Disorders of vasopressin Flashcards
What neurons in the hypothalamus stimulate AVP release, and where do they originate?
magnocellular neurons, in supraoptic and paraventricular nuclei
What are the 3 physiological effects of AVP?
Water reabsorption in collecting duct (V2 receptors), vasoconstriction (V1 receptors) and ACTH release
How would you view the posterior pituitary gland in imaging, and what is the bright spot?
MRI - appears as a bright spot // bright spot may not be visible for everyone, even in healthy patients
What are the two stimuli for vasopressin release, and what receptors detect this change?
increased plasma osmolality - osmoreceptors //
decreased atrial pressure - atrial stretch receptors
What are the two brain structures that store osmoreceptors and where are they located (with their special feature)?
Organum vasculosum of lamina terminalis & subfornical organ - around 3rd ventricle - no blood brain barrier
How do osmoreceptors regulate vasopressin?
When there is a high osmolality, water leaves osmoreceptor (causes shrinking), leads to more osmoreceptor firing, and hence AVP release
How do atrial stretch receptors regulate vasopressin?
Atrial stretch receptors detect pressure in atrium, when stretched there is firing via vagal afferents to inhibit vasopressin
Why is vasopressin released after a haemorrhage?
Lower atrial stretch receptor firing means less inhibition of vasopressin release
Why is vasopressin release useful after a haemorrhage?
V2 receptor for more water reabsorption - increases pressure in the circulation, V1 receptor for vasoconstriction - increases blood pressure
What is the physiological response to water restriction and how will concentrations of plasma and urine change?
Activation of osmoreceptors, increase AVP, there will be a slight increase in plasma osmolality (however body will stabilise) and increase in urine conc and decrease in urine volume
What are the three main symptoms of diabetes insipidus and what is the problem with this?
Polyuria, Nocturia, Polydipsia - all the same as diabetes mellitus which has a very different treatment plan
What is the clinical presentation of diabetes insipidus? x4
Dilute high volume urine, hyperosmolar plasma, hypernatraemia, normal glucose
What are the two types of diabetes insipidus?
Cranial DI - cannot make AVP //
Nephrological DI - cannot respond to AVP
What are three causes of CDI? (AVP-D)
pituitary surgery/trauma, metastasis,
autoimmune (sarcoidosis & TB)
What is an acquired cause of NDI? (AVP-R)
Lithium drugs (in schizophrenia)
What are the 4 blood tests you would do if you suspect DI and why?
blood glucose and HbA1c (for mellitus), sodium concentration (hypernatraemia), plasma osmolality
Why do people with DI have polydipsia?
Lose a lot of water in urine, osmoreceptors constantly fire leading to polydipsia
When can DI cause death?
When access to water is restricted - by losing all water in urine and not being replaced, plsma osmolarity increases
What is psychogenic polydipsia?
Too much water drinking - this leads to similar symptoms as DI
How would you differentiate DI and PP?
Water deprivation test - restrict water and monitor weight and urine osmolarity. DI will always stay a low osmolality whereas PP will increase over time. Patient with DI would have a progressive increase in plasma osmolality whereas PP will be lower than normal and increase to a reasonable level.
Why would you measure weight in this test?
People with DI can lose a lot of weight due to severe dehydration, stop the test if patient loses more than 3% bodyweight
How do you distinguish CDI and NDI?
Administer ddAVP (desmopressin). CDI will respond and urine osmolality will increase, whereas NDI will not
How do you treat CDI? (AVP-D)
Administer ddAVP either with a tablet or nasal spray
How do you treat NDI? (AVP-R)
rare and difficult to treat successfully
Thiazide diuretics (bendroflumethazide)
What is SIADH?
Syndrome of Inappropriate Anti-Diuretic Hormone - ie too much AVP
Excess water reabsorption from the kidney, causing concentrated urine, decreasing plasma osmolality and low sodium
What are some of the causes of SIADH?
Pituitary injury, pulmonary disease, malignancy, drug related, CNS (stroke, tumour)
What 2 ways do you manage SIADH?
Fluid restrict or vaptan (vasopressin antagonist). Latter is very expensive.
Arginine Vasopressin deficiency (AVP-D)
unable to make AVP
CDI
caused by issues with hypothalamus/ posterior pituitary
Arginine Vasopressin Resistance (AVP-R)
can make AVP
NDI
Kidney (collecting duct) unable to respond
Most common cause of polydipsia, polyuria and nocturia
Diabetes mellitus
symptoms due to osmotic diuresis not vasopressin
Congenital NDI
Rare
could be due to mutation in gene encoding V2 receptor
aquaporin 2 water channel
Response to desmopressin
AVP-D (CDI) - urine concentrates
AVP-R (NDI) - no increase in urine osmolarity as kidneys cannot respond
