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Aneesha Flashcards BRS 2 > Vasopressin disorders > Flashcards

Vasopressin disorders Flashcards

1
Q

Differences between the anterior pituitary and the posterior pituitary

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

What are hypothalamic magnocellular neurons

A

Contain AVP, oxytocin
Long, originate in supraoptic nuclei, paraventricular hypothalamic nuclei
Nuclei–>stalk–>posterior pituitary

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4
Q

what is the main physiological action of AVP

A

stimulation of water reabsorption in the renal collecting duct
This concentrates urine

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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 does vasopressin concentrate urine?

A

AVP from bloodstream binds to V2 receptors on basolateral membrane of renal collecting duct
This stimulates a signal cascade (G-protein binds adenylyl cyclase–>cAMP–>upregulates protein kinase A)
This stimulates Aquaporin-2 in cell to move to apical membrane, allowing water to enter cell, diffuse across and exit basolateral membrane via Aquaporin 3 into bloodstream

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9
Q

how do you see the posterior pituitary on MRI?

A

posterior bright spot, not always visible in healthy individuals

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10
Q

Stimulation for vasopressin release

A

osmotic- rise in plasma osmolality sensed by osmoreceptors
non-osmotic- decrease in atrial pressure sensed by atrial stretch receptors

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11
Q

where are atrial stretch receptors found?

A

right atrium

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12
Q

what are the organum vasculosum and subfornical organ important for?

A

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

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13
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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14
Q

what is the process for non-osmotic stimuli?

A

atrial stretch receptors in right atrium detect rise in pressure
This inhibits AVP release via vagal afferents to hypothalamus
Reduction in circulating volume eg haemorrhage means less stretch of these atrial receptors, so less inhibition of vasopressin

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15
Q

why is vasopressin released following a haemorrhage?

A

Vasopressin release results in increased water reabsorption in the kidney (some restoration of circulating volume) V2 receptors
vasoconstriction via V1 receptors
(NB renin-aldo system will also be important, sensed by JG apparatus)

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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 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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17
Q

what is the basis of diabetes insipidus?

A

vasopressin insufficiency or resistance

18
Q

what are the main symptoms of diabetes insipidus?
What is the difference in causation of these symptoms between diabetes mellitus and insipidus

A

polyuria
nocturia
thirst
polydypsia

In diabetes mellitus (hyperglycaemia), these symptoms are due to osmotic diuresis

In diabetes insipidus, these symptoms are due to a problem with arginine vasopressin

19
Q

what is cranial/ central diabetes insipidus?

A

problem with hypothalamus &/or posterior pituitary
vasopressin insufficiency

20
Q

what is nephrogenic diabetes insipidus?

A

vasopressin resistance
kidney (collecting duct) unable to respond to AVP

21
Q

what are the causes of cranial DI?

A

traumatic brain injury
pituitary surgery, tumours
metastasis to pituitary gland
granulomatous infiltration of pituitary stalk e.g. TB, sarcoidosis
autoimmune
rarely congenital

22
Q

what are the causes of nephrogenic DI?
Is it more/ less common than cranial DI?

A

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

Much less common than cranial DI

23
Q

how does diabetes insipidus often present?
What are the characteristics of urine and plasma?

A

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

24
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
If no access to water–> Dehydration and death

25
Q

what is psychogenic polydypsia?

A

patient always drinking water, no issues with AVP
usually comorbidity of mental illnesses

26
Q

how can you distinguish diabetes insipidus and psychogenic polydypsia?

A

water deprivation test

27
Q

how do you perform a water deprivation test?

A

no access to water
measure urine volumes, concentration and plasma concentration over time
weigh regularly and stop test if more than 3% body weight is lost–> marker of significant dehydration which can occur in diabetes insipidus

28
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

29
Q

how do you distinguish cranial DI from neurogenic DI?

A

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

30
Q

what is ddAVP

A

desmopressin, synthetic AVP that works only on V2 receptors

31
Q

Plasma osmolality in hydrated range, DI, and psychogenic polydipsia

A
32
Q

how do you treat cranial DI?
What receptors does this act on?

A

demopressin intranasal spray or tablets
Selective for V2 receptor (V1 receptor activation would be unhelpful)

33
Q

how do you treat nephrogenic DI?
What is the mechanism of action of this treatment?

A

difficult to treat successfully
thiazide diuretics e.g. bendofluthiazide
Paradoxical! Mechanism unclear

34
Q

what is SIADH

A

syndrome of inappropriate ADH - too much AVP

35
Q

what are the signs of SIADH

A

reduced urine output, water retention,low plasma osmolality, dilutional hyponaetraemia

36
Q

what are the causes of SIADH

A

CNS- head injury, stroke, tumour
pulmonary- pneumonia, bronchiectasis
malignancy- lung cancer (small cell)
drug related - carbamazepine, SSRIs
idiopathic - common in elderly

37
Q

how do you manage SIADH?

A

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

38
Q

why should desmopressin doses be tightly monitored?

A

too high may cause hyponatraemia, causing brain damage from swelling

39
Q

when should desmopressin doses be increased?

A

extreme exercise e.g marathons

40
Q

what tests should be ordered if DI is suspected?

A

paired plasma and urine osmolality
fasting/random glucose/oral glucose tolerance test

41
Q

why should DI not always be first suspected?

A

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

Aneesha Flashcards BRS 2 (47 decks)

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