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!!!!! BRS YR2 !!!!! > Gastro - Appetite > Flashcards

Gastro - Appetite Flashcards

1
Q

What are the 3 mechanisms through which thirst is regulated?

A

→ body fluid osmolality
→ blood volume is reduced
→ blood pressure is reduced

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2
Q

Which of the mechanisms is most potent?

A

→ plasma osmolality
→ change of 2-3% induces strong desire to drink
→ decrease of 10-15% in blood volume or arterial pressure is required to produce the same

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3
Q

What regulates osmolality?

A

ADH (anti-diuretic hormone) or vasopressin

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4
Q

What does ADH do?

A

acts on kidneys to regulate volume + osmolality of urine

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5
Q

Where in the kidneys does ADH act?

A

collecting duct, aquaporin 2 channel

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6
Q

How does low plasma ADH affect urine volume?

A

large volume of urine is excreted (water diuresis)

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7
Q

How does high plasma ADH affect urine volume?

A

small volume of urine is excreted (anti diuresis)

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8
Q

What receptors detect osmolality?

A

osmoreceptors

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9
Q

What are osmoreceptors?

A

Sensory receptors
Osmoregulation
Found in the hypothalamus

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10
Q

Where are osmoreceptors found?

A

in hypothalamus:
→ Organum vasculosum of the lamina terminalis (OVLT)
→ Subfornical Organ (SFO)

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11
Q

How do osmorecepetors stimulate ADH release?

A

→ Cells shrink when plasma more concentrated
→ Proportion of cation channels increases – membrane depolarizes
→ Send signals to the ADH producing cells to increase ADH
→ Fluid retention, Invokes drinking

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12
Q

How do osmorecepetors inhibit ADH release?

A

→ Cells are turgid/normal when plasma less concentrated
→ Proportion of cation channels decreases – membrane hype-polarises
→ No signals are sent to ADH producing cells, so ADH stays low

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13
Q

How is the sensation of thirst satisfied?

A

→ decreased by drinking even before sufficient water has been absorbed by the GI tract to correct plasma osmolality
→ Receptors in mouth, pharynx, oesophagus are involved
→ Relief of thirst sensation via these receptors is short lived.
→ Thirst is only completely satisfied once plasma osmolality is decreased or blood volume or arterial pressure corrected

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14
Q

Where is ADH stored?

A

posterior pituitary

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15
Q

What change in BP triggers the renin-angiotensin-aldosterone system?

A

decrease in blood pressure

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16
Q

What happens when BP decreases?

A

decrease in blood pressure causes JUXTAGLOMERULAR CELLS of renal afferent arterioles to produce RENIN

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17
Q

What does renin do?

A

renin is an enzyme that converts:
angiotensinogen —> angiotensin I
in the liver

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18
Q

What does angiotensin I do?

A

gets converted into angiotensin II by ACE in the lungs

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19
Q

What does angiotensin II cause?

A

→ vasoconstriction, increase in sympathetic activity
→ ADH secretion
→ H2O retention via Na+CL- absorption + K+ excretion
→ causes aldosterone to be released
→ Thirst

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20
Q

What else can stimulate aldosterone release?

A

increased potassium, decreased sodium levels

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21
Q

How is aldosterone released via angiotensin II? From where?

A

→ angiotensin II binds to intraglomerular messenger cells
→ cells contract + blood vessels around them contract
→ causes aldosterone to be released form zone glomerulosa of adrenal cortex

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22
Q

What does aldosterone do?

A

H2O retention via Na+CL- absorption + K+ excretion

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23
Q

What medications have an impact on the RAAS pathway?

A

→ ace inhibitors

→ direct renin inhibitors

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24
Q

Who studied body homeostasis in the 20th century?

A

→ Neuman 1902 – his weight was stable for a long time despite no conscious effort to balance out intake and expenditure
→ Passmore 1971 – most individual adults maintain a relatively stable weight over long periods

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25
Q

What does a reduction in fat mass result in?

A

increased food intake + reduced energy expenditure

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26
Q

What does adipose tissue expansion cause?

A

reduced food intake + increased energy expenditure

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27
Q

What systems are activated when weight is augmented? What is the result?

A

→ increased sympathetic nervous system activity
→ increased energy expenditure
→ decreased hunger/food intake
this all results in weight loss

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28
Q

What systems are activated when weight is reduced? What is the result?

A

→ decreased sympathetic nervous system activity
→ decreased energy expenditure
→ increased hunger/food intake
this all results in weight gain

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29
Q

What system mainly defend against the reduction of body fat?

A

central circuit

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30
Q

What system defends against rapid expansion?

A

yet to be discovered

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31
Q

What part of the body regulates appetite?

A

hypothalamus

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32
Q

What stimulants are necessary for hypothalamus to regulate appetite?

A

→ GHRELIN, PYY + other gut hormones
→ neural input from the periphery + other brain regions
→ LEPTIN

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33
Q

What parts of the hypothalamus are labelled here, 1-4?

A

1) paraventricular nucleus
2) ventromedial hypothalamus
3) lateral hypothalamus
4) arcuate nucleus

34
Q

What is the arcuate nucleus?

A

→ in the medial basal area, near 3rd ventricle
→ brain involved in regulation of food intake
→ incomplete BBB, allows access to peripheral hormones
→ integrates peripheral and central feeding signals
→ has 2 significant neuronal populations

35
Q

What are the 2 significant neuronal populations of the arcuate nucleus?

A

→ stimulatory (NPY/Agrp neuron)

→ inhibitory (POMC neuron)

36
Q

What is the NPY / Agrp neuronal population responsible for?

A

→ makes peptides that could potentially stimulate food intake
→ e.g. increases neuropeptide Y signalling + reduces melanocortin signalling via the release of Agrp

37
Q

What is NPY?

A

→ neuropeptide Y
→ released in many places in the body, found in high concentration in the arcuate nucleus
→ known as an orexigenic agent

38
Q

What is Agrp?

A

→ Agouti-related protein
→ produced in the brain by the AgRP/NPY neuron
→ synthesized in neuropeptide Y (NPY)-containing cell bodies located in the ventromedial part of the arcuate nucleus
→ increases appetite + decreases metabolism + energy expenditure

39
Q

What is the POMC neuronal population responsible for?

A

→ inhibits food intake, decreasing appetite, increasing metabolism + energy expenditure
→ produces peptides like POMC, then alpha-MSH to carry this out

40
Q

What is POMC?

A

pro-opiomelanocortin

41
Q

What is a melanocortin?

A

→ products of POMC cleavage

→ e.g. ACTH, MSH, alpha-MSH, etc.

42
Q

What is the melanocortin system?

A

→ POMC neurones in the brain release alpha-MSH melanocortin
→ MC4 receptors in the Paraventricular Nucleus detect alpha-MSH
→ positive stimulation causes it to go on to suppress food intake

43
Q

What is the paraventricular nucleus?

A

→ projects neurones into posterior pituitary to produce oxytocin, ADH
→ can also help regulate appetite + energy expenditure

44
Q

How is the paraventricular nucleus involved with the arcuate nucleus?

A

→ ArGP causes increased feeding when it stimulates the paraventricular nucleus
→ alpha-MSH from POMC stimulates decreased feeding through MC4R

45
Q

What parts of the arcuate nucleus have more NPY/ArGP neurones?

A

lateral

46
Q

What parts of the arcuate nucleus have more POMC/CART neurones?

A

ventromedial

47
Q

What is orexigenic?

A

agents that increase food intake

48
Q

What is anoretic?

A

agents that decrease food intake

49
Q

What is the benefits of the arcuate nucleus having access to the exposed BBB?

A

allows arcuate nucleus to interpret circulating factors, to see if feeding + appetite needs to be regulated

50
Q

What receptors do the 2 neuronal populations of the arcuate nucleus have?

A

→ receptors for Leptin + Insulin
→ decrease in Leptin or Insulin signalling causes more NPY + ArGP
→ increase in Leptin or insulin signalling causes more POMC

51
Q

What human CNS mutations can affect appetite?

A

→ No NPY or Agrp mutations associated with appetite discovered in humans
→ POMC deficiency and MC4-R mutations cause morbid obesity

52
Q

Are mutations responsible for the prevalence of obesity?

A

Mutations not responsible for the prevalence of obesity - but useful to explain signaling

53
Q

What higher parts of the brain are involved in appetite regulation?

A

→ amygdala
→ lateral + ventromedial hypothalamus
→ vagus nerve + brainstem

54
Q

What is the role of the amygdala in appetite regulation?

A

regulates appetite through reward + motivation pathways

55
Q

What is the role of the other parts of the hypothalamus in appetite regulation?

A

→ lateral = associated with orexigenic factors

→ ventromedial = associated with anoretic factors

56
Q

What is the role of the vagus nerve + brainstem in appetite regulation?

A

neuronal info from digestive tract is relayed through vagus nerve to brainstem to the hypothalamus

57
Q

What is the adipostat mechanism?

A

the body’s thermostat

how adipose tissue regulates the body’s adiposity and therefore appetite, feeding + energy expenditure

58
Q

How does the adipostat mechanism work?

A

→ Circulating hormone produced by fat
→ Hypothalamus senses the concentration of hormone.
→ Hypothalamus then alters neuropeptides to increase or decrease food intake.

59
Q

What could be hypothesised about the adipostat mechanism in obesity?

A

problem with the regulation of it could be causing the obesity

60
Q

What is the ob/ob mouse?

Why is it important?

A

→ obese mouse that ate excessively

→ lead to the discovery of leptin

61
Q

What is leptin?

A

→ hormone made by adipocytes in adipose tissue + enterocytes in small intestine
→ circulates in plasma
→ acts upon the hypothalamus regulating appetite + food intake + thermogenesis / energy expenditure
→ meaning thin, discovered in 1994
→ missing in the ob/ob mouse

62
Q

What does congenital leptin deficiency result in?

A

children will have normal body weight but insatiable hunger
will lead to excessive eating
results in them becoming obese

63
Q

How can congenital leptin deficiency be treated?

A

leptin is effective in reducing body weight

64
Q

What was the trend noticed by scientists concerning leptin in obesity?

A

high leptin levels were seen in those with high body fat

probably due to leptin resistance developed over time

65
Q

What is leptin’s mechanism of action?

A

→ adipose tissue releases leptin
→ leptin stimulates hypothalamus
→ decreases food intake
→ increases energy expenditure + fat + glucose metabolism

66
Q

What are the 3 things that can go wrong in leptin’s mechanisms to result in obesity?

A

→ absent leptin
→ regulatory defect in leptin levels
→ leptin resistance to high leptin levels

67
Q

What is leptin circulation in plasma proportional to?

A

→ Leptin circulates in plasma in concentrations proportional to fat mass
→ low leptin = low body fat mass
→ high leptin = high body fat mass

68
Q

Is leptin effective as a weight control drug?

A

no - usually obese people have sufficient leptin

69
Q

What is the purpose of GI hormones? What produces them?

A

→ secreted by entero-endocrine cells in the stomach, pancreas & bowels
→ controls various function of digestive organs

70
Q

Which GI hormones regulate appetite?

A

→ ghrelin

→ peptid YY

71
Q

What GI hormones does the stomach release?

A

→ ghrelin

→ gastrin

72
Q

What GI hormones does the pancreas release?

A 
→ insulin
→ glucagon
→ somatostatin
→ pancreatic polypeptide
→ amylin
73
Q

What GI hormones does the small intestine release?

A

→ cholecystokinin
→ secretin
→ GIP
→ motilin

74
Q

What GI hormones does the large intestine release?

A

→ GLP-1
→ GLP-2
→ oxyntomodulin
→ PYY 3-36

75
Q

What does ghrelin do?

A

→ stimulates + increases appetite

→ increases gastric emptying

76
Q

How does ghrelin stimulate appetite?

A

Directly modulates neurons in the arcuate nucleus
→ Stimulates NPY/Agrp neurons
→ Inhibits POMC neurons.

77
Q

When is Ghrelin levels the highest in the body? Why?

A

→ before a meal

→ help prepare for food intake by increasing gastric motility + acid secretion

78
Q

What else is ghrenlin useful for?

A

Regulation of reward, taste sensation, memory, circadian rhythm

79
Q

What is PPY?

A

→ peptide tyrosine tyrosine
→ released in terminal ileum + colon in response to food arrival
→ reduces appetite

80
Q

How does PYY reduce appetite?

A

→ inhibits NPY release

→ stimulates POMC neurones

81
Q

What comorbidities is obesity associated with?

A 
→ depression
→ sleep apnoea
→ MI
→ bowel cancer
→ osteoarthritis
→ gout
→ peripheral vascular disease
→ diabetes
→ hypertension
→ stroke

!!!!! BRS YR2 !!!!! (72 decks)

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