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302: Scientific Bases of Medicine > Diet, Physiology of appetite & weight > Flashcards

Diet, Physiology of appetite & weight Flashcards

1
Q

What are the various measurements of obesity?

A
  • Body mass index (BMI) kg / m2
    • < 18.5 underweight
    • 18.5-24.9 normal
    • 25-29.9 overweight
    • 30-39.9 obese
    • ≥40 morbid obesity
  • Waist circumference
  • Skin-fold thicknesses
  • Bioelectrical impedance analysis
  • Ethnicity specific cut-offs
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2
Q

What are the medical problems associated with Obesity?

A
  • Metabolic syndrome / type 2 diabetes
  • Cardiovascular disease
  • Respiratory disease
  • Liver disease
  • Cancer
  • Reproductive dysfunction
  • Joint problems
  • Psychological morbidity
  • the higher the BMI the greater the percentage of patients with co-morbidities
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3
Q

What is metabolic syndrome?

A
  • a constellation of closely associated CV risk factors
    • Visceral obesity
    • Dyslipidaemia
    • Hyperglycaemia
    • Hypertension
  • Insulin Resistance is the underlying pathophysiological mechanism
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4
Q

What is the epidemiology of Type 2 DM?

A
  • Risk is determined by
    • Age, Obesity, Family History, Ethnicity
  • Prevalent in
    • the rich in poor countries
    • in the poor in rich countries
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5
Q

What does CV disease cause

A

All the following are increased

  • ­ blood volume and blood viscosity
  • ­ vascular resistance
  • ­ hypertension
  • ­ left ventricular hypertrophy
  • ­ coronary artery disease
  • ­ stroke
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6
Q

How is the respiratory system effected in obesity?

A
  • Obstructive sleep apnoea
  • Hypoxia / hypercapnia
  • Pulmonary hypertension
    • Right heart failure
  • Accidents
    • Daytime somnolence
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7
Q

how does obesity effect the GI/ Liver

A
  • Non-alcoholic fatty liver
  • Non-alcoholic steatohepatitis
  • May progress to cirrhosis, portal hypertension, hepatocellular cancer
  • Gallstones
  • Reflux
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8
Q

Wha is the prevalence of cancer in obesity?

A
  • ~ 10% cancer deaths in non-smokers attributable to obesity
  • Types of cancer include
    • Breast, endometrial, oesophagus, colon, gall bladder, renal, thyroid
  • Mechanisms include
    • ­increase insulin, ­increase free IGF-I, ­increase oestrogen,
    • adipocytokines, reflux
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9
Q

How does obesity effect the reproductive system?

A
  • Polycystic ovarian syndrome
    • Oligomenorrhoea, hirsutism, acne
    • Subfertility
    • Endometrial hyperplasia
    • Insulin resistance
  • Male hypogonadism
  • Adverse pregnancy outcomes
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10
Q

How are joints affected by obesity?

A
  • Osteoarthritis
  • Gout
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11
Q

What psychological effects of obesity?

A
  • Depression
  • Eating disorders
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12
Q

What are the genetic components of obesity?

A
  • Rare
    • obesity-associated syndromes
      • Prader-Willi
      • Bardet-Biedl
  • Common
    • Polygenic
    • Susceptibility genes
    • Heritability of weight ~ heritability of height
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13
Q

What are other causes of obesity?

A
  • Hypothyroidism
  • Cushing’s syndrome
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14
Q

How does the environment contribute to obesity?

A
  • High fat
  • High sugar
  • ‘Coca-colonization’ of developing world
  • Socio-economic factors
  • 20-50% total energy expenditure
  • Obesity prevalence related to proxy measures of physical activity
    • Car ownership
    • TV viewing
  • Socio-economic factors
  • Social Networking
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15
Q

Explain Fetal programming and it’s relation to obesity

A
  • ‘Programming’: stimuli /insults at critical periods have persistent biological effects
  • ‘Stressors’ in utero
    • ?undernutrition, ?trace elements, ?other
    • crudely represented by birth weight
  • Mechanism: epigenetic modification of gene expression
  • Example:
    • ‘Programmed’ adrenal axis overactivity in adulthood
    • Causal factor for metabolic syndrome
    • Increased vulnerability to coronary heart disease
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16
Q

How does the ‘Life Course Model’ explain obesity?

A
  • factors operating at every stage of life affect health outcomes later in life
    • there is a ‘pathway of risk’ between events and health outcomes
  • the ‘worst outcomes’ are associated with:
    • low birth weight
    • excessive weight gain in infancy/childhood
    • adult obesity
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17
Q

Which hormones produced in the gut stimulate your appetite?

A

Ghrelin

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18
Q

Which Hormones in the gut suppress appetite?

A
  • Glucagon-like peptide 1
    (GLP-1)
  • Oxyntomodulin (OXM)
  • Cholecystokinin
    (CCK)
  • Glucose-dependent
  • insulinotropic
  • polypeptide (GIP)
  • Bile Acids
  • Neurotensin (NT)
  • Uroguanylin
  • Gastric leptin
  • Amylin
  • FGF19
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19
Q

How do Gut hormones work in the brain to produce their appetite-suppressing or inducing effect?

A
  • Ghrelin works centrally in the rain to stimulate appetite
  • the suppressors work in the Appetit centre of the brain
  • They interact with the gut microbiome as well
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20
Q

What are the positive effects of GLP-1

A

Pancreas

  • improves beta-cell function → increases insulin biosynthesis
  • increases glucose-dependent insulin secretion
  • decreases glucose-dependent glucagon secretion

Heart

  • decreases cardiovascular risk
  • decreases fatty acid metabolism
  • improves cardiac function
    • decreases systolic blood pressure
  • decreases inflammation

Brain

  • increases satiety
  • decreased body weight and food intake

Stomach

  • slows down gastric emptying

Liver

  • increased hepatic insulin sensitivity
  • decreases steatosis
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21
Q

What is Glucagon-like peptide-1 (GLP-1)?

what is its action?

A
  • It is produced and secreted by intestinal EEC- L cells and certain neurons within the nucleus of the solitary tract in the brainstem
  • Secreted in response to food consumption
  • Glucose-dependent insulinotropic peptide(GIP) is co secreted.
  • Enhances Insulin secretion in a glucose-dependent manner.
  • Numerous regulatory and protective effects
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22
Q

What is PYY

A
  • Belongs to NPY family
  • The release of PYY begins before nutrients arrive in the lower small intestine and the colon.
  • Further release of PYY is stimulated by nutrients within the lower small intestine and the colon.
  • PYY decreases food intake by inhibiting gut motility.
  • Blood remain high between meals
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23
Q

What are short term regulators of appetite?

and how do they work

A
  • Ghrelin
    • Rise precipitously when stomach is empty and fall rapidly when food consumed
    • Stimulates appetite by activating the NPY/AgRP-expressing neurons
  • Cholecystokinin
    • Released during eating
    • Promotes a sense of fullness that encourages an end to the meal
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24
Q

What are long term regulators of appetite?

A

Insulin and Leptin

both are released in proportion to the fat storage

they result in sustain inhibitory effects on food intake while increasing energy expenditure

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25
Q

How does the arcuate nucleus function?

A
  • Energy homeostasis
  • ‘Accelerator’ neurons produce NPY, which acts in the brain to stimulate feeding
  • “Brake”- Melanocortin peptides, which act on the same brain areas inhibit eating
  • NPY neurons also produce agouti-related peptide (AgRP) which blocks neuronal melanocortin receptors
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26
Q

What role does the Gut Microbiome play in Obesity and T2 Diabetes

A
  • Differences in gut bacteria
    • can be induced by diet e.g high-fat diet
  • Transplantation of faecal material alters insulin sensitivity
    • mice and humans
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27
Q

How are weight and appetite regulated?

A
  • slow-acting hormones that regulate body weight
    • Leptin
    • Insulin
  • Signal % body fat to the hypothalamus
    • decrease food intake
    • increase energy expenditure
  • Rapid-acting peptides that regulate meal sizes are released from GI tract
    • CCK: decreases eating
    • Ghrelin: increases eating
    • Peptide YY (PYY): decreases eating (up to 12 hours)
    • they act via the hypothalamus
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28
Q

How does the Hypothalamus control appetite?

A

Via the Arcuate nucleus

Increases eating

  • NPY (Neuropeptide Y)
    • increases eating
  • AgRP neurons
    • Blocks melanocortin receptor

Decreases eating

  • POMC neurons
  • Melanocortin peptides
    • alpha-MSH, CART
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29
Q

What is Leptins role in Obese humans?

A
  • usually acts as a starvation signal
  • Obesity rarely caused by
    • leptin deficiency
    • mutation of leptin receptor
  • Obesity usually caused by
    • increased leptin with increased fat
    • potentially leptin resistant
    • potentially decreased CNS leptin transport
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30
Q

How does Leptin function?

A
  • Leptin is secreted mainly by white adipose tissue, and levels are positively correlated with the amount of body fat
  • Central hypothalamic and peripheral tissues effects
  • Leptin interacts with the mesolimbic dopamine system, which is involved in motivation for and reward of feeding, and the nucleus of the solitary tract of the brainstem to contribute to satiety
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31
Q

Review this overview of how appetite is controlled

A
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32
Q

What pathways could be taken to control/ treat obesity?

A
  • Lifestyle modification
  • Pharmacological
  • Surgical
  • Public health/ Societal
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33
Q

What Lifestyle modifications need to be made in obese patients?

A
  • Diet
    • 500-1000 kcal energy deficiency
    • low energy density: decrease sat fat & sugar, increase fruit and veg
    • decreased portion sizes, decreased snacking
    • Structured meals/ meal replacements
  • Physical activity
    • exercise 7 days/wk
      • 30 mins moderate-high intensity or 60 mins low intensity
    • target 10,000 steps/day
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34
Q

What is a VLCD and what are it’s outcomes in T2 DM patients?

A
  • a very low-calorie diet used in patients diagnosed with T2DM <6 yrs prior
  • VLCD (830kcal/day) for 3-5 months
    • initially, total diet replacement with formulae
    • stepped food introduction
    • long term maintenance with structured support

Outcomes

  • 12 month outcomes reported
  • 24% of participants achieved 15 kg weight loss or more
  • 46% induced remission of T2DM
    • Normal HbA1c off all medication for 2 months
  • >10 kg weight loss: 73% remission
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35
Q

What are the usual targets and problems with Lifestyle Modification?

A
  • USUAL TARGETS
    • 10% weight loss (¹ ideal weight)
    • 1-2 lb (0.5 – 1 kg) per week
    • Some evidence that ‘ambitious’ goals promote more weight loss
  • PROBLEMS
    • Most patients can achieve ~ 5-10 % weight loss / 1 year
    • ‘Yo-yo’ dieting / regaining weight lost
    • ‘Obesogenic environment’
    • Weight loss results in increased ­hunger, increased satiety, increased metabolic rate
  • BEST HOPE
    • Sustainable lifestyle changes
    • Diet combined with exercise / physical activity
    • Ongoing management is required to maintain weight loss
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36
Q

What Anti-obesity agents are there?

A
  • CNS Stimulants
    • Eg- Phentermin/ Topiramate
    • Phentermine
    • Lorcaserin
    • Benzamphetamine
  • Anti-depressant/Dopamine re-uptake inhibitor/ Opioid antagonists- Bupropion/Naltrexone
  • GI Tract
  • Orlistat, GLP1 RA
    • Others- Metformin, Zonisamide, Amylin agonists, SGLT2 Inhibitors
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37
Q

What is the Mechanism of Orlistat?

A
  • BInds & inhibits lipases in the lumen of the gut
  • prevents the hydrolysis of dietary fat into absorbable free fatty acids/ glycerol
  • Excrete ~1/3 of dietary fat
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38
Q

What are the adverse effects of Orlistat?

A
  • Flatulence, oily faecal leakage
  • Diarrhoea
  • decreased absorption of fat soluble vitamins
    • vit. ADEK
    • take supplements
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39
Q

What is the indication of Metformin?

A
  • 1st line agent for over-weight/ obese patients with Type 2 diabetes
    • all other oral hypoglycaemic agents and insulin causes weight gain
  • used in diabetes prevention trials
  • recommended by NICE for prevention of T2DM in adults at high risk
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40
Q

What are the parameters in which surgical treatment of obesity is considered?

A
  • Patients with a body mass index (BMI) above 40
  • BMI between 35 and 39.9 and a severe obesity‐related comorbidity such as diabetes.
  • BMI between 30 and 34.9 and poorly controlled diabetes can also be considered.
  • BMI cutoffs may be lowered by 2.5 for patients of Asian descent
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41
Q

What 4 common surgical treatments can be done to treat obesity?

A
  • Laparoscopic adjustable banding (LAGB)
    • restrictive only- inject/withdraw saline to adjust the diameter of the band
  • Roux-en-Y gastric bypass
    • Gastric bypass partitioned
      • increased satiety
    • malabsorptive
      • micronutrient deficiencies: iron, B12, folate, Ca++, Vit D
    • alteration in gut hormones and bile acid flow contribute to weight loss
    • causes dumping syndrome
  • Sleeve Gastrectomy
    • restrictive surgery that creates a 100- 150 mL stomach - partial gastrectomy
  • Biliopancreatic diversion with duodenal switch BPD-DS
    • 50-80% gastrectomy is done
    • forward flow of bile and pancreatic juice in the biliopancreatic limb is believed to reduce complications of bacterial stasis
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42
Q

How does bariatric surgery facilitate weight loss?

A
  • Increases in satiety-promoting hormones
  • Reductions in hunger-promoting hormones
  • Reduced food intake
  • Central effects
  • Altered bile acid metabolism
  • Altered intestinal microbiota
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43
Q

What is the HIND gut Hypothesis

A

the hypothesis is that the improved glycaemic control is achieved as nutrients is delivered to the distal intestines sooner which augments the secretion of hormones that suppress appetite

  • The L cell -ileum and large intestine- secretes GLP‐1 and peptide YY, CCK.
    • GLP-1 being the main contributor: it stabilises glucose levels by enhancing glucose-stimulated insulin secretion and promoting the secretion of glucagon when glucose is low
  • GIP levels correlate with the length of the intestine that is exposed to ingested food
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44
Q

What are the pros and cons of surgical treatment for obesity?

A

Advantages

  • weight loss 25-30%
  • resolves or improve co-morbidities

Disadvantages

  • Perioperative mortality/morbidity
    • depends on the procedure and experience of the surgeon
  • Long-term follow-up
    • micronutrient deficiencies
  • Some weight re-gain
    • patients will still be obese
  • Expense
    • cost-effective after some time depending on co-morbidities
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45
Q

What are the NICE guidelines for bariatric surgery?

A

NICE 2006

  • After failure of other options if
    • BMI > 40 kg/m-2
    • BMI > 35 with co-morbid conditions
  • Or first line
    • BMI > 50 kg/m-2

NICE 2014

  • Recent onset T2DM:
    • Expedite bariatric surgery if BMI > 35
    • Consider surgery if BMI > 30
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46
Q

What are the NHS guidelines on bariatric surgery

A

NHS England 2013

  • As per NICE but…..
  • Must have been obese for at least 5 years
  • Must engage with non-surgical weight-loss programme for 12-24 months first
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47
Q

What are Public Health/ Societal approaches to tackling obesity?

A
  • Schools
    • PE, lunches, vending machines
  • Urban design
  • Marketing/ media/ social media
    • food labelling, food advertisements
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48
Q

What is the chemical name for Omega 6?

  • what is the final product?
A
  • Linoleic Acid
    • found in vegetable and safflower oils
  • converts to Arachidonic Acid
    • found in Meat, poultry and eggs
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49
Q

What is the chemical name for Omega 3

  • what are its final products when digested?
A
  • A-Linolenic Acid
    • found in leafy veg, canola, walnut and soybean oils
  • converts to Eicosapeanoic Acid then Docosahexaenoic acid
    • these are found in fish oils, there is a poor conversion of these therefore it is needed in the diet.
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50
Q

What is the function of dietary fat?

A
  • makes food taste better
  • carries important fat-soluble vitamins
    • vit A: night vision, and BW
    • vit D: hormone, bone health, immune system
    • vit E: antioxidant
    • vit K: blood clotting factors
  • component of the cell membrane
  • a precursor of steroid hormones and vitamin D
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51
Q

What are essential amino acids?

  • list them
A

Amino acids we need to get from our diet

  • Histidine
  • Isoleucine
  • Leucine
  • Methionine
  • Phenylalanine
  • Threonine
  • Tryptophan
  • Valine
  • Lysine
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52
Q

What are conditionally non-essential amino acids?

  • list them
A

The body can produce these with essential a.a acting as precursors

  • Arginine
    • produced from glutamate and glutamine in the intestines
  • Asparagine
  • Glutamine
  • Glycine
  • Proline
    • produced from glutamate and glutamine
  • Serine
  • Tyrosine
    • requires Phenylalanine: can have Phenylketonuria- genetic mutation makes you unable to carry out the conversion
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53
Q

What are non-essential amino acids?

  • list them
A

The body can produce these

  • Alanine
  • Aspartate
  • Cysteine
  • Glutamate
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54
Q

What enzymes are involved in Fat digestion?

A
  • In the Stomach: gastric lipase
    • produced from gastric cells in the fundic mucosa
  • The Liver and gallbladder: bile acids
    • cholic and chenodeoxycholic acid: form micelles, increasing the surface area
  • The Small Intestine: pancreatic lipase, pro colipase
    • pro-lipase converted to colipase by trypsin: colipase makes pancreatic lipase more effective
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55
Q

What is the product of Lipid digestion?

A
  • pancreatic lipase converts TG to
    • monoacylglycerol
    • fatty acids
    • glycerol
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56
Q

What enzymes are involved in Protein digestion?

A
  • In the Stomach: Pepsin
    • chief cells in the stomach produce pepsinogen
    • converted to pepsin in the presences of HCl ( released from parietal cells)
  • Pancrease secretions into the small intestine:
    • produces trypsinogen
      • converted to trypsin using enteropeptidase
    • trypsin goes on to convert proenzyme endopeptidases into their active form
      • chymotrypsin
      • elastase
      • carboxypeptidases
    • Exopeptidases are secreted at the brush border of the SI: (there are many of them)
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57
Q

What are the disaccharides and what are there monosaccharides?

A
  • Maltose
    • 2x Glucose
  • Sucrose
    • glucose, fructose
  • Lactose
    • glucose, galactose
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58
Q

What enzymes are involved in the final digestion of disaccharides digestion?

  • where are they found?
A
  • Sucrase-isomaltase
  • Lactase
  • Maltase-glucoamylase

> found on enterocytes, the digestions occur on the brush-border of the small intestine

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59
Q

How and where is COH absorbed?

A
  • occurs on the brush border of the small intestine
  • Glucose + galactose: via Na+ symport into the intestinal villi
  • Fructose: via GLUT 5 transporter into the intestinal villi
  • Both transported out of the villi into the lumen via GLUT 2 transporter
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60
Q

How is fat absorbed in the small intestine?

A
  • fatty acids enter the intestinal villi
  • endoplasmic reticulum and golgi body form them into chylomicrons: allows it to be water-soluble
  • chylomicrons leave villi and enter lymph in the lacteal, takes chylomicrons to the blood system
61
Q

How are proteins absorbed in the small intestine?

A
  • amino acids enter enterocytes by various transporters and leave the intestine into the blood via facilitated diffusion
  • di and tripeptides enter the enterocytes via Human peptide transporter 1 (PEPT1): then converted into amino acids and follow the same absorption process
  • the amino acids are transported to the liver through the hepatic portal system
62
Q

What happens to non-starch polysaccharides?

(Fibre)

A
  • not digested or absorbed
  • Soluble fibres (pectin/gum) are fermented by bacteria in the colon leads to the production of
    • CO2, H2, CH4
    • Short fatty acids
      • Acetate: enters peripheral circulation
      • Propionate: taken up by the liver
        • Butyrate: used as energy substrate by colonic cells (enhances microbial growth)
  • Insoluble fibres make up the cellulose in the diet
63
Q

What are the two severe forms of protein-calorie malnutrition (PCM)?

A
  • Marasmus
    • seen in early infancy
    • no oedema or skin changes
  • Kwashiorkor
    • 2+ years
    • growth retardation
    • skin changes
    • abnormal hair
    • hepatomegaly
    • apathy
64
Q

Which diseases is malnutrition most likely to occur in?

A
  • GI/ Liver disease
  • GI malignancy
  • Oesophageal
  • Gastric
  • Pancreatic
  • Colorectal
  • surgery patients are also at risk
65
Q

What are the mechanisms behind malnutrition?

A
  • Inadequate intake
  • Impaired nutrient digestion/ processing
  • Excess losses
  • Altered requirements
66
Q

Give examples of impaired nutrient digestion and processing

A
  • Gastritis
    • can lead to gastric atrophy
      • Pernicious Anaemia: intrinsic factors isn’t secreted –> B12 not absorbed
    • gastric barrier
  • Peptic Ulcer
    • caused by H. pylori, irritation, poor blood supply, high acid and pepsin content
  • can also be from the intestines, pancreas or liver
67
Q

Give examples of Excess Loss that would cause malnutrition

A
  • vomiting
  • NG tube drainage
  • Diarrhoea
  • Surgical drains
  • Fistulae
  • Stomas
68
Q

Give examples of altered/ increased metabolic demand that would cause malnutrition

A
  • inflammation
  • cancer
  • burns/ wounds
  • brain injury
69
Q

What are the two types of fasting?

and what are the differences?

A
  • Uncomplicated fasting
    • uses ketogenesis using fatty stores, reduces gluconeogenesis
      • less protein used, less protein mass used
  • Stress fasting
    • a smaller proportion of energy from fat stores and ketogenesis
      • more amnio acids lost is stress starvation
    • a bit lower nitrogen balance
    • significant increase in salt and water retention- more likely to have oedema
70
Q

What is the impact of uncomplicated starvation in healthy people?

A
  • Decreased skeletal and muscle mass in the first day
    • muscle function reduces by day 5
  • 18% loss of muscle mass leads to physiological disturbance
    • cardiac output reduces by 45%
    • respiratory/ diaphragmatic muscular mass and contractility reduces
    • Gut and immune function reduce
  • ~40% weight loss is fatal
71
Q

What things need to be monitored when trying to prevent malnutrition?

A
  • low weight
  • weight loss
  • poor intake or predicted to become poor (surgery)
  • poor absorptive capacity
  • High nutrient losses
  • increased nutritional needs - burns, sepsis

“End-of-the-bed-o-gram”

72
Q

What measurements/ anthropometry are taken when monitoring malnutrition?

A
  • BMI
    • can estimate using mid-upper arm circumference (MUAC)
      • < 23.5 cm, likely to be < 20kg/m3
      • >32.0 cm, likely to be >30kg/m3
  • Estimating height from ulna length (patients that cannot stand)
73
Q

Explain the MUST screening tool for malnutrition

A
  • Add the following scores from each category
    • BMI score: 0-2 score
    • Weight loss score (unplanned weight loss in the last 3-6 months): 0-2 score
    • Acute diseases effect score: if present score 2
  • Overall risk
    • 0 = low risk
    • 1 = medium risk
    • 2+ = high risk
74
Q

What is the action plan when the risk of malnutrition is established?

A
  • 0- Low risk
    • repeat screening
      • weekly if in the hospital
      • monthly in care homes
      • annually in the community
  • 1- Medium risk
    • diet diary for 3 days
    • if the diet is ok repeat the screening
    • if it isn’t alright follow local guidelines/ increase intake
  • 2+ - High risk
    • refer to a dietitian, nutritional support team/ implement local policy
    • set goals to improve, monitor and review
75
Q

What are the routes of feeding?

A
  • Oral
    • safest, cheapest, most acceptable
    • contraindications: unsafe to swallow, damaged/ non-functioning gut
  • Enteral: using the gut
    • Percutaneous/ Nasal
    • Gastric/ Jejunal
    • Endoscopic/ interventional radiology access
  • Parenteral: bypassing the gut
    • total parenteral nutrition: fluid with nutrients
76
Q

What is refeeding syndrome?

A

Severe electrolyte and fluid shifts associated with metabolic abnormalities in malnourished patients undergoing refeeding

  • this can be orally, generally or parenterally
77
Q

What is the physiological cause of re-feeding syndrome?

A
  • during starvation, trans-membrane pumps aren’t active to conserve energy
    • Na and water drift intracellularly
    • K and Phos drift intracellularly and are excreted to keep plasma levels stable
  • as soon as energy is restored through feeding they are switched on causing
    • a sudden drop in plasma K ad Phos –> arrhythmias
    • a sudden surge in plasma nad water –> overload
78
Q

How is refeeding syndrome treated/ avoided?

A
  • be aware of the risk and check electrolytes before feeding
  • begin electrolyte replacement before feeding
  • refeed slowly and gradually
  • continue to monitor and replace as needed
79
Q

What micronutrient deficiency are there in the UK population?

A
  • iron-deficiency anaemia in adult women and older girls
    • periods and strict diets)
  • low vitamin D- increased risk of
    • rickets in young people
    • osteomalacia in adulthood
  • functional riboflavin (B2) deficiency
    • older children
    • adults
80
Q

What micronutrient deficiencies are associated with

  • Alcohol liver disease
  • IBS
  • Obesity
A
  • Alcohol liver disease
    • thiamine (B1)
    • vitamin D
  • IBS
    • iron
    • B12, B6, B1
    • vitamin D
    • vitamin K
    • folic acid
    • Selenium, zinc
  • Obesity
    • vit D
    • copper
    • Zinc
81
Q

How is vitamin C absorbed?

A
  • transport occurs at the brush border in the small intestine
  • occurs through a carrier-mediated Na dependant mechanism
  • SVCT1, SVCT2 (vitamin C transporter-1/2)

water soluble

82
Q

What is Biotin, what are it’s sources and what could its deficiency result in?

A
  • Vitamin H or B7
  • Water soluble
  • Found in
    • liver
    • egg yolk
    • soybeans
    • milk and meat
  • Deficiency causes
    • dermatitis
    • anorexia
    • alopecia
    • myalgia
    • paraesthesia
83
Q

Hows is Biotin absorbed and acquired?

A
  • Acquired through
    • the diet
    • and bacterially
  • absorbed via carried mediated Na dependent process
    • SMVT- sodium-dependent multivitamin transporter
84
Q

What is Cobalamin and how is it obtained?

A
  • vitamin B12: important for the formation of red blood cells
  • Water-soluble
  • obtained from animal products and from the colon microbiome
    • dietary B12 binds to protein heptocorrin
    • released from this complex in the Si in trypsin
    • then binds to the gastric intrinsic factor
85
Q

What is Folic Acid and how is it acquired?

A
  • vitamin M or B9
    • acquired from the diet from poly and mono-glutamate
    • also synthesised in the colons microbiome
    • water soluble
  • folate hydrolase releases folate from its conjugated polyglutamate form in the upper SI
  • folate has three carriers
    • FOLT: folate reduced carrier
    • PCFT/HCP1: proton-coupled folate transporter
    • FOLR1: GPI-anchored folate receptor
86
Q

What causes Folic acid malabsorption and what malaise would it cause?

A

Causes of Malabsorption

  • Tropical sprue
  • Gluten induced enteropathy
  • Bowel resections or diseases i.e crohns
  • alcohol
  • Phenytoin: epilepsy drug
  • Cytotoxic drugs

Causes macrocytic anaemia

87
Q

What is Niacin, how is it acquired?

A
  • Vitamin B3/ Nicotinic acid
    • water-soluble
    • used in NAD
  • Acquired directly from diet and endogenously
    • Tryptophane converted to Niacin through the kynurenine pathway
88
Q

What is Niacin deficiency associated with?

A
  • Pellagra
  • Dermatitis
  • Diarrhoea
  • Dementia
89
Q

What is Riboflavin, how is it acquired?

A
  • Vitamin B2
    • water-soluble
    • used to form FMN –> FAD
  • Acquired from diet
    • diary products
    • eggs
    • meats
    • leafy greens
  • absorbed via RFVT 3 into the intestine
  • RFVT1/2 from the intestine into the blood
  • RFVT1 from blood to tissue
90
Q

What is Riboflavin deficiency associated with?

A
  • may be associated IBS
  • chronic alcoholism
91
Q

What is thiamin, how is it acquired and what is its deficiency associated with?

A
  • vitamin B1
    • water-soluble
    • acquired from whole grains, nuts, dried legumes
  • absorbed via THTR1 and THTR2 transporters
    • expressed throughout the GI tract
  • deficiency can be genetic in rare cases
    • usually related to poor dietary intake
    • excessive alcohol use
  • causes Wernicke-Korsakoff syndrome
92
Q

What is Vitamin A, and how is it absorbed?

A
  • Retinol
    • lipid-soluble
  • From the diet absorbed as either Retinylester or Cartenoids (pro-vitamin A)
    • ​Retinyl ester: Liver, egg, butter, milk, fortified cereal
    • Carotenoids: Carrots spinach, collards, pumpkins, squash
      • conversion to vitamin A takes place in enterocytes
93
Q

What is vitamin D, what is the impact of its deficiency?

A
  • Lipid-soluble
  • Presents in two forms vitamin D2- ergocalciferol and vitamin D3- cholecalciferol
    • D3 is from UV rays
    • D2 is dietary which is then converted to D3 in the digestive system
  • Deficiency: effects Ca++ and Pi homeostasis
94
Q

What is vitamin E and what is its action?

A
  • Found as Tocopherol or tocotrienols
    • alpha, beta, delta, gamma
    • the alpha-tocopherol is predominant in foods apart from in soy where it is the gamma version
  • lipid-soluble
  • membrane-bound
  • powerful antioxidant: protects from ROS
95
Q

What is vitamin K? Explain its importance in our diet

A
  • fat soluble
  • presents as vit K1 (more active) and vit K2 (usually storage form, less active)
  • used to form clotting factors
    • newborns are at risk of haemorrhagic disease due to limited vit. k placenta permeability and breast milk. therefore they receive an injection
96
Q

How is calcium absorbed?

A
  • Site of absorption
    • Dairy products: primarily in the duodenum, jejunum
    • Plant products: fermentation of plant products in the colon
  • Mechanism of absorption
    • 20-30% absorbed in an acid medium
      • it was a vitamin D-dependent calcium transport system when intake is low and the requirement is high
      • happens in the duodenum
    • passively intake in the jejunum when intake is high
97
Q

How is Iron absorbed?

A
  • Site of absorption
    • the end of the proximal small intestine for both harm and non-haem sources
  • Mechanism of absorption
    • Haem absorbed as an intact porphyrin complex
    • Non-haem ironized from ferric to ferrous form: 35% of this absorbed when stores are low
98
Q

What are the six mechanisms of Malabsorption?

A
  • Mal-digestion
    • poor secretion of digestive enzymes
  • Inadequate absorptive surface
    • SI damage, infection, or removal
  • Bile Salt Deficiency
    • effects lipid digestion and fat-soluble vitamins
  • Lymphatic obstruction
    • impact on lipid absorption
  • Vascular disease
    • due to hypovolaemia
  • Mucosal disease
99
Q

What diseases cause Mal-digestion malabsorption?

A
  • Chronic pancreatitis
  • Cystic fibrosis
  • Pancreatic carcinoma
100
Q

What diseases cause malabsorption due to an inadequate absorptive surface?

A
  • Intestinal resection
  • Gastro colic fistula
  • Jejuno-ileal bypass
101
Q

What diseases cause malabsorption due to Bile salt deficiency?

A
  • Cirrhosis
  • Cholestastasis
  • Bacterial overgrowth
  • Impaired ileal reabsorption
  • Bile salt binders
102
Q

What diseases cause malabsorption due to lymphatic obstruction?

A
  • Lymphoma
  • Whipple’s disease
  • Intestinal lymphangiectasia
103
Q

What disease cause malabsorption due to Vascular disease?

A
  • Constructive pericarditis
  • Right-sided heart failure
  • Mesenteric arterial
  • Venous insufficiency
104
Q

What diseases cause malabsorption due to Mucosal disease?

A
  • Infection: giardia, Whipple’s disease, tropical sprue)
  • Inflammatory diseases
  • Radiating enteritis
  • Eosinophilic enteritis
  • Ulcerative jejunitis
105
Q

How does critical illness effect the human growth hormone?

A
  • cytokines released in illness, causing decreased GH sensitivity
    • decreased synthesis of GH-binding protein
    • decreased expression of GH-receptors
      • causes decreased hepatic sensitivity to GH:
      • IGF-1, IGFBP-1 and ALS synthesis decreased
      • decreased skeletal muscle hypertrophy/ protein catabolism isn’t inhibited
  • Overall increases the synthesis of GH due to negative feedback system
    • GH-activated tyrosine kinases inhibit Insulin activated PI3-kinase
    • the action of Insulin is inhibited
106
Q

What are clinical manifestations of growth hormone dysregulation?

A
  • Hyperglycaemia
  • Hyperlipidaemia
  • Hyperbolic rate
  • Muscle rate
  • Poor myotrophic response to exercise
107
Q

Why is it important to consider the nutritional needs of acutely and chronically ill patients?

A
  • may have a higher catabolic state: make patients weaker may hamper their recovery
  • may have a reduced appetite due to the illness ( or age)
  • their treatment may require ‘nil by mouth’, must consider this in older frailer patients, and younger patients
108
Q

What are five major classes of Lipoprotein

A
  • Chylomicrons (CM)
  • Very low-density lipoprotein (VLDL)
  • Intermediate density lipoprotein (IDL)
  • Low density lipoprotein (LDL)
  • High density lipoprotein (HDL)
109
Q

What is the absorptive and post-absorptive phase?

A
  • Absorptive is after a meal, energy source for most cells is glucose, glucose is being converted into storage molecules
  • Post-absorptive phase is a while after the meal, the stored materials are converted to glucose, most source of energy is from triglycerides
110
Q

Explain metabolism in the Fed state in the Liver

A
  • High insulin, glucagon ratio - glucose → glycogen and TGs as VLDL
  • some glucose enters the TCA cycle - glycerol from peripheral tissues → triacylglycerol
  • excess amino acids → pyruvate and enter TCA or converted to triacylglycerols
111
Q

Explain metabolism in the Fed state in Muscles

A
  • glucose enters muscles via insulin stimulated Glut 4 receptors
  • Glu is converted to glycogen or metabolised via glycolysis and TCA cycle
  • Fatty acids from the diet enter via chylomicrons and from the liver as VLDL
  • they are oxidised via Beta-oxidation to acetyl Co-a to produce ATP
  • the Liver Protein Lipase channel protein is increased in the high insulin to glucagon state
112
Q

Explain metabolism in the Fed state in Adipose tissue

A
  • Glucose enters the adipose by the insulin-dependent Glut 4 transport system
  • converted to Acetyl CoA and then fatty acids and triacylglycerol via glycolysis and PDH
  • Fatty acids enter from VLDL and chylomicrons and are converted to triacylglycerol
  • Glycerol released from TAGs is returned to Liver for re-use
113
Q

What is the source, trigger and effect of the hormone Glucagon on glycogenolysis and gluconeogenesis?

A

Source: Pancreatic alpha-cells

Trigger: Hypoglycaemia Effect: rapid activation

114
Q

What is the source, trigger and effect of the hormone Adrenaline on glycogenolysis and gluconeogenesis?

A

Source: Adrenal medulla

Trigger: Stress, hypoglycaemia Effect: Rapid activation

115
Q

What is the source, trigger and effect of the hormone Cortisol on glycogenolysis and gluconeogenesis?

A

Source: Adrenal Cortex

Trigger: Stress Effect: Chronic activation

116
Q

What is the source, trigger and effect of the hormone Insulin on glycogenolysis and gluconeogenesis?

A

Source: Pancreatic Beta-cells

Trigger: Hyperglycaemia Effect: Inactivation

117
Q

Explain in general reciprocal regulation of phosphorylase and glycogen synthase by phosphorylation

A
  • Glucagon (liver) and adrenaline (muscle) activate glycogen breakdown and inhibit synthesis by activating cAMP PK with ultimate phosphorylation of phosphorylase and glycogen synthase
  • Mimicked by increasing Ca2+ during contraction
  • Insulin activates protein phosphatase to reverse these effects
118
Q

What are the irreversible steps in the glycolytic pathway? including enzymes

A
  • Glucose -(Hexokinase/Glucokinase)→ G-6-P
  • F-6-P –(PFK1)-→ F-1,6-P2
  • PEP –(Pyruvate kinase)–> Pyruvate
119
Q

What is gluconeogenesis?

A
  • production of glucose from non-carbohydrate precursors
    • lactate from glycolysis,
    • amino acids from protein breakdown,
    • glycerol (not fatty acids) from fat metabolism
  • these provide the carbon skeleton for the glucose
120
Q

What stimulates gluconeogenesis in the short term?

A
  • glucagon and adrenaline
  • changes in protein phosphorylation or mobilisation fatty acids and production of acetyl CoA
121
Q

What stimulates gluconeogenesis in the long term?

A

enzyme induction by

  • glucagon -
  • glucocorticoids -
  • thyroid hormones
122
Q

What inhibits gluconeogenesis in the short term?

A
  • insulin → via dephosphorylation and suppression of lipolysis
123
Q

What inhibits gluconeogenesis in the long term?

A
  • suppression of gluconeogenic enzymes
124
Q

Explain the urea cycle

A
  • increased gluconeogenesis = increased urea -
  • amino acids need to be transaminated to lose their ammonia
  • NH3 +CO2 + 2H2O + 3ATP +asparate → urea + fumerate + 2ADP+ AMP + 2Pi+ PPi
    • fumerate converted to OAA int the cytoplasm generating a substrate for gluconeogenesis
125
Q

What is the difference between Liver and muscle glycogen?

A
  • Liver: used to maintain plasma glucose -
  • Muscle: used for muscle contraction
126
Q

What product does glycogenolysis produce?

A
  • converts glycogen to glucose-1-phosphate
  • can then be converted to free glucose
127
Q

What enzyme is important for mobilisation in the liver?

A
  • glucose-6-phosphatase - removes the phosphate from gluc-6-phosphate
  • muscles do not express this enzyme
128
Q

What is the normative range for blood glucose?

A

2.5-8mM

129
Q

Name the hormones that increase the blood glucose levels?

A
  • Glucagon
  • Cortisol (adrenal glands)
  • Growth hormone
  • Catecholamines (adrenal glands, stress)
130
Q

What are healthy cholesterol limits?

A

serum cholesterol level is < 5.0 mmol/L in individuals without cardiovascular disease

131
Q

What is the relationship between serum cholesterol and CHD risk

A
  • the lowest risk for CHD is below 5mmol/L of serum cholesterol
  • the risk doubles between 5-6.5 mmol/L
  • and quadruples between 5-7.8 mmol/
132
Q

What are the helathy limits for Triglycerides

A

the upper limit of normality in fasting serum lipids is 1.7mmol/L

133
Q

What is a healthy limit for HDL-C?

A

the lower limit of normal is 0.9mmol/L in mend and 1.2mmol/L in women

134
Q

What does the Framingham Heart study show about the association between blood lipid and cholesterol levels and CHD?

A
  • Low HDL-C predicts CHD independent of LDL-C in men aged 50-70 years
  • HDL-C is inversely correlated with CAD risk
135
Q

What is Familial Hypercholesterolaemia?

A
  • Autosomal dominant disorder of lipid metabolism
  • effects up to 1 in 270 people in the UK
  • Features are: raised blood cholesterol specifically LDL and tendon and skin xanthomata
136
Q

What are Physical signs of Familial Hypercholesterolemia?

A
  • Xanthomata on the hands, around the eyes at the Achilles tendon and corneal arches
137
Q

What are genetic mutations implicated in Familial Hyperlipidemia?

A
  • APOB
  • the protein that binds to the LDL receptor 9 mutations described
  • PCSK9
  • a protein involved in receptor degradation 6 mutations described
  • LDLR
  • Over 1000 mutations spread throughout gene described
138
Q

What are causes of secondary Dyslipidaemias?

A

Hypertriglyceridaemia

  • Obesity
  • Diabetes mellitus
  • XS alcohol
  • Renal failure
  • Gout
  • Drug treatment (thiazides, beta-blockers, retinoic acid derivatives, oestrogen therapy, antipsychotics)

Hypercholesterolaemia

  • Hypothyroidism
  • Nephrotic syndrome
  • High saturated fat diet
  • Cholestatic liver disease
  • Anorexia nervosa
139
Q

What types of obesity are there?

A

Visceral (Intra-abdominal) fat

Subcutaneous fat

140
Q

What is the common result of Abdominal obesity?

A
  • Abdominal obesity is the most common cause of this cluster of metabolic abnormalities increasing risk of coronary heart disease in type 2 diabetic patients.
141
Q

What is the difference in Obese patients presenting with Visceral fat vs Subcutaneous fat?

A
  • Obese patients with a high accumulation of visceral adipose tissue show a significantly greater glycemic response in the presence of marked hyperinsulinemia
    • predictive of determination in glucose tolerance in the presence of marked hyperinsulinemia

hence a greater disturbance in glucose-insulin homeostasis is seen in those resenting with a visceral fat phenotype

142
Q

What is the Q Risk 2 Score

A

This score tells you you likelyhood/ risk of developing CVD in the next 10 years

  • Age
  • Total serum cholesterol/ HDL cholesterol
  • Systolic Blood Pressure
  • Smoking status
  • Sex
  • Left ventricular hypertrophy
  • Type 2 Diabetes mellitus
  • Body mass index
  • Family history
  • Deprivation score
  • Ethnicity
  • Atrial fibrillation
  • Renal disease
  • Rheumatoid arthritis
143
Q

What is the epidemiology of obesity in England?

A
  • 1: 4 men and women
144
Q

What is the effect of a low energy diet on your brain and your gut hormones?

A
  • Increased hunger and increased desire and urge to eat.
  • Significant reduction in PYY, cholecystokinin (CCK), insulin, leptin and amylin levels
  • Ghrelin, GIP and pancreatic polypeptide (PP) increased.
145
Q

What is the effect of exercise on your brain and your gut hormones?

A
  • Increase in circulating PYY levels
  • Suppression in appetite and ghrelin following exercise eg low volume sprint and endurance exercises
146
Q

What is the effect of obesity on your brain and your gut hormones?

A
  • Intestinal EECs ( Entero Endocrine cells) responsiveness is reduced in people with obesity
  • Blunted ghrelin reductions post-meal
  • Loss of pre-meal peaks, along with reduced diurnal variability
    • Contributes to the lack of regular meals and the frequent snacking behaviour often observed in individuals with obesity
  • Reduced circulating baseline and meal-stimulated levels of anorectic peptides PYY, GLP-1 and Neurotensin (NT), compared to individuals with normal weight
  • Leptin resistance in common obesity
147
Q

What Drug classes induce weight gain?

A
  • Antipsychotics
    • Risperidone, Lithium, Quetiapine, Aripiprazole, Olanzapine, Valproic acid
  • Antidepressants
    • Citalopram, Duloxetine, Venlafaxine
  • Sleep inducing drugs
    • Zopiclone, Zolpidem, Trazadone
  • Neuropathic agents
    • Pregabalin, Gabapentin
  • Steorids
  • Insulin
148
Q

What Drug classes induce weight gain?

A
  • Antipsychotics
    • Risperidone, Lithium, Quetiapine, Aripiprazole, Olanzapine, Valproic acid
  • Antidepressants
    • Citalopram, Duloxetine, Venlafaxine
  • Sleep inducing drugs
    • Zopiclone, Zolpidem, Trazadone
  • Neuropathic agents
    • Pregabalin, Gabapentintin
  • Steorids
  • Insulin

302: Scientific Bases of Medicine (9 decks)

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