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
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
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
4
Q
What is the accepted units of alcohol in a week?
A
14 unis for men and women
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 Iād 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 ā> caries and refer to alcohol awareness or charities
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
7
Q
what makes a nutriton āessentialā
A
we cannot make it in the body and need it for normal bodily function
8
Q
what is the difference between undernutrition and malnutrition
A
under - not enough food
mal - the wrong nutrients/unhealthy
9
Q
define Anabolism
A
forming of larger nutrients from smaller
10
Q
define catabolism
A
breaking down of molecules
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
12
Q
what is NSP
A
non-soluble polysaccharide
13
Q
what is GI for a food
A
Glycemic index is how fast the carbohydrate reaches the bloodstream as glucose
14
Q
why are carbohydrates classed as a protein sparer and how much of daily energy should come from free sugar
A
āprotein sparerā means it prevents the breakdown of proteins
<5% and to be reduced through life
15
Q
what are vitamins
A
Vitamins are organic (or related) substances with specific biochemical functions
essential for normal metabolism (promote reaction/s)
16
Q
what are minerals
A
Minerals are essential constituents of soft tissues, fluids, skeleton, teeth
17
Q
what are the water soluble and water soluble vitamins
A
water soluble are B and C
fat soluble are ADEK
18
Q
what is your basal metabolism
A
amount of energy required for basic life processes e.g. heartbeat, respiration, cellular activity.
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
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
21
Q
when is overuse of vitamin supplements most likely to cause toxicity
A
during pregnancy for the foetus
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
23
Q
where do we get vitamin D
A
mushrooms
sunlight
24
Q
what is the function of vitamin D
A
absorption of calcium and phosphates affecting mineralization of bone+tooth
immune function
25
vitamin D deficency?
rickets
| reduced immune response
26
explain rickets
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
27
what are the anti-oxidant vitamins
A C and E
28
where do we find vitamin K
fortified cereals
leafy greens
oils
29
what is the function of vitamin K (2)
precursor for blood clotting factors
coenzyme for post translational carboxylation of glutamate to y carboxy glutamate
stops proteins binding to phosphoilipd membranes (preventing clotting)
30
what is a deficiency in Vitamin K and who is more at risk
haemorrhagic disease
| new-borns particularly at risk, given Vit K at birth
31
what is vitamin C and where do we find it
Ascorbic acid
| colourful citrus fruit and vegetables
32
what is the function of vitamin C
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)
33
what are signs of vitamin C deficency
bleeding gums
anaemia
tired and weak
poor wound healing
34
why is the face and oral cavity sensitive to nutritional vitamin deficiencies
mucous membrane has rapid turnover of epithelium so needs lots of vitamins and protein to form new cells (vitamin A)
35
what vitamins are important for tongue health
B and iron
36
what is the importance of iron and where do we get it
used to form haemoglobin which is the main carrier of oxygen around the body essential for respiration
green leafy vegetables, meat,
37
why are calcium and phosphate important and what vitamin helps their absorption
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
38
what are oral manifestations of vitamin B/iron defiecncies
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)
39
why might the tongue be smooth?
atrophiy of filiform papillae caused by deficency in vitamin B and iron
40
what is malar pigmentation and what is the cause
blue/brown spots freckled in patches on the face
| deficency in B6, iron, niacin
41
what are the main 3 vitamin deficiencies that affect oral/facial structures
iron, B6 and niacin
42
what is the general function of vitamin B
immune and nervous function
Cell function and growth
B9 (folate) important for neural tube health in pregnancy
43
what happen if we have too high/low blood glucose levels
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
44
what does glucagon do
covnert glycogen stores from cells into glucose
45
what does insulin do
convert blood glucose to glycogen for short term storage
46
what are the three soruces of glucose
diet
glycogen degradation
gluconeogenesis
47
which part of the body cannot be supplied by fats for fuel? why?
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
48
SOME fibre gets broken down in the digestive tract. How?
some fibre is fermented by bacteria in the gut to make short chain fatty acids
49
when does the fasting period start and how long can we last without food
2 hours after eating
| 40 days
50
which hormone other than insulin and glucagon affects glucose blood levels?
adrenaline increases glycogen degradation
| It can override glucagon and insulin temporarily
51
what is gluconeogenesis and when does it begin
formation of glucose from non-carbohydrate sources mainly in the liver
30 hours after eating when glycogen levels are low
52
name three things that can be turned into glucose for gluconeogenesis
amino acids - mainly alanine
lactate formed by anaerobic respiration in intense muscle exercise
glycerol from fatty acids
53
some energy is required to initiate gluconeogenesis. Where does this come from
beta oxidation of fatty acids
54
what mechanisms is gluconeogenesis regulated by (2)
substrate availability e.g. insulin, glucagon, glycogen, ATP, lactate, amino acids
regulatory irreversible steps e.g. glucose - 6 -phosphate to glucose
55
f
56
what is a triglygeride
1 glycerol bound to 3 fatty acid chains by ester bonds
57
what forms of lipids are there
triglycerides - unsatured and saturated
phospholipids
steroids e.g. cholesterol
58
how can lipids be gained for the body
diet
| carbohydrate --> lipid in liver
59
explain how we absorb lipids
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
60
why can micelles cross membranes
they have phospholipid non-polar heads on their outer surface so pass through non-polar lipid membranes
61
what are nascent chyomircons and where are they formed
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
62
what happens to nascent chylomicrons
enter lymphatic system
get thongs added to them to become mature chylomicrons
travel to cells needing fats
63
what is LPL and what is its function
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
64
what is LPL and what is its function and wjat controls this
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
65
how are triglycerides and cholesterol transported
chylomicrons
66
where do chylomicrons remnants like excess FA, glycerol and cholesterol go?
liver for metabolism and recycle
67
what are endogenous lipids
lipids formed from glucose/triglycerides formed in the liver
68
what are the three main fates of triglycerides
stored as triglycerides
beta-oxidised for ATP fuel
used as structural components e.g. phospholipids
69
how are endogenous lipids stored and transported? same as dietary lipids?
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
70
how are lipids used for energy and what stimulates this process
beta oxidation
| glucagon, ADP
71
how do fatty acids enter cells
fatty acids bind with ATP to form fatty acyl-CoA
| diffuse across membrane
72
explain beta-oxidation
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
73
why is cholesterol important
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
74
how is cholesterol absorption controlled and why is this important
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
75
defects to enterocyte proteins affect what
increased cholesterol levels
76
how is cholesterol synthesised and where
liver converts acetyl-CoA into cholester by HMG-CoA Reductase
77
what things affect HMG-CoA Reductase
```
(HMG CoA reductase converts NADH into cholesterol)
insulin excites
glucagon inhibits
cholesterol-lowering drugs inhibits
cholesterol inhibits
```
78
how is cholesterol transported from the liver and what are their fates
bile salts stored in gallbladder used to aid digestion of lipids
cholesterol esters implemented into VLDL (and chylomicrons but not from liver)
79
what happens to the remnants of VLDL/Chylomicrons (expand on cholesterol)
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
80
how do cells get more cholesterol if needed?
- LDL activated to adhere and break down VLDL or Chylomicrons
- apoproteins on cells LDL receptors break down LDL
81
what happens to excess LDL
macrophages phagocytose the LDL
82
explain how pathogenic blood clots form in blood vessels
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
83
what plaque and where, does LDL cause
atherosclerotic plaque on blood vessel walls
84
what are ketone bodies
Ketone bodies are water-soluble molecules that contain the ketone groups produced from fatty acids breakdown in the liver.
85
why might a patient have a bad breath/nail polish remover/acetone smell
when ketone bodies are broken down acetone is released
excess ketone
sign of poorly controlled diabetes or severe starvation/eating disorder
86
when are ketone bodies used
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
87
Which cells of the pancreas make insulin and glucagon
alpha cells make glucagon
| beta cells make insulin
88
what are the major symptoms of diabetes mellitus
```
high blood glucose levels
sweet urine
ithcy skin
blurry vision
increased thirst and urination
reccuring gum/bladder infection
```
89
what are the normal fed and fasting blood glucose levels for a person with and without diabetes
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
90
What are some major complications of diabetes mellitus
```
peripheral vascular disease (cold extremities)
stroke
sugar induced coma
nerve damage
ulceration
```
91
Briefly explain type 1 diabetes
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
92
briefly explain type II diabetes
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
93
What is gestational diabetes
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
94
why does gestational diabetes occur and what affect does it have on the baby and mother
hormonal changes alter the bodies response to insulin leading to hyperglaecemia
baby will be larger
mother has higher chances of developing type 2 diabetes
95
what is pre-diabetes and what is the difference of IGT and IFG
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.
96
how do we test for diabetes
fasting glucose levels
oral glucose tolerance testing 2h and 8h after eating
random plasma glucose check
97
what is glycated haemoglobin check and what does it test and what normal/diabetic readings do we get
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
98
how do we manage diabetes
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
99
what is the function of oral medications for diabetes (2)
Drugs that decrease gluconeogenesis in the liver
| Drugs that increase insulin production in the pancreas
100
how does diabetes affect the oral cavity
```
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
```
101
What is Orthorexia Nervosa
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)
102
what is Anorexia Nervosa
eating disorder where a patient feels more overweight than they are
may eat secretly and discretely
103
what are the signs of anorexia nervosa
```
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
```
104
what can anorexia lead to (4)
cardiac problems due to body breaking down cardiac muscle
Malnutrition leading to deficencies
dehydration as most water comes from food
infertilitiy and periods stop
105
how can we manage eating disorders
```
'no blame' approach
group monitoring
diet plans and management
weekly weigh ins
councelling
```
106
What is bulimia Nervosa
where a patient binge eats and eats until painfully full and then makes themself be sick
107
what are the signs of bulimia
```
obsessive exercise and laxatives
Ulceration of mouth and hands due to stomach acid
high caries
high erosion of teeth
parotid gland enlargement
```
108
How can we treat the oral manifestations of bulimia
Ask patient to brush teeth with high flouride mouthwash after being sick and apply flouride varnish on all surfaces to prevent caries ad TSL
109
What is binge eating disorder
similar to bulimia without purging
| patient hoards food and eats it slowly over time with social withdrawl, feels bad about eating
110
What are the signs of binge eating disorder
weight gain
bad skin
constipation
caries due to constant acid attack
111
how do we manage binge eating disorder
dont diet advise just provide a time schedule to eat at specific times
112
what classes someone as obese
BMI over 30
113
explain the 5 steps of CBT
```
Make a list
list unproductive thoughts
create replacement thoughts
read the list often
reflect and replace thoughts
```
114
How do we speak to a patient we suspect to have an eating disorder
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
what organs are involved in the GI tract
```
mouth
oesophagus
stomach
small intestine
large intestine/colon
rectum
accessory organs e.g. gall bladder, pancreas, glands
```
116
what is the general structure of all of the GI tract
good blood supply for glandular secretions
significant nervous supply within submucosal plexus
glands intermittent
Mucosal epithelium with underlying lamina propria - loose connective tissue
117
what epithelium is mucosal lining
non-keratinized squamous epithelium
118
how much liquid do we absorb in a day and how much is from idet, where is the rest from?
9L a day
2L from diet
rest is reabsorbed gastric jucies
119
what is deglutition and what are the 3 stages
swallowing
stage 1 = oral phase
stage 2= pharyngeal
stage 3 = oesophageal
120
why is swallowing so tightly regulated
as food and liquid goes very close to the airway which must be tightly controlled and prevented
121
describe the oral phase of degluttation
```
voluntary
tongue presses against hard palate
compresses bolus
retraction of tongue pushes bolus into pharynx
respiration inhibited
```
122
describe the pharyngeal stage of deglutition
involuntary from stimulus when food hits pharynx
soft palate reflects closing nasopharynx
Epiglottis closes the airway
trigger to oesophageal phase
123
describe the oesophageal phase of degluttation
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
how are all passages apart from the oesophagus blocked during the oesophageal phase of degluttation
soft palate reflecting prevents passage into nasopharynx
tongue against palate prevents exit into oral cavity
epiglottis reflects preventing passage into airway
125
what prevents reflux of material back into oesophagus and why is it special
lower oesophageal sphincter or cardiac sphincter
| has a squamocolumnar junction between squamous mucosal epithelium and columnar stomach epithelium
126
what are the four parts of the J shaped stomach
1st cardiac (cardiac sphincter)
2nd (upper right) Fundus
3rd body
4th pylorus (pyloric sphincter)
127
what is gastric accomodation
stomachs ability to store food and begin mechanical digestion
control of chyme into small intestine
128
what are the functions of the stomach
gastric accommodation
protection against bacteria - low pH
absorption of fatty acids and alcohol
digestion of proteins with gastric juice
129
explain the surface of the stomach in relation to gastric release
stomach has single cell columnar epithelium
ruggae on surface that can stretch
gastric glands in lamina propria open at pits
130
where are gastric glands found
lamina propria of stomach
131
what is the composition of gastric juice
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
what is the role of HCL in GI tract
prevent growth of most bacteria
| catalyse cleavage of pepsinogen to pepsin
133
what is the role of mucous in the GI tract
line and protect gastric mucosa
134
what is the role of gastrin
regulates secretion of acid
135
what is the role of intrinsic factor and where is it secreted
helps absorption of B12 in ileum
| secreted from the stomach
136
what parts of the nervous system is the GI tract controlled by
Enteric nervous system
137
what parts of the nervous system control digestion (3)
```
autonomic nervous system
-sympathetic: inhibit digestion
-parasympathetic initiates digestion
central nervous system
enteric nervous system
```
138
what is the function of the enteric nervous system, what is it composed of and roughly how many nerve fibres are involved
~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
what is the effect of CNS on digestion
sight, smell, taste all act as external stimulus
alters activity of enteric nervous system through long reflexes
changing motility and secretion
140
what does the LI absorb
water and salts
141
what nerves control the oesophageal phase of degluttation
primary peristalsis is controlled by vagus nerve
| secondary peristalsis is controlled by enteric nervous system
142
what cells control release of hormones into GI tract and how are they controlled
enteroendocrine cells
| negative feedback through enteric nervous system feedback loops
143
what is the function of enteroendocrine cells
detect the luminal contents
release hormones in response
link capillaries and lumen
144
what is a gastric glands
pit in the epithelium of the GI tract that invaginates the lamina propria
fully made of single celled columnar epithelium with goblet cells
145
what cells can be found in gastric glands and what do they produce (4)
chief cells produce pepsinogen
parietal cells produce HCL and intrinsic factor
G cells produce gastrin
mucous neck cells produce mucous
146
describe motility of the stomach
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
what is the gastric phase
where food entering the stomach triggers peristalsis and release of gastrin (to release gastric juice)
148
what is the intestinal phase of digestion
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
what is gastric inhibitory peptide
hormone that inhibits motility
| released when food enters the duodenum
150
what happens in the lag phase of stomach digestion
food is churned, motility occurs
151
where is the antrum found and why is it relevant
within the pylorus
| antral systole is contractions aiding motility and gastric emptying
152
when do gastric ulcers occur and where do they occur
break in the mucosal barrier exposing the underlying connective tissue to acidic corrosion
stomach or small intestine
153
what are symptoms of gastric ulcers
abdominal pain
anaemia
haemorrage
H.Pylori bacteria
154
what increases the chances of gastric ulcers
Anxiety, diet and NSAIDs.
155
what affect does diet have on forming gastric ulcers
coffee and alcohol stimulate parietal cells which release gastric acid
alcohol also damages other cells in the stomach
156
what type of drug increases risk of gastric ulcer and why
NSAIDs
decrease prostaglandin production
which decreases inhibition of acid production
157
why does anxiety cause gastric ulcers
Anxiety increases parasympathetic output (increases gastrin)
| Stress increased sympathetic output which decreases mucus and carbonate ions secretion
158
which bacteria causes gastric ulcers and why
H.Pylori
can survive in the stomach and have a strong role in peptic ulcer
as they release proteases and endotoxins.
159
what are the exocrine secretions of pancreas, how are they released, what cells are involved and what is their function?
bicarbonate ions to neutralise gastric acid and enzymes for digestion lipase, amylase, protease
released via gall bladder
acinar cells
160
what are the exocrine secretions of the pancreas and what cells produce these
insulin produced by beta cells in the iselts of langerhans
| glucagon produced by alpha cells in the iselts of langerhans
161
where does the gall bladder release its contents into and what feeds into the gall bladder
liver and pancreas
| into the duodenum
162
what is the function of CCK hormone
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
how does the pancreas know when to release bicarbonates for stomach acid neutralisation
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
what does the liver release into the digestive system
bile salts for emulsification of fats
bile to neutralise stomach acid
excretion of waste productions e.g. cholesterol
165
what is the function of the gall bladder
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
what is secretin
stimulates liver to produce bile and gall bladder to release bile
stimulated by fats and acid
167
how does the duodenum control digestion
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
explain how glucose and amino acids are absorbed in the SI
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
how do we end up with up to 4 litres of gas in the digestion tract
swallowing air
diffusion of CO2
neutralisation and acids
production of CO2 from bacteria
170
what is absorbed in the LI
water and ions
171
how does fibre aid digestion and prevent cancers
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
how is continence maintained
rectal accommodation
| anal sphincter contraction
173
how does defecation occur and what nervous systems are responsible
stretching of rectum signals CNS to defecate
voluntary nervous system anal sphincter relaxation
sympathetic and parasympathetic colorectal contraction
raised abdominal pressure
174
what is emesis
feeling that we are going to be sick
| protective mechanism to protect GI tract from absorbing toxins
175
what are the first and second line emesis defences
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
how do we vomit
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
what oral mechanisms occur when vommiting
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
other than toxins , what causes vomitting and what is the mechanism
irradiation of abdomen
infection
injury
causes release of proteins that act on the vomiting centre in brain
178
other than toxins , what causes sickness and what is the mechanism
irradiation of abdomen
infection
injury
causes release of proteins that act on the vomiting centre in brain
179
what oral manifestations prevent a baby breasfeeding
cleft palate
180
why can babies not eat straight away (3)
kidneys cannot regulate high solute load in blood
GIT is too immature to digest
neuromuscular pathways to swallow whole food is not complete
181
at 1 year old, whys is 500ml of milk a great food source
high calcium
high vitamin B
1/4 of energy needs
182
why is tea not recommended for children
tannins in tea prevent iron absorption
| iron is vital in child growth for haemoglobin production and respiration for bodily function
183
at what age do we swap from whole to semi-skimmed milk
5
184
at what age do we need 50% of our diet to be protein
11-14 puberty (more for males)
185
signs of vitamin C deficency
poor wound healing (collagen III to collagwn I), anaemia (poor uptake of iron) and scurvvy. bleeding gums
186
is there a link between high calcium/vitamin D in children or their mother and tooth strength?
no evidence for childs diet
| evidence suggests mothers diet greatly affects tooth health of child
187
what is SACN
scientific advisory committee on nutrition
188
what is change for life now called
better food, healthier families
189
what have been some government changes to increase healthier diet for children
sugar tax to increase prices of foods containing sugar
banning unhealthy adverts
less fast food outlets near schools
healthier school meals
190
what is the BNF (2)
British nutrition foundation
advise on healthy eating
AND British national formulae
give interactions with medications
191
what is FSA and what do they do
```
food standards agency
encourage healthier eating
Eatwell plate
traffic light system
ensure saftety and 'healthiness' of foods
```
192
name some food/nutrition agencies
FSA - food standards agency
BNF - British nutritional foundation
SACN - scientific advisory committee for nutrition
193
what are the government guidelines on healthy school meals
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
what improvement could be made to food labels with sugar contents of foods
separate free sugar from contained sugar
195
how does smoking affect HDL and LDL
smoking decreases HDL (that has no link to CHD) and increase LDL and makes it more sticky (increasing CHD)
196
what affect does saturated fats have on diet
increase LDL which are linked to CHD and high blood pressure
197
during fertility what do men and women need to have more of
men - zinc
women - folic acid, vitamin A, oily fish, high calcium
vitamin A protects sperm from anti-oxidants reducing miscaraige
198
how much energy should we get from fat and unsaturated fat
35% fat
| 10% saturated fat
199
if a women has osteoporosis and low oestrogen, what food source can be helpful and why
calcium to aid bone health
soy protein contain phytoestrogens which mimic oestrogen and will reduce symptoms of heart disease, osteoporosis and cancer.
200
what are phytoestrogens
found in soy protein, phytoestrogens mimic oestrogen
| reduce symptoms of heart disease, osteoporosis and cancer.
201
if a patient is house boud and old, what vitamin supplement is most important
vitamin D as they experience no light
202
what vitamins and macronutrients are elderly patients likely lacking and why
vitamin D due to being inside more and not experiencing sunlight vitamin D synthesis
iron/proteins due to inability to chew meat
203
what problems alter the eating habits of the elderly
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
what age group is best before date most important for and why
elderly 70+
| listeria
205
what nutritional needs change as we get older
same nutritional needs
less energy needs
less vitamin A to avoid fractures
206
how can we fight malnutrition in elderly
lunch clubs
health care assistants
meals on wheels
207
what dietary factors have been found to decrease incidence of colorectal cancer
high fibre
| calcium and dairy products
208
should we advise breastfeeding if able? why? until when?
yes
decreases chances of breast cancer
decreases babies chances of being overweight
Passes antibodies to baby (natural passive immunity)
until 6 months
209
what is someone's 'diet'
the sum of everything we ingest
| habitual eating pattern
210
how does vitamin D deficiency in childhood/pregnancy affect tooth development and what is VDRR
- 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
where do we get fluoride in our diet
```
water (<1ppm)
salt
tea 200mg/Kg
oily fish
children's school milk in Scotland 2.65pmm reduced bioavailability
```
212
what happens if we have excess flouride in our diet whilst growing?
fluorosis of the teeth
hypo mineralisation of enamel
white staining on teeth that is susceptible to brown stainig if coffee/smoke
213
what percent of the UK population has fluoridated water
10% at 1ppm
214
what are risk factors of erosion form the things we injest
citrus fruits (>2)
vegetarians/vegans
fizzy pop (>4 a day increases 252%)
polypharmacy leads to acid reflux
215
where are good sources of calcium and phosphates
milk
fortified bread/cereals
cod liver oil
216
what cells were greatly affected within tooth formation in rats with vitamin A deficiency
ameloblasts
217
how does severe undernourishment affect growth of teeth and their structure
underdeveloped
thin, weak hypoplastic enamel
delayed dental eruption
218
how do fibrous foods helps our oral cavity (2)
they improve periodontal health maintaining pressure on alveolar bone
increase salivary output
219
if you are PEG fed what does this mean
fed via a tube
220
how do PEG fed patients get calculus but no caries
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
why does vitamin C deficency lead to its oral manifestations
bleeding gums
loose teeth
due to disturbed collagen formation
222
what is folic acid important for (oral and non-oral) and what manifestations in the mouth do we get with folate deficency
foetal development
integrity of oral cell epithelium
ulcers and depapilation of the tongue
223
what folate B9 oral medicines are given to pregnant women and why
folic acid mouthwash to decrease pregnancy gingivitis
224
a patient has come in with red/black/blood stained teeth, what is the likely cause
chewing tabacco/betel quid
225
which vitamin deficiencies lead to bleeding gums
```
vitamin C (disrupted collagen formation)
vitamin K (clotting factors)
```
226
a patient has a swollen tongue (oedema), what deficency can lead to this
protein - kwaishikor
227
a patient has recurring ulcers. what should we do
give a diet diary and investigate diet
228
what deficencies can lead to ulcers
iron, b12, b9
229
what deficiency can lead to angular chelitis
B2, B12 and iron
230
a patient has burning mouth syndrome. What is the cause and what is another likely symptom
vitamin deficency: iron, B9, B12
| depapilation of the tongue - smooth tongue
231
where do we get b12
meat, poultry, eggs
232
what is an OFG
orofacial granuloma
233
what foods likely cause OFG
benzoates - preservatives in everything, especially in fizzy pop E210-219
cocoa
cinammon
234
what are symptoms of an OFG
```
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
what is the treatment for OFG
exclusive diet
symptomatic relifef (painkillers)
steroids
immunosepressants
236
what causes OFG
delayed hypersensivity reaction
possibly immunorepsonse
identified triggers are benzoates e.g. E210-219, cinnamon, cocoa
237
how does vitamin C affect wound healing
vitamin C is needed for forming cross links between collagen I fibres making it stronger
238
What curve shows pH against diet
Stephan curve
239
what are 3 ways for the body to get amino acids
diet
synthesis
recycled protein turnover
240
if amino acids are not needed, what happens to them
cannot be stored
| either rapidly used for energy or excreted in urine
241
what are essential and conditionally essential amino acids
```
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
how are amino acids achieved from the diet
we ingest protein
hydrolysis by proteases releases amino acids
cotransporter with ions (Na+/Cl-) into duodenum
243
what do we need for amino acid synthesis
glucose and a nitrogen source
244
where do we get nitrogen sources for amino acid synthesis
degradation of proteins or ammonia
245
how are non-essential amino acids made in the body
breakdown and reformation of essential amino acids
246
what are the 2 ways of amino acid degredation
glucogenic - carbons converted to pyruvate or acetyl Co-A --> citrate cycle = glucose
ketogenic - converted to acetyl CoA ketone bodies
247
what is transamination
amino group form one amino acid is moved to another
248
what is the fate of nitrogen from amino acids and what controls this
glutamate dehydrogenase converts nitrogen to ammonia in liver
enters urea cycle to be excreted
controlled by ATP (inhibits) and ADP (activates)
249
how is glucogenic amino acid degradation controlled
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
what enzyme aids degradation of nitrogen from amino acids to urea
glutamate dehydogenase
251
how is nitrogen received off of amino acids
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
what is nitrogen balance and why is it important
nitrogen ingested = nitrogen excreted
| NH4+ is very toxic to bodily tissues and we cannot store nitrogen
253
who should be in positive nitrogen balance and why
children, building muscle and pregnant women (anywhere in growth)
ingested nitrogen > excreted nitrogen
being used for amino acids for growth
254
who would have negative nitrogen balance
people in malnutirtion
255
what is the main function of urea cycle
convert ammonia NH3 form amino acid degredaiton into urea for excretion
256
how would you describe the type of system that is the urea cycle and explain
feed forward
| the more ammonia present, the faster the reaction goes
257
what is the glucose alanine cycle and when is it important
cycle of nutrients from muscles to the liver
| involving transamination releasing energy for muscles when glucose levels are low
258
what are some causes of b12 deficiency
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
where do we find folate
fresh fruit and veg
260
what is polyuria
weeing a lot
261
what is polydipsia
drinking a lot
262
What grpah shows plaque pH in response to food
Stephan curve
263
what fruit should we avoid on warfarin
grapefruit
| makes action of warfarin accelerate
264
what 3 hormones aid plasma calcium levels
calcitrol (vit D derived from liver and kidneys) - increases plasma levels
calcitonin - decreases calcium plasma levels
PTH - increased plasma levels
265
where do we get calcitriol
liver and kidneys synthesise this hormone from vitamin D
| upregulates absorption of calcium
266
which vitamin has most use in the immune system
vitamin A
267
what is healthy BMI
18-25
268
what is overweight and obeses BMI
25-30
| 31+
269
what classes as underweight on the BMI scale
<18.5
