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203: Theme 1 - 304 - Endocrinology > Physiology of Appetite and Weight > Flashcards

Physiology of Appetite and 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
17
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
18
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
19
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
20
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
21
Q

Review this overview of how appetite is controlled

A
22
Q

What pathways could be taken to control/ treat obesity?

A
  • Lifestyle modification
  • Pharmacological
  • Surgical
  • Public health/ Societal
23
Q

What Lifestyle modifications need to be made?

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
24
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
25
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
26
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
27
Q

What are the adverse effects of Orlistat?

A
  • Flatulence, oily faecal leakage
  • Diarrhoea
  • decreased absorption of fat soluble vitamins
    • vit. ADEK
    • take supplements
28
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
29
Q

What surgical treatment can be done to treat obesity?

A
  • Laparoscopic adjustable banding
    • restrictive only- inject/withdraw saline to adjust the diameter of the band
  • Roux-en-Y gastric bypass
    • Restrictive
      • 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
30
Q

What are the pros and cons of surgical treatment?

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
31
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
32
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
33
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

203: Theme 1 - 304 - Endocrinology (15 decks)

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