Disorders of Vasopressin Flashcards
What tissue is the posterior pituitary made from?
Neuronal tissue
It is also anatomically continuous with the hypothalamus
What are the posterior pituitary neurones and what do they contain?
Hypothalamic magnocellular neurons containing AVP or oxytocin:
-Long, originate in supraoptic and paraventricular hypothalamic nuclei
-Nuclei → stalk →posterior pituitary
What is the physiological action of vasopressin?
Other name = Anti-Diuretic Hormone
Diuresis = production of urine
Main physiological action = stimulation of water reabsorption in the renal collecting duct
This concentrates urine
Acts through the V2 receptor in the kidney
Also a vasoconstrictor (via V1 receptor)
Stimulates ACTH release from anterior pituitary
How does vasopressin concentrate urine?
How do you visualise the posterior pituitary on MRI?
What are the stimuli for vasopressin release?
Osmotic
-Rise in plasma osmolality sensed by osmoreceptors
Non-osmotic
-Decrease in atrial pressure sensed by atrial stretch receptors
What senses plasma osmolality for osmotic stimulation of vasopressin release?
Organum vasculosum & subfornical organ
-both nuclei which sit around the 3rd ventricle (‘circumventricular’)
-no blood brain barrier – so neurons can respond to changes in the systemic circulation
-highly vascularised
-neurons project to the supraoptic nucleus - site of vasopressinergic neurons
How do osmoreceptors regulate vasopressin?
How does non-osmotic stimulation of vasopressin release
Atrial stretch receptors detect pressure in the right atrium
Inhibit vasopressin release via vagal afferents to hypothalamus
Reduction in circulating volume eg haemorrhage means less stretch of these atrial receptors, so less inhibition of vasopressin
Why is vasopressin released following a haemorrhage
(ie reduction in circulating volume)?
Vasopressin release results in increased water reabsorption in the kidney (some restoration of circulating volume) V2 receptors
vasoconstriction via V1 receptors
(NB renin-aldo system will also be important, sensed by JG apparatus)
What is the physiological response to water deprivation
What are the clinical symptoms for diabetes insipidus?
Polyuria
Nocturia
Thirst – often extreme
Polydispia
In diabetes mellitus (hyperglycaemia), these symptoms are due to osmotic diuresis
In diabetes insipidus, these symptoms are due to a problem with arginine vasopressin
Remember – the most common cause of polyuria, nocturia & polydipsia is diabetes mellitus, NOT diabetes insipidus
Urine
-Very dilute (hypo - osmolar)
-Large volumes
Plasma
-Increased concentration (hyper-osmolar) as patient becomes dehydrated
-Increased sodium (hypernatraemia)
-Glucose normal (make sure you ALWAYS check this in a patient with these symptoms)
What are the two types of diabetes insipidus?
Cranial (central) and nephrogenic
What is cranial diabetes insipidus?
Problem with hypothalamus &/or posterior pituitary
Unable to make arginine vasopressin
‘VASOPRESSIN INSUFFICIENCY’
What is nephrogenic diabetes insipidus?
Can make arginine vasopressin (normal hypothalamus & posterior pituitary)
Kidney (collecting duct) unable to respond to it
‘VASOPRESSIN RESISTANCE’
What are the acquired causes of cranial diabetes insipidus?
Traumatic brain injury
Pituitary surgery
Pituitary tumours
Metastasis to the pituitary gland eg breast
Granulomatous infiltration of pituitary stalk eg TB, sarcoidosis
Autoimmune
Why do these symptoms occur in diabetes insipidus?
How does diabetes insipidus cause death?
How do the symptoms in psychogenic polydipsia arise?
What would a graph of water deprivation by urine osmolality look like?
How do we distinguish between cranial & nephrogenic diabetes insipidus?
How to distinguish between diabetes insipidus and psychogenic polydipsia
What is the treatment of diabetes insipidus - cranial?
Want to replace vasopressin
Desmopressin
Selective for V2 receptor (V1 receptor activation would be unhelpful)
Different preparations
-Tablets
-Intranasal
