Vasopressin disorders Flashcards
differences between the anterior pituitary and the posterior
posterior anatomically and embryologically distinct from anterior
posterior continuous with hypothalamus
posterior not dependent on blood/portal supply
what are the posterior pituitary hormones
arginine vasopressin
oxytocin
where do hypothalamic magnocellular neurones originate?
supraoptic nuclei
paraventricular nuclei
what is the main physiological action of AVP
stimulation of water reabsorption in the renal collecting duct
what receptor does AVP bind to for water reabsorption
V2
what receptor does AVP bind to for vasoconstriction
V1
what is the smaller effects of AVP
vasoconstriction
stimulates ACTH release from anterior pituitary
how do you see the posterior pituitary on MRI?
bright spot, not always visible in healthy individuals
what are the two stimuli for release of AVP
osmotic, rise in plasma osmolality sensed by osmoreceptors
non-osmotic, decrease in arterial pressure sensed by arterial stretch receptors
where are atrial stretch receptors found?
right atrium
what are the organum vasculosum and subfornical organ important for?
osmotic receptors around 3rd ventricle with neurones projecting to the supraoptic nucleus (site of vasopressinergic neurones)
no BBB - detect changes to systemic circulation
what is the process for osmotic stimuli?
a rise in plasma osmolality (increase in extracellular Na+) causes water to flow out of the osmoreceptors
osmoreceptor shrinks, triggering increased osmoreceptor firing
increased osmoreceptor firing causes AVP release from hypothalamic neurones in supraoptic nucleus
what is the process for non-osmotic stimuli?
atrial stretch receptors in right atrium detect rise in pressure
AVP release inhibited by vagal nerve stimulation
or atrial stretch receptors detect fall in pressure
AVP release less inhibited by less vagal nerve stimulation
why is vasopressin released following a haemorrhage?
to make up for lost blood volume and vasoconstrict
vasopressin release results in increased water reabsorption in the kidney (V2 receptors)
vasoconstriction via V1 receptors to increase blood pressure (acts along with adrenaline etc)
what is the physiological response to water deprivation?
increased plasma osmolality -> stimulation of osmoreceptors -> thirst, increased AVP release -> increased water reabsorption from renal collecting ducts -> reduced urine volume, increase in urine osmolality -> reduction in plasma osmolality (back to normal ish)
what is the basis of diabetes insipidus?
vasopressin insufficiency or resistance
what are the main symptoms of diabetes insipidus?
polyuria
nocturia
thirst
polydypsia
what is cranial diabetes insipidus?
problem with hypothalamus &/or posterior pituitary
vasopressin insufficiency
what is nephrogenic diabetes insipidus?
vasopressin resistance
kidney (collecting duct) unable to respond to AVP
what are the causes of cranial DI?
traumatic brain injury pituitary surgery, tumours metastasis to pituitary gland granulomatous infiltration of pituitary stalk autoimmune rarely congenital
what are the causes of nephrogenic DI?
drugs e.g lithium rarely congenital (mutation in gene encoding V2, aquaporin 2)
how does diabetes insipidus often present?
similar to DM, polyuria, nocturia, polydypsia, thirst
large volumes of hypoosmolar urine (dilute)
hyperosmolar plasma, hypernaetraemia
glucose NORMAL
what is the process of diabetes insipidus?
AVP issue -> impaired urine concentration -> large volumes of hypotonic urine -> increased plasma osmolality -> stimulation of osmoreceptors -> thirst -> circulating volume maintained if patient has access to water
what is psychogenic polydypsia?
patient always drinking water, no issues with AVP
usually comorbidity of mental illnesses
how can you distinguish diabetes insipidus and psychogenic polydypsia?
water deprivation test
how do you perform a water deprivation test?
no access to water
measure urine volumes, concentration and plasma concentration over time
stop test if more than 3% body weight is lost
how do water deprivation tests of psychogenic polydypsia and diabetes insipidus differ?
psycho- urine volume decreases, plasma osmolality stays similar and urine osmolality increases
DI - urine volume stays same, plasma osmolality increases and urine osmolality stays same
how do you distinguish cranial DI from neurogenic DI?
give ddAVP
cranial - pass smaller urine volumes, urine osmolality increases
nephrogenic - urine volume and osmolality stay the same
what is ddAVP
desmopressin, synthetic AVP that works only on V2 receptors
how do you treat cranial DI?
demopressin intranasal spray or tablets
how do you treat nephrogenic DI?
difficult to treat successfully
thiazide diuretics
what is SIADH
syndrome of inappropriate ADH - too much AVP
what are the signs of SIADH
reduced urine output, water retention, hyponaetraemia
what are the causes of SIADH
head injury, stroke, tumour pneumonia, bronchiectasis lung cancer drug related - carbamazepine, SSRIs idiopathic - common in elderly
how do you manage SIADH?
fluid restriction (500ml max) vaptan - vasopressin antagonist (v expensive)
why should desmopressin doses be tightly monitored?
too high may cause hyponatraemia, causing brain damage from swelling
when should desmopressin doses be increased?
extreme exercise e.g marathons
what tests should be ordered if DI is suspected?
paired plasma and urine osmolality
fasting/random glucose/oral glucose tolerance test
why should DI not always be first suspected?
glucose should always be checked - DM is far more common explanation for presenting symptoms
