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brs2 > Appetite > Flashcards

Appetite Flashcards

1
Q

the body regulates/controls thirst through which main triggers?

A

body fluid osmolality
blood volume is reduced
blood pressure is reduced

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2
Q

why is plasma osmolality the most potent stimulus in thirst

A

change of 2-3% induces strong desire to drink

- 10-15% decrease in blood vol/pressure required to produce same response

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3
Q

what is the role of adh in thirst and osmolality

A

acts on collecting duct in kidneys - aquaporin 2 channels

and regulates olume and osmolality of urine

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4
Q

what is water diuresis

A

when plasma ADH is low and water is excreted

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5
Q

what is anti diuresis

A

when plasma ADH is high, small volume of urine is excreted

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6
Q

where is adh stored

A

posterior pituitary gland

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7
Q

what are osmoreceptors

A

sensory receptors
responsible for osmoregulation
found in the hypothalamus

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8
Q

which regions of hypothalamus are osmoreceptors found?

A

organum vasculosum of lamina terminalis

subfornical organ

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9
Q

how do osmoreceptors regulate adh release

A

cells shrink when plasma is more concentrated
proportion of cation channels increases - membrane depolarises
sends signals to adh producing cells
fluid retention invokes drinking

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10
Q

when is thirst completely satisfied

A

once plasma osmolality is decreased/ blood vol/arterial pressure is corrected

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11
Q

what happens in kidneys when blood pressure drops

A

juxtaglomerular apparatus secretes renin which activates angiotensin system by cleaving angiotensinogen to angiotensin1 which is converted to angiotensin2 by ACE

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12
Q

What are the effects of angiotensin 2

A

induces thirst

most important effect is on aldosterone

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13
Q

what is the role of aldosterone

A

influences reabsorption of sodium and potassium excretion influencing water retention

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14
Q

what is role of angiotensin 2

A

vasoconstriction - increases sympathetic activity

adh secretion

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15
Q

what 2 gut hormones are involved in peripheral signalling in appetite regulation

A

ghrelin
pyy
- travels through vagus nerve which connects to brainstem which communicates with hypothalamus - cns e.g amygdala

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16
Q

what is the long term hormones involved in appetite regulation

A

leptin

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17
Q

what is orexigenic

A

appetite stimulant

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18
Q

what is anorectic

A

appetite suppressive

19
Q

what does the lateral hypothalamus produce

A

orexigenic petides

20
Q

what is the ventromedial hypothalamus associated with

A

satiety

- lesions can lead to severe obesity

21
Q

when does food intake decrease

A

when arcuate nucleus pro opio melanocortin neurones activate

22
Q

what are some other hypothalamic factors which implicate appetite regulations

A

endocannabinoids
amp - activated protein kinase
protein tyrosine phosphotase

23
Q

what is the arcuate nucleus

A

brain area involved in regulation of food intake
incomplete bbb - allows access to peripheral hormones
- integrates peripheral and central feeding signals

24
Q

what are the 2 neuronal populations in the arcuate nucleus

A

stimulatory - NPY/agrp neuron

inhibitory - pomc neurone

25
Q

where are npy/agrp neurones found

A

only in arcuate nucleus in hypothalamus

26
Q

what is the role of npy/agrp neurones

A

potentially stimulate food intake by increasing neuropeptide y signalling and reducing melanocortin signalling

27
Q

what is agrp

A

endogenous melanocortin receptor antagonist

28
Q

what effect does leptin have on npy/agrp

A

inhibitory effects

29
Q

what effect does leptin have on pomc/cart

A

stimulatory effects

30
Q

what conditions can cause increased food intake via leptin mechanism

A

fasting
uncontrolled diabetes
genetic leptin deficiency

31
Q

other than feeding what are 2 factors the arcuate nucleus is responsible for

A

fertility and cardiovascular regulation

32
Q

what is the central melanocortin system

A

collection of central nervous circuits e.g npy/agrp and pomc

33
Q

what is melanocortin

A

product of pomc gene

34
Q

what are some human cns mutations affecting appetite

A

no npy/agrp mutations associated with appetite

  • pomc deficiency and mc4r mutations cause morbid obesity
  • mutations not responsible for obesity - but useful to explain signalling
35
Q

what is the adipostat mechanism

A

circulating hormone produced by fat

- hypothalamus senses concentration of hormone and then alters neuropeptides to increase/decrease food intake

36
Q

what is leptin

A

hormone made by adipocytes in white adipose tissue and enterocytes
circulates in plasma
acts on hypothalamus regulating appetite and thermogenesis

37
Q

what is congenital leptin deficiency

A

rare condition

causes severe obesity very early in life

38
Q

what is leptin resistance

A

leptin circulates in plasma in conc proportional to fat mass
obesity due to leptin resitance
leptin is ineffective as weight control drug

39
Q

why do we feel less hungry after a meal

A

hormone signals from gut aka gi hormones

40
Q

what are gi hormones secreted by

A

enteroendocrine cells in stomach, pancreas and sb

41
Q

what gi hormones is appetite regulated by

A

ghrelin - stimulates appetire, increases gastric emptying

peptide yy - inhibits food intake

42
Q

what is ghrelin

A

*help prepare food intake by increasing gastric mobility and acid secretion
directly modulates neurones in arcuate nucleus
stimulates npy/agrp neurones
inhibits pomc neurones
- increases appetite
- regulation of reward, taste sensation, memory and circadian rhythm

43
Q

what is peptide tyrosine tyrosine

A

short peptide released in terminal ileum and colon in response to feeding
reduces appetite
food arriving at ti and colon results in pyy release
inhibits npy release
stimulates pomc neurones

44
Q

what cormobidities is obesity associated with

A 
depression
sleep apnoea
bowel cancer
stroke
mi
osteoarthiritis
peripheral vascular disease
gout
hypertension
diabetes

brs2 (65 decks)

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