15 Appetite Flashcards
Q: 3 forms of appetite regulation.
A: The control of thirst Hypothalamic circuits controlling body weight Peripheral signals of body homeostasis Long Term- Leptin Short term – Ghrelin, PYY
Q: When does an individual perceive thirst? (3) What induces a strong desire to drink? (2)
A: Body fluid osmolality is increased.
Blood volume is reduced.
Blood pressure is reduced.
Plasma osmolality increased is the more potent stimulus – change of 2-3%
would need same response with decrease of 10-15% in blood volume or arterial pressure
Q: What are the 2 key organs involved in water regulation? Actions? (3) What is tightly regulated? why? (3) how?
A: gut and kidney
absorption, reabsorption and excretion
osmolality (concentration) of blood is very tightly regulated (285-295 mOsm/kg) to maintain solute gradients, a suitable haematocrit and the ideal viscosity.
kidneys can produce urine of wildly different osmolalities (50-1200 mOsm/kg).
Q: What can sense change in solute concentration? Smaller sensor?
A: osmoreceptors in the brain adjacent to structures with an incomplete blood brain barrier.
Principally the hypothalamus, within the OVLT and SFO regions.
During (even mild) dehydration, the hypothalamic response is considerably more sensitive than peripheral baroreceptors (which respond to changes in blood volume and pressure).
Q: Where is vasopressin produced? goes to? What are its primary functions? (2) Similar to? aim? Minor action?
A: Vasopressin (antidiuretic hormone; ADH) = hormone
in the hypothalamus and released from the posterior pituitary gland.
Its primary functions are:
- insert aquaporin-2 channels into the collecting duct of renal nephrons to increase water reabsorption
- stimulate vasoconstriction
These mechanisms (in a similar way to angiotensin II) combine to conserve blood volume and to increase blood pressure.
Beyond stimulating water retention, they stimulate THIRST to increase behaviours that will lead to increased fluid intake.
Q: Describe urine produced when we have high ADH production. Low. What are they both called?
A: 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)
Q: What is diuresis?
A: increased or excessive production of urine
Q: What regulates the production of ADH? Describe the location of this structure. (4) 3 examples.
A: Osmoreceptive cells
- in the brain -> have
- cell bodies outside of the blood brain barrier that are
- bathed in the extracellular fluid (ECF)
- ie adjacent to structures with an incomplete blood brain barrier.
Principally the hypothalamus, within the OVLT and SFO regions (Circumventricular organs)
Q: 3 step process to how osmoreceptors regulate ADH production. What does increased ADH lead to? (2)
A: 1. These cells are very sensitive to their local environment and quickly equilibrate with it.
- If the ECF varies from about 290 mOsm/kg, the cells will proportionately grow (in response to reduced osmolality) or shrink (in response to increased osmolality) by osmosis.
- These changes will affect the firing rate of these cells, which will adjust the basal level of ADH being secreted.
Increased ADH secretion will lead to water retention (and a decreased osmolality).
Q: What does increased plasma osmolarity invoke? (2) result?
A: Invokes drinking and ADH release
Increased ADH stimulates kidney to conserve water
Q: What does decreased plasma osmolarity invoke? (2) result?
A: Thirst is suppressed and ADH release decreased
Absence of ADH the kidney excretes more water
Q: What are the 2 ways thirst can be satiated (satisfied, quenched)? Which is short term? long term? Mechanism? (2)
A: the presence of water in the GI tract can quench thirst, for a short period of time at least. This is thought to results from receptors in the upper GI tract (mouth to oesophagus) - short term feedback
once the original stimulus (osmolality or blood pressure) has been corrected, then the perception of thirst is no longer felt - long term feedback
Q: What are the 6 functions of angiotensin II?
A: 1. It binds to receptors on vascular smooth muscle cells to stimulate vasoconstriction
- It upregulates activity of the sympathetic nervous system, which largely promotes vasoconstriction
- It stimulates aldosterone secretion, which increases sodium reabsorption in the nephron, which creates an osmotic gradient for water reabsorption
- It directly influences sodium reabsorption, causing water reabsorption
- It stimulates ADH release and stimulates thirst
- Activates SFO neurons
Q: When is ANG II released? 3 needed components to make?
A: when blood volume and pressure are reduced.
- juxtaglomerular cells of renal afferent arteriole make renin
- liver makes angiotensinogen
- cleaving-> ANG I
- Angiotensin converting E (expressed on the vascular endothelial cells of the pulmonary and renal microvessels) -> ANG II
Q: What structure is responsible for body weight homeostasis? 3 inputs. 2 outputs.
A: hypothalamus
inputs from periphery:
- hormones: GHRELIN, PYY & other gut hormones
- Neural input from the periphery and other brain regions
- leptin
- control of food intake
- control of energy expenditure
