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BRS YR2 > Appetite > Flashcards

Appetite Flashcards

1
Q

What are the 3 main triggers of the control of thirst?

A
  • plasma osmolality
  • reduced blood volume
  • reduced blood pressure
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2
Q

What is the most potent stimulus for thirst control?

A

Plasma osmolality

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3
Q

What change in plasma osmolality is required to induce thirst?

A

2-3%

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4
Q

What change in blood volume/arterial pressure is required to induce thirst?

A

10-15%

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5
Q

How does the body regulate osmolality?

A

Anti-diuretic hormone (ADH)/vasopressin

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6
Q

Where does ADH act?

A
  • on the kidneys to regulate the volume and osmolality of urine
  • collecting duct, V2 receptor
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7
Q

What happens when ADH is low?

A

large volumes of urine is excreted (water diuresis)

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8
Q

What happens when ADH is high?

A

small volumes of urine are excreted (anti-diuresis)

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9
Q

Where is ADH stored?

A

in the posterior pituitary gland

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10
Q

How does the body measure osmolality?

A

via osmoreceptors in the hypothalamus

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11
Q

What are osmoreceptors? DELETE

A
  • sensory receptors
  • involved in osmoregulation
  • found in the hypothalamus
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12
Q

Where are osmoreceptors in the hypothalamus?

A
  • Organum vasculosum of the lamina terminalis (OVLT)
  • Subfornical Organ (SFO)
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13
Q

How is ADH release regulated in a dehydrated condition?

A
  • cells shrink when plasma is more concentrated
  • the proportion of cation channels increases, and the membrane depolarizes
  • sends signals to ADH producing cells to increase ADH
  • fluid retention, invokes drinking
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14
Q

How is ADH release regulated in a hydrated condition?

A
  • cells expand when plasma is less concentrated
  • cation channels are inhibited, the membrane is hyperpolarised
  • inhibits signals
  • excretion of fluid
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15
Q

What causes a decrease in thirst?

A

drinking

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16
Q

What detects that drinking has occured in order to stop thirst?

A

receptors in the mouth, pharynx and oesophagus

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17
Q

When is thirst completely satisfied?

A

when plasma osmolality is decreased or blood volume/arterial pressure is corrected

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18
Q

What type of relief is provided by mouth/pharynx/oesophagus receptors?

A

temporary

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19
Q

What else can prompt thirst?

A
  • habit
  • cravings
  • desire
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20
Q

What are the negatives of excessive fluid consumption?

A
  • energy wastage
  • decreased plasma osmolarity
  • interference with nutrient absorption (dependent/driven by sodium)
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21
Q

What system responds to changes in blood pressure/volume?

A

the renin-angiotensin-aldosterone system

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22
Q

What happens when blood pressure drops?

A

juxtaglomerular apparatus secretes renin

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23
Q

Where is the juxtaglomerular apparatus?

A

The hilus of the glomerulus

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24
Q

What happens when renin is released?

A

activates the renin-angiotensin system by cleaving angiotensinogen into angiotensin I

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25
Q

What secretes angiotensinogen?

A

the liver

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26
Q

What happens to angiotensin I?

A

it is converted into angiotensin II by (angiotensin converting enzyme) in the lungs

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27
Q

What is the effects of angiotensin II?

A
  • induces thirst
  • release of aldosterone
  • ADH secretion
  • vasoconstriction (increased sympathetic activation)
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28
Q

What does aldosterone do?

A 
Influences:
- sodium reabsorption
- potassium excretion
and therefore, 
- water retention
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29
Q

What happens when there is a reduction in fat mass?

A
  • increase in food intake
  • reduction in energy expenditure
  • reduces the effect of the thyroid gland
  • sympathetic inhibition
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30
Q

What happens when there is adipose tissue expansion?

A
  • reduces food intake
  • increases energy expenditure
  • sympathetic activation
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31
Q

What is the impact of changes in adipose tissue?

A

activates responses that favour the return to the previous/original weight

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32
Q

Which part of the brain regulates hunger?

A

hypothalamus

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33
Q

What are the 2 main gut hormones involved in appetite regulation (peripheral signalling)?

A
  • Ghrelin
  • PYY
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34
Q

What is the long term hormonal appetite regulation?

A

leptin system

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35
Q

What are the 3 main factors involved in appetite regulation?

A
  • Ghrelin/PYY
  • neural input from periphery/other brain regions
  • Leptin
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36
Q

What does orexigenic mean?

A

appetite stimulant

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37
Q

What does anorectic mean?

A

appetite supressive

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38
Q

What is the role of the arcuate nucleus?

A
  • regulation of food intake
  • both orexigenic and anorectic
  • integrates peripheral and central feeding signals
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39
Q

How does the arcuate nucleus allow access to peripheral hormones?

A

Incomplete blood-brain barrier

40
Q

What are the two neuronal populations of the arcuate nucleus?

A
  • stimulatory NPY/AGRP neuron
  • inhibitory POMC neuron
41
Q

What is the role of the paraventricular nucleus?

A
  • neurones to the posterior pituitary (oxytocin)
  • regulates appetite
42
Q

What is the role of the lateral hypothalamus?

A

produces orexigenic peptides

43
Q

What is the role of the ventromedial hypothalamus?

A

satiety

44
Q

What is the effect of lesions in the ventromedial hypothalamus?

A

severe obesity

45
Q

What is the effect of arcuate nucleus pro-opiomelanocortin (POMC) neurones?

A

reduced food intake

46
Q

What is also thought to be implicated in appetite regulation?

A
  • endocannabinoids
  • AMP (activated protein kinase)
  • protein tyrosine phosphokinase
47
Q

Where are NPY/Agrp neurones found?

A

only in the arcuate nucleus

48
Q

How do NPY/Agrp neurones stimulate food intake?

A

make peptides that:
- increase NPY signaling
- reducing melanocortin signaling
by AGRP release

49
Q

What is ARGP?

A

an endogenous melanocortin receptor antagonist

50
Q

What can activate NPY/Agrp neurones?

A

decrease in:

  • leptin
  • insulin
51
Q

What conditions cause an increase in food intake by impacting the NPY/Agrp neurones?

A
  • fasting
  • uncontrolled diabetes
  • genetic leptin deficiency
52
Q

What is the arcuate nucleus involved in?

A
  • feeding
  • fertility
  • cardiovascular regulation
53
Q

What is in the central melanocortin system?

A
  • NPY
  • AGRP neurones
  • POMC
54
Q

What are melanocortins?

A

products of the POMC

55
Q

What is an example of melanocortin

A

alpha-MSH

56
Q

What is the role of the central melanocortin system?

A

central regulator of energy balance
including:
- feeding behaviours
- energy expenditure

57
Q

Where are melanocortin-4 receptors expressed?

A

paraventricular nucleus

58
Q

What stimulates melanocortin-4 receptors?

A

serotonin

59
Q

What is the effect of the stimulation of melanocortin-4 receptors?

A
  • reduction of appetite
  • weight loss
  • reduced food intake
60
Q

What has a encouraging/stimulating effect on melanocortin-4 receptor?

A

alpha-MSH

61
Q

What has a inhibiting effect on melanocortin-4 receptor?

A

Agrp

62
Q

What is the effect of Agrp and NPY mutations?

A

No associated effects to appetite

63
Q

What is the effect of POMC deficiency and MC4-R mutations?

A

causes morbid obesity

64
Q

What role does the amygdala play?

A

controls reward related motivation pathways, affects appetite

65
Q

How is neural information from the digestive tract passed on to the hypothalamus?

A

carried by the vagus to the brain stem and eventually the hypothalamus

66
Q

What is the adipostat mechanism?

A
  • circulating hormones are produced by adipose tissue (more=more hormone)
  • concentration sensed by the hypothalamus
  • hypothalamus alters neuropeptides to change food intake
67
Q

What produces leptin?

A
  • adipocytes in white adipose tissue
  • enterocytes
68
Q

What does leptin do?

A
  • acts on the hypothalamus
  • decreases appetite (intake)
  • increases thermogenesis (expenditure)
69
Q

When is leptin low or high?

A
  • low when low body fat
  • high when high body fat
70
Q

Where in the hypothalamus does leptin act?

A
  • arcuate nuclei
  • ventromedial nuclei
71
Q

What is the role of leptin?

A
  • regulation of adipose tissue mass
  • development of atherosclerosis (innate system)
72
Q

What conditions have been associated with low levels of leptin?

A
  • Alzheimer’s disease
  • Depression
73
Q

What happens in congenital leptin deficiency?

A

RARE
morbid/severe obesity
low serum leptin levels

74
Q

How can congenital leptin deficiency be managed?

A

leptin replacement to reduce body weight

75
Q

What happens to serum leptin in obesity?

A
  • serum leptin concentration is correlated to the body fat %
  • obesity due to leptin resistance
76
Q

What are the mechanisms of leptin in obesity?

A
  • absent leptin
  • leptin resistance
  • regulatory defect in leptin (signalling issue)
77
Q

Would leptin be an effective weight control drug?

A

No, due to leptin resistance

78
Q

What reduces hunger after a meal?

A

hormonal signalling from the gut

79
Q

What secretes gut hormones?

A

enteroendocrine cells in:

  • stomach
  • pancreas
  • small intestine
80
Q

What are the roles of the gut hormones?

A
  • motility regulation
  • appetite regulation
  • satiety
  • salivation
81
Q

What is the effect of Ghrelin?

A
  • stimualtes appetite
  • increases gastric emptying
82
Q

What is the effect of Peptide YY?

A

inhibits food intake

83
Q

When is Ghrelin highest?

A
  • before meals
  • increases gastric motility and acid secretion
  • prepares for food intake
84
Q

What impact does Ghrelin have in the hypothalamus?

A
  • stimulates NPY/Agrp neurones
  • inhibits POMC neurones
85
Q

What does Ghrelin regulate?

A
  • reward
  • taste sensation
  • memory
  • circadian rhythm
  • increases appetite
86
Q

What rhythm is seen by Ghrelin levels?

A

diurnal rhythm

87
Q

What does circulating Ghrelin correlate with?

A
  • time of day
  • positive with age
88
Q

What is the physiological role of Ghrelin?

A

meal initiation

89
Q

Where is Peptide tyrosine tyrosine (PYY) released?

A
  • terminal ileum and colon
  • response to feeding
90
Q

What is the effect of PYY in the hypothalamus?

A
  • stimulates POMC neurones
  • inhibits NPY release
91
Q

What types of food trigger PYY release?

A
  • dietary fibres
  • wholegrains
  • enzymatic breakdown of crude fish proteins
92
Q

What does PYY do?

A

induces satiety/reduces appetite

93
Q

What is the degree of PYY release proportional to?

A

calorie intake

94
Q

What are the side effects of PYY?

A
  • nausea
  • fullness
  • less hunger
  • early fullness
95
Q

What co-morbidities are associated with obesity?

A
  • depression
  • stroke
  • sleep apnoea
  • MI
  • hypertension
  • diabetes
  • bowel cancer
  • osteoarthritis
  • peripheral vascular disease
  • gout
96
Q

Which factors are most dominant in terms of increasing risk of obesity?

A

environmental factors and genetic predisposition

BRS YR2 (67 decks)

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