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BDS 2 > Nutrition and Digestion > Flashcards

Nutrition and Digestion Flashcards

1
Q

Why are diet diaries important

A

Help identify cariogenic foods
Help patient realise what they eat
Help understand amount of cariogenic attacks
Identify malnutrition or lack of parent support

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2
Q

What instructions do we give with a diet diary

A
  • 2 week days and 1 weekend
  • fill in every time we eat or drink
  • amount, type of food, time
  • add in when we brush/mouthwash
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3
Q

When we receive a diet diary, what are the steps to how we deal with it?

A
  • thank patient for bringing it back
  • see if it is filled completly and correctly
  • find something good to congradulate patient
  • find hidden sugars
  • ask patient to highlight cariogenic food and then correct if wrong
  • give individualised improvements on erosion and caries feedback
  • dont be extreme, ask to cut down, not quit
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4
Q

What is the accepted units of alcohol in a week?

A

14 unis for men and women

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5
Q

What do we do with patients who say the drink more than 14 units?

A

Ask them if they are concerned with how much they drink and I’d they have ever thought about reducing and if they say no, leave it. If they say yes, make them aware of risks with oral cancer and sugar –> caries and refer to alcohol awareness or charities

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6
Q

If a patient says they smoke, what do we do?

A

Ask if they have ever thought of quitting or if they want to, and if they say yes offer them our smoking cessation services

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7
Q

what makes a nutriton ‘essential’

A

we cannot make it in the body and need it for normal bodily function

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8
Q

what is the difference between undernutrition and malnutrition

A

under - not enough food

mal - the wrong nutrients/unhealthy

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9
Q

define Anabolism

A

forming of larger nutrients from smaller

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10
Q

define catabolism

A

breaking down of molecules

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11
Q

why is it important to balance fibre and NSP

A

NSP are good for:

  • preventing constipation
  • act against carcinogens
  • make us feel fuller

too much NSP binds to minerals and makes them unavailable

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12
Q

what is NSP

A

non-soluble polysaccharide

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13
Q

what is GI for a food

A

Glycemic index is how fast the carbohydrate reaches the bloodstream as glucose

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14
Q

why are carbohydrates classed as a protein sparer and how much of daily energy should come from free sugar

A

‘protein sparer’ means it prevents the breakdown of proteins

<5% and to be reduced through life

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15
Q

what are vitamins

A

Vitamins are organic (or related) substances with specific biochemical functions
essential for normal metabolism (promote reaction/s)

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16
Q

what are minerals

A

Minerals are essential constituents of soft tissues, fluids, skeleton, teeth

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17
Q

what are the water soluble and water soluble vitamins

A

water soluble are B and C

fat soluble are ADEK

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18
Q

what is your basal metabolism

A

amount of energy required for basic life processes e.g. heartbeat, respiration, cellular activity.

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19
Q

what are some general guidelines of the eatwell plate

A 
2 portions of fish a week
5-7 portions of fruit and veg a day
cut down saturated fat and sugar
limit alcohol
dont skip breakfast
base meals on starchy foods
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20
Q

what is bioavailability of a vitamin and which is the most bioavailable vitamin

A

the relative absorption of the vitamin from the diet
the abundance of naturally occuring vitamin
D as we synthesise it from the sun

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21
Q

when is overuse of vitamin supplements most likely to cause toxicity

A

during pregnancy for the foetus

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22
Q

what is vitamin A, where do we find it, what is its function and what is its deficency

A

precursor for retinoids
leafy greens, fish, oils, milk, eggs
bind to proteins in retina to form visual pigments and role in cell signalling
Vital for epithelial cell integrity
severe deficency = blindness, poor turnover of epithelium
low deficiency = poor vision in low light

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23
Q

where do we get vitamin D

A

mushrooms

sunlight

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24
Q

what is the function of vitamin D

A

absorption of calcium and phosphates affecting mineralization of bone+tooth
immune function

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25
Q

vitamin D deficency?

A

rickets

reduced immune response

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26
Q

explain rickets

A

Vitamin D/calcium deficency
reduced absorption of calcium and phosphates
reduced bone formation and mineralization
bones weak and cant support body and start to bend

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27
Q

what are the anti-oxidant vitamins

A

A C and E

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28
Q

where do we find vitamin K

A

fortified cereals
leafy greens
oils

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29
Q

what is the function of vitamin K (2)

A

precursor for blood clotting factors
coenzyme for post translational carboxylation of glutamate to y carboxy glutamate
stops proteins binding to phosphoilipd membranes (preventing clotting)

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30
Q

what is a deficiency in Vitamin K and who is more at risk

A

haemorrhagic disease

new-borns particularly at risk, given Vit K at birth

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31
Q

what is vitamin C and where do we find it

A

Ascorbic acid

colourful citrus fruit and vegetables

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32
Q

what is the function of vitamin C

A

synthesis of adrenaline and noradrenaline
maturation of connective tissue - cross linkage of collagen I
increases iron uptake (keeps iron as Fe2+ not Fe3+ increasing absorption)

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33
Q

what are signs of vitamin C deficency

A

bleeding gums
anaemia
tired and weak
poor wound healing

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34
Q

why is the face and oral cavity sensitive to nutritional vitamin deficiencies

A

mucous membrane has rapid turnover of epithelium so needs lots of vitamins and protein to form new cells (vitamin A)

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35
Q

what vitamins are important for tongue health

A

B and iron

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36
Q

what is the importance of iron and where do we get it

A

used to form haemoglobin which is the main carrier of oxygen around the body essential for respiration
green leafy vegetables, meat,

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37
Q

why are calcium and phosphate important and what vitamin helps their absorption

A

vital for proper neuromuscular function
vital for good bone formation and mineralisation
vitamin D helps absorption of these minerals
Calcium important for coagulation cascade and wound healing

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38
Q

what are oral manifestations of vitamin B/iron defiecncies

A

Glossitis (tongue is inflammed and red)
Smooth tongue
Cheilosis (swelling and fissuring of lips)
Angular Chelitis
Malar pigmentation
Nasolabial seborrhea (red, flaked skin - dermititis around nose)

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39
Q

why might the tongue be smooth?

A

atrophiy of filiform papillae caused by deficency in vitamin B and iron

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40
Q

what is malar pigmentation and what is the cause

A

blue/brown spots freckled in patches on the face

deficency in B6, iron, niacin

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41
Q

what are the main 3 vitamin deficiencies that affect oral/facial structures

A

iron, B6 and niacin

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42
Q

what is the general function of vitamin B

A

immune and nervous function
Cell function and growth
B9 (folate) important for neural tube health in pregnancy

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43
Q

what happen if we have too high/low blood glucose levels

A

too high pulls water out of cells due to osmosis destroying the cells
too low –> low ATP –> brain has no fuel so goes into coma and lack of oxygen leads to cell death

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44
Q

what does glucagon do

A

covnert glycogen stores from cells into glucose

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45
Q

what does insulin do

A

convert blood glucose to glycogen for short term storage

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46
Q

what are the three soruces of glucose

A

diet
glycogen degradation
gluconeogenesis

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47
Q

which part of the body cannot be supplied by fats for fuel? why?

A

the brain
fatty acids produce ATP straight away without glucose
glucose travels to the brain cells to provide ATP at the cells
ATP cannot cross into the brain

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48
Q

SOME fibre gets broken down in the digestive tract. How?

A

some fibre is fermented by bacteria in the gut to make short chain fatty acids

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49
Q

when does the fasting period start and how long can we last without food

A

2 hours after eating

40 days

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50
Q

which hormone other than insulin and glucagon affects glucose blood levels?

A

adrenaline increases glycogen degradation

It can override glucagon and insulin temporarily

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51
Q

what is gluconeogenesis and when does it begin

A

formation of glucose from non-carbohydrate sources mainly in the liver
30 hours after eating when glycogen levels are low

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52
Q

name three things that can be turned into glucose for gluconeogenesis

A

amino acids - mainly alanine
lactate formed by anaerobic respiration in intense muscle exercise
glycerol from fatty acids

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53
Q

some energy is required to initiate gluconeogenesis. Where does this come from

A

beta oxidation of fatty acids

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54
Q

what mechanisms is gluconeogenesis regulated by (2)

A

substrate availability e.g. insulin, glucagon, glycogen, ATP, lactate, amino acids
regulatory irreversible steps e.g. glucose - 6 -phosphate to glucose

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55
Q

f

A
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56
Q

what is a triglygeride

A

1 glycerol bound to 3 fatty acid chains by ester bonds

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57
Q

what forms of lipids are there

A

triglycerides - unsatured and saturated
phospholipids
steroids e.g. cholesterol

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58
Q

how can lipids be gained for the body

A

diet

carbohydrate –> lipid in liver

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59
Q

explain how we absorb lipids

A

eat fatty foods
CCK –> gallbladder releases bile salts emulsify lipids
Pancrease –> lipases and co-lipases break down into triglycerides
further breakdown into micelles that diffuse into SI
bile salts re-absorbed and triglycerides reform in cells
go to SER to form nascent chylomicrons
apoporeins added in RER and golgi alter proteins for recognition

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60
Q

why can micelles cross membranes

A

they have phospholipid non-polar heads on their outer surface so pass through non-polar lipid membranes

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61
Q

what are nascent chyomircons and where are they formed

A

formed in the smooth endoplasmic reticulum
transporters of triglycerides
outer surface formed by phospholipids
contain free triglycerides and cholesterol
apoproteins added by RER to be identified by cells requiring lipids

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62
Q

what happens to nascent chylomicrons

A

enter lymphatic system
get thongs added to them to become mature chylomicrons
travel to cells needing fats

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63
Q

what is LPL and what is its function

A

lipoprotein lipase found on cells requiring lipids
adheres to chylomicrons and VLDL
breakdown lipids and release triglycerides from chylomicrons
found on cells like adipose tissue, glands, muscle

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64
Q

what is LPL and what is its function and wjat controls this

A

lipoprotein lipase found on cells requiring lipids
breakdown lipids and release triglycerides from chylomicrons
found on cells like adipose tissue, glands, muscle
insulin and glucagon control release of this

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65
Q

how are triglycerides and cholesterol transported

A

chylomicrons

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66
Q

where do chylomicrons remnants like excess FA, glycerol and cholesterol go?

A

liver for metabolism and recycle

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67
Q

what are endogenous lipids

A

lipids formed from glucose/triglycerides formed in the liver

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68
Q

what are the three main fates of triglycerides

A

stored as triglycerides
beta-oxidised for ATP fuel
used as structural components e.g. phospholipids

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69
Q

how are endogenous lipids stored and transported? same as dietary lipids?

A

in liver combined with proteins and glycerol-3-phosphate from citrate cycle, cholesterol and apoproteins to form
VLDL very low density lipids
Very similar to chylomicrons but different still

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70
Q

how are lipids used for energy and what stimulates this process

A

beta oxidation

glucagon, ADP

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71
Q

how do fatty acids enter cells

A

fatty acids bind with ATP to form fatty acyl-CoA

diffuse across membrane

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72
Q

explain beta-oxidation

A

fatty acids bind with ATP to form fatty-acylCoA
move into mitochondria
All carbons converted to Acetyl-coA used in the citrate/TCA cycle to produce NADH and FADH2 forming ATP
Lots of carbons within fatty acid chains so produces a lot of ATP

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73
Q

why is cholesterol important

A

stabilises fluidity of phospholipid membranes
blood lypoprotein transport of triglycerides in chylomicrons/VLDL
precursor of bile salts
precurser of Vit D
Useful for formation of steroid hormones

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74
Q

how is cholesterol absorption controlled and why is this important

A

small lipid diffusion into lumen SI
Enterocytes transport excess cholesterol back into lumen

important as cannot be fully metabolised so cholesterol levels depend on initial absorption

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75
Q

defects to enterocyte proteins affect what

A

increased cholesterol levels

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76
Q

how is cholesterol synthesised and where

A

liver converts acetyl-CoA into cholester by HMG-CoA Reductase

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77
Q

what things affect HMG-CoA Reductase

A 
(HMG CoA reductase converts NADH into cholesterol)
insulin excites
glucagon inhibits
cholesterol-lowering drugs inhibits
cholesterol inhibits
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78
Q

how is cholesterol transported from the liver and what are their fates

A

bile salts stored in gallbladder used to aid digestion of lipids
cholesterol esters implemented into VLDL (and chylomicrons but not from liver)

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79
Q

what happens to the remnants of VLDL/Chylomicrons (expand on cholesterol)

A

taken to liver
usually high in cholesterol
Can be turned into bile salts or vitamin D
converted to intermediate density lipid (IDL) and further to low density lipid (LDL) which is very high in cholesterol
LDL can be used to form VLDL or for cells needing cholesterol

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80
Q

how do cells get more cholesterol if needed?

A
  • LDL activated to adhere and break down VLDL or Chylomicrons
  • apoproteins on cells LDL receptors break down LDL
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81
Q

what happens to excess LDL

A

macrophages phagocytose the LDL

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82
Q

explain how pathogenic blood clots form in blood vessels

A

macrophages phagocytose excess LDL - high in cholesterol
macrophages become foamy cells and stick to blood vesel walls
forms atherosclerotic plaque that forms a lump in the blood vessels
High BP hits the plaque forming small thrombosis
continuous repair of epithelium leads to larger clot
blood clot

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83
Q

what plaque and where, does LDL cause

A

atherosclerotic plaque on blood vessel walls

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84
Q

what are ketone bodies

A

Ketone bodies are water-soluble molecules that contain the ketone groups produced from fatty acids breakdown in the liver.

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85
Q

why might a patient have a bad breath/nail polish remover/acetone smell

A

when ketone bodies are broken down acetone is released
excess ketone
sign of poorly controlled diabetes or severe starvation/eating disorder

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86
Q

when are ketone bodies used

A

when the body has very low glucose blood levels
They can be converted into Acetyl-CoA which enters the citrate cycle to produce ATP.
The brain uses ketone bodies for energy as fatty acids cannot cross the blood brain barrier but ketone bodies can

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87
Q

Which cells of the pancreas make insulin and glucagon

A

alpha cells make glucagon

beta cells make insulin

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88
Q

what are the major symptoms of diabetes mellitus

A 
high blood glucose levels
sweet urine
ithcy skin
blurry vision
increased thirst and urination
reccuring gum/bladder infection
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89
Q

what are the normal fed and fasting blood glucose levels for a person with and without diabetes

A

Without diabetes:
Fasting : 3-4mmol/l
Fed 90 minutes post: <10 mmol/l

With diabetes:
Fasting: 4-7mmol/l
Fed 90 minutes post: >20mmol/l

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90
Q

What are some major complications of diabetes mellitus

A 
peripheral vascular disease (cold extremities)
stroke
sugar induced coma
nerve damage
ulceration
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91
Q

Briefly explain type 1 diabetes

A

chronic disease emerging in childhood or pregnancy
lack of insulin produced
though to be because of attack on beta cells in pancreas autoimmune
family history increases risk

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92
Q

briefly explain type II diabetes

A

Environmental factors like obesity and high sugar diets increase defects in response to insulin leading to hyperglycaemia
Comes on usually in adulthood after high glucose exposure
Insulin response decreases over time

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93
Q

What is gestational diabetes

A

diabetes that onsets in the 2nd trimester of pregnancy
2-5% of all pregnancies
age>35, ethnicity and obesity predisopose
no obvious symptoms but sometimes classic diabetes symptoms

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94
Q

why does gestational diabetes occur and what affect does it have on the baby and mother

A

hormonal changes alter the bodies response to insulin leading to hyperglaecemia
baby will be larger
mother has higher chances of developing type 2 diabetes

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95
Q

what is pre-diabetes and what is the difference of IGT and IFG

A

impaired glucose tolerance and impaired fasting glyceamia
IGT = abnormally high glucose levels after eating but not high enough to = diabetes. Increased risk of cariovascular
IFG = impaired fasting glycaemia is higher than normal fasting glucose blood levels but not high enough to = diabetes. Control diet and exercise.

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96
Q

how do we test for diabetes

A

fasting glucose levels
oral glucose tolerance testing 2h and 8h after eating
random plasma glucose check

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97
Q

what is glycated haemoglobin check and what does it test and what normal/diabetic readings do we get

A

best way of checking if diabetes is under control
RBC last 8-12 weeks
addition of glucose to haemoglobin is irreversible
Normal: 3.5-5.5% glycated haemoglobin
Diabetes: ~6.5% glycated haemoglobin

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98
Q

how do we manage diabetes

A

type 1:

  • insulin injections
  • monitor glucose levels
  • diet and exercise

type 2:

  • manage diet
  • exercise to burn glucose

General:

  • low sugar and cholesterol diets
  • regular meal times
  • monitor blood glucose levels
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99
Q

what is the function of oral medications for diabetes (2)

A

Drugs that decrease gluconeogenesis in the liver

Drugs that increase insulin production in the pancreas

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100
Q

how does diabetes affect the oral cavity

A 
Higher risk of bleeding when brushing
Red swollen gums
Higher tooth decay and plaque on teeth
Higher amount of alveolar bone loss.
Increased periodontitis 
Changes in blood flow and innervation
Changes in immune response and increased inflammation
Decreased salivary flow so dry mouth
Increased bleeding time during surgery
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101
Q

What is Orthorexia Nervosa

A

Not clincially seen as an eating disorder
Patient keeps strict diet and feels guilty for bad diet
Way of keeping control of themself
Can lead to other eating disorders
Malnutrition presents as ulceration or angular chelitis (vit B/iron deficency)

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102
Q

what is Anorexia Nervosa

A

eating disorder where a patient feels more overweight than they are
may eat secretly and discretely

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103
Q

what are the signs of anorexia nervosa

A 
loss of weight
thin layer of hair over skin (insulation)
social withdrawal
loss of head hair
decreased bone mass
acetone smell (ketone body)
angular chelitis
dry mouth
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104
Q

what can anorexia lead to (4)

A

cardiac problems due to body breaking down cardiac muscle
Malnutrition leading to deficencies
dehydration as most water comes from food
infertilitiy and periods stop

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105
Q

how can we manage eating disorders

A 
'no blame' approach
group monitoring
diet plans and management
weekly weigh ins
councelling
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106
Q

What is bulimia Nervosa

A

where a patient binge eats and eats until painfully full and then makes themself be sick

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107
Q

what are the signs of bulimia

A 
obsessive exercise and laxatives
Ulceration of mouth and hands due to stomach acid
high caries
high erosion of teeth
parotid gland enlargement
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108
Q

How can we treat the oral manifestations of bulimia

A

Ask patient to brush teeth with high flouride mouthwash after being sick and apply flouride varnish on all surfaces to prevent caries ad TSL

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109
Q

What is binge eating disorder

A

similar to bulimia without purging

patient hoards food and eats it slowly over time with social withdrawl, feels bad about eating

110
Q

What are the signs of binge eating disorder

A

weight gain
bad skin
constipation
caries due to constant acid attack

111
Q

how do we manage binge eating disorder

A

dont diet advise just provide a time schedule to eat at specific times

112
Q

what classes someone as obese

A

BMI over 30

113
Q

explain the 5 steps of CBT

A 
Make a list
list unproductive thoughts
create replacement thoughts
read the list often
reflect and replace thoughts
114
Q

How do we speak to a patient we suspect to have an eating disorder

A

sensitively
in private room, not in clinic or possibly not in front of family
x-ray room is good opportunity
avoid commenting on physical appearance/clothing
don’t focus on weight

115
Q

what organs are involved in the GI tract

A 
mouth
oesophagus
stomach
small intestine
large intestine/colon
rectum
accessory organs e.g. gall bladder, pancreas, glands
116
Q

what is the general structure of all of the GI tract

A

good blood supply for glandular secretions
significant nervous supply within submucosal plexus
glands intermittent
Mucosal epithelium with underlying lamina propria - loose connective tissue

117
Q

what epithelium is mucosal lining

A

non-keratinized squamous epithelium

118
Q

how much liquid do we absorb in a day and how much is from idet, where is the rest from?

A

9L a day
2L from diet
rest is reabsorbed gastric jucies

119
Q

what is deglutition and what are the 3 stages

A

swallowing
stage 1 = oral phase
stage 2= pharyngeal
stage 3 = oesophageal

120
Q

why is swallowing so tightly regulated

A

as food and liquid goes very close to the airway which must be tightly controlled and prevented

121
Q

describe the oral phase of degluttation

A 
voluntary
tongue presses against hard palate
compresses bolus
retraction of tongue pushes bolus into pharynx
respiration inhibited
122
Q

describe the pharyngeal stage of deglutition

A

involuntary from stimulus when food hits pharynx
soft palate reflects closing nasopharynx
Epiglottis closes the airway
trigger to oesophageal phase

123
Q

describe the oesophageal phase of degluttation

A

upper oesophageal sphincter relaxes, bolus enters oesophagus
vagus nerve triggers primary peristalsis
Enteric nervous system triggers secondary peristalsis of oesophagus pushing bolus down
lower oesophageal sphincter opens

124
Q

how are all passages apart from the oesophagus blocked during the oesophageal phase of degluttation

A

soft palate reflecting prevents passage into nasopharynx
tongue against palate prevents exit into oral cavity
epiglottis reflects preventing passage into airway

125
Q

what prevents reflux of material back into oesophagus and why is it special

A

lower oesophageal sphincter or cardiac sphincter

has a squamocolumnar junction between squamous mucosal epithelium and columnar stomach epithelium

126
Q

what are the four parts of the J shaped stomach

A

1st cardiac (cardiac sphincter)
2nd (upper right) Fundus
3rd body
4th pylorus (pyloric sphincter)

127
Q

what is gastric accomodation

A

stomachs ability to store food and begin mechanical digestion
control of chyme into small intestine

128
Q

what are the functions of the stomach

A

gastric accommodation
protection against bacteria - low pH
absorption of fatty acids and alcohol
digestion of proteins with gastric juice

129
Q

explain the surface of the stomach in relation to gastric release

A

stomach has single cell columnar epithelium
ruggae on surface that can stretch
gastric glands in lamina propria open at pits

130
Q

where are gastric glands found

A

lamina propria of stomach

131
Q

what is the composition of gastric juice

A

water
ions
HCL preventing bacterial growth and catalysed cleavage of
pepsinogens into pepsins
Mucous to protect gastric mucosa
gastrin stimulates release of more acid
intrinsic factor helps absorption of vitamin B12

132
Q

what is the role of HCL in GI tract

A

prevent growth of most bacteria

catalyse cleavage of pepsinogen to pepsin

133
Q

what is the role of mucous in the GI tract

A

line and protect gastric mucosa

134
Q

what is the role of gastrin

A

regulates secretion of acid

135
Q

what is the role of intrinsic factor and where is it secreted

A

helps absorption of B12 in ileum

secreted from the stomach

136
Q

what parts of the nervous system is the GI tract controlled by

A

Enteric nervous system

137
Q

what parts of the nervous system control digestion (3)

A 
autonomic nervous system
     -sympathetic: inhibit digestion
     -parasympathetic initiates digestion
central nervous system
enteric nervous system
138
Q

what is the function of the enteric nervous system, what is it composed of and roughly how many nerve fibres are involved

A

~100 million similar to spinal chord
2 nervous plexuses
controls short nerve impulses, detects food in GI tract and what food
controls muscles and glands

139
Q

what is the effect of CNS on digestion

A

sight, smell, taste all act as external stimulus
alters activity of enteric nervous system through long reflexes
changing motility and secretion

140
Q

what does the LI absorb

A

water and salts

141
Q

what nerves control the oesophageal phase of degluttation

A

primary peristalsis is controlled by vagus nerve

secondary peristalsis is controlled by enteric nervous system

142
Q

what cells control release of hormones into GI tract and how are they controlled

A

enteroendocrine cells

negative feedback through enteric nervous system feedback loops

143
Q

what is the function of enteroendocrine cells

A

detect the luminal contents
release hormones in response
link capillaries and lumen

144
Q

what is a gastric glands

A

pit in the epithelium of the GI tract that invaginates the lamina propria
fully made of single celled columnar epithelium with goblet cells

145
Q

what cells can be found in gastric glands and what do they produce (4)

A

chief cells produce pepsinogen
parietal cells produce HCL and intrinsic factor
G cells produce gastrin
mucous neck cells produce mucous

146
Q

describe motility of the stomach

A

bolus enters stomach through pyloric sphincter
fundus and body relaxes and food enters the fundus through gastric accommodation
peristalsis (muscle contraction) occurs in middle of stomach and pushes food toward pylorus
Antral Systole - peristaltic wave pushes contents back into the body, some chyme moves into the duodenum

147
Q

what is the gastric phase

A

where food entering the stomach triggers peristalsis and release of gastrin (to release gastric juice)

148
Q

what is the intestinal phase of digestion

A

the arrival of food in duodenum triggers release of hormones (gastric inhibitory peptide GIH) which inhibit motility
Triggers release of bile and pancreatic enzymes for digestion and absorption

149
Q

what is gastric inhibitory peptide

A

hormone that inhibits motility

released when food enters the duodenum

150
Q

what happens in the lag phase of stomach digestion

A

food is churned, motility occurs

151
Q

where is the antrum found and why is it relevant

A

within the pylorus

antral systole is contractions aiding motility and gastric emptying

152
Q

when do gastric ulcers occur and where do they occur

A

break in the mucosal barrier exposing the underlying connective tissue to acidic corrosion
stomach or small intestine

153
Q

what are symptoms of gastric ulcers

A

abdominal pain
anaemia
haemorrage
H.Pylori bacteria

154
Q

what increases the chances of gastric ulcers

A

Anxiety, diet and NSAIDs.

155
Q

what affect does diet have on forming gastric ulcers

A

coffee and alcohol stimulate parietal cells which release gastric acid
alcohol also damages other cells in the stomach

156
Q

what type of drug increases risk of gastric ulcer and why

A

NSAIDs
decrease prostaglandin production
which decreases inhibition of acid production

157
Q

why does anxiety cause gastric ulcers

A

Anxiety increases parasympathetic output (increases gastrin)

Stress increased sympathetic output which decreases mucus and carbonate ions secretion

158
Q

which bacteria causes gastric ulcers and why

A

H.Pylori
can survive in the stomach and have a strong role in peptic ulcer
as they release proteases and endotoxins.

159
Q

what are the exocrine secretions of pancreas, how are they released, what cells are involved and what is their function?

A

bicarbonate ions to neutralise gastric acid and enzymes for digestion lipase, amylase, protease
released via gall bladder
acinar cells

160
Q

what are the exocrine secretions of the pancreas and what cells produce these

A

insulin produced by beta cells in the iselts of langerhans

glucagon produced by alpha cells in the iselts of langerhans

161
Q

where does the gall bladder release its contents into and what feeds into the gall bladder

A

liver and pancreas

into the duodenum

162
Q

what is the function of CCK hormone

A

duodenum releases it if there are fats or proteins in the chyme entering SI
feeds back to pancreas to release proteases and lipases via gall bladder

163
Q

how does the pancreas know when to release bicarbonates for stomach acid neutralisation

A

if there is HCL in the chyme entering the duodenum
acid enters the blood stream lowering pH
activates ductal cells in the pancreas to secrete bicarbonate ions

164
Q

what does the liver release into the digestive system

A

bile salts for emulsification of fats
bile to neutralise stomach acid
excretion of waste productions e.g. cholesterol

165
Q

what is the function of the gall bladder

A

store bile and enzymes released by pancreas and liver
alters the bile composition and delivery by absorbing NA, Cl, H20 to concentrate bile. It secretes H+ and mucin to neutralise alkaline bile and protect surface epithelium.

166
Q

what is secretin

A

stimulates liver to produce bile and gall bladder to release bile
stimulated by fats and acid

167
Q

how does the duodenum control digestion

A

when high fats and proteins release CCK which stimulates pancreas to release proteases and lipases
when high stomach acid, secretin released to stimulate gall bladder to contract and release bile
when glucose detected, pancreas cells in islets of Langerhans to produce insulin
chime entering the duodenum initiates gastric inhibitory enzyme which makes us feel full and inhibits motility

168
Q

explain how glucose and amino acids are absorbed in the SI

A

ions are proton pumped out into the lumen of SI

they then diffuse back in through co-transport enzymes with attached amino acids and glucose

169
Q

how do we end up with up to 4 litres of gas in the digestion tract

A

swallowing air
diffusion of CO2
neutralisation and acids
production of CO2 from bacteria

170
Q

what is absorbed in the LI

A

water and ions

171
Q

how does fibre aid digestion and prevent cancers

A

slows digestion by holding onto water and decreases gastric emptying preventing stomach cancer
holds onto water and slows absorption of nutrients creating a slow and steady absoprtion
acts as a substrate for bacteria

172
Q

how is continence maintained

A

rectal accommodation

anal sphincter contraction

173
Q

how does defecation occur and what nervous systems are responsible

A

stretching of rectum signals CNS to defecate
voluntary nervous system anal sphincter relaxation
sympathetic and parasympathetic colorectal contraction
raised abdominal pressure

174
Q

what is emesis

A

feeling that we are going to be sick

protective mechanism to protect GI tract from absorbing toxins

175
Q

what are the first and second line emesis defences

A

first line:
-pre-ingestive senses smelling, tasting, seeing and deciding not to eat

second line:

  • detection of absorbed toxins by chemoreceptors
  • trigger zones outside the brain barrier induces nausea to prevent further ingestion and activates vomiting centres.
176
Q

how do we vomit

A
  1. giant retrograde contractions of the intestines return material to the stomach
  2. Relaxation of the pyloric sphincter
  3. antral mobility inhibited to prevent gastric emptying
  4. stomach relaxes to accommodate for returning material
  5. Relaxation of the lower oesophageal sphincter
  6. retrograde peristalsis of oesophagus and contraction of diaphragm/abdominal wall expels chyme
177
Q

what oral mechanisms occur when vommiting

A

soft palate raised to protect nasopharynx
glottis closed to close respiratory tract
increased salivation
air and saliva drawn down into oesophagus to protect oesophagus and decrease oesophageal pressure

178
Q

other than toxins , what causes vomitting and what is the mechanism

A

irradiation of abdomen
infection
injury
causes release of proteins that act on the vomiting centre in brain

178
Q

other than toxins , what causes sickness and what is the mechanism

A

irradiation of abdomen
infection
injury
causes release of proteins that act on the vomiting centre in brain

179
Q

what oral manifestations prevent a baby breasfeeding

A

cleft palate

180
Q

why can babies not eat straight away (3)

A

kidneys cannot regulate high solute load in blood
GIT is too immature to digest
neuromuscular pathways to swallow whole food is not complete

181
Q

at 1 year old, whys is 500ml of milk a great food source

A

high calcium
high vitamin B
1/4 of energy needs

182
Q

why is tea not recommended for children

A

tannins in tea prevent iron absorption

iron is vital in child growth for haemoglobin production and respiration for bodily function

183
Q

at what age do we swap from whole to semi-skimmed milk

A

5

184
Q

at what age do we need 50% of our diet to be protein

A

11-14 puberty (more for males)

185
Q

signs of vitamin C deficency

A

poor wound healing (collagen III to collagwn I), anaemia (poor uptake of iron) and scurvvy. bleeding gums

186
Q

is there a link between high calcium/vitamin D in children or their mother and tooth strength?

A

no evidence for childs diet

evidence suggests mothers diet greatly affects tooth health of child

187
Q

what is SACN

A

scientific advisory committee on nutrition

188
Q

what is change for life now called

A

better food, healthier families

189
Q

what have been some government changes to increase healthier diet for children

A

sugar tax to increase prices of foods containing sugar
banning unhealthy adverts
less fast food outlets near schools
healthier school meals

190
Q

what is the BNF (2)

A

British nutrition foundation
advise on healthy eating

AND British national formulae
give interactions with medications

191
Q

what is FSA and what do they do

A 
food standards agency
encourage healthier eating
Eatwell plate
traffic light system
ensure saftety and 'healthiness' of foods
192
Q

name some food/nutrition agencies

A

FSA - food standards agency
BNF - British nutritional foundation
SACN - scientific advisory committee for nutrition

193
Q

what are the government guidelines on healthy school meals

A

high-quality meat, poultry or oily fish
fruit and vegetables
bread, other cereals and potatoes
no drinks with added sugar, crisps, chocolate or sweets in school meals and vending machines
no more than 2 portions of deep-fried, battered or breaded food a week
children lacking in nutritional support or financial support can claim free school dinners

194
Q

what improvement could be made to food labels with sugar contents of foods

A

separate free sugar from contained sugar

195
Q

how does smoking affect HDL and LDL

A

smoking decreases HDL (that has no link to CHD) and increase LDL and makes it more sticky (increasing CHD)

196
Q

what affect does saturated fats have on diet

A

increase LDL which are linked to CHD and high blood pressure

197
Q

during fertility what do men and women need to have more of

A

men - zinc
women - folic acid, vitamin A, oily fish, high calcium
vitamin A protects sperm from anti-oxidants reducing miscaraige

198
Q

how much energy should we get from fat and unsaturated fat

A

35% fat

10% saturated fat

199
Q

if a women has osteoporosis and low oestrogen, what food source can be helpful and why

A

calcium to aid bone health
soy protein contain phytoestrogens which mimic oestrogen and will reduce symptoms of heart disease, osteoporosis and cancer.

200
Q

what are phytoestrogens

A

found in soy protein, phytoestrogens mimic oestrogen

reduce symptoms of heart disease, osteoporosis and cancer.

201
Q

if a patient is house boud and old, what vitamin supplement is most important

A

vitamin D as they experience no light

202
Q

what vitamins and macronutrients are elderly patients likely lacking and why

A

vitamin D due to being inside more and not experiencing sunlight vitamin D synthesis
iron/proteins due to inability to chew meat

203
Q

what problems alter the eating habits of the elderly

A

loss of sight smell alter our motivation to eat
arthritis may hurt chewing tough things like meat
less energy to cook leads to ready meals with worse nutrition

204
Q

what age group is best before date most important for and why

A

elderly 70+

listeria

205
Q

what nutritional needs change as we get older

A

same nutritional needs
less energy needs
less vitamin A to avoid fractures

206
Q

how can we fight malnutrition in elderly

A

lunch clubs
health care assistants
meals on wheels

207
Q

what dietary factors have been found to decrease incidence of colorectal cancer

A

high fibre

calcium and dairy products

208
Q

should we advise breastfeeding if able? why? until when?

A

yes
decreases chances of breast cancer
decreases babies chances of being overweight
Passes antibodies to baby (natural passive immunity)
until 6 months

209
Q

what is someone’s ‘diet’

A

the sum of everything we ingest

habitual eating pattern

210
Q

how does vitamin D deficiency in childhood/pregnancy affect tooth development and what is VDRR

A
  • vitamin D resistant rickets VDRR
  • delayed tooth development
  • hypoplastic enamel
  • large pulp horns and chambers
  • microscopic cracks causing pulp infection leading to spontaneous abscesses in 25% of child VDRR primary teeth
211
Q

where do we get fluoride in our diet

A 
water (<1ppm)
salt
tea 200mg/Kg
oily fish
children's school milk in Scotland 2.65pmm reduced bioavailability
212
Q

what happens if we have excess flouride in our diet whilst growing?

A

fluorosis of the teeth
hypo mineralisation of enamel
white staining on teeth that is susceptible to brown stainig if coffee/smoke

213
Q

what percent of the UK population has fluoridated water

A

10% at 1ppm

214
Q

what are risk factors of erosion form the things we injest

A

citrus fruits (>2)
vegetarians/vegans
fizzy pop (>4 a day increases 252%)
polypharmacy leads to acid reflux

215
Q

where are good sources of calcium and phosphates

A

milk
fortified bread/cereals
cod liver oil

216
Q

what cells were greatly affected within tooth formation in rats with vitamin A deficiency

A

ameloblasts

217
Q

how does severe undernourishment affect growth of teeth and their structure

A

underdeveloped
thin, weak hypoplastic enamel
delayed dental eruption

218
Q

how do fibrous foods helps our oral cavity (2)

A

they improve periodontal health maintaining pressure on alveolar bone
increase salivary output

219
Q

if you are PEG fed what does this mean

A

fed via a tube

220
Q

how do PEG fed patients get calculus but no caries

A

calculus is mineralized plaque biofilm
PEG fed means fed through a tube
caries requires cariogenic food e.g. sugar/carbohydrates which patient doesn’t get
still has bacteria from external environment that are calcified by minerals in saliva

221
Q

why does vitamin C deficency lead to its oral manifestations

A

bleeding gums
loose teeth
due to disturbed collagen formation

222
Q

what is folic acid important for (oral and non-oral) and what manifestations in the mouth do we get with folate deficency

A

foetal development
integrity of oral cell epithelium

ulcers and depapilation of the tongue

223
Q

what folate B9 oral medicines are given to pregnant women and why

A

folic acid mouthwash to decrease pregnancy gingivitis

224
Q

a patient has come in with red/black/blood stained teeth, what is the likely cause

A

chewing tabacco/betel quid

225
Q

which vitamin deficiencies lead to bleeding gums

A 
vitamin C (disrupted collagen formation)
vitamin K (clotting factors)
226
Q

a patient has a swollen tongue (oedema), what deficency can lead to this

A

protein - kwaishikor

227
Q

a patient has recurring ulcers. what should we do

A

give a diet diary and investigate diet

228
Q

what deficencies can lead to ulcers

A

iron, b12, b9

229
Q

what deficiency can lead to angular chelitis

A

B2, B12 and iron

230
Q

a patient has burning mouth syndrome. What is the cause and what is another likely symptom

A

vitamin deficency: iron, B9, B12

depapilation of the tongue - smooth tongue

231
Q

where do we get b12

A

meat, poultry, eggs

232
Q

what is an OFG

A

orofacial granuloma

233
Q

what foods likely cause OFG

A

benzoates - preservatives in everything, especially in fizzy pop E210-219
cocoa
cinammon

234
Q

what are symptoms of an OFG

A 
orofacial granuloma
Diffuse facial swelling
Lip enlargement + vertical fissuring
Angular cheilitis
Oedema of buccal mucosa
Mucosal tags
Aphthous-like ulceration
Buccal cobblestoning/tags (lumpy cheeks)
differential diagnosis to vitamin disorders
235
Q

what is the treatment for OFG

A

exclusive diet
symptomatic relifef (painkillers)
steroids
immunosepressants

236
Q

what causes OFG

A

delayed hypersensivity reaction
possibly immunorepsonse
identified triggers are benzoates e.g. E210-219, cinnamon, cocoa

237
Q

how does vitamin C affect wound healing

A

vitamin C is needed for forming cross links between collagen I fibres making it stronger

238
Q

What curve shows pH against diet

A

Stephan curve

239
Q

what are 3 ways for the body to get amino acids

A

diet
synthesis
recycled protein turnover

240
Q

if amino acids are not needed, what happens to them

A

cannot be stored

either rapidly used for energy or excreted in urine

241
Q

what are essential and conditionally essential amino acids

A 
essential = amino acids we cannot produce e.i. have to get from diet
conditionally = needed more at certain parts of life e.i. high growth rates like puberty
242
Q

how are amino acids achieved from the diet

A

we ingest protein
hydrolysis by proteases releases amino acids
cotransporter with ions (Na+/Cl-) into duodenum

243
Q

what do we need for amino acid synthesis

A

glucose and a nitrogen source

244
Q

where do we get nitrogen sources for amino acid synthesis

A

degradation of proteins or ammonia

245
Q

how are non-essential amino acids made in the body

A

breakdown and reformation of essential amino acids

246
Q

what are the 2 ways of amino acid degredation

A

glucogenic - carbons converted to pyruvate or acetyl Co-A –> citrate cycle = glucose
ketogenic - converted to acetyl CoA ketone bodies

247
Q

what is transamination

A

amino group form one amino acid is moved to another

248
Q

what is the fate of nitrogen from amino acids and what controls this

A

glutamate dehydrogenase converts nitrogen to ammonia in liver
enters urea cycle to be excreted
controlled by ATP (inhibits) and ADP (activates)

249
Q

how is glucogenic amino acid degradation controlled

A

ATP and ADP levels
ATP means high energy so inhibits this pathway
ADP means low ATP so excited this pathway to get energy from carbon backbone of amino acids

250
Q

what enzyme aids degradation of nitrogen from amino acids to urea

A

glutamate dehydogenase

251
Q

how is nitrogen received off of amino acids

A

amino acids undergo transamination where amino group is swapped
nitrogen removed and collected by glutamate
glutamate dehydrogenase breaks down glutamate and nitrogen to ammonia
ammonia enters urea cycle

252
Q

what is nitrogen balance and why is it important

A

nitrogen ingested = nitrogen excreted

NH4+ is very toxic to bodily tissues and we cannot store nitrogen

253
Q

who should be in positive nitrogen balance and why

A

children, building muscle and pregnant women (anywhere in growth)
ingested nitrogen > excreted nitrogen
being used for amino acids for growth

254
Q

who would have negative nitrogen balance

A

people in malnutirtion

255
Q

what is the main function of urea cycle

A

convert ammonia NH3 form amino acid degredaiton into urea for excretion

256
Q

how would you describe the type of system that is the urea cycle and explain

A

feed forward

the more ammonia present, the faster the reaction goes

257
Q

what is the glucose alanine cycle and when is it important

A

cycle of nutrients from muscles to the liver

involving transamination releasing energy for muscles when glucose levels are low

258
Q

what are some causes of b12 deficiency

A

diet - veganism (B12 from animal products, bacteria, cereals)
pernicious anaemia - inhibits binding of intrinsic factor and b12
lack of intrinsic factor
lack of absorption in ileum - TB, Crohns

259
Q

where do we find folate

A

fresh fruit and veg

260
Q

what is polyuria

A

weeing a lot

261
Q

what is polydipsia

A

drinking a lot

262
Q

What grpah shows plaque pH in response to food

A

Stephan curve

263
Q

what fruit should we avoid on warfarin

A

grapefruit

makes action of warfarin accelerate

264
Q

what 3 hormones aid plasma calcium levels

A

calcitrol (vit D derived from liver and kidneys) - increases plasma levels
calcitonin - decreases calcium plasma levels
PTH - increased plasma levels

265
Q

where do we get calcitriol

A

liver and kidneys synthesise this hormone from vitamin D

upregulates absorption of calcium

266
Q

which vitamin has most use in the immune system

A

vitamin A

267
Q

what is healthy BMI

A

18-25

268
Q

what is overweight and obeses BMI

A

25-30

31+

269
Q

what classes as underweight on the BMI scale

A

<18.5

BDS 2 (13 decks)

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