appetite & disorders Flashcards

(46 cards)

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
what hormone is related to obesity
lepin resistance
26
what is secondary polydipsia
due to a medical issue disruptinf any step in osmoregulation or alter ADH
27
causes of secondary polydipsia
``` diabetes I and M kidney failure conns syndrome addisons disease sickle cell diuretics and laxatives antidepressants dehydration ```
28
name some causes of dehydration
``` sweating acute illness fevers vomiting diarrhoea underhydration ```
29
causes of primary polydipsia
its mentaw iwwness innit brain injuries organic brain damage
30
what issues may be caused by polydipsia
``` hyponatraemia causing: kidney/bone damage headaches nausea/cramps slowed reflexes/slurred speech low energy confusion/seizures ```
31
what is adipsia
absence of thirst
32
categories of anorexia nervosa
mild - BMI >17 moderate 16-16.99 severe - 15-15.99 extreme <15
33
signs of anorexia nervosa
``` low BMI continuous weight loss amenorrhoea halitosis mood swings dry hair/skin/ thinning ```
34
causes of anorexia nervosa
genetic environmental psychological sociological
35
what is an eating disorder
mental illness characterised by altered eating habits
36
what is the mechanism behind anorexia
serotonin
37
what is the treatment of obesity?
best results - diet and exercise | bariatric surgery if severe
38
when is bariatric surgery offered to an obese individual
BMI 40+ OR 35+ Comorbidities
39
most common bariatric surgery
roux-en Y gastric bypass | 2nd most - sleeve gastrectomy
40
what are the hormonal changes after bariatric surgery
ghrelin reduced | Glucagon-like peptide 1&2, PYY elevated
41
role of lateral hypothalamus in appetite
produce only orexigenic (appetite) peptides
42
role of ventromedial hypothalamus in appetite
produce anorexigenic peptides only
43
types of appetite stimuli
``` ghrelin - orexigenic PYY - anorexigenic vagus nerve - mechanoreceptors in stomach (increased firing = anorexigenic) leptin - adipose tissue anorexigenic insulin - anorexigenic ```
44
mechanisms of leptin dysfunction
not enough produced receptor signalling defective decreased sensitivity to leptin
45
levels of leptin depend on
levels of body fat - doesnt fluctuate much during day | high fat = high leptin
46
what is congenital leptin deficiency
constant hunger as a result of no leptin circulating body | leptin effective when replaced in body - body weight reduced