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BRS Year 2 > appetite & disorders > Flashcards

appetite & disorders Flashcards

1
Q

what is the strongest stimulus for thirst

A

plasma osmolarity

over blood volume/arterial pressure

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2
Q

action of vasopressin

A

regulates volume and osmolarity of urine
via aquaporin 2 channels on collecting duct
more adh = small amount of urine (less water)

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3
Q

where are the osmoreceptors?

A

organum vasculosum of lamina terminalis
subfornical organ
within hypothalamus

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4
Q

stimulus of thirst?

A

cells shrink via osmosis if plasma is more concentrated (no BBB)
proportion of cation channels increases - membrane depolarises
sends signals to ADH producing cells for ADH release
fluid retention and invokes drinking

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5
Q

how is the sensation of thirst satiated?

A

decreased by drinking (before sufficient water has yet been absorbed to correct osmolarity)
receptors in mouth, pharynx and oesophagus
but SHORT LIVED release - only completely satiated when plasma osmolarity decreased/blood volume/arterial pressure

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6
Q

how is a reduction in blood pressure regulated by the body, starting in the kidney

A

fall in bp detected by juxtaglomerular cells in renal afferent arteriole
renin produced
angiotensinogen converted to angiotensin I in liver
angiotensin I- II in lungs by ACE
results in vasoconstriction, thirst, stimulation of aldosterone secretion in zona glomerulosa, H2O retention and Na retention, ADH secretion

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7
Q

where in the brain is responsible for appetite

A

hypothalamus:
arcuate nucleus
lateral hypothalamus (feeding centre)
ventromedial hypothalamus (satiety centre)

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8
Q

what is the arcuate nucleus

A

brain area involved with regulation of food intake (via lateral and ventromedial hypothalamus)
with 2 neuron groups: neuropeptide Y/agouti-related peptide and POMC

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9
Q

how is appetite regulated by the hypothalamus

A

stimuli - insulin and leptin (levels of circulating factors)ghrelin, vagus nerve stimulation of AN

arcuate nucleus - orexigenic and anorectic neurons send signals to inhibit/stimulate:

paraventricular nucleus - ADH

lateral hypothalamus - orexigenic peptides (feeding centre)

ventromedial hypothalamus - anorexigenic peptides /melanocortins (satiety centre)

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10
Q

where is the arcuate nucleus

A

medial-basal part of hypothalamus, adjacent to 3rd ventricle

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11
Q

what is the paraventricular nucleus

A

collection of neurons around 3rd ventricle in hypothalamus
controls energy expenditure and appetite
produces ADH and oxytocin
terminal field of arcuate nucleus neurons (appetite neurons)

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12
Q

what mechanisms of weight homeostasis kick in if weight reduces

A

reduced sympathetic activity
reduced energy expenditure
reduced thyroid activity
increased hunger/food intake

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13
Q

what weight homeostasis mechanisms kick in when weight is increased?

A

increased sympathetic activity
increased energy expenditure
reduced hunger/food intake

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14
Q

how does peripheral input for appetite reach the brain (not through blood)

A

vagus nerve

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15
Q

what are the orexigenic neurons

A

neuropeptide Y and AGRP neurons

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16
Q

what are the anorexic neurons

A

POMC neurons

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17
Q

how do melanocortins produce their effect

A

alpha-MSH (melanocyte stimulating hormone) released by POMC neurons in arcuate nucleus
binds to MC4R in paraventricular nucleus
this decreases appetite and suppresses food intake

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18
Q

how does the arcuate nucleus know to increase appetite?

A

receptors for insulin and leptin

decrease of either will stimulate NPY/AGRP neurons to increase appetite

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19
Q

what is leptin

A

anorexigenic hormone made by adipocytes
proportional to body fat
inhibits NPY and AGRP, stimulates POMC neurons

20
Q

what is ghrelin

A

orexigenic gut hormone from enteroendocrine cells

increase before every meal

21
Q

how does ghrelin work for appetite

A

stimulates NPY/AGRP neurons
inhibits POMC neurons
increases gastric motility and secretions
displays a diurnal rhythm

22
Q

what is peptide YY

A

anorexigenic gut hormone produced by terminal ileum and colon
suppresses appetite
inhibits NPY, stimulates POMC

23
Q

how does peptide YY work for appetite

A

inhibits NPY neurons
stimulates POMC neurons
suppresses appetite

24
Q

what gene mutations are associated with obesity?

A

POMC neuron mutations

25
Q

what hormone is related to obesity

A

lepin resistance

26
Q

what is secondary polydipsia

A

due to a medical issue disruptinf any step in osmoregulation or alter ADH

27
Q

causes of secondary polydipsia

A 
diabetes I and M
kidney failure
conns syndrome
addisons disease
sickle cell
diuretics and laxatives
antidepressants
dehydration
28
Q

name some causes of dehydration

A 
sweating
acute illness
fevers
vomiting
diarrhoea
underhydration
29
Q

causes of primary polydipsia

A

its mentaw iwwness innit
brain injuries
organic brain damage

30
Q

what issues may be caused by polydipsia

A 
hyponatraemia causing:
kidney/bone damage
headaches
nausea/cramps
slowed reflexes/slurred speech
low energy
confusion/seizures
31
Q

what is adipsia

A

absence of thirst

32
Q

categories of anorexia nervosa

A

mild - BMI >17
moderate 16-16.99
severe - 15-15.99
extreme <15

33
Q

signs of anorexia nervosa

A 
low BMI
continuous weight loss
amenorrhoea
halitosis
mood swings
dry hair/skin/ thinning
34
Q

causes of anorexia nervosa

A

genetic
environmental
psychological
sociological

35
Q

what is an eating disorder

A

mental illness characterised by altered eating habits

36
Q

what is the mechanism behind anorexia

A

serotonin

37
Q

what is the treatment of obesity?

A

best results - diet and exercise

bariatric surgery if severe

38
Q

when is bariatric surgery offered to an obese individual

A

BMI 40+ OR 35+ Comorbidities

39
Q

most common bariatric surgery

A

roux-en Y gastric bypass

2nd most - sleeve gastrectomy

40
Q

what are the hormonal changes after bariatric surgery

A

ghrelin reduced

Glucagon-like peptide 1&2, PYY elevated

41
Q

role of lateral hypothalamus in appetite

A

produce only orexigenic (appetite) peptides

42
Q

role of ventromedial hypothalamus in appetite

A

produce anorexigenic peptides only

43
Q

types of appetite stimuli

A 
ghrelin - orexigenic
PYY - anorexigenic
vagus nerve - mechanoreceptors in stomach (increased firing = anorexigenic)
leptin - adipose tissue anorexigenic
insulin - anorexigenic
44
Q

mechanisms of leptin dysfunction

A

not enough produced
receptor signalling defective
decreased sensitivity to leptin

45
Q

levels of leptin depend on

A

levels of body fat - doesnt fluctuate much during day

high fat = high leptin

46
Q

what is congenital leptin deficiency

A

constant hunger as a result of no leptin circulating body

leptin effective when replaced in body - body weight reduced

BRS Year 2 (67 decks)

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