamel formation stage to pregnant women, causes enamel staining

210
Q

What is the percentage reduction in caries with fluoride?

A

15-50% reduction in caries

excess fluorosis, GIT upset, respiratory arrest and death

211
Q

What can patients with vit D resistant rickets present with in their teeth?

A 
Large pulp chambers
Large/promininent pulp horns
Enamel hypoplasia 
Clefts and tubular defects in dentine
may present with spontaneous dental abscesses
212
Q

What are the risk factors for a vitamin D deficiency?

A

high BMI, low fish consumption, low educational level, and limited skin exposure

213
Q

What is the evidence for the role of calcium and phosphates in dental development?

A

There was a significant decrease in prevalence of enamel hypoplasia in children (1929-1943) following introduction of:
Cheap milk
Cod liver oil for pregnant women and young children
Bread fortified with calcium

Patients with disorders of calcium and phosphate metabolism (x-linked hypophosphatasia, hypoparathyroidism) show significant increases in enamel defects (hypoplasias)

214
Q

What was the evidence for the role of vitamin D in dental development?

A

Historically, May Mellanby (early 1900s) found that dogs fed on diets deficient in vit D had:
Delayed dental development
Deficient (hypoplastic) enamel

215
Q

What was the evidence for the role of vitamin A in dental development?

A

Severe changes in ameloblasts occurs in rats fed with diet deficient in vitamin A – with resultant defective enamel and dentine formation
No evidence for the role of vit A in human tooth formation

216
Q

What is the evidence for the role of malnutrition in dental development?

A

Nigerian study (1973) found the following dental defects in malnourished children (severe lack of protein)
Enamel hypoplasia (linear grooves) involving primary incisors
Generalised enamel hypoplasias in 20% of children
Delayed dental eruption

217
Q

What are some extrinsic dietary causes of erosion?

A

Acidic drinks (most fruit-flavoured or carbonated drinks)
Acidic food (citrus fruits, yoghurts)
Vit C tablets
Pickled foods + vinegar

> 2 citrus fruits daily
Vegetarians/vegans
4 carbonated drinks daily: 252% increased risk

218
Q

What is the link between food consistency and periodontla health?

A

In (some) animals there is evidence that a fibrous diet will help reduce incidence of plaque-related gingivitis and periodontal disease

no evidence in humans but eating fibrous foods may help to maintain the supporting tissues of the periodontium, and increased salivary flow from eating fibrous foods may have some beneficial effects on oral health generally

219
Q

What do children who are PEG fed readily develop?

A

excessive calculus deposits on all tooth surfaces

220
Q

What is vitamin C deficiency related to?

A

poor peridontal health

Disturbed collagen formation
Bleeding and swollen gums, loose teeth
First seen in sailors (now seen in people with very deficient diets: homeless, fussy teenagers!)

221
Q

What is the most deficient nutrient in adults?

A

Folic acid and periodontal health
Primarily concerned with DNA synthesis and cell turnover
Probably plays a role in periodontal health by maintaining epithelial integrity and attachment
Folate mouthwashes and supplements have been shown to reduce pregnancy-related gingivitis

222
Q

Name some foods rich in folate?

A

leafy greens, asparagus, broccoli, oranges, avocado, seeds and nuts, brussel sprouts, cauliflower, bell peppers

223
Q

What are the oral mucosa manifestations of vitamin B12, C, K, folic acid, iron and protein deficiencies?

A 
Vitamin B12 (glossitis, fissured tongue, burning mouth, erosive or ulcerative lesions)
Vitamin C (haemorrhage and swelling)
Vitamin K (gingival bleeding)
Folic acid (ulcers, burning mouth, depapillation of tongue)
Iron (ulcers, glossitis, burning mouth)
Protein deficiency/kwashiokor (oedema of tongue, atrophy of papillae, circumoral hypopigmentation)
224
Q

What is orofacial granulomatosis and what are some agents that trigger it?

A

Probable delayed hypersensitivity reaction

agents identified - benzoates E210-219, cocoa, cinnamon, carvone (found in essental oils - caraway, spearmint, dill)

225
Q

What are the clinical signs of orofacial granulomatosis?

A 
Diffuse facial swelling
Lip enlargement + vertical fissuring
Angular cheilitis
Oedema of buccal mucosa
Mucosal tags
Aphthous-like ulceration
226
Q

How can you investigate and confrim orofacial granulomatosis?

A

Biopsy – non-caseating granulomata
Bloods
Patch-testing

227
Q

How do you manage orofacial granulomatosis?

A

Exclusion diet
Symptomatic relief (difflam, gengigel)
Immunosupresants
Steroids (mouthwash, systemic)

228
Q

What are the problems with diet diaries?

A

They forget to return their diet sheet or lose it
They change their eating habits (subconsciously or consciously)
They may be observing a religious festival or be on a special diet at the time of the diet diary
They write what they think you would like to see
They forget details
There may be literacy or language difficulties

229
Q

What is the 3 step approach from a diet diary analysis?

A 
Identify and target at-risk patients (high caries experience or erosion)
Ask them (or guardian) to keep a written record of everything they eat and drink for 3 days (including one weekend day)
Ask them to return it for you to appraise and give feedback
230
Q

What is the cochrane evidence for dietary analysis?

A

2012

interventions to change diet in a dental care environment
Review aimed to determine whether efforts by dentists and other dental staff members are successful in changing patients’ diets

5 studies identified – 2 concerned with diet advice given concerning general health (one was about alcohol and one was about fruit and vegetable consumption). In both these studies there was a change to healthier behaviour following the advice.

Most of the studies concerning sugar consumption are of relatively weak quality.
The evidence for dietary advice aiming to change sugar consumption is poor. Further studies in this area should be considered

231
Q

What are the dietary recommendations in dental practice in relation to dental erosion?

A

discourage frequency and amount of acid drinks and foods consumed

discourage adding acidic drinks to infant feeding bottles

promote chilling of drinks, use at one go and limit to mealtimes any soft drinks consumed

discourage use of acidic sweets especially inbetween meals

promote drinking water, also nutritious drinks e.g. milk, also promote fresh fruits as part of a healthy diet

promote use of neutralising food e.g. cheese after having an acidic food or drink

use of a straw

refrain from toothbrushing straight after an acid attack

232
Q

What are the steps after the diet diary has been returned to you?

A

step 1 - thank the person for returning the diet sheet and show a genuine interest, tell them you would like some time to look at it before their next visit and give them feedback

gain a general idea of whether the sheet has been completed thoroughly or not, could ask some follow up questions at their next visit e.g. do they take sugar in their tea

step 3 - find some positive/ good about their diet history to feedback

step 4 - identify all the cariogenic/erosive food or drinks that are taken outside of a mealtime, count up episodes

step 5 - hidden sugars, cereals ketchup flavoured crisps, fruit yoghurt, dried fruit

step 6 - ideally provide individualised written and verbal feedback so that the patient can take something away with to help them remember your advice

step 7 - feedback about caries:
say something nice
explain that frequency of sugar attacks need to be reduced to prevent decay
offer safe altenratives
advice against drinks for infants in a bottle
recommend general healthy eating guidelines ( 5 a day)
reinforce toothbrushing with F toothpast twice a day

step 8 - reinforcement - repeat the exercise at a recall visit

233
Q

What are some ‘safe’ snacks and drinks?

A

Water/milk/tea with no sugar (or sweetners for older patients)
Fresh fruit/veg
Cheese/meat
Bread/breadstick
(Plain crisps)
Nuts (for older patients, with no nut allergy!)

234
Q

What are the general principles for dietary analysis?

A

Keep it simple (avoid too much information at once)
Don’t be judgemental
Be positive and encouraging
Give practical alternatives
Accept that there may be medical reasons that override your diet advice for dental health
Reinforce your advice

MDENT210 (7 decks)

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