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BRS Year 2 > Disorders of Vasopressin > Flashcards

Disorders of Vasopressin Flashcards

1
Q

What are hypothalamic magnocellular neurons?

A

Hypothalamic magnocellular neurons contain AVP or oxytocin
They’re long, originate in supraoptic and paraventricular hypothalamic nuclei

Nuclei → stalk →posterior pituitary

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2
Q

What is vasopressin also known as?

A

Also known as antidiuretic hormone (diuresis means producing urine so non- urine producing hormone)

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3
Q

What is the physiological action of vasopressin?

A

Stimulation of water reabsorption in the renal collecting duct
This concentrates urine
Acts through the V2 receptor in the kidney

Also a vasoconstrictor (via V1 receptor)
Stimulates ACTH release from anterior pituitary

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4
Q

How does vasopressin concentrate urine?

A

AVP (arginine vasopressin) travels from blood and binds to V2 receptor on collecting duct
This causes an intracellular signalling cascade which causes the insertion of aquaporin 2 on tubular luminal membrane
This causes reabsorption of water through the aquaporin across the conc. gradient and out through aquaporin 3 channels into circulation

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5
Q

How does the posterior pituitary appear on an MRI?

A

Appears as a bright spot

Not visualised in all healthy individuals, so absence may be normal variant

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6
Q

What stimuli are there 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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7
Q

How does osmotic stimulation of vasopressin release work?

A

Plasma osmolality is sensed by oroganum vasculosum & subfornical organ
They are both nuclei which sit around the 3rd ventricle (‘circumventricular’)
There’s no blood brain barrier – so neurons can respond to changes in the systemic circulation
Highly vascularised
neurons project to the supraoptic nucleus - site of vasopressinergic neurons

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8
Q

How do osmoreceptors regulate vasopressin?

A

Increase in extracellular Na and plasma osmolality
Water moves out of osmoreceptor (along conc. gradient) causing the osmorector to shrink
This causes increased osmoreceptor firing
This causes AVP release from hypothalamic neurons

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9
Q

How does Non-osmotic stimulation of vasopressin release work?

A

Atrial stretch receptors: detect high pressure in the right atrium
This inhibits vasopressin 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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10
Q

Why is vasopressin released in response to haemorrhage?

A

Haemorrhage leads to a reduction in circulating volume

Vasopressin release leads to 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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11
Q

What is the physiological response to water deprivation?

A

Increased plasma osmolarity
Stimulation of osmoreceptors
Thirst and increased AVP release
Increased water reabsorption from renal collecting ducts
Reduced urine volume, increase in urine osmolality

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12
Q

What are symptoms of diabetes insipidus?

A

Polyuria
Nocturia
Thirst – often extreme
Polydispia

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13
Q

What’s the difference between diabetes mellitus and diabetes insipidus?

A

In diabetes mellitus (hyperglycaemia) these symptoms are due to osmotic diuresis
In diabetes insipidus, these symptoms are due to a problem with arginine vasopressin

Remember – the most common cause of polyuria, nocturia & polydipsia is diabetes mellitus, NOT diabetes insipidus

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14
Q

What are the different types of diabetes insipidus?

A

Cranial (central) diabetes insipidus

Nephrogenic diabetes insipidus

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15
Q

What is cranial diabetes insipidus?

A

Problem with hypothalamus &/or posterior pituitary
Unable to make arginine vasopressin
‘VASOPRESSIN INSUFFICIENCY’

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16
Q

What is nephrogenic diabetes insipidus?

A

Can make arginine vasopressin (normal hypothalamus & posterior pituitary)
Kidney (collecting duct) unable to respond to it
‘VASOPRESSIN RESISTANCE

17
Q

What are causes of cranial diabetes insipidus?

A

Acquired (more common):

Traumatic brain injury
Pituitary surgery
Pituitary tumours
Metastasis to the pituitary gland eg breast
Granulomatous infiltration of pituitary stalk eg TB, sarcoidosis
Autoimmune

Congenital rare

18
Q

What are causes of nephrogenic diabetes insipidus?

A

Much less common than cranial diabetes insipidus

Congenital:
rare (e.g. mutation in gene encoding V2 receptor, aquaporin 2 type water channel)

Acquired:
Drugs (e.g. lithium- often used to treat mental health)

19
Q

How does diabetes insipidus present?

A

Urine:
Very dilute (hypo - osmolar)
Large volumes

Plasma:
Increased concentration (hyper-osmolar) as patient becomes dehydrated
Increased sodium (hypernatraemia) 
 Glucose normal (make sure you ALWAYS check this in a patient with these symptoms)
20
Q

Why do these symptoms occur in diabetes insipidus?

A
  1. Arginine vasopressin problem: not enough (CDI) or not responding (NDI)
  2. Impaired conc. of urine in renal collecting duct
  3. Large volumes of dilute urine
  4. Increase in plasma osmolality
  5. Stimulation of osmoreceptors
  6. Thirst- Polydipsia
  7. Maintains circulating volume as long as patient has access to water
21
Q

What is the biggest consequence of diabetes insipidus?

A

Polydipsia can lead to dehydration and death

22
Q

What is psychogenic polydipsia?

A

Similar presentation to diabetes insipidus
Polydipsia
Polyuria
Nocturia
Unlike diabetes insipidus – no problem with arginine vasopressin
Problem is that the patient drinks all the time, so passes large volumes of dilute urine

23
Q

How do symptoms arise in psychogenic polydipsia?

A
  1. Increased drinking (polydipsia)
  2. Plasma osmolality falls
  3. Less AVP secreted by post. pituitary
  4. Large volumes of dilute urine
  5. Plasma osmolality returns to normal
24
Q

How can we distinguish between diabetes insipidus and psychogenic polydipsia?

A

We carry out a water deprivation test:

No access to anything to drink
Over time we measure:

  • Urine volumes
  • Urine concentration (osmolality)
  • Plasma concentration (osmolality)

In a patient with psychogenic polydipsia urine osmolality increases but in a patient with diabetes insipidus it won’t because no release of AVP or resistance to AVP

25
Q

What is monitored during the water deprivation test to ensure the patient does not become dangerously dehydrated?

A

Body weight is measured regularly

Test is stopped if patient loses >3% of body weight

26
Q

How can we distinguish between cranial diabetes insipidus and nephrogenic diabetes insipidus?

A

Give ddAVP
This will work ‘like’ vasopressin
Cranial diabetes insipidus – response to ddAVP – urine concentrates
Nephrogenic diabetes insipidus – no increase in urine osmolality with ddAVP, as kidneys can’t respond

27
Q

How does plasma osmolality vary for diabetes insipidus and psychogenic polydipsia?

A

In diabetes insipidus its >290 mOsm/kg H2O

In psychogenic polydipsia its <270 mOsm/kg H2O

Normal range around 280 mOsm/kg H2O

28
Q

How is cranial diabetes insipidus treated?

A

Want to replace vasopressin
Desmopressin (ddAVP)
Selective for V2 receptor (V1 receptor activation would be unhelpful)
Different preparations:
- Tablets
- Intranasal (prevents it from being broken down in stomach)

ddAVP adjusted based on lifestyle (if drinking a lot take less)

29
Q

How is nephrogenic diabetes insipidus treated?

A

Luckily this is very rare – difficult to treat successfully
Thiazide diuretics eg bendofluazide
We dont know why it works

30
Q

What is Syndrome of Inappropriate Anti-Diuretic Hormone (SIADH)?

A

Too much arginine vasopressin

Symptoms:

  • Reduced urine output
  • Water retention
  • High urine osmolality
  • Low plasma osmolality
  • Dilutional hyponatraemia
31
Q

What are causes of SIADH?

A 
CNS
Head injury, stroke, tumour, 
Pulmonary disease
Pneumonia, bronchiectasis
Malignancy
Lung cancer (small cell)
Drug-related
Carbamazepine, Serotonin Reuptake Inhibitors (SSSRIs)
Idiopathic (not sure why)
32
Q

How is SIADH managed?

A

Common cause of prolonged hospital stay
Fluid restriction
Can use a vasopressin antagonist (vaptan) – binds to the V2 receptors in the kidney (expensive)

BRS Year 2 (110 decks)

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