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203: Reproduction and endocrinology > T1 L11:APPETITE AND WEIGHT > Flashcards

T1 L11:APPETITE AND WEIGHT Flashcards

1
Q

what measures can you use to measure someone’s weight

A

Body mass index (BMI)
kg / m2
Waist circumference

Skin-fold thicknesses

Bioelectrical impedance analysis

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2
Q

what groups do we have to be careful when measuring weight

A

Ethnic groups

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3
Q

what are the 5 ranges of BMI that someone can fall into

A 
< 18.5 underweight
18.5-24.9 normal
25-29.9 overweight
30-39.9 obese
≥40 morbid obesity
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4
Q

what percentage of adults are obese in England

A

25%

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5
Q

what are the health risks of obesity (3)

A 
Metabolic syndrome / type 2 diabetes
Cardiovascular disease
Respiratory disease
Liver disease
Cancer
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6
Q

what BMI category can health risks start from

A

overweight category
Men -25
women -24

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7
Q

what is metabolic syndrome

A

Constellation of closely associated CV risk factors and T2 diabetes

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8
Q

what is the underlying pathophysiological mechanism
of metabolic syndrome

(there are 2, 1 of which has 2 consequences the other has examples)

(3 marks )

A

Insulin resistance :
 Gluconeogenesis
 Dyslipidaemia

Pro-inflammatory cytokines
TNF-, IL-6 (from ‘overloaded’ white adipose tissue)

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9
Q

what are the signs associated with metabolic syndrome

4 marks

A

Visceral obesity
Dyslipidaemia
Hyperglycaemia
Hypertension

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10
Q

what type of body fat shape is metabolic syndrome associated with? and what type of fat distribution and BMI as well?

A

apple shape

Central (visceral) fat
Body mass index > 30

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11
Q

what can adipocyte cells release that influences hormones

A

ADIPOCYTOKINES

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12
Q

what is the risk of D2

A

AGE
OBESITY
FAMILY HISTORY
ETHNICITY

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13
Q

what are the symptoms of CVD and metabolic syndrome

4 marks

A 
increased:
 
blood volume and blood viscosity
 vascular resistance
 hypertension
 left ventricular hypertrophy
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14
Q

what respiratory symptoms link with metabolic syndrome

4 marks

A

Obstructive sleep apnoea
Hypoxia / hypercapnia
Pulmonary hypertension
-ight heart failure

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15
Q

what can obesity do to the liver

3m

A

Non-alcoholic fatty liver
Non-alcoholic steatohepatitis
May progress to cirrhosis, portal hypertension, hepatocellular cancer

Gallstones

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16
Q

what are the types of cancer associated with obesity and what mechanisms are associated as well?

A

Types of cancer include

Breast, endometrial, oesophagus,
colon, gall bladder, renal, thyroid

Mechanisms include- increase in
 insulin,  free IGF-I,  oestrogen,
adipo-cytokines, reflux

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17
Q

How can obesity affect the reproductive system

A

Polycystic ovarian syndrome

  • oligomenorrhoea hirsutism, acne
  • Subfertility
  • Endometrial hyperplasia
  • Insulin resistance

Male hypogonadism

Adverse pregnancy outcomes

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18
Q

what can obesity cause to the joints

A

Osteoarthritis

Gout

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19
Q

what psychological features can obesity cause

A

Depression

Eating disorders

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20
Q

what are the rare and common genetics associated with obesity

A

Rare :
Obesity-associated syndromes
Prader-Willi

COMMON
Polygenic
Susceptibility genes
Heritability of weight ~ heritability of height

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21
Q

what are the thyroid and adrenal related causes of obesity

A

Hypothyroidism

Cushing’s syndrome

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22
Q

what are the 2 main environmental features that contribute to obesity

A

Diet

physical activity

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23
Q

what type of diet leads to obesity

A

High fat

High sugar

24
Q

what % can physical activity count for total energy expenditure

A

20-50% total energy expenditure

25
Q

what is the SOCIAL NETWORKING: theory of obesity

A

Those with more obese friends tend to be obese

26
Q

what is FETAL PROGRAMMING

A

stimuli/insults at critical periods that have persistent biological effects

27
Q

what is the mechanism of fetal programming

A

Mechanism: epigenetic modification of gene expression

28
Q

give examples of fetal programming

3marks

A

Example: (3)
programmed’ adrenal axis overactivity in adulthood
Causal factor for metabolic syndrome
Increased vulnerability to coronary heart disease

29
Q

describe the association between cortisol and fetal weight with 9am levels

A

Babies with a lower birth weight have a higher cortisol level

30
Q

what is the LIFE COURSE MODEL

A

Factors operating at every stage of life affect health outcomes later in the future

‘PATHWAY OF RISK’ between events and health outcomes

31
Q

what is the 3 possible worst outcomes of the life course model associated with

A

Worst outcome’ associated with: (3)
Low birth weight
Excessive weight gain in infancy / childhood
Adult obesity

32
Q

How does the gut microbe influence diabetes t2 and metabolic syndrome

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

33
Q

what are the slow acting hormones and what do they signal

A

LEPTIN
INSULIN

decrease food intake

increase body expenditure

34
Q

what are the Rapid-acting peptides that regulate meal sizes

A

Released from GI tract
Cholecystokinin (CCK)
-reduce eating

Ghrelin
-increase eating

PYY-via hypothalamus
-decrease eating for up to 12 hours

35
Q

what type of neurons originate from the HYPOTHALAMUS(ARCUATE NUCLEUS)

A

‘Accelerator neurons’
AgRP neurons- release NPY
Nyp-increases eating by decreasing satiety
AGRP- blocks the melanocortin receptor

Brake neurons’
POMC neurons
-these are melanocortin peptides that decrease eating sensation

36
Q

what is the LEPTIN (MICE))experiment

A

‘ob/ob mouse’

  • Leptin deficient

‘db/db mouse’

-Mutation of leptin receptor

‘ob’ gene product = leptin

Mouse models of obesity

37
Q

what does leptin treatment do in mice

A

It reduces obesity in the ob/ob mouse

38
Q

what does Leptin do in humans

A

it behaves as the starvation signal and it causes permissive effect on puberty

39
Q

what causes obesity in humans that is related to Leptin

A

Leptin deficiency due to mutation of receptor

40
Q

how do you treat Obesity via lifestyle (diet)

4marks

A

DIET

-500-1000 kcal energy deficiency
-Low energy density
low sat fat, low sugar
 fruit & veg (substitute for other foods)

  • decrease portion sizes, decrease snacking
  • Structured meals / meal replacements may help promote greater weight loss
41
Q

how do you treat Obesity via lifestyle Pt 2

A

PHYSICAL ACTIVITY
Exercise 7 days / wk
30 mins moderate-high intensity OR
60 mins low intensity

10,000 steps

42
Q

what is the concept of a VLCD

A

Primary care programme
Patients with T2DM diagnosis < 6 years prior
VLCD (830 kcal/day) for 3-5 months

  • Initially, total diet replacement with formulae
  • Then stepped food reintroduction (2-8 weeks)
  • Long-term maintenance with structured support
43
Q

what is the target for lifestyle modification

A
  • 10% weight loss ( ideal weight)
  • 1-2 lb (0.5 – 1 kg) per week
  • Some evidence that ‘ambitious’ goals promote more weight loss
44
Q

what are the problems with lifestyle mods

4marks

A
  • Most patients can achieve ~ 5-10 % weight loss / 1 year
  • ‘Yo-yo’ dieting / regaining weight lost
  • ‘Obesogenic environment’
  • Weight loss results in hunger, satiety, metabolic rate
45
Q

what are the best outcomes for lifestyle modifications

3marks

A
  • Sustainable lifestyle changes
  • Diet combined with exercise / physical activity
  • Ongoing management is required to maintain weight loss
46
Q

what does Orlistat do

A

MECHANISM
Binds & inhibits lipases in the lumen of the gut
Prevents the hydrolysis of dietary fat into absorbable free fatty acids / glycerol
Excrete ~ 1/3rd dietary fat

47
Q

adverse effects of orlistat

A

Flatulence, oily faecal leakage, diarrhoea

decreased absorption fat soluble vitamins so :

ADEK
Supplement

48
Q

what does Metformin do

A

oral hypoglycaemic agents

49
Q

PHARMACOLOGICAL THERAPY-evaluate

A

PROBLEMS

  • Can only increase by 3-4 fold the proportion of patients who achieve 5% weight loss in a year
  • Weight re-gain after treatment stopped

THE FUTURE
All identified gut peptides / neuropeptides / their receptors are potential therapeutic targets / options!
-Gut hormones in combination most likely way forwards…

50
Q

what are the surgical treatments available

A

Laparoscopic adjustable banding

Roux-en-Y gastric bypass

51
Q

what is the Laparoscopic adjustable banding

A

Restrictive only

Inject / withdraw saline to adjust the diameter of the band

52
Q

what is the Roux-en-Y gastric bypass

A
  • Restrictive
  • Malabsorptive
  • Alterations in gut hormones and bile acid flow contribute to weight loss

Micronutrient deficiencies
-Supplement with iron, B12, folate, calcium, vitamin D
Dumping syndrome
-GI & vasomotor symptoms

53
Q

why is the Roux-en-Y gastric bypass better long term than Laparoscopic adjustable banding

A

Endocrine factors important in effects

  • Plasma from operated rats to sham-operated rats
  • Ate 1/3rd less

Increased satiety seems to be key

  • “I don’t like burgers any more……”
  • F-MRI studies
54
Q

Evaluate SURGICAL TREATMENT

A

ADVANTAGES

-Weight loss 25-30%
-Resolve or improve co-morbidities
Brings cost savings

DISADVANTAGES
-Perioperative mortality / morbidity
--Depends on procedure and experience of surgeon
-Long-term follow-up
Micronutrient deficiencies
-Some weight re-gain
--Patients will still be obese
-Expense
--Though cost effective by 2 - 5 years, depending on co-morbidities and weight
55
Q

what are the UK NICE guidelines for surgery

A 
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

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

56
Q

what is the UK Position bariatric surgery:NHS guidelines

A
  • 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
57
Q

What is the expected % weight loss from

  • Lifestyle interventions
  • Bariatric surgery
A

Weight loss 25-30%-surgery

10% weight loss

203: Reproduction and endocrinology (53 decks)

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