Disorders Of Vasopressin Flashcards
Describe physiology of posterior pituitary
Posterior pituitary is anatomically continuous with hypothalamus
Hypothalamic magnocellular neurons containing AVP or oxytocin
Long originate in supraoptic and paraventricular hypothalamic nuclei
Action of vasopressin
Aka ADH produces urine by stimulating water reabsorption in the renal collecting duct. This concentrates urine by acting through the v2 receptor in kidney
Also a vasoconstrictor stimulating ACTH release from anterior pituitary
How vasopressin worksheets
- AVP binds to v2 receptor in collecting duct
2.stimulates intracellular cascade
3.promotes movement of aquaporin 2 to apical membrane
4.water flows out of cell via aquaporin 3 channels into plasma
5.more concentrated urine
Describe the osmotic and non-osmotic stimuli for vasopressin release
Osmotic-rise in plasma osmolality sensed by osmoreceptors
Non osmotic-decrease in atrial pressure sensed by atrial stretch receptors
Organum vasculosum and subfornical organ- both nuclei which sit around the third ventricle. No blood brain barrier so neurons can respond to changes in systemic circulation. Highly vascularised, neurons project to supraoptic nucleus
Why is vasopressin released following a haemorrage
Causes increased water reabsorption in the kidney via v2 receptor
Vasoconstriction via v1 receptor
Physiological response to water deprivation
Increased plasma osmolality causes stimulation of osmoreceptors which causes thirst increasing AVP release. Increased water reabsorption from renal collecting duct causes reduced urine volume and increase in urine osmolality reducing plasma osmolality
Symptoms of diabetes
Polyuria
Nocturia
Thirst
Polydipsia
Due to osmotic diuresis in diabetes mellitus
In insipidus due to problem with AVP
Types of diabetes mellitus
Vasopressin insufficiency
-cranial diabetes insipidus problem with hypothalamus/posterior pituitary. Can’t make AVP
Vasopressin resistance
-nephrogenic diabetes insipidus problem. Can make AVP but kidney collecting duct unable to respond to it
Causes of diabetes insipidus
Cranial
Traumatic brain injury,pituitary surgery,pituitary tumours,metastasis to pituitary gland,autoimmune,granulomatous infiltration if pituitary stalk eg TB
Nephrogenic
Congenital rare eg mutation in gene encoding V2 receptor,aquaporin 2 water channel
Acquired via drugs eg lithium
Presentation of vasopressin deficiency
-urine
Very dilute
Large volumes
-Plasma
I ceased concentration (hyperosmolar) as patient becomes dehydrated
Increased sodium (hypernaetraemia)
Glucose normal
Why do these symptoms occur in diabetes insipidus or
AVP problem->impaired conc of urine in renal collecting duct ->large volumes of dilute urine ->increase in plasma osmolality causes->stimulation of osmoreceptors which->thirst (polydipsia->maintains circulating volume as long as patient has access to water
Psychogenic polydipsia
Similar presentation to diabetes
No problem with AVP
Problem is that patient drinks all the time so passes large volumes of dilute urine
Diabetes insipidus vs psychogenic polydipsia
Water deprivation test
No access to water or anything to drink
Measure urine volumes urine concentration plasma concentration
Weigh regularly : stop test if lose more than 3 percent body fat which is a marker of severe dehydration which can occur in diabetes insipidus
Cranial vs nephrogenic diabetes insipidus
Give ddAVP
This will work like vasopressin
Cranial will respond to it thus urine concentrates (deficiency)
Nephrogenic causes no increase in urine osmolality as kidneys can’t respond (resistance)
Treatment for DI cranial
Want to replace vasopressin
Desmopressin
Selective for v2 receptor
