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Gastro BSc > Module 1.1: Nutrition > Flashcards

Module 1.1: Nutrition Flashcards

1
Q

Define malnutrition

A

a state where deficiency, excess or imbalance of energy, protein or other nutrient (inc vits and mins) causes measurable effects on body function and clinical outcome

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2
Q

Describe the clinical relevance of nutritional care

A

50% of people overweight or obese –> increased risk of co-morbidities

5% underweight/borderline underweight - chronic protein-energy undernutrition risk

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3
Q

Describe the complications of undernutrition

A
  1. impaired immune response
    a. predisposes to infection
  2. decreased muscle strength
    a. increased fatiguability –> inactivity –> inability to work effectively –> poor self care –> abnormal muscle function –> falls
    b. poor cough pressure –> predisposing and prolonging respiratory infections
    c. bed sores and thromboembolism
  3. poor thermoregulation
    a. hypothermia
  4. poor wound healing
    a. prolonged recovery from illness
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4
Q

effects of <10% WL in hospitalised pts

A 
o	Increased mortality 
o	Prolonged stay 
o	Increased readmission rate
o	Morbidity from chest and wound infections 
o	Wound breakdown and pressure sores
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5
Q

Complications/Chronic Conditions related to Overweight/Obesity

A
  • Metabolic disorders (T2DM and dyslipidaemias)
  • Cardiovascular disease and hypertension
  • Respiratory problems (obstructive sleep apnoea)
  • Certain cancers

• Musculoskeletal problems (osteoarthritis)
o Orthopaedic surgeons often recommend those overweight to have surgery to reduce BMI as this is associated with fewer complications from osteoarthritis

  • Gastrointestinal disorders (gallstones, GORD)
  • Reproductive disorders ( fertility)
  • Psychological disorders
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6
Q

Health Benefits from 5-10% Weight Loss in an Obese Individual

A

o Angina reduced by 91%
Better than drug therapy

o Exercise tolerance ­up by 33%

o Fasting plasma glucose down by 30-50%

o Systolic & diastolic blood pressure down 10mmHg
Better than drug therapy

o LDL down 50%; TG down 30%; HDL up ­ 8%

o improved quality & quantity of sleep; ¯ snoring
o ­ improved mobility; decrease in pain
o ­improvement in menstrual regularity; ­ in fertility

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7
Q

Summarise how nutrition can be assessed

A

History

Anthropometry

Biochemical measurements - albumin, urinary nitrogeni calorimetry

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8
Q

What is the MUST tool?

A

Malnutrition Universal Screening Tool

  1. Step 1: Work out BMI
    a. BMI >20 = 0 points
    b. BMI of 18.5-20 = 1 point
    c. BMI < 18.5 = 2 points
  2. Step 2: Weight Loss Score
    a. <5% unintentional weight loss = 0 points
    b. 5-10% unintentional weight loss = 1 point
    c. >10% unintentional weight loss = 2 points
  3. Step 3: Acute disease effect
    a. if patient acutely ill and there has been or is likely to be on no nutritional intake for >5 days = 2 points

Overall Risk:
• Score of 0 = LOW  Routine clinical care + repeat screening
• Score of 1 = MEDIUM  Document intake + assess improvement + repeat
• Score of 2 = HIGH  refer to nutrition team + increase intake + monitor and review

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9
Q

What can be seen in the examination of a malnourished pt?

A

muscle wasting

loss of fat

oedema/ascites due to low albumin

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10
Q

Descrbe the symptoms and signs of nutrient deficiencies

general, skin, hair, eyes, mouth, neuro

A

General: weakness, muscle wasting, WL

SKIN:
pallor
follicular hyperkeratosis - vit A/C
perifollicular petechiae - vit C
dermatitis - protein/calorie/iacin/riboflavin/Zn/vit A
Bruising - vit C/K

HAIR:
alopecia - protein/Zn/biotin
corkscrew hairs - Copper

EYES:
night blindless/photophobia - Vit A
conjunctival inflammation - vit A

MOUTH:
Glossitis - Vit A/riboflavin
bleeding gums - fibovlavin/niacin/folate/B12/protein
decreased taste - Vit A/C/K/folate
sore mouth and tongue - Zn/Vit A
Angular stomatitis - vit B12/C/niacin/Folate/Fe etc

NEURO:
tetany - Ca/Mg
paresthesias - Thiamine/pyridoxine/B12/E
Loss of reflexes - Niacin/B12
Dementia - vitE/thiamine
Opthalmoplegia - Thiamine
Depression - biotin/folate/B12
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11
Q

Describe the need for increased micro and macronutrient requirements

A

FATS - lipid malabsorption

PROTEINS - growth, injury repair, protein loss, burns

CARBS - energy/heat generation, activity, growth, malnutrition

ELECTROLYTES - renal disease, vomiting, diarrhoea, GI losses

MINERALS - pregnancy and lactation, growth, blood loss, malabsorption

TRACE ELEMENTS - Zn/Cu - pregnancy and lactation, malabsorption

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12
Q

Classes of Vit A

A

Retinoids and Carotenoids

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13
Q

Classes of Vit B

A 
B1 - thiamine
B2 - riboflavin
B3 - niacin
B5 - panthothenic acid
B6 - pyridoxine
B7 - biotin
B9 - folate
B12 - cobalamin
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14
Q

Names of vit C, D, E

A

C - ascorbic acid
D - cholecalciferol
E - tocopherol

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15
Q

Describe the causes of poor nutiritonal intake

A

1- ANOREXIA:
drugs, cancer, depression, fear, debilitation, surgery

2- INABILITY TO SWALLOW
CVA, MS/MND, mechanical ventilation, head/neck surgery

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16
Q

Describe the causes of increased nutritional losses

A

short bowel syndrome

Crohns

UC

Pancreatitis

Gut infection

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17
Q

Describe the causes of increased nutritional requirements

A

burns

head injury

decompensated liver disease

sepsis

pneumonia

infection

acute pancreatitis complications

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18
Q

Complications related to % loss of lean body mass

10%
20%
30%
40%

A

10 - impaired immunity, increased infection - 10% mortality

20 - decreased healing, weakness, infection - 30% mortality

30 - too weak to sit, pressure sores, pneumonia, no healing, 50% mortality

40 - death, usually from pneumonia - 100% mortality

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19
Q

Indications for Nutrition Support

A

• People who are malnourished, as defined by any of the following:
o BMI < 18.5 kg/m2
o Unintentional weight loss greater than 10% within the last 3–6 months
o BMI < 20 kg/m2 and unintentional weight loss greater than 5% within the last 3–6 months.

• People at risk of malnutrition , as defined by any of the following:
o Eaten little or nothing for >5 days and/or are likely to eat little or nothing for the next 5 days or longer
o Poor absorptive capacity, and/or have high nutrient losses and/or have increased nutritional needs e.g. catabolism

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20
Q

Aims of Nutrition Support

A
  • Improve nutritional status
  • Maintain nutritional status
  • Minimise losses in nutritional status
  • Provide comfort and maintain dignity and quality of life
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21
Q

Assessment for Nutrition Support

A

• ABCD
• Anthropometrics
– Weight loss / BMI/ MUAC/ handgrip strength/ estimation/ extremes of BMI. Subjective global assessment
• Biochemistry
– Hydration, U+Es, vitamins and minerals, LFTs , inflammatory markers
• Clinical
– Bowels, fluid balance, medications, NEWS + obs, blood glucose monitoring
• Diet
– Requirements, diet history, feeding regimen, SLT assessment , refeeding syndrome

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22
Q

NICE guidelines on route of nutritional support

A
  • Malnourished Patients with a safe swallow should be considered for oral nutritional support
  • Inadequate or unsafe oral intake patients should be considered for a 2-4 week trial of NG feeding
  • Post-abdominal surgical patients should be considered for post-op oral intake within 24 hours
  • Malnourished patients with inadequate intake or unsafe swallow with a functional GI tract should be considered for enteral tube feeding
  • If long term feeding tube placed i.e. PEG, can be used for feeding 4h post insertion.
  • Consider motility agents in ICU patients with delayed gastric emptying.
  • Major abdominal surgery - do not give tube feeding to patients within 48h of surgery unless malnourished with inadequate oral intake/swallow and a functional gut.
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23
Q

Oral Nutrition Support

A

o Fortified diets: texture modified diets – puree, fork-mash, soft options, normal (available for cultural meals, private patients have their own menu)
o Nutritional supplements: milk-based, juice-based, puddings, powders, soups (available on ward or on prescription)

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24
Q

when is enteral tube feeding considered

A

• Inadequate or unsafe oral intake

AND

• A functional, accessible GI tract

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25
Q

Indications for NG tubes

A

• For individuals who are requiring nutritional support for <1 month

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26
Q

Indications for Nasoduodenal/Nasojejunal

A

problems with gastric reflux or has delayed gastric emptying

failure to tolerate NG tube with high GI aspirates

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27
Q

Indications for Gastrostomy (RIG/PEG)

A

• Considered in patients with long-term enteral feeding >1 month

low morbidity associated with placement (2%)

require surgical or laparoscopic procedure

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28
Q

Indications for Jejunostomy Tubes (PEG-J or surgical JEJ)

A

o There is an upper GI obstruction or fistulae

o Early post-op feeding

o Complicated hepatobiliary surgery

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29
Q

Complications associated with enteral feeding

A

vomiting
gastric distension

 Stop feed
 Review infusion rate
 Start slowly and gradually build up to prescribed infusion
 Consider prokinetic medication

diarrhoea

 Review medication
 Re-hydrate patient
 Complete clinical assessment on ‘stool assessment chart’
 Consider anti-diarrhoeal medication if no infection
 Dietitian review infusion rate and feed

reflux

 Reduce infusion rate
 Confirm tube position
 Consider prokinetics and post-pyloric feeding

drug/nutrient interaction

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30
Q

Indications for panteral feeding

A

Are malnourished or at risk of malnutrition
AND
• Have inadequate or unsafe oral and/or enteral nutritional intake
AND
• Have a non-functional, inaccessible or perforated (leaking) GI tract

  • GI obstruction/ileus
  • High output fistula (>500ml in 24 hours)
  • Anastomotic breakdown after GI surgery
  • Short bowel syndrome (<100cm viable bowel)
  • Unable to tolerate enteral feeding (hyperemesis)
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31
Q

Define parenteral nutrition

A

Direct perfusion of nutrients into the circulatory system bypassing the GI system

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32
Q

pros and cons of parenteral nutrition

A

• Pros:
o Do not need gut
o Can provide nutritional needs

• Cons:
o Line complications: length of insertion, pneumothorax, catheter blockage, central vein thrombosis, line sepsis
o Metabolic: hyperglycaemia, lipaemia, deranged LFTs
o Fluid overload
o Electrolyte imbalance
o Expensive (~£100 per normal bag, if specialised can cost more – supplement drinks can be as little as 1p per bottle)

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33
Q

Define refeeding syndrome

A

Severe fluid and electrolyte shifts and related metabolic disturbances found in malnourished patients being re-fed.

• Can lead to severe fluid and electrolyte shifts in malnourished patients

  • It is caused by a switch in metabolism from fat (starvation) to glucose (refeeding)
  • Insulin is released with cellular glucose uptake which causes intracellular shifts in potassium (K+), magnesium (MG2+) and phosphate (PO4-)
  • Can have metabolic, cardiac, renal neuromuscular and Gi complications as a result
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34
Q

Stimulators of appetite

A

Neuropeptide Y (NPY), Melanin concentrating hormone (MCH), Agouti-related Protein (AGRP), Orexins, Grehlin, Galanin

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35
Q

Inhibitors of appetite

A

alpha-MSH (melanocyte-stimulating hormone), Glucagon-Peptide 1 (GLP-1), CART, Leptin, CCK, Corticotrophin Releasing Factor (CRH)

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36
Q

Summarise the anatomy of hypothalamus

A

see notes pg 131

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37
Q

Describe role of NPY in appetite control

A
  • Produced in the arcuate nucleus/co-expression with AgRP
  • NPY Receptors are found in the PVN and ARC
  • It is the most potent orexigen known
  • Increased levels in genetic models of obesity e.g. ob/ob mouse

• Six defined receptors for NPY: Y1-Y6.
o Y1, Y2 and Y5 found in hypothalamus – mediate effects of FI

• NPY orexigenic effects are via Y1 & Y5 as selective antagonism of Y1 and Y5 decreases nocturnal feeding.

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38
Q

Summarise findings in NPY knockout mice

A
  • NPY knockout mice had normal feeding/body weight  this was felt to be due to compensation during development therefore may not see expected phenotype
  • Y1 knockout mice show reduced food intake/metabolic rate and reduced responses to fasting
  • Y5 knockout mice are found to have normal food intake but has reduced response to exogenous NPY
  • Y1/Y5 knockouts are both mildly obese –> thought to be due to upregulation of other orexigenic peptides
  • However, when NPY is injected into the arcuate nucleus, this overexpression of NPY is shown to have a cumulative effect on weight gain in mice
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39
Q

Describe role of the melanocortin system in appetite control

A
  • Overexpression of Agouti protein in this mouse antagonizes the Melanocortin-4 receptor (MC-4 R) and leads to obesity
  • MC-4 receptor is expressed within hypothalamus (PVN)

• Endogenous ligands for MC-4R are POMC (a-MSH) gene products.
o a-MSH potently inhibits feeding
o Produced in lateral part of Arcuate Nucleus
o Endogenous ligand for hypothalamic MC-4 receptor
o Agouti mouse over expresses of Agouti protein which is a melanocortin receptor 4 antagonist.

  • MC-4 receptor knockout mouse are obese and hyperphagic
  • In humans, MC-4 receptor & POMC mutations are a frequent cause of morbid obesity
  • Mice lacking POMC are obese & have increased food intake
40
Q

Describe role of the Agouti Related Protein in appetite control

A
  • Agrp presents naturally in hypothalamus
  • High expression within the Arcuate nucleus.
  • Agrp is selective MC-4 receptor antagonist and blocks a-MSH binding.
  • Curtails restraint of inhibitory effects of a-MSH
  • Overexpressing Agrp mouse is fat.
  • Intracerebral injection of AgRP increases food intake
41
Q

Describe role of the Melanin-Concentrating Hormone (MCH) in appetite control

A
  • Expressed in LH
  • Projections throughout the brain.
  • Highly conserved.
  • Increased expression in fasted animals  suggests a physiological effect
  • Increased feeding ICV.
  • MCH knockout mice – Hypophagic, lean.
  • MCH overexpressing mouse – Obese, Diabetic

• The MCH receptor is found in all areas that control food intake: PVN, LH, VMH

  • MCH knockout mice has inappropriately high metabolic rate
  • MCH overexpressing mouse appears to have reduced energy expenditure

• MCH may therefore reduce energy expenditure  via thyroid axis, as it is involved in control of metabolism

42
Q

Describe role of the CART in appetite control

A
  • CART mRNA and peptide levels are detected in the hypothalamus in feeding related sites (PVN, ARC, VMN, DMN)
  • There is a decrease in arcuate CART mRNA following food deprivation.
  • Intracerebral injections of CART reduces normal and fasting-induced feeding.
  • Blocks NPY-induced feeding response
  • Immunoblockade of endogenous CART increases feeding.]
43
Q

Describe role of the GLP-1 in appetite control

A
  • Product of proglucagon processing in gut and CNS
  • Synthesised in vagal complex and projects to PVN
  • GLP-1 receptor expression in PVN & ARC
  • Intracerebral injection of GLP-1 decreases food intake  dose-response effect
  • Chronic GLP-1 injections in mice studies show that this has a significant effect in reducing body weight
Exendin (9-39)
•	Specific GLP-1 receptor antagonist
•	Found in Gila monster venom
•	Blocks effects of GLP-1
•	Physiological role of GLP-1 as an anorectic peptide has been suggested by observation that exendin 9-39 stimulates feeding in satiated rats
44
Q

Summarise hypothalamis appetite control circuits

A

IMAGE p133

45
Q

What is metabolic syndrome

A

a clustering of risk factors including diabetes and pre-diabetes, abdominal obesity, high cholesterol and high blood pressure

  • Link with PCOS, certain cancers e.g. colorectcal cancer, NAFD, and dementia (how much of this is vascular dementia is uncertain)
  • Early ageing process (biologically speaking)

International Diabetes Federation (IDF) definition of Metabolic Syndrome:

  1. Central obesity (defined by waist circumference)
  2. Plus 2 of the following:
    a. High TG level or low HDL level
    b. High systolic BP
    c. High fasting plasm glucose (or previously diagnosed T2DM)
46
Q

Prevalence of Metabolic syndrome

A

25% of the world

47
Q

role of adipocytes in metabolic syndrome

A
  • Adipocytes (and to a certain extent monocytes) are thought to be the culprits of the Metabolic Syndrome
  • Adipocytes can release cytokines such that they can exert all the different factors that cause the metabolic syndrome
  • Fantuzzi G, J Allergy Clin Immunol. 2005: Adipocytes are not just stores of excess fat and inert but are very active tissues which participate in regulating physiological and pathological processes including: immunity and inflammation producing a variety of pro-inflammatory and anti-inflammatory factors
  • Antuna-Puente B, Diabetes Metab. 2008: Adipocytes/Adipose tissue-infiltrated macrophages release adipocytokines/adipokines that lead to a chronic subinflammatory state and are believed to play a central role in the development of insulin resistance and type 2 diabetes, and increased risk of CVD associated with obesity.
48
Q

Describe the role of beta cell dysfunction in T2DM

A

• Type 2 diabetes occurs due to chronic hyperglycaemia, and is a combination of insulin resistance and beta-cell dysfunction with a genetic predisposition  these can be changed by weight loss for up to 10 years of chronic hyperglycaemia

• Reduced ability of b-cells to secrete insulin in response to hyperglycaemia
o Glucotoxicity
o Genetic predisposition
• As long as β-cells are able to compensate for the insulin resistance by enhancing insulin secretion and increasing β-cell mass, euglycemia can be maintained
• Assaults to the β-cells include: genes, nutritients, fetal life, cytokines, physical activity, obesity and metabolites

• Over 60 genes are associated with T2DM
• Vast majority are involved in the working of pancreatic beta-cells and production of insulin rather than specifically insulin resistance
• Hence you need to have susceptible genes  vulnerable beta-cells
o Where you put your fat is important  genetically determined

, the phenotype is determined by the environment and one of the biggest fuels to the rise of obesity and T2DM is the environment in utero

Obese and diabetic mothers mean that their children have an epigenetic susceptibility to T2DM and obesity

49
Q

Normal Calcium Physiology

A
  • 1kg in adults (99% of which is in bone; 1% or 1gram of which is in blood)
  • Has crucial roles in intracellular signaling
  • 300-1300g per day = normal dietary intake; much of this passes through the kidneys; most is re-absorbed, 150g is lost
  • Small amount secreted in GI fluids (100-150g)
  • 25g lost through the skin
50
Q

Roles of Vit D

A

• Has classical roles in intestine, kidney and bone
• Also has immune functions: expressed in macrophages, monocytes, dendritic cells (important in granuloma formation in sarcoid/TB) as well as lymphocytes (implicated in immune disorders e.g. IBD, MS, DM)
• Lack of vitamin D in children leads to rickets whilst in adults it leads to osteomalacia
o These are “lack of bone calcification” due to lack of vitamin D
• May have a role in proliferation/cancer prevention e.g. in psoriasis, CRC, breast cancer

51
Q

Vitamin D Pathway

A
  • 7-decholesterol in skin –> sunlight –> pro-vitamin D3 –> vitamin D3 –> vitamin D
  • Dietary sources = Vitamin D3 (animals) or vitamin D2 (plants) –> vitamin D
  • Vitamin D –> liver –> hydroxylated by 25-hydroxlase to 25-hydroxyD3 = Major circulating type
  • 25-hydroxyD3 –> kidney –> hydroxylated by 1alpha-hydroxylase to 1,25-dihydroxyD3 = ACTIVE
  • Breakdown of 1,25-dihydroxyvitD by 24-hydroxylase (expressed in vit D target tissues) to calcitroic acid and is added on to bile to be excreted
52
Q

Describe the structure of the vit d receptor

A

intracellular “steroid hormone” family receptor which dimerises with retinoid X receptor (RXR)

53
Q

types of VDRE

A 
o	Direct Repeat
	spaced by 3 (DR3) 
	very strong: consensus RGKTSA 
•	where R = purine i.e. A or G, K = keto i.e. G or T and S = strong i.e. G or C
•	example: AGGTCA  nnn  AGGTCA

o Inverted Palindrome
 spaced by 9 (IP9)
 strength unknown
 example: TGACCT nnnnnnnnn AGGTCA

54
Q

Calcium Absorption

A
  • Only a proportion of calcium in GI tract is absorbed
  • This difference in variation is not due to vitD3, though calcium absorption does correlate with VitD3 - Gallagher et al J Clin Invest 1979 (key paper)

1) Calcium is absorbed at the brush border down the steep concentration gradient (10^-310^-7) through TRPV6
2) It binds calbindin-DK9 in the enterocyte
3) Transported from enterocyte cytoplasm across basolateral membrane against steep concentration gradient (10^-710^-3) via PMCA1 (ATP2B1), an ATPase with greatest expression in the duodenum (i.e. pumped out)

55
Q

Examples of genes with VDREs

A
  • 25-hydroxylase
  • TRPV6
  • Osteocalcin, Osteopontin
  • PTH
  • Cathelicidin
  • C-Fos, Beta-2 integrin etc.
56
Q

Osteoporosis diagnosis criteria

A

• Z-score = age-matched normal standard deviate; T-score = young adult normal standard deviate
• WHO definitions: (using Caucasians)
o Osteopenia as T = -1 to -2.5
o Osteoporosis as T = -2.5

• Considerations
o Ethnicity
o Normal/abnormal ageing
o Sex should also be considered (men and AC have higher bone density)

57
Q

Osteoporosis and Coeliac Disease

A

o Ca malabsorption due to:
 Loss of proximal villous cells where calcium is absorbed
 Increased calcium binding to unabsorbed fatty acids hence reduced availability for absorption

o Ca deficiency due to:
 Gluten free diet
 Associated lactose intolerance

o Vitamin D deficiency due to:
 Reduced sunlight exposure
 Secondary hyperPTH following low calcium levels

Molteni et al. Am J Gastro. 2005: Calcium absorption is reduced in untreated Coeliac Dsease in females, this increases once put on a gluten free diet (after 1 year)`

58
Q

Osteoporosis due to non-intestinal factors:

A

o Generalized malnutrition
o Reduced bone growth factors e.g. IGF1
o Increased bone resorption due to cytokines and secondary hyperPTH
o Reduced physical activity
o Hypogonadism (low testosterone in men, delayed menarche, early menopause)

59
Q

Osteoprosis and lactose tolerance

A

Di Stefano, 2002: Lactose intolerance and BMD: it was found that if you are lactose intolerant you have a lower BMD and increased risk of fractures of neck of femur and lumbar spine. However if you are lactose tolerant (but not absorber) you have the same risk as those who are lactose absorbers.

60
Q

Vitamin D and Colorectal Cancer

A
  • Gorham et al, American Journal of Preventative Medicine, 2007: quantitative meta-analysis that looked at risk of CRC and vitamin D and found that those with the highest quintiles of vitamin D in serum had the lowest risk of CRC
  • EPIC study, Brit Med J, 2010: big European study of 500000 subjects (case control): found that highest quintile of serum vitamin D had 40% incidence compared with the lowest. It also found that these were not significant in rectal cancer only. Dietary intake was also not significant. However, there were other significantly positive interactions with high dietary calcium and retinol.
61
Q

Role of ghrelin in appetite regulation

A

• 28 amino-acid, orexigenic peptide hormone
• Secreted by gastric mucosa oxyntic cells (and small intestine)
• Acts on GH receptors (growth hormone)
• ­ during fasting, peak level before meal, fall rapidly after meal
• Two major roles:
o GH regulation
o Energy balance
• Plasma grehlin level in relation to meal: increases just prior to meal and decreases once one has eaten –> adaptable so those who don’t eat breakfast in the morning don’t feel hungry because their grehlin levels are not so high

62
Q

How does Grehlin increase appetite?

A

Grehlin increases activity of AgRP/PYY to increase food intake.

63
Q

Role of CCK in appetite regulation

A

• Cholecystokinin released from I cells of the duodenum in response to fat entry
• Allows for: gallbladder contraction  to allow for emulsify fats through BA secretion
• Direct effect on feeding centre through VAGUS to reduce feeding but also blood-borne signals
• Clinical trials disappointing
o People ate less during a meal but frequency of meals increased

64
Q

Role of Insulin in appetite regulation

A
  • Secretion in response to: glucose, arginine, and fatty acids
  • Secretion tracks insulin secretion
  • Actions: decreases food intake, decreases glucagon release, decreases gastric emptying
  • Steven R. Smith et al. Am J Physiol Endocrinol Metab 2007: Pramlintide (analogue of amylin) reduced food intake when compared to placebo
  • Matthew Riddle et al. Dia Care, 2009: Pramlintide vs. Insulin decreases weight when compared to insulin, as well as improving HbA1c
65
Q

Role of PYY3-36 in appetite regulation

A

peptide synthesised by specialised endocrine cells (L cells) in the gut

  • PYY is made in response to food entering the GIT especially from ileum and colon
  • Binds to an inhibitory receptor (autoreceptor = Y2 receptor) on NPY/AgRP  decreased inhibitory secretion of NPY and AgRP  reduced hunger
  • This in turn also activates POMC neurones
  • Le Raux et al. Endocrinology. 2006: the more PYY administered the less people ate.
  • If one exceeds the dose of PYY, past the point of satiety, patients will throw up as this signal will induce nausea (aversion signal)
  • People have not been able to create a drug analogue of PYY due to pharmacokinetic problems
66
Q

Why is there so much PYY produced in the rectum?

A

PYY is produced in response to protein and fat, which is normally absorbed in the small intestine. If there is undigested fat and protein in the colon due to malabsorption e.g. tropical diarrhoea, PYY is stimulated and stops us from eating, and can even makes us feel nauseous.

67
Q

Role of GLP1 in appetite regulation

A

• Produced from L-cells in the ileum  precursor is proglucagon
• GLP-1 has two effects: appetite and diabetes:
o GLP-1 has an incretin function, that is they find pancreatic beta cells, causing insulin production

 Beta-cell: enhances glucose-dependent insulin secretion in the pancreas
 Alpha-cell: suppresses post-prandial glucagon secretion
 Liver: reduces hepatic glucose output
 Stomach: slows rate of gastric emptying
 Brain: promotes satiety and reduces appetite

68
Q

Role of GIP in appetite regulation

A
  • Mainly involved with glucose regulation
  • Increased insulin release in response to glucose (incretin effect)
  • Stimulates lipogenesis
  • Unclear role in body weight regulation
69
Q

Role of Oxyntomodulin in appetite regulation

A
  • Produced by L-cells
  • Has both aspects of GLP-1 and glucagon in its structure
  • Stimulates GLP-1 receptors at the arcuate nucleus to increase satiety via vagus
  • ALSO causes increased energy expenditure i.e. upregulates metabolic rate
70
Q

Role of leptin in appetite regulation

A
  • Hypothalamus senses energy storage through the actions of leptin
  • Leptin is a peptide hormone released from adipose tissue
  • ↑ adipose tissue leads to ↑ in LEPTIN production
  • Coded by ob gene
  • Acts on hypothalamus to decrease food intake and increase energy expenditure
  • Stimulates POMC/CART, inhibits AgRP/NPY  satiety
  • Does not work pharmacologically because fat people have lots of leptin and are leptin resistance  hence administration does not have a net effect on weight
71
Q

Summary of GI endocrine appetite regulation

A

Leptin and insulin circulate in the blood at concentrations proportionate to body-fat mass. They decrease appetite by inhibiting neurons (centre) that produce the molecules NPY and AgRP, while stimulating melanocortin-producing neurons in the arcuate-nucleus region of the hypothalamus, near the third ventricle of the brain.

NPY and AgRP stimulate eating, and melanocortins inhibit eating, via other neurons (top). Activation of NPY/AgRP-expressing neurons inhibits melanocortin-producing neurons. The gastric hormone ghrelin stimulates appetite by activating the NPY/AgRP-expressing neurons. Batterham et al.1 have now shown that PYY3-36, released from the colon, inhibits these neurons and thereby decreases appetite for up to 12 hours. PYY3-36 works in part through the autoinhibitory NPY receptor Y2R.

72
Q

what is the Barker Hypothesis

A

• Postulates that growth in utero dictates development of later chronic diseases of adulthood e.g. diabetes and CHD
• 2 phases
o Poor growth in utero leads to lower than expected birth weight
o Catch up or accelerated postnatal growth
• Both phases probably work together  small birth weight (BW) children tend to catch up due to excess of nutrients

73
Q

short and long term outcomes of breast feeding

A 
•	For baby
o	Decreased risk of infection
o	Later heart disease
•	For mother
o	Decreased risk of breast cancer 
o	Improved bone health
74
Q

Reasons for increased energy needs in pregnancy

A

• Increased energy cost of movement (note: women do not move around as much to compensate)
o Extra weight

• Deposition of tissue mass
o Mother (includes 2kg adipose for lactation)
o Increased for foetus

• Increased basal metabolic rate
o But for women with low BMI, their BMR may be even lower in pregnancy due to nutrition going to the baby rather than the fat stores of the mother  BMR depends on pre-pregnancy BMI

75
Q

What can compromise fetal nutrition

A

o HTN
o Smoking (causes poor vascular blood flow)
o Maternal infection e.g. CMV, toxoplasmosis, rubella
o Maternal chronic illness e.g. SLE, malignancy
o Unknown maternal factors (genetics?)

76
Q

Protein requirements in pregnancy

A
  • Extra 6g/day
  • Most accreted during last trimester

Supplementation
• Not recommended
• Motherwell study, Kerr Grieve: High protein diet  low birth weight babies
• Excess protein diets linked to low BW, increased BP and adverse events

77
Q

Ca requirements in pregnancy

A
  • Main increase in requirement in third trimester = 3mmol/kg/day
  • No recommendations for increased intake
  • Close monitoring needed when cows milk is excluded  due to low calcium and vitamin D intake`
78
Q

VitA requirements in pregnancy

A

• Recommended 100mug/day increase raising intake to 700mug/day

79
Q

Vitamin B (folate) requirements in pregnancy

A

• Reduced risk of NTD; hence general females should have 0.4mg/day, for those with Hx of NTD = 4mg/day

  • No increased intake recommended of thiamine, niacin, pyridoxine
  • Riboflavin and folate increase recommended
80
Q

Vitamin C requirements in pregnancy

A
  • Increase of 10mg/day recommended but only in the last trimester
  • BUT: Women in UK have enough intake
81
Q

Vitamin D requirements in pregnancy

A
  • Abrams 2007 AJCN: Maternal vitamin D status may affect child’s long-term bone health
  • Lercherbaum & Obermayer Pietsch 2012 EJEndo: deficiency implicated in infertility
  • Additional 10mug/day recommended
  • SACN 2016: advise daily supplement for all UK population (400IU/day)
82
Q

Teace element requirements in pregnancy

A

• No supplements required in UK

83
Q

GI Changes in Pregnancy (throughout pregnancy)

A
  • Loss of smooth muscle tone
  • Reduced peristaltic activity
  • Richter et al 2005: Delayed gastric emptying and gut transit
  • Marrero et al 1992: Decrease LOS pressure (mechanism: progestore?)
  • Quartarone et al 2013: High incidence of heartburn: 17-80%
84
Q

Avoidances during Pregnancy

A

• Alcohol
o Excess – foetal alcohol syndrome and developmental delay
o Data uncertain about intakes under 1 unit/day
o Recommendation is to avoid completely – CMO Report 2016, Bailey & Sokol 2008 Clin Obs Gynae

• Caffeine
o Crosses placenta
o Boylan et al 2008 BMJ, Bakker et al 2010 AJCN: May cause spontaneous abortion and low BW + low length
o Committee on toxicity of chemicals in food (2001) recommend: <200mg/day

85
Q

At-risk Groups in Pregnancy

A

• Teenagers – Baker et al 2009
o Have high requirements themselves
o Associated with other risk factors e.g. smoking, low SE class, poor diet
o Smith & Pell BMJ 2001: 2nd teenage birth = increased risk of preterm delivery and still birth

• Obese
o Galtier et al 1995 Int J Obesity: Higher risk of NTD and other problems
o Cnattingius et al 1998 NEJM: Higher risk of late foetal death
o Soltani et al 2000 BJN: Higher risk of maternal central obesity
o Juonala et al 2013 J Ped: Higher risk of gestational diabetes if genetically predisposed
o Crisham-Janik et al 2013 JPeds: Higher risk of cerebral palsy

86
Q

effect of alcohol and caffeine on LACTATION

A

• ALCOHOL
o Enters breast milk; anecdotal reports of increased infant sleeping (bad), decreased suckling and decreased milk supply

• CAFFEINE
o Enters breast milk; anecdotal reports of infant distress when mother takes excess caffeine hence <150mg/day recommended

87
Q

Describe oral problems associated with nutrition in ageing

A
  • Soreness and ulceration  ill-fitting dentures, poor dental health, occasionally vitamin deficiencies
  • Problems with salivation  directly related to ageing, also due to drug side-effects

• Mastication and dental health  loss of teeth (25% >60s edentate), fillings, gum disease, poorly fitting dentures
o The more natural teeth present, the less chewing problems occur
o Edentate people are shown to consume less energy, calcium, iron, vitamins A, C, E & B complex, fibre (quite difficult to chew fibre) and protein
o Edentate people have a lower BMI

• Difficulty swallowing  neurological e.g. stroke
o Guyomard et al, J Am Geriatr Soc, 2009: patients with dysphagia have worse outcomes in terms of patient mortality and length of stay in hospital than those without (OR for death: 12.5; OR for increased length of stay = 3.9)

• Decreased taste and smell – decreases pleasure of eating
o This is directly related to ageing  trigger cephalic phase response is reduced in older persons which is needed to optimise gut for food ingestion and appetite
o Disease and drugs can also affect taste and smell

88
Q

Solutions of oral issues in ageing

A

• Management of dysphagia
o Targeting the cause (when possible) is it pharyngeal or oesophageal? (SALT)
o Eating appropriate food and liquid consistencies
o Monitor and control progression symptoms
o Consult with a speech therapist or gastro team
o Have someone to eat with the older adult
o If oesophageal spasm is present, CCBs may be useful
• Regular dental reviews
• Good mouth hygiene
• Artificial saliva  or even sucking on sugar-free sweets, frozen berries etc to stimulate saliva production
• Enhancing food flavour has been shown to increase intake with poor taste
• Have favourite foods

89
Q

oesophagus issues in ageing

A

o GORD
 10-20% of adults experience symptoms equally
 15-40% experience symptoms monthly
 Aetiology: reduced saliva production, delayed gastric emptying, altered anti-reflux barrier
 Medications used for HTN, CVD and depression reduced the LOS pressure promoting GORD
o Oesophagitis
o Malignancy

90
Q

Solutions of oesophagus issues in ageing

A
  • Weight loss if overweight
  • Reduction in meal volume
  • Avoidance of irritants (alcohol, coffee, citrus, spicy, onions, peppermint)
  • Raise head off the bed
  • Increased physical activity (but not straight after meals)
  • Reduction in dietary fat
  • Avoid laying down for at least 3 hours after eating
  • Medication review
91
Q

stomachissues in ageing

A
  • Gastric atrophy, with decreased secretion of gastric acid, pepsin and mucus
  • Reduced gastric emptying
  • Reduced blood supply
  • Peptic ulcer disease
  • H. Pylori infection
92
Q

small intestine issues in ageing

A 
•	Causes of malabsorption in older persons include:
o	Coeliac disease
o	SIBO 
o	Crohn’s disease
o	Infections 
o	Cholestasis 
o	Pancreatic insufficiency
93
Q

large intestine issues in ageing

A

• Changes in gut microflora
o Solutions may be probiotics or bio-yogurts  evidence is sketchy

• Constipation
o Causes: medication, lack of movement, suppressing the need to go, reduced fibre intake due to oral issues
o Dietary advice
o Medicines

• IBS
o Diet and psychological management

• Diverticular disease
o Management through diet  high fluid and high fibre

• Colorectal cancer
o Dietary management
o Oncology care

• Pelvic floor disorders/autonomic neuropathy (incomplete evacuation of the rectum)
o Physiotherapy  pelvic floor exercises
o Medication

94
Q

Drug Side-Effects and Ageing

A
  • NSAIDs  can cause mucosal injury
  • Neomycin, methotrexate and olmessartan  can cause drug-induced villous atrophy
  • Narcotics and neuroleptics  decline in colonic transit
  • Metformin  can induce nausea and vomiting
  • PPIs  can lead to SIBO which cause gas, bloating and a change in bowel habit
95
Q

social issues in ageing

A

• Isolation
o Those living alone have lower energy intake
o Bereavement
• Poverty
o Lower income groups found to have lower energy, protein, fibre and many micro-nutrient intakes
• Reduced ADLs
o Shopping, cooking  affected in diseases such as arthritis

96
Q

Psychological Issues in ageing

A
  • Depression thought to be a major cause of reduced intake and weight loss in the elderly
  • Weight loss and altered eating behaviour is a recognised characteristic of the dementing process
  • Dementia is common in late stages but may appear early
  • Lowest weight patients are those with most behavioural problems

Gastro BSc (13 decks)

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