Control of Plasma Osmolarity Flashcards
1
Q
Explain how changes in plasma osmolarity are detected in the body
A
- Detected by hypothalamic osmoreceptors
- Located in the OVLT of the hypothalamus
- Fenestrated leaky endothelium exposed directly to systemic circulation (on plasma side of blood brain barrier)
- Sense changes in plasma osmolarity
- Signal secondary responses - ADH and thirst
- Cells of the supraoptic nucleus lie close to OVLT with input from baroreceptors
- Reduce ADH when plasma levels low to draw water back
2
Q
Distinguish the factors that regulate thirst and cause secretion of ADH
A
- ADH secreted in the short term and secreted unconsciously
- Made in the hypothalamus and stored/secreted from the posterior pituitary
- Goes to the kidney and increases renal water reabsorption
- Thirst acts as the 2nd line of defence and involves behavioural change
- Brain stimulates drinking behaviour and water intake occurs
3
Q
Outline how osmolarity is sacrificed for volume in extreme scenarios
A
- A decrease in extracellular volume - set point is shifted to lower osmolarity values and the slope of the relationship is steeper (low osmolarity)
- When faced with circulatory collapse, the kidneys continue to conserve water even though this will reduce osmolarity of body fluids
- An increase in pressure or volume has the opposite effect (high osmolarity)
- Set point is shifted higher and slope decreases
- Fluid needs to be removed from the plasma, causing high plasma osmolarity
- Volume is more important than osmolarity - if volume crashes, then life threatening
4
Q
State the locations of the aquaporins in the collecting duct
A
- Aquaporin 2 (AQP2) located on apical side
- Increased expression of AQP2 with ADH - decides amount of water reabsorbed
- Aquaporin 3 and 4 located on basolateral side
5
Q
Explain the effect of ADH when plasma osmolarity decreases
A
- No ADH stimulation means no aquaporin 2 in apical membrane
- Limited water reuptake in latter DCT and limited in collecting duct
- Tubular fluid rich in water passes through the hyperosmotic renal pyramid with no change in water content
- Loss of large amount of hypo osmotic (dilute) urine
- Diuresis
6
Q
Explain the effect of ADH when plasma osmolarity increases
A
- Body needs to produce a hyperosmotic urine
- Kidney must reabsorb as much water as possible from the kidney tubule
- Water will move out of collecting duct into hyperosmotic environment if there are aquaporin channels in both the apical and basolateral epithelium in the tubule cells
- Release of ADH causes insertion of AQP2 channels into apical membrane
7
Q
State the osmolality in the cortico-medullary border, tip of descending limb and start of DCT
A
- Isotonic (300 mOsm/Kg) at cortico-medullary border
- 1200 mOsm/Kg at the tip of descending limb
- Fluid entering the DCT has low osmolality of 100 mOsm/Kg
8
Q
Describe how the descending and ascending limb help generate the medullary gradient
A
- Descending limb highly permeable to water due to AQP1 which is always open
- Not permeable to sodium ions so filtrate concentration in loop of Henle increases further into the medulla
- Ascending limb actively transports NaCl out of tubular lumen into interstitial fluid
- Impermeable to water
- Removes solute without water and therefore increases osmolarity of the interstitium
- As NaCl leaves, water remains so osmolality decreases in the ascending limb
9
Q
What factors help generate the vertical osmotic gradient
A
- Active NaCl transport in thick ascending limb
- Recycling of urea
- Vasa recta blood moves in the opposing direction the loop of Henle it is next to
10
Q
Outline how recycling of urea helps generate vertical osmotic gradient
A
- Urea reabsorption from medullary collecting duct
- Cortical collecting duct cells are impermeable to urea
- Movement into interstitium (high salt concentration) and diffusion back into loop of Henle
11
Q
How does ADH influence urea recycling
A
- Under the influence of ADH, fractional excretion of urea decreases and urea re-cycling increases
- ADH released which causes more water to be reabsorbed - increases concentration of urea in collecting duct
- Therefore higher concentration increases driving force of diffusion into interstitial space
- ADH also expresses urea transporters and aquaporin in collecting duct to further increase urea reabsorption into interstitial space
12
Q
Outline how the counter current multiplication system occurs
A
See onenote
13
Q
Explain the role of the vasa recta as a counter current exchanger
A
- Along the descending loop of Henle, water immediately enters the vasa recta
- Osmolality within vasa recta very high to attract water
- Blood ascending towards cortex will have higher solute content than surrounding interstitium
- Driving force created by salts entering previously
- Maintains the high osmolality of the interstitial space as water does not remain in interstitium
- Osmolality within vasa recta very high to attract water
- Along the ascending loop of Henle, salts enter vasa recta from high osmolality interstitium
- Increases the osmolality inside the vasa recta
14
Q
State the causes of diabetes insipidus
A
- Damage done to hypothalamus or pituitary glands
- A brain injury - particularly fracture of the base of the skull
- Tumour
- Sarcoidosis or tuberculosis
- Aneurysm
- Forms of encephalitis or meningitis
- Langerhans cell histiocytosis
15
Q
Explain the pathogenesis of diabetes insipidus and its presentation
A
- Central diabetes insipidus results when plasma ADH levels are too low
- Nephrogenic diabetes insipidus cause by an acquired insensitivity of the kidney to ADH
- In both, water is inadequately reabsorbed from the collecting ducts, so a large quantity of urine is produced
- Patients may present with severe thirst, frequent urination, high serum osmolality
- Managed clinically by ADH injections or by ADH nasal spray treatments
