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BRS 1b > Apetite > Flashcards

Apetite Flashcards

1
Q

What are the three factors that regulate thirst?

A

1) Plasma osmolarity
2) Hypovolaemia
3) Hypotension

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2
Q

Where is vasopressin released from?

A

Herring bodies of the posterior pituitary gland i

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3
Q

Which types of neurones release vasopressin?

A

Magnocellular hypothalamic neurones

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4
Q

Which hypothalamic nuclei release vasopressin?

A

Supraoptic and paraventricular nuclei

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5
Q

Which receptors are stimulated by vasopressin?

A

V2 receptors on tubule cells of the collecting duct and distal convoluted tubule

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6
Q

Which types of channels are synthesised in response to vasopressin?

A

Aquaporin-2 channel expression to increase water permeability and reabsorption

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7
Q

What is the effect of low plasma ADH?

A

Water diuresis

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8
Q

What is the effect of high plasma ADH?

A

Anti-diuresis

Small volume of concentrated urine

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9
Q

Where are osmoreceptors found?

A

Circumventricular residing within the organum vasculosu, and the subfornical organ

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10
Q

How do osmoreceptors induce ADH release?

A
  1. Detection of increased plasma osmolarity.
  2. Osmoreceptor cell shrinkage (due to water diffusing into extracellular environment).
  3. Conformational change increases proportion of cation channels expressed on the cell surface membrane.
  4. Increased influx of cations  Membrane depolarisation.
  5. Transmits action potentials to ADH producing magnocellular hypothalamic neurones
  6. Improved fluid retention
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11
Q

What happens to the osmoreceptor when there is an increase in plasma osmolarity?

A

Cell shrinkage, due to water diffusing into extracellular environment.

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12
Q

What happens to the osmoreceptors when there is conformational change?

A

Causes an increase in the expression of cation channels expressed on the cell surface membrane
-influx of cations, causing membrane depolarisation

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13
Q

What effect does ADH do in hypertonic conditions?

A

increased fluid retention, by stimulating water reabsorption

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14
Q

What happens in hypotonic conditions to ADH>

A

In hypotonic conditions, osmoreceptor cells maintain their structural shape, and cation channels are inhibited  Reduced cation influx induces a state of hyperpolarisation to inhibit firing.

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15
Q

Where are thirst receptors located?

A

Mouth, pharynx, and oesophagus

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16
Q

What is the effect of the stimulation of thirst receptors?

A

They are stimulated by detecting water consumption, and relieve the sensation of thirst in the short-term

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17
Q

How is thirst sensation completely satisfied?

A

• Thirst sensation is completely satisfied once plasma osmolarity is corrected or blood volume/arterial pressure is restored to normal.

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18
Q

What is the response to low renal perfusion pressure by JG cells?

A

Renin is secreted (increased sympathetic activity by stimulating beta-1 receptors).

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19
Q

What is the effect of renin?

A

Converts angiotensinogen into angiotensin-I

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20
Q

What is the effect of ACE?

A

Converts angiotensin-I to angiotensin-II

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21
Q

What is the effect of angiotensin-II?

A

A potent vasoconstriction to increase systemic blood pressure and increases sympathetic activity.

  • Promotes thirst
  • Promotes ADH secretion
  • Promotes aldosterone synthesis
  • Increased sodium reabsorption
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22
Q

What effect does aldosterone have on tubule cells of the distal convoluted tubule?

A

Sodium reabsorption

Potassium secretion

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23
Q

What is the effect of ACE-inhibitors?

A

Inhibit the conversion of angiotensin -I to angiotensin-II
reduces vasoconstrictive properties of angiotensin-II
vasodilator

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24
Q

What is an ARB?

A

Angiotensin-receptor blocker

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25
Q

Where is aldosterone synthesised?

A

In the zona glomerulosa of the adrenal cortex

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26
Q

What is the mechanism of an ARB?

A

• Angiotensin-II receptor blockers are receptor antagonists which prevent angiotensin-II from exerting hypertensive effects.

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27
Q

What is adipose tissue expansion?

A

Reduces food intake and increases energy expenditure.

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28
Q

What happens to energy expenditure when there is a reduction in fat mass?

A

Reduction in fat mass - Increased

29
Q

What is the ventromedial nucleus?

A

Ventromedial nucleus is associated with inducing a state of satiety, a lesion to the ventromedial nuclei increases the sensation to intake food contributing to severe obesity.

30
Q

What is the impact to a lesion to the ventromedial nucleus?

A

Increases the sensation of food intake - leading to severe obesity

31
Q

What is the role of the ventromedial nucleus?

A

Induces a state of satiety

32
Q

What type of factor is released from the lateral hypothalamic nucleus?

A

Releases orexigenic factors

33
Q

What is an orexigenic factor?

A

Behaves as an appetite stimulant

34
Q

Which structure includes both orixgenic and anorexigenic neurones?

A

Arcuate nucleus

35
Q

What are orexigenic neurones?

A

are appetite stimulating – releasing neuropeptide Y and agouti-related peptides. (LHN)

36
Q

Which peptides are released from orexigenic neurones?

A

Neuropeptide Y and agouti-related peptides (LHN)

37
Q

What are anorexigenic neurones?

A

POMC/CART neurones are appetite suppressive – releasing MSH. (VHN). These neurones are directly innervated and inhibited by the NPY neurones.

38
Q

Which peptides are released from anorexigenic neurones?

A

Alpha-MSH

39
Q

What directly inhibits POMC neurones?

A

NPY neurones

40
Q

Where do the neuronal projections terminate at?

A

Paraventricular nucleus of the hypothalamus, adjacent to the third ventricle.

41
Q

What does the paraventricular nucleus secrete?

A

Oxytocin and ADH

42
Q

How does the arcuate nucleus receive hormonal stimulation?

A

There is an incomplete blood brain barrier - enabling access for the arcuate nucleus to interact with circulating hormones

43
Q

Which hormones inhibit orexigenic neurones?

A

Leptin, peptide YY, and insulin

44
Q

Which hormone stimulates orexigenic neurones?

A

Ghrelin

45
Q

What is the hunger reflex?

A

Hunger:

  1. Decreased stimulation of mechanoreceptors within the stomach
  2. Decreased firing frequency of the vagal nerve to the solitary nucleus.
  3. Solitary nucleus relays information to the arcuate nucleus within the hypothalamus
  4. Activates the lateral hypothalamic nucleus via orexigenic factors
  5. Supresses the ventromedial nucleus via the anorectic factors.
46
Q

Which nucleus relays information to the arcuate nucleus?

A

Solitary nucleus

47
Q

Which nucleus is activated during hunger?

A

Lateral hypothalamic nucleus

48
Q

Which factors are released during hunger from the lateral hypothalamic nucleus?

A

Orexigenic factors

49
Q

Which centres are suppressed during hunger?

A

Ventromedial nucleus

50
Q

Which hormone is released during hunger?

A

Ghrelin - stimulates the arcuate nucleus

51
Q

What effect does leptin have on appetite sensation?

A

Inhibits appetite sensation (binds to leptin receptors on both NPY and POMC neurones)

52
Q

Which peptide is released from POMC neurones?

A

POMC neurones of the arcuate nucleus release alpha-MSH peptides which induce an anorexigenic effect

53
Q

What type of effect is exerted by alpha-MSh neurones?

A

Anorexigenic effect on the paraventricular nucleus

54
Q

What type of receptors does alpha-MSH bind to?

A

MC-4, triggers the sensation of satiety

55
Q

What happens in an NPY and Agrp mutation?

A

This is associated with reduced appetite.

56
Q

What is the effect of a POMC deficiency or MC4-R mutation?

A

Cause obesity given that the induction of satiety is lost

57
Q

Which cells release leptin and circulating hormones?

A

Adipocytes

58
Q

Which tissue synthesises leptin?

A

White adipose tissue

59
Q

What is the effect of leptin?

A

Regulate intake and thermogenesis by inhibiting orexigenic neurones (NPY, AGRP) within the arcuate nucleus and lateral hypothalamic area

Stimulates the anorexigenic neurones

60
Q

What is congenital leptin deficiency?

A

There is a significant reduction in circulating leptin, thus the inhibitory effect on orexigenic neurones is lost - promoting feeding behaviour and intake

Manifests as severe early age obesity

61
Q

What is the treatment of congenital leptin deficiency?

A

Leptin injections can reduce body weight

62
Q

What is the relationship between serum leptin and body fat?

A

Serum leptin is higher in comparison to baseline patients in obesity, suggesting that hypothalamus is insensitive to endogenous leptin production

63
Q

What is the effect of Ghrelin?

A

Stimulates appetite and increases gastric emptying

  • Directly modulates neurones in the arcuate nucleus. Stimulates NPY/Agrp neurones.
  • Inhibits POMC neurones.
  • Increases appetite
  • Regulation of reward, taste sensation memory, circadian rhythm
64
Q

What is the relationship between plasma ghrelin and pre-prandial?

A

Plasma ghrelin increases twofold pre-prandially

Decreases thereafter post-prandially

65
Q

What rhytmn is exhibited by ghrelin inter-prandially?

A

Diurnal

66
Q

Which cells secrete peptide YY?

A

Enteroendocrine L cells, throughout the mucosa of the terminal ileum, colon and rectum

67
Q

What is the effect of peptide YY?

A

Increases post-prandially, to reduce appetite and food intake

Inhibits NPY orexigenic release

Stimulates POMC anorexigenic releases

N.B: Also reduces intestinal motility, gall bladder contractions and inhibits pancreatic exocrine secretion.
-Can cause nausea.

68
Q

What comorbidities are associated with obesity?

A 
Depression
Sleep apnoea
Bowel cancer
Stroke
Osteoarthritis
Gout
Peripheral vascular disease
Diabetes
Hypertension
MI

BRS 1b (62 decks)

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