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BRS YR2 > Appetite > Flashcards

Appetite Flashcards

1
Q

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

A
  • body fluid 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, aquaporin 2 channel
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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?

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
  • ## 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 renal afferent arterioles

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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 lung

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27
Q

What is the effects of angiotensin II?

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

How does angiotensin II trigger the release of aldosterone?

A
  • binds onto receptors on the intraglomerular messenger cells
  • cell contraction
  • release of aldosterone in the zona glomerulosa of the adrenal cortex
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29
Q

What does aldosterone do?

A 
Influences:
- sodium reabsorption
- potassium excretion
and therefore, 
- water retention
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30
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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31
Q

What happens when there is adipose tissue expansion?

A
  • reduces food intake
  • increases energy expenditure
  • sympathetic activation
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32
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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33
Q

Which part of the brain regulates hunger?

A

hypothalamus

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34
Q

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

A
  • Ghrelin

- PYY

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35
Q

What is the long term hormonal appetite regulation?

A

leptin system

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36
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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37
Q

What does orexigenic mean?

A

appetite stimulant

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38
Q

What does anorectic mean?

A

appetite supressive

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39
Q

What is the role of the arcuate nucleus?

A
  • regulation of food intake

- both orexigenic and anorectic

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40
Q

What is the role of the paraventricular nucleus?

A
  • neurones to the posterior pituitary (oxytocin)

- regulates appetite

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41
Q

What is the role of the lateral hypothalamus?

A

produces orexigenic peptides

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42
Q

What is the role of the ventromedial hypothalamus?

A
  • satiety
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43
Q

What is the effect of lesions in the ventromedial hypothalamus?

A

severe obesity

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44
Q

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

A

reduced food intake

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45
Q

What is also thought to be implicated in appetite regulation?

A
  • endocannabinoids
  • AMP (activated protein kinase)
  • protein tyrosine phosphokinase
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46
Q

What is so advantageous about the arcuate nucleus?

A
  • incomplete blood-brain barrier
  • allows access to the peripheral hormones in the plasma
  • able to integrate peripheral and central feeding signals
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47
Q

What are the 2 different types of neurones in the arcuate nucleous?

A 
Stimulatory 
- Neuropeptide Y (NPY)
- Agouti-related peptide (Agrp neuron)
Inhibitory
- pro-opiomelanocortin sensitising (POMC neuron)
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48
Q

Where are NPY/Agrp neurones found?

A

only in the arcuate nucleus

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49
Q

How do NPY/Agrp neurones stimulate food intake?

A

make peptides that:
- increasing neuropeptide Y signaling
- reducing melanocortin signaling
by AGRP release

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50
Q

What is ARGP?

A

an endogenous melanocortin receptor antagonist

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51
Q

What can activate NPY/Agrp neurones?

A

decrease in:

  • leptin
  • insulin
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52
Q

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

A
  • fasting
  • uncontrolled diabetes
  • genetic leptin deficiency
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53
Q

What is the arcuate nucleus involved in?

A
  • feeding
  • fertility
  • cardiovascular regulation
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54
Q

What is the central melanocortin system?

A

collection of:

  • NPY
  • AGRP neurones
  • POMC
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55
Q

What are melanocortins?

A

products of the POMC

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56
Q

What is an example of melanocortin

A

alpha-MSH

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57
Q

What is the role of the central melanocortin system?

A

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

58
Q

Where are melanocortin-4 receptors expressed?

A

paraventricular nucleus

59
Q

What stimulates melanocortin-4 receptors?

A

serotonin

60
Q

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

A
  • reduction of appetite
  • weight loss
  • reduced food intake
61
Q

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

A

alpha-MSH

62
Q

What has a inhibiting effect on melanocortin-4 receptor?

A

Agrp

63
Q

What is the effect of Agrp and NPY mutations?

A

No associated effects to appetite

64
Q

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

A

causes morbid obesity

65
Q

What role does the amygdala play?

A

controls reward related motivation pathways, affects appetite

66
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

67
Q

What is the adipostat mechanism?

A
  • circulating hormones are produced by adipose tissue (more=more hormone)
  • sensed by the hypothalamus
  • hypothalamus alters neuropeptides to change food intake
68
Q

What produces leptin?

A

made by:

  • adipocytes in white adipose tissue
  • enterocytes
69
Q

What does leptin impact?

A

acts on the hypothalamus to regulate:

  • decreases appetite (intake)
  • increases thermogenesis (expenditure)
70
Q

Where in the hypothalamus does leptin act?

A

cell receptors in:

  • 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 to reduce body weight

75
Q

What happens to serum leptin in obesity?

A

serum leptin concentration is correlated to the body fat %

- obesity, leptin resistance

76
Q

What is the mechanism 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
  • colon
80
Q

What are the roles of the gut hormones?

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

What gut hormones regulate appetite?

A
  • Ghrelin

- Peptide YY (PYY)

82
Q

What is the effect of Ghrelin?

A
  • stimualtes appetite

- increases gastric emptying

83
Q

What is the effect of Peptide YY?

A
  • inhibits food intake
84
Q

When is Ghrelin highest?

A
  • before meals
  • increases gastric motility and acid secretion
  • prepares for food
85
Q

What impact does Ghrelin have in the hypothalamus?

A
  • stimulates NPY/Agrp neurones

- inhibits POMC neurones

86
Q

What does Ghrelin regulate?

A
  • reward
  • taste sensation
  • memory
  • circadian rhythm
87
Q

What rhythm is seen by Ghrelin levels?

A

diurnal rhythm

88
Q

What does circulating Ghrelin correlate with?

A
  • time of day

- positive with age

89
Q

What is the physiological role of Ghrelin?

A

meal initiation

90
Q

Where is Peptide tyrosine tyrosine (PYY) released?

A
  • terminal ileum and colon

- response to feeding

91
Q

What is the effect of PYY in the hypothalamus?

A
  • stimulates: POMC neurones

- inhibits: NPY release

92
Q

What types of food trigger PYY release?

A
  • dietary fibres
  • wholegrains
  • enzymatic breakdown of crude fish proteins
93
Q

What does PPY do?

A

induces satiety

94
Q

What is the degree of PPY release proportional to?

A

calorie intake

95
Q

What is the impact of PPY on food/calorie intake?

A

reduces it

96
Q

What are the side effects of PYY?

A
  • nausea
  • fullness
  • less hunger
  • early fullness
97
Q

What co-morbidities are associated with obesity?

A
  • depression
  • stroke
  • sleep apnoea
  • MI
  • hypertension
  • diabetes
  • bowel cancer
  • osteoarthritis
  • peripheral vascular disease
  • gout
98
Q

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

A

environmental factors and genetic predisposition

99
Q

What is polydipsia?

A

excessive thirst or drinking

100
Q

What is adipsia?

A

inappropriate lack of thirst

- consequent failure to drink

101
Q

What is anorexia?

A

loss/lack of appetite for food

102
Q

What is obesity?

A

abnormal or excessive fat accumulation that presents health risks

103
Q

What can cause secondary polydipsia?

A
  • chronic medical issues that disrupt any step in osmoregulation or alter ADH
  • medications
  • dehydration
104
Q

What does ADH do?

A

regulates the volume and osmolality of urine

105
Q

Where does ADH act?

A

Aquaporin 2 channel of the collecting duct in the kidneys

106
Q

What happens when ADH is low?

A

large volume of urine excretion (water diuresis)

107
Q

What happens when ADH is high?

A

small volume of urine excreted (anti-diuresis)

108
Q

Where is ADH stored?

A

in the posterior pituitary

109
Q

What chronic medical conditions can cause secondary polydipsia?

A
  • Diabetes Insipidus and Mellitus
  • Kidney failure
  • Conn’s syndrome
  • Addison’s disease
  • Sickle cell anaemia
110
Q

What medications can cause secondary polydipsia?

A
  • diuretics
  • laxatives
  • antidepressants
111
Q

What chronic medical conditions can cause dehydration?

A
  • acute illness
  • sweating
  • fevers
  • vomiting
  • diarrhoea
  • underhydration
112
Q

What is the difference between diabetes insipidis and mellitus?

A

DM: blood sugar
DI: impaired ADH production

113
Q

What are the symptoms of diabetes?

A
  • always tired
  • frequent urination
  • sudden weight loss
  • wounds that don’t heal
  • sexual dysfunction
  • constant hunger
  • blurry vision
  • numb of tingling peripherals
  • constant thirst
  • vaginal infections
114
Q

What is Conn’s syndrome?

A

primary aldosteronism

115
Q

What is Addison’s syndrome?

A

hypoadrenocorticism

116
Q

What are the causes of primary polydipsia?

A
  • mental illness
  • brain injuries
  • organic brain damage
117
Q

What mental illnesses can cause primary polydipsia?

A
  • psychogenic polydipsia
  • schizophrenia
  • mood disorders (depression and anxiety)
  • anorexia
  • drug use
118
Q

What can polydipsia cause?

A
  • kidney and bone damage
  • headache
  • nausea
  • cramps
  • slow reflexes
  • slurred speech
  • low energy
  • confusion
  • seizures
119
Q

What can cause adipsia?

A
  • increased osmolality of urine
  • stimulates the secretion of ADH
  • water retention
  • decreased thirst sensation
120
Q

How many different types of adipsia are there?

A

4

121
Q

What receptors are used to detect ADH levels?

A

osmoreceptors

122
Q

What triggers the release of ADH?

A
  • cells shrink when plasma is more concentrated
  • proportion of cation channels increases - depolarizing the membrane
  • sends signals to the ADH producing cells to increase ADH
  • fluid retention that invokes drinking
123
Q

What is an eating disorder?

A

a mental disorder defined by abnormal eating habits

124
Q

What are some examples of eating disorders?

A
  • binge eating disorder
  • anorexia nervosa
  • bulimia nervosa
  • PICA
  • rumination syndrome
  • avoidant/restrictive food intake disorder
125
Q

What are the signs of anorexia?

A
  • Low BMI
  • continuous weight loss
  • amenorrhea
  • halitosis
  • mood swings
  • dry hair
  • skin and hair thinning
126
Q

What are the causes of anorexia?

A
  • genetic
  • environmental
  • psychological
  • sociological
127
Q

What is the mechanism of anorexia?

A

serotonin

128
Q

What BMI would classify anorexia as mild?

A

> 17

129
Q

What BMI would classify anorexia as moderate?

A

16-16.99

130
Q

What BMI would classify anorexia as severe?

A

15-15.99

131
Q

What BMI would classify anorexia as extreme?

A

<15

132
Q

What co-morbidities are associated with anorexia?

A
  • depression
  • sleep apnoea
  • bowel cancer
  • osteoarthritis
  • gout
  • peripheral vascular disease
  • diabetes
  • hypertension
  • MI
  • stroke
133
Q

What is included in a screening for obesity?

A
  • height
  • weight
  • abdominal girth
  • BMI
    Medical history
  • dietary and physical activity
  • psychosocial factors
  • weight-gaining medications
  • familial traits
134
Q

What is necessary for a classification of obesity?

A

BMI >/= 30
or
BMI >/= 25 + co-morbidity/risk factor

135
Q

What is involved in the treatment of obesity?

A 
Lifestyle modification
- diet
- exercise
Surgical treatment
- gastric bypass
- gastric sleeve
136
Q

What is needed to qualify for bariatric surgery for obesity treatment?

A

BMI >40
or
BMI >35 + co-morbiditiesx

137
Q

What is the effect of GLP1 and GLP2?

A
  • stimulate insulin release

- inhibit glucagon release

138
Q

What is the effect of ghrelin?

A

NPY activation to initiate appetite

139
Q

What is the effect of PYY?

A
  • satiety

- anorexgenic

140
Q

What is the impact of bariatric surgery on Ghrelin?

A
  • decreases

stomach fills easier/quicker therefore, when full ghrelin inhibition

141
Q

What is the impact of bariatric surgery on GLP1/2 and PYY?

A
  • increases

BRS YR2 (70 decks)

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