Aspects of Obesity Flashcards

1
Q

how does the body use up energy?

A
basal metabolism (60-75%)
thermogenesis (including digestion) = 10%
physical activity = 15-30%
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2
Q

what gene is associated with obesity and why?

A

FTO gene

may cause people to eat more

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3
Q

what may be a link between obesity and cancer?

A

high insulin and oestrogen levels

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4
Q

name 4 obesity co-morbidities that are only associated with increased fat mass?

A

OA
back pain
Asthma
Sleep apnoea

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5
Q

how does obesity progress to hyperglycaemia?

A

obesity leads to insulin resistance
causes compensatory hyperinsulinaemia
eventually pancreas cant keep up and patient becomes hyperglycaemic and develops diabetes

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6
Q

what does adipose tissue secrete?

A
leptin
adiponectin
CRP
TNF alpha
IL-6
PAI-1
Oestrogen
Cortisol
free fatty acids
many more
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7
Q

what is leptin?

A

hormone produced by adipose tissue

tells body how fat you are or how thin you are

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8
Q

what are the effects of a leptin deficiency or lack of leptin receptors in brain?

A

brain thinks that you are starving so increases hunger and food intake and decreases thermogenesis to reduce burning of fat

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9
Q

what are the effects of too much leptin?

A

doesn’t have the opposite effect to low leptin

once you get up to a certain amount of leptin it levels out so appetite is not decreased

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10
Q

how are adipocytes and macrophages related?

A

share a lot of overlapping functions
both can secrete cytokines (IL-6, TNF alpha etc)
both can store fat
become more alike in obesity as adipocytes secrete cytokines and macrophages store fat forming foam cells leading to atherosclerotic plaques

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11
Q

what can trigger inflammation in obesity?

A

adipocytes secrete cytokines attracting macrophages which then infiltrate adipose tissue
cellular stress can trigger - if the ER in adipocytes cant cope with metabolic demands of expanding fat mass then it activates pathways involved in inflammation and insulin resistance
these metabolic changes in the acute phase are also proatherogenc

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12
Q

what are the steps in the formation of an atherosclerotic plaque?…

A

1 = endothelial dysfunction

  • chronic endothelial injury leads to endothelial dysfunction. LDL migrates into the intima. This attracts macrophages and lymphocytes which then migrate into the intima
    2. Fatty streak formation
  • monocytes eat LDL and form foam cells, creating a fatty streak in the vessel wall
    3. Smooth muscle cells migrate over the surface of the plaque forming a cap (thick = stable, thin = unstable)
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13
Q

how is very low calorie diets used?

A

only short term (6-8 weeks)

not sustainable as only amounts to around a glass of milk per day

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14
Q

options for hypocaloric diets?

A
portion control/calorie counting
low carbs
low fat
very low calorie diet (VLCD)
meal replacement (e.g slim fast)
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15
Q

how does orlistat work?

A

blocks lipase so inhibits absorption of dietary fat

loose up to 1/3rd of ingested fat in faeces

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16
Q

what are the 3 most common bariatric surgeries in the UK?

A

gastric band = restrictive
gastric bypass = restrictive and malabsorptive
sleeve gastrectomy = restrictive

17
Q

common problem with gastric band?

A

band slipping

18
Q

which is the most effective approach to weight loss?

A

gastric bypass as both restrictive and malabsorptive

all surgical approaches are more effective than medications and lifestyle

19
Q

what is basal metabolic rate?

A

amount of energy expended at rest

= minimum energy consumption

20
Q

what contributes to resting metabolic rate?

A

fat mass and fat free mass

21
Q

how does resting metabolic rate change with weight?

A

higher in obesity

lower in weight loss

22
Q

what is adaptive thermogenesis?

A

the large fall in resting metabolic rate seen in weight loss which exceeds predicted fall

23
Q

what are the implications of adaptive thermogenesis?

A

means weight loss will level off even if youre still doing the same things