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endo > 1B disorders of vasopressin > Flashcards

1B disorders of vasopressin Flashcards

1
Q

How does the posterior pituitary work?

A
  • It’s anatomically continuous with the hypothalamus
  • Hypothalamic magnocellular neurons containing AVP or oxytocin
  • Long, originate in supraoptic and paraventricular hypothalamic nuclei
  • Nuclei → stalk → posterior pituitary
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2
Q

What is the physiological action of vasopressin aka ADH?

A
  • Stimulation of water reabsorption in renal collecting duct which concentrates urine- acts through V2 receptor in the kidney
  • Also a vasoconstrictor via V1 receptor
  • Stimulates ACTH release from anterior pituitary
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3
Q

How does the posterior pituitary come up on MRI?

A
  • As a bright spot
  • Not visualised in all healthy individuals, so absence may be normal variant
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4
Q

What are the 2 triggers for vasopressin release?

A
  • osmotic: rise in plasma osmolality (conc) sensed by osmoreceptors
  • non-osmotic
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5
Q

What nuclei sense plasma osmolality and how are they adapted for their job?

A
  • Organum vasculosum and subfornical organ- both sit around 3rd ventricle (circumventricular)
  • Neurons project to supraoptic nucleus- site of vasopressinergic neurons
  • No BBB- so neurons can respond to changes in the systemic circulation
  • Highly vascularised
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6
Q

How do osmoreceptors regulate vasopressin?

A
  • Increase in plasma osmolality (e.g. increase in extracellular Na+ in diagram)
  • Via osmosis, water flows out of osmoreceptor
  • Osmoreceptor changes shape and shrinks
  • Increases osmoreceptor firing
  • AVP release from hypothalamic neurons
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7
Q

How does a non-osmotic trigger for vasopressin release work?

A
  • Decrease in atrial pressure sensed by atrial stretch receptors in right atrium
  • Stretch receptors usually inhibit vasopressin release via vagal afferents to hypothalamus
  • Reduction in circulating volume e.g. haemorrhage means less stretch of these atrial receptors, so less inhibition of vasopressin
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8
Q

What does the release of vasopressin help do?

A
  • Vasopressin release results in increased water reabsorption in the kidney (some restoration of circulating volume) via V2 receptors
  • Vasoconstriction via V1 receptors (renin-aldo system will also be important, sensed by JG apparatus)
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9
Q

What is the physiological response to water deprivation?

A

1) Increased plasma osmolality

2) stimulation of osmoreceptors, leading to thirst

3) increased AVP release

4) increased water reabsorption from renal collecting ducts

5) reduced urine volume, increase in urine osmolality

6) reduction in plasma osmolality

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10
Q

What are the symptoms of Arginine Vasopressin Deficiency/Resistance?

A
  • Polyuria
  • Nocturia
  • Polydipsia (thirst- often extreme)
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11
Q

What happens to urine in AVP-D/R?

A

Very dilute (hypoosmolar) and large volumes

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12
Q

What happens to plasma in AVP-D/R?

A

Increased concentration (hyperosmolar) as patient becomes dehydrated, increased sodium (hypernatraemia), glucose is normal

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13
Q

Why do patients with AVP-D/R have polydipsia, polyuria and nocturia?

A

1) Arginine vasopressin problem- either not enough (CDI) or not responding (NDI)

2) Impaired conc of urine in renal collecting duct

3) large volumes of dilute (hypotonic) urine

4) Increase in plasma osmolality and sodium

5) Stimulation of osmoreceptors

6) Thirst- polydipsia

7) Maintains circulating volume as long as patient has access to water

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14
Q

When does AVP-D/R lead to death?

A

When there is no access water, the patient dehydrates and dies.

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15
Q

Why are symptoms different in diabetes mellitus (hyperglycaemia) vs insipidus (AVP disorders)?

A

In mellitus (hyperglycaemia), the symptoms arise due to osmotic diuresis.

In insipidus, these symptoms are due to problems with arginine vasopressin.

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16
Q

Which is more common out of diabetes mellitus and diabetes insipidus for these symptoms?

A

Diabetes mellitus is much more common.

  • If you see a patient with these symptoms, check their blood sugar first because of this
  • Preventing a patient with insipidus from drinking or not giving fluids if unable to drink can cause death
17
Q

What are the two types of diabetes insipidus?

A
  • Cranial (central) diabetes insipidus/ AVP-D
  • Nephrogenic diabetes insipidus/ AVP-R
18
Q

What is AVP-D?

A
  • Problem with hypothalamus and/or posterior pituitary
  • Unable to make arginine vasopressin

therefore vasopressin insufficiency

19
Q

What are the two causes of AVP-D?

A
  • Acquired (common)
  • Congenital (rare)
20
Q

What are examples of acquired causes of AVP-D?

A
  • Traumatic brain injury
  • Pituitary surgery
  • Pituitary tumours
  • Metastasis to the pituitary gland e.g. breast
  • Granulomatous infiltration of pituitary stalk e.g. TB, sarcoidosis
  • Autoimmune
21
Q

What is the treatment for AVP-D?

A
  • Want to replace vasopressin with something selective for V2 receptor (V1 receptor activation would be unhelpful)
  • Desmopressin
  • Different preparations- tablets or intranasal
22
Q

What is AVP-R?

A
  • Can make arginine vasopressin (normal hypothalamus and posterior pituitary)
  • Kidney (collecting duct) unable to respond to it

therefore vasopressin resistance

23
Q

What are the causes of AVP-R?

A
  • Much less common than cranial diabetes insipidus
  • Acquired- drugs e.g. lithium
  • Congenital- rare- e.g. mutation in gene encoding V2 receptor, aquaporin 2 type water channel
24
Q

What is the treatment for AVP-R?

A
  • Very rare disease: difficult to treat successfully
  • Thiazide diuretics e.g. bendofluazide works
  • Paradoxical: mechanisms unclear
25
Q

What is psychogenic polydipsia?

A
  • Similar presentation to diabetes insipidus
  • Polydipsia, polyuria, nocturia symptoms
  • Unlike diabetes insipidus- no problem with arginine vasopressin
  • Problem is that patient is drinking water all the time, so passes large volumes of dilute urine
26
Q

How does psychogenic polydipsia lead to its symptoms?

A

1) Increased drinking (polydipsia)

2) plasma osmolality falls

3) less AVP secreted by posterior pituitary

4) large volumes of dilute (hypotonic) urine

5) plasma osmolality returns to normal

27
Q

How do we distinguish between diabetes insipidus and psychogenic polydipsia?

A
  • Water deprivation test- no access to anything to drink
  • Over time, measure urine volumes, conc (osmolality) and plasma conc (osmolality)
  • Weigh regularly- stop test if patient loses >3% body weight (a marker of significant dehydration which can occur in diabetes insipidus)
28
Q

Graph of normal vs psych poly vs insipidus urine osmolality

A
29
Q

How do we distinguish between AVP-D and AVP-R?

A
  • Give ddAVP during water deprivation test- this’ll work like vasopressin
  • CDI- response to ddAVP- urine concentrates
  • NDI- no increase in urine osmolality with ddAVP as kidneys can’t respond
30
Q

Graph of urine osmolality of normal patient, AVP-D patient and AVP-R patient

A
31
Q

Difference in plasma osmolality between psych poly and insipidus?

A
32
Q

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

A
  • Too much AVP
  • Reduced urine output
  • Water retention
  • High urine osmolality
  • Low plasma osmolality
  • Dilutional hyponatraemia- big problem, esp in elderly
33
Q

What are the causes of SIADH?

A
  • CNS- head injury, stroke, tumour
  • Pulmonary disease- pneumonia, bronchiectasis
  • Malignancy- lung cancer (small cell)
  • Drug related- carbamazepine, serotonin reuptake inhibitors (SSRIs)
  • Idiopathic (we don’t know)
34
Q

What is the management of SIADH?

A
  • Common cause of prolonged hospital stay
  • Fluid restrict
  • Can use a vasopressin antagonist (vaptan)- binds to V2 receptors in the kidney- very expensive

endo (12 decks)

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