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Gastroenterology > Apetite > Flashcards

Apetite Flashcards

1
Q

What changes can stimulate control of thirst?

A

Body fluid osmolality increased
Blood volume is reduced
Blood pressure is reduced

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2
Q

What is the most potent stimulus for controlling thirst?

A

Plasma osmolality increase is the more potent stimulus – change of 2-3% induces strong desire to drink
Decrease of 10-15% in blood volume or arterial pressure is required to produce the same response

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3
Q

What hormone is used to regulate osmolality?

A

Antidiuretic hormone (ADH) or vasopressin

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4
Q

Describe the mechanism by which ADH regulates osmolality

A
  • ADH is stored in the posterior pituitary
  • Acts on the kidneys to regulate the volume & osmolality of urine
    (Collecting duct - Aquaporin 2 channel)
  • When plasma ADH is low a large volume of urine is excreted (water diuresis)
  • When plasma ADH is high a small volume of urine is excreted (anti diuresis).
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5
Q

What type of receptors help regulate osmolality?

A

Osmoreceptors:
Sensory receptors
Osmoregulation
Found in the hypothalamus

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6
Q

Which regions in the hypothalamus are the osmoreceptors found?

A

Organum vasculosum of the lamina terminalis (OVLT)

Subfornical Organ (SFO)

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7
Q

Describe the mechanism by which osmoreceptors lead to ADH release

A
  1. Cells shrink when plasma more concentrated
  2. Proportion of cation channels increases – membrane depolarizes
  3. Send signals to the ADH producing cells to increase ADH
  4. Fluid retention- Invokes drinking
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8
Q

How is the sensation of thirst relieved?

A
  • Thirst is decreased by drinking even before sufficient water has been absorbed by the GI tract to correct plasma osmolality
  • Receptors in mouth, pharynx, oesophagus are involved
  • Relief of thirst sensation via these receptors is short lived
  • Thirst is only completely satisfied once plasma osmolality is decreased or blood volume or arterial pressure corrected.
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9
Q

How are changes in blood pressure detected by the renin-angiotensin-aldosterone system?

A
  1. BP decreases
  2. Detected by the Muacula densa which sends signals to the juxtaglomerular cells of renal afferent arteriole
  3. Releases renin
  4. Renin converts angiotensinogen into angiotensin I
  5. ACE enzyme (released from lung) converts angiotensin I into angiotensin II
  6. Angiotensin II stimualtes: Vasoconstriction, increase sympathetic activity, thirst, ADH secretion, aldosterone release (aldosterone released from the zona glomerulosa of adrenal cortex- leads to H2O retention via Na+CL- absorption and K+ excretion
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10
Q

Describe the general central control of body weight

A
  1. in the Underfed state:
    - “A reduction in fat mass increases food intake and reduces energy expenditure”
    - decreased sympathetic NS activity
    - Increased hunger
  2. in the Overfed state:
    - “Adipose tissue expansion reduces food intake and increases energy expenditure”
    - Increased sympathetic NS activity
    - Decreased hunger
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11
Q

What factors regulate appetite in the body?

A
  1. Gut hormones: Ghrelin, PYY and others
  2. Leptin
  3. Neural input from the periphery and other brain regions
    (all act on the hypothalamus to regulate food intake and energy expenditure)
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12
Q

Describe the mechanism of action of Ghrelin

A
  1. Ghrelin is released from the stomach (it is an orexigenic hormone)
  2. Hypothalamus senses the circulating hormone/ concentration of hormone
  3. Information first received in the arcuate nucleus: Ghrelin stimulates the NPY/AGRP neurons found in the arcuate nucleus AND inhibit the POMC/CART neurons also found in the arcuate nucleus
  4. Info is then fed to the paraventricular nucleus
  5. PN feeds the info to the posterior pituitary
  6. STIMULATES appetite (increases feeding & reduces energy expenditure)
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13
Q

What are the features of the arcuate nucleus?

A

Brain area involved in the regulation of food intake
Incomplete blood brain barrier, allows access to peripheral hormones.
Integrates peripheral and central feeding signals
Two neuronal populations:

Stimulatory (NPY/AGRP neuron)
Inhibitory (POMC neuron)

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14
Q

Describe “The melanocortin system”

A

a.k.a the mechanism of action of leptin in the overfed state

  1. Leptin is released by adipocytes in white adipose tissue and enterocytes (circulates in plasma).
  2. Hypothalamus senses the circulating hormone/ concentration of hormone
  3. Information first received in the arcuate nucleus:
    Leptin stimulates the POMC/CART neurons & promote processing of POMC to the mature hormone α-MSH
    (Also inhibits the NPY/AGRP neurons)
  4. This then binds to melanocortin- 4 receptor (MC4R) in the paraventricular nucleus
  5. SUPPRESSES appetite (decreased food intake & increased energy expenditure)
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15
Q

What CNS mutations can occur to affect appetite?

A
  1. No NPY or Agrp mutations associated with appetite in humans.
  2. POMC deficiency and MC4-R mutations cause morbid obesity.

Mutations not responsible for the prevalence of obesity - but useful to explain signaling.

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16
Q

What other signals from brain regions (other than the hypothalamus) affect appetite?

A
  1. Higher centres
  2. Amygdala- emotion, memory.
  3. Other parts of the hypothalamus, e.g. lateral hypothalamus and ventromedial hypothalamus
  4. Vagus to brain stem to hypothalamus.
17
Q

Describe how the levels of Leptin change in the body

A

Leptin circulates in plasma in concentrations proportional to fat mass

Low when low body fat
High when high body fat

18
Q

What disorders associated with Leptin can occur?

A
  1. Congenital leptin deficiency (children can’t produce leptin but still respond to it- can be given as treatment)
  2. Leptin resistance (hormone is present but doesn’t signal effectively & Leptin is ineffective as a weight control drug.)

both can lead to obesity

19
Q

Why do we feel less hungry after a meal?

A

Hormonal Signal from the gut
(2 gut hormones: Ghrelin and peptide YY in this case PYY reduces food intake after feeding)

20
Q

What is the role of Peptide YY?

A
  • Short peptide released in the terminal ileum (TI) and colon in response to feeding (36 Amino acids)
  • Inhibits food intake
  • can be digested or injected IV
  • (inhibits NPY/AGRP neurons and stimulates the POMC/CART neurons)
21
Q

What is the role of Ghrelin and describe how the levels of Ghrelin change in the body

A

Stimulates appetite, increases gastric emptying
(increases gastric mobility and acid secretion)

Blood levels of ghrelin are highest before meals (Spikes at breakfast, lunch and dinner + rapid drop later)

22
Q

What are the comorbidities associated with obesity

A
  • Depression
  • Sleep apnoea
  • Bowel cancer
  • osteoarthritis
  • Gout
  • peripheral vascular disease
  • diabetes
  • hypertension
  • myocardial infarction
  • stroke
23
Q

What factors contribute to obesity

A

Environmental + genetic

24
Q

Define “polydipsia”

A

extreme thirst

25
Q

Define “adipsia”

A

A disease characterized by the absence of thirst even in the presence of body water depletion or salt excess

26
Q

define “anorexia”

A

an eating disorder characterized by low weight

27
Q

define obesity

A

definedas abnormal or excessive fat accumulation that presents a risk to health BMI over 30

28
Q

List some causes of “primary polydipsia”

A
  1. Psychogenic polydipsia
  2. Obsessive-compulsive disorder
  3. Anorexia
  4. Anxiety
  5. Drug use
  6. Organ (brain) damage/ trauma
29
Q

What is “primary polydipsia”?

A

Primary polydipsia is a condition that involves drinking more water than your body needs or should have. Secondary polydipsia is drinking excess water due to medical issues that disrupt any step in osmoregulation or alter ADH, prompted by an actual need for water.

30
Q

List conditions that can lead to secondary polydipsia

A

Cranial diabetes insipidus
Type 2 diabetes
nephrogenic diabetes insipidus
Chronic kidney disease
Chronic heart failure
Medication: diueretics, laxatives
Conn’s syndrome

31
Q

Define the BMI needed to be diagnosed “underweight”

A

Underweight= less than 18.5
Normal= 18.5 to 24.9

32
Q

Define the BMI of a healthy weight range/ normal

A

Normal= 18.5 to 24.9

33
Q

Define the BMI needed to be diagnosed “overweight” but not obese

A

Overweight= 25.0 to <30

34
Q

Define the BMI needed to be diagnosed in the first classes of obesity

A

Obesity:
Class 1= 30 to < 35
Class 2= 35 to < 40
Class 3= BMI of 40 or higher.

Gastroenterology (9 decks)

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