Endo - Vasopressin Flashcards

1
Q

What is the other name of AVP?

A

→ argenine vasopressin

→ anti-diuretic hormone

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2
Q

What is the main physiological action of AVP?

A

Stimulation of water reabsorption in the renal collecting duct

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3
Q

What impact does vasopressin have on urine?

A

Concentrates urine

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4
Q

What is another purpose of AVP?

A

→ Vasoconstrictor

→ stimulates ACTH release from anterior pituitary

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5
Q

By what mechanism does AVP concentrate urine?

A

→ 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

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6
Q

How does vasopressin act as a vasoconstrictor?

A

Via v1 receptor

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7
Q

How does posterior pituitary show up on MRI?

A

“bright spot” but not visualised in all healthy individuals

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8
Q

What is the osmotic stimuli for vasopressin release?

A

Rise in plasma osmolality sensed by osmoreceptors

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9
Q

What is the non-osmotic stimuli for vasopressin release?

A

Decrease in atrial pressure sensed by atrial stretch receptors

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10
Q

What are the nuclei that respond to the osmotic stimuli?

A

→ organum vasculosum

→ subfornical organ

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11
Q

Where are the two nuclei located?

A

Around the 3rd ventricle “circum ventricular”

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12
Q

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

A

→ 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

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13
Q

How do osmoreceptors regulate vasopressin?

A

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

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14
Q

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

A

→ 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

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15
Q

Why is vasopressin released after a haemorrhage?

A

→ to restore some circulating volume

→ vasopressin release = increased water reabsorption in kidneys + vasoconstriction

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16
Q

What is the physiological response to water deprivation?

A

→ 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

17
Q

What are the symptoms of diabetes insipidus?

A

→ polyuria
→ nocturia
→ thirst - often extreme
→ polydipsia

18
Q

What are the two different types of DI?

A

→ cranial

→ nephrogenic

19
Q

What is cranial DI?

A

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

20
Q

What is nephrogenic DI?

A

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

21
Q

What is the rarest cause of CDI?

A

congenital

22
Q

What are the acquired causes of CDI?

A
→ traumatic brain injury
→ pituitary surgery
→ pituitary tumours
→ metastasis to pituitary gland
→ granulomatous infiltration of pituitary stalk
→ autoimmune
23
Q

What are the causes of NDI?

A

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

24
Q

How does DI present differently to DM?

A

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

25
Q

Why do these symptoms occur in DI?

A
→ 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
26
Q

What can mimic DI?

A

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

27
Q

How does psychogenic polydipsia present with the same symptoms?

A
→ increased drinking
→ plasma osmolality falls
→ less AVP secreted
→ large volumes of dilute urine
→ plasma osmolality returns to normal
28
Q

How do you distinguish between DI and PP?

A

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

29
Q

How do you distinguish between CDI and NDI?

A

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

30
Q

How is CDI treated?

A

replace vasopressin with Desmopressin (tablets or intranasal)

31
Q

How is NDI treated?

A

thiazide diuretics (paradoxical - mechanism still unclear)

32
Q

What is SIADH?

A

Syndrome of Inappropriate ADH

→ too much AVP

33
Q

What does SIADH cause?

A
→ reduced urine output
→ water retention
→ high urine osmolality
→ low plasma osmolality
→ dilutional hypoatraemia
34
Q

What are the causes of SIADH?

A
→ head injury, stroke, tumour
→ pneumonia, bronchiectasis
→ lung cancer
→ drug-related (carbamazepine, SSRIs)
→ idiopathic
35
Q

How is SIADH treated?

A

→ fluid restriction

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