Endo - Vasopressin Flashcards
What is the other name of AVP?
→ argenine vasopressin
→ anti-diuretic hormone
What is the main physiological action of AVP?
Stimulation of water reabsorption in the renal collecting duct
What impact does vasopressin have on urine?
Concentrates urine
What is another purpose of AVP?
→ Vasoconstrictor
→ stimulates ACTH release from anterior pituitary
By what mechanism does AVP concentrate urine?
→ acts on V2 receptors in kidney
→ after the cascade of proteins, aqua-porin 2 + transports the H2O from the urine into cells
→ aqua-porin 3 transports it back to plasma
How does vasopressin act as a vasoconstrictor?
Via v1 receptor
How does posterior pituitary show up on MRI?
“bright spot” but not visualised in all healthy individuals
What is the osmotic stimuli for vasopressin release?
Rise in plasma osmolality sensed by osmoreceptors
What is the non-osmotic stimuli for vasopressin release?
Decrease in atrial pressure sensed by atrial stretch receptors
What are the nuclei that respond to the osmotic stimuli?
→ organum vasculosum
→ subfornical organ
Where are the two nuclei located?
Around the 3rd ventricle “circum ventricular”
What makes the two nuclei good at responding to osmotic stimuli?
→ no blood brain barrier, neurones respond to change into systemic circulation
→ highly vascularised + has osmoreceptors
→ neurones project to the supraoptic nucleus - site of vasopressinergic neurones
How do osmoreceptors regulate vasopressin?
→ osmoreceptors respond to increase in extracellular Na+ causing water to exit
→ osmoreceptor shrinks
→ osmoreceptor firing increases
→ AVP released from hypothalamic neurones
How does the mechanism of non-osmotic stimulation of vasopressin work?
→ atrial receptors detect pressure in right atrium
→ inhibit vasopressin release via vagal afferent to hypothalamus
→ reduction in circulating volume e.g. haemorrhage, means less stretch of these atrial receptors
→ leads to less inhibition of vasopressin
Why is vasopressin released after a haemorrhage?
→ to restore some circulating volume
→ vasopressin release = increased water reabsorption in kidneys + vasoconstriction
What is the physiological response to water deprivation?
→ increased plasma osmolality
→ stimulation of osmoreceptors
→ thirst + increased AVP release
→ increased h2o reabsorption from the renal collecting duct
→ reduced urine volume, increase in urine osmolality
→ reduction in plasma osmolality
What are the symptoms of diabetes insipidus?
→ polyuria
→ nocturia
→ thirst - often extreme
→ polydipsia
What are the two different types of DI?
→ cranial
→ nephrogenic
What is cranial DI?
→ problem w hypothalamus and/or posterior pituitary
→ unable to make AVP
→ “vasopressin insufficiency”
What is nephrogenic DI?
→ can make AVP
→ kidney doesn’t respond to it
→ “vasopressin resistance”
What is the rarest cause of CDI?
congenital
What are the acquired causes of CDI?
→ traumatic brain injury → pituitary surgery → pituitary tumours → metastasis to pituitary gland → granulomatous infiltration of pituitary stalk → autoimmune
What are the causes of NDI?
→ congenital = rare (e.g.mutation in gene encoding V2 receptor, aquaporin 2 type water channel)
→ acquired = drugs (e.g. lithium)
How does DI present differently to DM?
→ very dilute large volumes of urine
→ increased plasma osmolality
→ increased sodium levels
→ normal glucose levels
Why do these symptoms occur in DI?
→ not enough AVP / not responding to AVP → impaired conc. of urine in RCD → large volumes of dilute urine → increase in plasma osmolality → stimulation of osmoreceptors → thirst = polydipsia → circulating volume can only be maintained if patient has access to water → no access to water = dehydration + death
What can mimic DI?
psychogenic polydipsia
→ has similar presentation
→ but no problem with AVP
→ patients drink too much water all the time
How does psychogenic polydipsia present with the same symptoms?
→ increased drinking → plasma osmolality falls → less AVP secreted → large volumes of dilute urine → plasma osmolality returns to normal
How do you distinguish between DI and PP?
water deprivation test
→ no access to anything to drink
→ measure urine volume + urine conc/osmolality + plasma conc/osmolality over time
→ PP should see urine osmolality increase + return back to normal
→ DI can’t due AVP problems
weigh regularly
→ stop test if lost >3% body weight due to dehydration
How do you distinguish between CDI and NDI?
give ddAVP
→ works like AVP
→ CDI will respond + urine osmolality will increase
→ NDI won’t + urine osmolality wil decrease
How is CDI treated?
replace vasopressin with Desmopressin (tablets or intranasal)
How is NDI treated?
thiazide diuretics (paradoxical - mechanism still unclear)
What is SIADH?
Syndrome of Inappropriate ADH
→ too much AVP
What does SIADH cause?
→ reduced urine output → water retention → high urine osmolality → low plasma osmolality → dilutional hypoatraemia
What are the causes of SIADH?
→ head injury, stroke, tumour → pneumonia, bronchiectasis → lung cancer → drug-related (carbamazepine, SSRIs) → idiopathic
How is SIADH treated?
→ fluid restriction
→ vasopressin antagonist (vaptan) (binds to V2 receptors in kidneys)
