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BRS Year 2 > Vasopressin disorders > Flashcards

Vasopressin disorders Flashcards

1
Q

differences between the anterior pituitary and the posterior

A

posterior anatomically and embryologically distinct from anterior
posterior continuous with hypothalamus
posterior not dependent on blood/portal supply

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2
Q

what are the posterior pituitary hormones

A

arginine vasopressin

oxytocin

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3
Q

where do hypothalamic magnocellular neurones originate?

A

supraoptic nuclei

paraventricular nuclei

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4
Q

what is the main physiological action of AVP

A

stimulation of water reabsorption in the renal collecting duct

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5
Q

what receptor does AVP bind to for water reabsorption

A

V2

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6
Q

what receptor does AVP bind to for vasoconstriction

A

V1

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7
Q

what is the smaller effects of AVP

A

vasoconstriction

stimulates ACTH release from anterior pituitary

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8
Q

how do you see the posterior pituitary on MRI?

A

bright spot, not always visible in healthy individuals

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9
Q

what are the two stimuli for release of AVP

A

osmotic, rise in plasma osmolality sensed by osmoreceptors

non-osmotic, decrease in arterial pressure sensed by arterial stretch receptors

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10
Q

where are atrial stretch receptors found?

A

right atrium

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11
Q

what are the organum vasculosum and subfornical organ important for?

A

osmotic receptors around 3rd ventricle with neurones projecting to the supraoptic nucleus (site of vasopressinergic neurones)
no BBB - detect changes to systemic circulation

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12
Q

what is the process for osmotic stimuli?

A

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

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13
Q

what is the process for non-osmotic stimuli?

A

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

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14
Q

why is vasopressin released following a haemorrhage?

A

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)

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15
Q

what is the physiological response to water deprivation?

A

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)

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16
Q

what is the basis of diabetes insipidus?

A

vasopressin insufficiency or resistance

17
Q

what are the main symptoms of diabetes insipidus?

A

polyuria
nocturia
thirst
polydypsia

18
Q

what is cranial diabetes insipidus?

A

problem with hypothalamus &/or posterior pituitary

vasopressin insufficiency

19
Q

what is nephrogenic diabetes insipidus?

A

vasopressin resistance

kidney (collecting duct) unable to respond to AVP

20
Q

what are the causes of cranial DI?

A 
traumatic brain injury
pituitary surgery, tumours
metastasis to pituitary gland
granulomatous infiltration of pituitary stalk
autoimmune
rarely congenital
21
Q

what are the causes of nephrogenic DI?

A 
drugs e.g lithium
rarely congenital (mutation in gene encoding V2, aquaporin 2)
22
Q

how does diabetes insipidus often present?

A

similar to DM, polyuria, nocturia, polydypsia, thirst
large volumes of hypoosmolar urine (dilute)
hyperosmolar plasma, hypernaetraemia
glucose NORMAL

23
Q

what is the process of diabetes insipidus?

A

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

24
Q

what is psychogenic polydypsia?

A

patient always drinking water, no issues with AVP

usually comorbidity of mental illnesses

25
Q

how can you distinguish diabetes insipidus and psychogenic polydypsia?

A

water deprivation test

26
Q

how do you perform a water deprivation test?

A

no access to water
measure urine volumes, concentration and plasma concentration over time
stop test if more than 3% body weight is lost

27
Q

how do water deprivation tests of psychogenic polydypsia and diabetes insipidus differ?

A

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

28
Q

how do you distinguish cranial DI from neurogenic DI?

A

give ddAVP
cranial - pass smaller urine volumes, urine osmolality increases
nephrogenic - urine volume and osmolality stay the same

29
Q

what is ddAVP

A

desmopressin, synthetic AVP that works only on V2 receptors

30
Q

how do you treat cranial DI?

A

demopressin intranasal spray or tablets

31
Q

how do you treat nephrogenic DI?

A

difficult to treat successfully

thiazide diuretics

32
Q

what is SIADH

A

syndrome of inappropriate ADH - too much AVP

33
Q

what are the signs of SIADH

A

reduced urine output, water retention, hyponaetraemia

34
Q

what are the causes of SIADH

A 
head injury, stroke, tumour
pneumonia, bronchiectasis
lung cancer
drug related - carbamazepine, SSRIs
idiopathic - common in elderly
35
Q

how do you manage SIADH?

A 
fluid restriction (500ml max)
vaptan - vasopressin antagonist (v expensive)
36
Q

why should desmopressin doses be tightly monitored?

A

too high may cause hyponatraemia, causing brain damage from swelling

37
Q

when should desmopressin doses be increased?

A

extreme exercise e.g marathons

38
Q

what tests should be ordered if DI is suspected?

A

paired plasma and urine osmolality

fasting/random glucose/oral glucose tolerance test

39
Q

why should DI not always be first suspected?

A

glucose should always be checked - DM is far more common explanation for presenting symptoms

BRS Year 2 (67 decks)

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