Endo - Vasopressin

Question 1

What is the other name of AVP?

Answer 1

→ argenine vasopressin

→ anti-diuretic hormone

Question 2

What is the main physiological action of AVP?

Answer 2

Stimulation of water reabsorption in the renal collecting duct

Question 3

What impact does vasopressin have on urine?

Answer 3

Concentrates urine

Question 4

What is another purpose of AVP?

Answer 4

→ Vasoconstrictor

→ stimulates ACTH release from anterior pituitary

Question 5

By what mechanism does AVP concentrate urine?

Answer 5

→ acts on V2 receptors in kidney
→ after the cascade of proteins, aqua-porin 2 + transports the H2O from the urine into cells
→ aqua-porin 3 transports it back to plasma

Question 6

How does vasopressin act as a vasoconstrictor?

Answer 6

Via v1 receptor

Question 7

How does posterior pituitary show up on MRI?

Answer 7

“bright spot” but not visualised in all healthy individuals

Question 8

What is the osmotic stimuli for vasopressin release?

Answer 8

Rise in plasma osmolality sensed by osmoreceptors

Question 9

What is the non-osmotic stimuli for vasopressin release?

Answer 9

Decrease in atrial pressure sensed by atrial stretch receptors

Question 10

What are the nuclei that respond to the osmotic stimuli?

Answer 10

→ organum vasculosum

→ subfornical organ

Question 11

Where are the two nuclei located?

Answer 11

Around the 3rd ventricle “circum ventricular”

Question 12

What makes the two nuclei good at responding to osmotic stimuli?

Answer 12

→ no blood brain barrier, neurones respond to change into systemic circulation
→ highly vascularised + has osmoreceptors
→ neurones project to the supraoptic nucleus - site of vasopressinergic neurones

Question 13

How do osmoreceptors regulate vasopressin?

Answer 13

→ osmoreceptors respond to increase in extracellular Na+ causing water to exit
→ osmoreceptor shrinks
→ osmoreceptor firing increases
→ AVP released from hypothalamic neurones

Question 14

How does the mechanism of non-osmotic stimulation of vasopressin work?

Answer 14

→ atrial receptors detect pressure in right atrium
→ inhibit vasopressin release via vagal afferent to hypothalamus
→ reduction in circulating volume e.g. haemorrhage, means less stretch of these atrial receptors
→ leads to less inhibition of vasopressin

Question 15

Why is vasopressin released after a haemorrhage?

Answer 15

→ to restore some circulating volume

→ vasopressin release = increased water reabsorption in kidneys + vasoconstriction

Question 16

What is the physiological response to water deprivation?

Answer 16

→ increased plasma osmolality
→ stimulation of osmoreceptors
→ thirst + increased AVP release
→ increased h2o reabsorption from the renal collecting duct
→ reduced urine volume, increase in urine osmolality
→ reduction in plasma osmolality

Question 17

What are the symptoms of diabetes insipidus?

Answer 17

→ polyuria
→ nocturia
→ thirst - often extreme
→ polydipsia

Question 18

What are the two different types of DI?

Answer 18

→ cranial

→ nephrogenic

Question 19

What is cranial DI?

Answer 19

→ problem w hypothalamus and/or posterior pituitary
→ unable to make AVP
→ “vasopressin insufficiency”

Question 20

What is nephrogenic DI?

Answer 20

→ can make AVP
→ kidney doesn’t respond to it
→ “vasopressin resistance”

Question 21

What is the rarest cause of CDI?

Answer 21

congenital

Question 22

What are the acquired causes of CDI?

Answer 22

→ traumatic brain injury
→ pituitary surgery
→ pituitary tumours
→ metastasis to pituitary gland
→ granulomatous infiltration of pituitary stalk
→ autoimmune

Question 23

What are the causes of NDI?

Answer 23

→ congenital = rare (e.g.mutation in gene encoding V2 receptor, aquaporin 2 type water channel)
→ acquired = drugs (e.g. lithium)

Question 24

How does DI present differently to DM?

Answer 24

→ very dilute large volumes of urine
→ increased plasma osmolality
→ increased sodium levels
→ normal glucose levels

Question 25

Why do these symptoms occur in DI?

Answer 25

``` → not enough AVP / not responding to AVP → impaired conc. of urine in RCD → large volumes of dilute urine → increase in plasma osmolality → stimulation of osmoreceptors → thirst = polydipsia → circulating volume can only be maintained if patient has access to water → no access to water = dehydration + death ```

Question 26

What can mimic DI?

Answer 26

psychogenic polydipsia → has similar presentation → but no problem with AVP → patients drink too much water all the time

Question 27

How does psychogenic polydipsia present with the same symptoms?

Answer 27

``` → increased drinking → plasma osmolality falls → less AVP secreted → large volumes of dilute urine → plasma osmolality returns to normal ```

Question 28

How do you distinguish between DI and PP?

Answer 28

water deprivation test → no access to anything to drink → measure urine volume + urine conc/osmolality + plasma conc/osmolality over time → PP should see urine osmolality increase + return back to normal → DI can't due AVP problems weigh regularly → stop test if lost >3% body weight due to dehydration

Question 29

How do you distinguish between CDI and NDI?

Answer 29

give ddAVP → works like AVP → CDI will respond + urine osmolality will increase → NDI won't + urine osmolality wil decrease

Question 30

How is CDI treated?

Answer 30

replace vasopressin with Desmopressin (tablets or intranasal)

Question 31

How is NDI treated?

Answer 31

thiazide diuretics (paradoxical - mechanism still unclear)

Question 32

What is SIADH?

Answer 32

Syndrome of Inappropriate ADH | → too much AVP

Question 33

What does SIADH cause?

Answer 33

``` → reduced urine output → water retention → high urine osmolality → low plasma osmolality → dilutional hypoatraemia ```

Question 34

What are the causes of SIADH?

Answer 34

``` → head injury, stroke, tumour → pneumonia, bronchiectasis → lung cancer → drug-related (carbamazepine, SSRIs) → idiopathic ```

Question 35

How is SIADH treated?

Answer 35

→ fluid restriction | → vasopressin antagonist (vaptan) (binds to V2 receptors in kidneys)