Control of Plasma Osmolarity Flashcards
What is the osmolality of body fluids in comparison to intracellular osmolality and which is the exception?
Most bodily fluids are isotonic to cells Osmolality. The exception is urine. If water intake is less than water excretion then osmolality will increase and vice versa this is because we change the amount of water we excrete but not the number of osmoles of solute.
Where are osmoreceptors found?
Osmoreceptors are found in the hypothalamus, in the organum vasculosum of the lamina terminalis (OVLT). OVLT is anterior and ventral to the third ventricle.
How do osmoreceptors detect changes in osmolality?
Fenestrated leaky endothelium are exposed directly to systemic circulation on the plasma side of BBB. It senses changes in plasma osmolarity and signals secondary responses which are mediated via two pathways leading to concentration of urine and the feeling of thirst.
Where are cells of the supraoptic nucelus found?
Cells of the supraoptic nucleus lie close to the OVLT with input from baroreceptors.
How does the hypothalamus respond to high osmolality?
Under conditions of predominant loss of water osmoreceptors in the hypothalamus increase release of ADH from posterior pituitary. ADH then inhibits excretion of water in the kidneys. Low Osmolarity inhibits ADH secretion this creates a negative feedback loop.
What happens when the blood volume or pressure changes?
When the blood volume or pressure changes there is a change in the set point for ADH so that the Osmolarity may change. This is to prevent circulatory collapse because volume is more important than Osmolarity.
When does thirst behavior occur, what else does it stimulate and when does it stop?
This occurs when there are large deficits in water (or salt) that is only partially compensated for by ADH in the kidneys. It is stimulated by an increase in fluid Osmolarity but also by reduced ECF volume. Salt ingestion acts like thirst in that it prevents water loss. Thirst stops when sufficient fluid has been consumed but before GI tract has absorbed as this would take too long and we’d potentially overshoot. Salt intake is stimulated by a natural appetite for it.
Describe ADH and how it works
Produced by neurosecretory cells in the hypothalamus but secreted form the posterior pituitary gland. Peptide that is 9 amino acids long and is also known as Arginine Vasopressin, Vasopressin and Argipressin.
ADH increases the permeability of the collecting duct to water and urea. Low plasma ADH = diuresis and high plasma ADH = anti-diuresis.
What is central diabetes insipidus?
This is when plasma ADH levels are too low. This occurs due to damage to the brain, tumour, sarcoidosis or tuberculosis, aneurysms, some forms of encephalitis or meningitis and rare disease of langerhans cell histiocytosis.
What is nephrogenic diabetes insipidus?
Is from an acquired insensitivity of the kidneys to ADH.
In both these cases water is inadequately reabsorbed from the collecting duct so a large volume of urine is produced. Managed clinically by ADH injections or nasal sprays.
What is SIADH?
Syndrome of inappropriate antidiuretic hormone secretion. Characterised by excessive release of ADH form the PP gland or another source. This results in large retention of water and so a dilution of all the solutes. Specifically, this causes hyponatremia.
What symptoms are there of hyponatraemia?
Symptoms of hyponatremia include nausea and vomiting, headache, confusion, lethargy, fatigue, appetite loss, restlessness and irritability, muscle weakness, spasms, cramps, seizures and decreased consciousness or coma.
What are aquaporin channels?
Many different types found all over the body it is effectively a hole in the membrane that only allows water through.
Where are the different aquaporin channels found?
AQP1 is found on both the apical and basolateral membrane of the PCT and descending limb of the loop of Henle. AQP2, AQP3 and AQP4 are all found in the latter DCT and collecting duct with AQP3 and AQP4 on the basolateral side and AQP2 on the apical side.
How does low ADH effect aquaporin channels?
No ADH stimulation means no AQP2 on apical membrane of the latter DCT and collecting ducts. Ths limits water reuptake in the latter DCT and in the collecting duct. Tubal fluid rich in water passes through the hyperosmotic renal pyramid with no change in water content. Loss of large amounts of hypo-osmotic (dilute) urine. This is diuresis.
