vasopressin

Question 1

What is the relation of the posterior pituitary and hypothalamus?

Answer 1

continuous with eachother

Question 2

What is origin or posterior pituitary?

Answer 2

neural origin

Question 3

What does posterior pituitary look like on MRI? What would absence mean on MRI?

Answer 3

bright spot on MRI

-not always visualised so absence could be normal

Question 4

What are hypothalamic neurones containing posterior pituitary hormones called / which hormones do they contain / where do they originate. Where do they go?

Answer 4

Hypothalamic Magnocellular neurones contain AVP and oxytocin. Magnocellular neurones originate in supraoptic and paraventricular nuclei in hypothalamus. They go down pituitary stalk to the posterior pituitary.

Question 5

vasopressin mechanism of action?

Answer 5

Vasopressin acts on V2 receptors in the kidneys collecting ducts to increase water reabsorption. Acts on V1 receptors for vasoconstriction. Vasopressin binds to V2 receptors on collecting duct basolateral membrane, initiating a signalling cascade which generates aquaporin 2 channels leading to reabsorption of water.

Question 6

What are the triggers for vasopressin release?

Answer 6

1. Osmotic - increased plasma osmolarity sensed by osmoreceptors. 2. non-osmotic - decreased atrial pressure sensed by atrial stretch receptors

Question 7

How is osmotic stimulation sensed? How can they do this?

Answer 7

increased plasma osmolarity sensed by organum vasculosum & subfornical organ nuclei which sit around 3rd ventricle. They have no BBB so they can sense changes in systemic circulation. The neurones then project to supraoptic nucleus where AVP is produced

Question 8

How do osmoreceptors act?

Answer 8

Osmoreceptors sense the plasma osmolarity. Increased plasma osmolarity so water leaves osmoreceptor by osmosis and shrinks, increasing osmoreceptor firing, which triggers AVP release from hypothalamic nuclei

Question 9

How do atrial stretch receptors work? What would happen in major haemorrhage?

Answer 9

Atrial stretch receptors are found in the right atrium. Normally they inhibit AVP release. Less circulating pressure means less stimulation of the atrial stretch receptor, so less inhibition of AVP release, leading to more AVP release from hypothalamic nuclei. In case of haemorrhage, this AVP would act both on V2 receptors in collecting duct to increase water reabsorption, but also V1 receptors for vasoconstriction

Question 10

What would happen in case of water deprivation?

Answer 10

increased plasma osmolarity sensed by osmoreceptors, increasing firing and AVP release and also stimulating thirst.

Question 11

What are the symptoms of diabetes insipidus?

Answer 11

polyuria, nocturia, thirst, polydipsia

Question 12

What happens in cranial/central diabetes inspidius? What are potential causes? What is the treatment?

Answer 12

AVP is not produced due to problem with hypothalamus or pituitary gland. Causes: brain damage, pituitary damage, hypothalamic damage, pituitary tumours or metastasis to pituitary (eg by breast cancer), granulomatous infiltration of pituitary stalk in TB or sarcoidosis, autoimmune or congenital. Treatment is desmopressin (vasopressin replacement) which is specific for V2 receptor.

Question 13

what is nephrogenic diabetes inspidus? What are causes? What is treatment?

Answer 13

AVP is produced but collecting duct doesn’t respond to it (vasopressin resistance). Causes can be congenital (mutation in gene encoding V2 receptor but this is rare), more common is drug like lithium used in psychiatric disorders. Treatment is thiazide diuretics (eg. Bendrofluazide)

Question 14

What is the distinguishing test between cranial and nephrogenic diabetes insipidus? What happens in each case

Answer 14

Give ddAVP (synthetic vasopressin), in cranial diabetes inspidus urine should concentrate (osomolarity should increase) but in nephrogenic there would be no change because kidney cant react to ddAVP.

Question 15

What is the presentation of diabetes inspididus? Why are they thirsty?

Answer 15

They present with large amounts of dilute urine, polydipsia, thirst, nocturia, hypernatraemia (getting rid of a lot of fluid), glucose is normal, thirst because osmoreceptors are being stimulated but no AVP is produced/responded too

Question 16

Is circulating volume maintained in diabetes inspidus? When can it be dangerous?

Answer 16

Circulating volume is maintained with access to water but it is dangerous when deprived of water.

Question 17

What happens in psychogenic polydipsia?

Answer 17

There is no problem with AVP but the patient keeps drinking a lot of water and therefore passes large amounts of urine.

Question 18

How do you distinguish between psychogenic polydipsia and diabetes insipidus? What are considerations for this test? What happens in each case.?

Answer 18

water deprivation test. Look at urine output and osmolarity. In water deprivation test, in psychogenic polydipsia the urine will concentrate because AVP is present so over time urine will decrease in volume / increase in osmolarity. This wont happen with diabetes inspidus, need to be careful to weigh them regularly and stop if they lose more than 3% of body weight (make sure they don’t become too dehydrated can be dangerous)

Question 19

what is syndrome where too much vasopressin?

Answer 19

SIADH Syndrome of inappropriate anti-diuretic hormone

Question 20

What happens in SIADH - how does it present?

Answer 20

There is increased vasopressin produced leading to increased water retention, reduced urine output, dilutional hyponatreamia. Common in elders. Urine concentration will be high

Question 21

What are causes of SIADH

Answer 21

idiopathic, drug related (carbamazepine, SSRI), lung cancer (small cell), pulmonary diseases like pneumonia & bronchiectasis, CNS (stroke, tumour, injury)

Question 22

What is treatment of SIADH

Answer 22

fluid restriction. vasopressin antagonist (vaptan) - very expensive