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BS - Gastrointestinal System pt.1 > Obesity & Metabolic Syndrome Etc. > Flashcards

Obesity & Metabolic Syndrome Etc. Flashcards

1
Q

Why does body weight barely change over many years?

A

There is a good feedback system in the body

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2
Q

What happens to energy that is consumed by the body?

What equation demonstrates this?

A

Energy that is consumed is either used or stored

Energy in = energy used + energy stored

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3
Q

Why do people tend to gain weight as they get older?

A

Often a reduction in exercise/physical activity is not matched by a change in diet

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4
Q

What is involved in balancing appetite?

A

Appetite is balanced by the hypothalamus balancing signals that encourage eating and signals that prevent it

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5
Q

What are the main signals that feed into the hypothalamus which prevent eating?

A
  1. neural signals from the gut

2. circulating hormones, such as insulin and CCK

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6
Q

What are the centres in the hypothalamus involved with appetite regulation?

A

The hunger and satiety centres

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7
Q

What would happen if either the hunger or satiety centre was completely burned out?

A

If the hunger centre was burnt out, this would lead to complete termination of eating

If the satiety centre was burnt out, this would lead to constant eating

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8
Q

What is meant by satiety?

A

Satiety is the feeling of fullness and the suppression of hunger for a period of time after a meal

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9
Q

What is ghrelin?

Where is it produced?

A

It is a 28 amino acid peptide

It is produced from neuroendocrine cells in the stomach

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10
Q

When is ghrelin released?

A

It is released when the stomach is empty

It is also present as a neuropeptide in the brain

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11
Q

What are the functions of ghrelin?

A
  1. it is a growth hormone secretagogue

2. it is a powerful hypothalamic orexigenic agent

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12
Q

What is an orexigenic agent?

A

It is an appetite-inducing agent

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13
Q

What is an anorexigen?

A

An agent that suppresses appetite

Many of the gut/pancreatic peptides are anorexigens

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14
Q

What are the most common anorexigens?

A
  1. CCK
  2. insulin
  3. GLP-1
  4. Peptide YY
  5. Oxyntomodulin
  6. somatostatin
  7. foodstuffs
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15
Q

How can foodstuffs act as anorexigens?

A

Hypothalamic areas are outside the blood-brain barrier so can detect foodstuffs in the blood

Glucose, amino acids and lipids have direct actions on the hypothalamus

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16
Q

What is the role of peptide YY?

A

It is produced from the colon and provides the ileal brake

It also suppresses appetite

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17
Q

What triggers hunger?

What happens after eating?

A

Ghrelin in the stomach triggers hunger

During/after eating, ghrelin levels will fall

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18
Q

What happens to CCK/insulin/amylin levels after eating?

What does this produce?

A

Levels rise steeply during eating

CCK and insulin induce a feeling of satiation

This is uncomfortable fullness

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19
Q

What happens to PYY/GLP-1?oxyntomodulin levels after eating?

What does this produce?

A

They begin to rise after a meal has been eaten

They produce the feeling of satiety

This is a more comfortable feeling of being full

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20
Q

What is the role of adipokines produced from fat?

A

They tell the body how much fat that you have, and are involved in the control of obesity

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21
Q

What is the role of leptin produced by adipocytes?

A

It potentiates insulin and signals about how much fat there is in the body

it will inhibit hunger

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22
Q

Why will someone with a defect in the leptin receptor become obese?

A

When there is a defect in the receptor, more leptin is produced

This leads to weight gain as the leptin cannot be detected

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23
Q

What is another adipokine with similar effects to leptin?

A

Adiponectin

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24
Q

What adipokines act as pro-inflammatory cytokines?

What is their role?

A

TNF-alpha and IL-6

They will inhibit insulin and leptin

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25
Q

Where is the nucleus of the solitary tract?

What is its role?

A

It is in the medulla

It collects central and peripheral messages from the gut, including anorexinogens

It passes these signals to the arcuate nucleus

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26
Q

What are the two projections from the arcuate nucleus?

A
  1. satiety centre in the ventromedial nucleus

2. hunger centre in the lateral hypothalamic centre

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27
Q

What are the 2 types of neurones contained within the arcuate nucleus?

A
  1. anorexigenic neurones

2. orexigenic neurones

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28
Q

What is secreted by anorexigenic neurones in the arcuate nucleus?

A
  1. proopiomelanocortin (POMC)

2. cocaine-amphetamine-related-transcript (CART)

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29
Q

What is secreted by orexigenic neurones in the arcuate nucleus?

A
  1. Agouti-related peptide (AGRP)

2. neuropeptide Y (NPY)

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30
Q

What is the role of Agouti-related peptide?

A

It inhibits melanocortin receptors

This stimulates appetite

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31
Q

What are melanocortins?

A

a group of peptide hormones which are derived from proopiomelanocortin (POMC)

They decrease appetite

32
Q

In what order are different stores used up during starvation?

A

Starvation uses up muscle, fat and then muscle again

33
Q

Why is muscle broken down initially during starvation?

A

The brain needs glucose - which is provided by gluconeogenesis

Glycerol from fat is used in gluconeogenesis

This does not produce sufficient glucose so muscle is broken down to produce amino acids

Amino acids are processed in the liver to be converted to glucose

34
Q

Why does starvation move from using up muscle to using up fat?

A

Ketone bodies begin to be produced in the liver

The brain shifts to use these as a primary food source

Muscles are no longer degraded as ketone bodies are made from fatty acids

35
Q

What smell on the breath is a sign of starvation?

A

Smelling acetone on the breath is sign that someone hasn’t eaten for 3-4 days

This is due to ketone body production

36
Q

Why does muscle begin to be used up again during starvation?

A

Muscle begins to be consumes again when fat stores are exhausted

37
Q

How does muscle wasting in extreme starvation affect the body?

A
  1. muscle fatigue and reduced exercise capacity
  2. diminished respiratory capacity
  3. slowed heart rate and reduced contractility
38
Q

Why does extreme starvation lead to loss of heat-generating capacity?

A

A drop in thyroid hormone levels leads to loss of heat generating capacity and apathy

39
Q

What usually causes death in extreme starvation?

A

Respiratory or cardiac failure

Or infection

40
Q

Why are extremely starved people more prone to infection?

A

Cortisol and stress hormone production leads to immunosuppression

They are less able to fight infection

41
Q

What is meant by an ‘eating disorder’?

A

A voluntary/deliberate maintenance of a low dietary intake, which may lead to a low body weight, or may result in bingeing and purging

42
Q

What are the psychological and psychiatric characteristics associated with eating disorders?

A
  1. low self esteem
  2. perfectionism
  3. desire to control their environment
  4. depression
  5. distorted body image
43
Q

What is weight loss like in anorexia nervosa?

What must body weight be like?

A

Weight loss is due to VOLUNTARY abstinence

Body weight is more than 15% below standard - BMI < 17.5

44
Q

How do people with anorexia nervosa perceive themselves?

A

They have a distorted body image and a morbid fear of fatness

45
Q

What is the death risk carried with anorexia?

A

2-5% suicide risk, or they may die of starvation

46
Q

How does bulimia nervosa differ from anorexia nervosa?

A

Someone with bulimia does not necessarily have a low body weight

47
Q

What is the formula for BMI?

A

BMI =

(weight in kg) / (height in m)^2

48
Q

What is normal BMI?

What is overweight, obese and underweight?

A

Underweight = < 18.5

Normal = 18.5 - 24.99

Overweight = 25 - 29.99

Obese = > 30

49
Q

How does BMI give an indication of mortality?

A

Being underweight increases mortality rate by a small amount

The relative risk increases massively with obesity

50
Q

What does having a high BMI greatly increase the risk of?

A

It massively increases the risk of type 2 diabetes

It also increases the risk of hypertension, coronary heart disease and gallstones

51
Q

What may a tiny fraction of obesity be due to?

How can this be identified?

A

Specific genetic defects

In this case, obesity happens very early on in life (age 4/5) and very quickly

52
Q

What are levels of leptin and ghrelin like in obese patients?

A

Levels of leptin and ghrelin rise and fall appropriately

Leptin is high and ghrelin is low

53
Q

Other than hunger ,what other factors may influence dietary intake?

A
  1. habit
  2. society and socialising
  3. opportunity (e.g. free food)
  4. hedonism (pursuit of pleasure)
54
Q

How does obesity affect the musculoskeletal system?

A

It causes osteoarthritis and lower back pain

This is due to the load on the joints being increased with weight gain

55
Q

How does obesity affect the circulatory system?

A
  1. hypertension which leads to coronary heart disease, stroke and renal failure
  2. deep vein thrombosis
  3. pulmonary embolism
56
Q

Why does obesity cause hypertension and DVT?

A

The circulatory system is strained and the heart must work harder as fat has a rich blood supply

DVT is due to the flow of blood coming back from the legs being slower

57
Q

How does obesity affect the metabolic and endocrine systems?

A
  1. type 2 diabetes risk raised
  2. dyslipidemia
  3. metabolic syndrome
58
Q

What is dyslipidemia?

A

an abnormal amount of lipids in the blood

59
Q

What cancers does obesity increase the risk of?

A
  1. endometrial
  2. breast
  3. colon
60
Q

How does obesity affect the reproductive and urological systems?

A
  1. stress incontinence and menstrual abnormalities
  2. polycystic ovarian syndrome
  3. infertility
  4. erectile dysfunction
61
Q

How does obesity affect the respiratory system?

A

Fat around the airways can cause them to collapse and make breathing more difficult

This causes sleep apnoea

62
Q

How does obesity affect the GI tract and liver?

A
  1. non-alcoholic fatty liver disease
  2. gastro-oesophageal refluc
  3. gallstones
63
Q

How does obesity cause psychological and social problems?

A
  1. stress
  2. low self-esteem
  3. social disadvantage
  4. depression
  5. reduced libido
64
Q

What is metabolic syndrome characterised by?

A

A patient must have at least 3 out of 5 of:

  1. obesity (waist circumference)
  2. type 2 diabetes
  3. hypertension
  4. high plasma triglycerides
  5. low plasma HDL cholesterol

(high LDL:HDL ratio)

65
Q

How does the handling of fat differ depending on where it is located?

A

Fat may be subcutaneous - under the skin layer

This is ‘healthy’ adipose tissue

Fat may be around the viscera

This is ‘dysfunctional’ adipose tissue

66
Q

What leads to the development of visceral obesity?

A

Energy-dense food and lack of physical activity lead to subcutaneous and visceral obesity

Visceral obesity is caused by:

  1. smoking
  2. maladaptive response to stress
  3. unfavourable genotype
67
Q

How does visceral fat differ to subcutaneous fat?

A

Visceral fat is less responsive to insulin

It produces more non-esterified fatty acids (NEFA)

68
Q

How does the distribution of fat lead to a normal metabolic profile?

A

If there is no ectopic fat and only subcutaneous fat:

  1. low muscle fat
  2. low epicardial fat
  3. low liver fat and normal function

this leads to a normal metabolic profile

69
Q

How can the distribution of fat lead to metabolic syndrome?

A

If there is lipid overflow and ectopic fat:

  1. increased muscle fat
  2. increased epicardial fat
  3. increased liver fat and altered function

This leads to an altered metabolic profile

70
Q

How does the production of cytokines and adipokines vary in visceral fat?

A
  1. production of more proinflammatory cytokines
    e. g. IL-1, IL-6, TNF-a
  2. produces less adiponectin
71
Q

What is the effect of visceral fat producing more non-esterified fatty acids?

A

NEFA makes the liver less sensitive to insulin

It also impairs B-cell insulin release

This leads to more gluconeogenesis and type II diabetes

72
Q

What is the effect on the plasma of increasing insulin resistance?

A
  1. higher plasma insulin

2. higher plasma glucose

73
Q

What induces an inflammatory response after insulin-resistance is induced?

A

Advanced glycation endproducts (AGEs) act via a receptor (RAGE) to induce an inflammatory response

AGEs are produced from glucose reacting with proteins

74
Q

What is the result of the inflammatory response induced by AGEs?

A

Cytokines produced from the inflammatory response, and central adipocytes, cause the production of reactive oxygen species

75
Q

What is thought to underlie the increase in atheroma and cardiovascular disease in obesity?

A

A combination of dyslipidemia and oxidative stress

BS - Gastrointestinal System pt.1 (22 decks)

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