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GI > Obesity and metabolic syndrome > Flashcards

Obesity and metabolic syndrome Flashcards

1
Q

where is the hunger centre located in the hypothalamus?

A

lateral area

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2
Q

where is the satiety centre located in the hypothalamus?

A

ventro-medial nucleus

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3
Q

what do positive signals to the satiety centre stimulate a felling of?

A

fullness

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4
Q

what are the circulating hormones that makes you feel hungry?

A

orexigens

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5
Q

what are the circulating hormones that makes you feel full?

A

anorexigens

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6
Q

where are orexigens produced?

A

neuroendocrine cells in stomach, neuropeptide in brain

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7
Q

name some anorexigens

A

SST, CCK, Peptid YY (ileal break), oxyntomodulin, GLP-1

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8
Q

are foodstuffs like AAs lipids and glucose anorexigens or orexigens?

A

anorexigens

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9
Q

what does ghrelin stimulate?

A

hunger

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10
Q

where is the arcuate nucleus found and where does it receive messages from?

A

medulla, receives central and peripheral messages and messages from annorexigens

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11
Q

what does the arcuate nucleus communicate with?

A

hunger centre in the hypothalamus

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12
Q

What do anorexigenic neurones release?

A

POMC (–> aMSH) and CART

go to hypothalamic areas

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13
Q

what do orexigenic neurones release?

A

AGRP and NPY that modify function

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14
Q

what effect does AGRP have on melanocortin receptors?

A

inhibitory

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15
Q

What hormones are involved in the overall long term integrating signal for eating?

A

leptin and adipokines

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16
Q

which cells produce leptin?

A

adipocytes

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17
Q

what is the effect of leptin?

A

potentiates insulin

central effects

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18
Q

which hormone is similar to leptin?

A

adiponectin

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19
Q

which pro-inflammatory cytokines inhibit leptin and insulin and therefore worsen obesity

A

TNF-a and IL-6

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20
Q

which neurones does leptin stimulate?

A

anorexigenic neurones –> feel full so don’t eat

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21
Q

what is the order of metabolites used in starvation?

A

glucose fat (ketone bodies to brain glycerol to gluconeogenesis) muscle (AAs to gluconeogenesis)

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22
Q

what happens in severe starvation?

A

apathy, decreased heart rate, muscle wasting, muscle fatigue, decreased respiratory capacity, decreased exercise capacity, cardiac failure, respiratory failure, infection, decreased heat generating capacity

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23
Q

which 3 out of 5 conditions are required to have the metabolic syndrome?

A

DMT2, obesity (waist circumference), low HDL cholesterol, hypertension, high plasma triglycerides

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24
Q

what disease is the metabolic syndrome associated with?

A

CVS disease

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25
Q

why is visceral fat around organs more dangerous?

A

less responsive to insulin, hyperlipolytic state, more NEFAs produced, less adiponectin produced, more pro-inflammatory cytokines produced

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26
Q

what effect do non-esterified fatty acids (NEFA) have on the body?

A

liver is less sensitive to insulin, alters lipid handling, impairs beta cell insulin release

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27
Q

which pro-inflammatory cytokines does visceral fat increase the levels of?

A

TNF-a, IL-6, IL-1 (amplified by invading macrophages)

28
Q

Why does insulin resistance lead to protein glycation?

A

increased plasma glucose levels results in advanced glycation endproducts (AGEs)

29
Q

what is the term for glycated proteins?

A

AGEs (advanced glycation endproducts)

30
Q

via which receptor do AGEs induce an inflammatory response?

A

RAGE

31
Q

how do AGEs increase the risk of CHD and atheroma?

A

via the RAGE receptor –> induce an inflammatory response –> reactive oxygen species –> CHD, atheroma

32
Q

which other factors contribute to CHD and atheroma formation?

A

dislipidaemias, oxidative stress

33
Q

which hormone do obese mice lack?

A

leptin

34
Q

which receptor do diabetic mice lack?

A

leptin receptors

35
Q

What do most obese people have high levels of?

A

ghrelin and low leptin

36
Q

how is the energy used for an activity per day calculated?

A

PAR (physical activity ratio) x BMR/hr x hours

37
Q

how is BMI calculated?

A

weight/ height^2

38
Q

what are the risks associated with obesity?

A

DMT”, CHD, gout, hypertension, sleep apnoea, cancer, stroke, MI, osteoarthritis, retinopathy, hypertension, reproductive and urological problems, musculoskeletal problems

39
Q

What are the 3 factors that characterise anorexia nervosa?

A

active maintenance of low body weight,

40
Q

What are the characteristics of anorexia nervosa?

A

peaks at 15-18years, 0.5% girls 15-18 years get it, 95% female

41
Q

how is bullimia nervosa distinguished from binge eating bisorder?

A

no compensatory behaviour after binge

42
Q

what binge frequency is required to diagnose bullimia nervosa?

A

frequency of one per week for 3 weeks

43
Q

what are the characteristics of bulimia nervosa?

A

recurrent binge eating, compensatory behaviours, extreme shape and weight concern

44
Q

What are the characteristics of binge eating disorder?

A

recurrent binge eating, binge episodes, marked distress regarding bingeing, no compensatory behaviour, no BN or AN

45
Q

who typically gets bulimia nervosa?

A

late adolescents, 1-3% or 18-25, 95% female

46
Q

what is OSFED?

A

Other specified feeding and eating disorders
disordered eating such as bingeing or restriction but criteria for AN or BN not met
AN but >85% body weight
BN but less frequent episodes

47
Q

what are the common features of eating disorders?

A

behaviour around food, levels of distress, overvaluation of shape and weight

48
Q

Who devised the Socio-cultural model and what are the 4 main components of it that increase the likelihood to dieting?

A

Stice, 1994

socio-cultural environnment, carriers (peers media), mediators (self esteem body weight), individual

49
Q

who devised the theory that dieting is a main pathway leading to eating disorders?

A

Patton et al 1999
2000 15 year olds over 3 year cohort study
moderate dieting increased risk 5x severe dieting increased risk 18x

50
Q

in the study by patton et al 1999 what effect did poor mental health have on the frequency of eating disorders?

A

increased risk 6x

51
Q

who devised the model for specific and non-specific risk?

A

connors, 1996

52
Q

what are the non-specific factors that contribute to risk of eating disorder?

A

self-regulatory risk factors that lead to low self esteem, affective dysregulation and insecure attachment

53
Q

what are the specific factors that contribute to risk of eating disroders?

A

body dissatisfaction risk factors leading to negative body image and weight preoccupation

54
Q

what is an eating disorder a combination of in regard to the specific and non-specific risk theory?

A

body dissatisfaction and low self esteem or other psychological problems

55
Q

Why are eating disorders a particular problem with adolescent girls?

A

shape and weight concern acted out through food, often framed as ‘healthy’, food autonomy from parents, peer impression management

56
Q

why might eating disorders develop?

A

as a way of managing a problom for example feeling in control by stopping eating, bingeing to regualate negative emotional state

57
Q

what was the minnesota experiment?

A

ancxel keys

starved men during the war to look into physical and psychological effects of starvation

58
Q

who delevoped the motivated eating restraint theory?

A

palmer 2000

59
Q

what is motivated eating restraint?

A

pre-cursor to AN and BN with similar motivations of “sitting on top of hunger” AN is successful BN breaks out with binges

60
Q

what are the negatives associated with eating diorders?

A

prevents socialising, lost freedom, moody, guilty, controls life

61
Q

when are drugs considered to reat obesity?

A

BMI 25-30 and high waist crcumference and co-morbidities

62
Q

when is bariatric surgery recommended?

A

BMI > 40 or 35-40 with co-morbidities and other significant disease, generally fit for surgery and anaesthesia., commits to long term follow up

63
Q

how did the foresight report of 2007 change the way we tackle obesity?

A

treating obesity as physiology

highlighted an obesogenic environment

64
Q

what were the 7 main themes outlined by the foresight report of october 2007?

A

passive weight gain is a biological adaptation to biology, food consumption, individual psychology, activity environment, societal influences, food production, individual activity, activity environment

65
Q

what 5 factors are required before a person can begin weight loss treatment?

A
  1. physical and emotional circumstances 2. eating disorders 3. own initiatives/ pressured? 4. realistic expectations (10% loss) 5. understanding of what’s needed

GI (10 decks)

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