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BRS YR2 > Disorders of Vasopressin > Flashcards

Disorders of Vasopressin Flashcards

1
Q

What neurones are present in the hypothalamus and the posterior pituitary gland?

A

Hypothalamic magnocellular neurons

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2
Q

What do hypothalamic magnocellular neurons contain?

A

AVP or oxytocin

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3
Q

Describe hypothalamic magnocellular neurons?

A

Long, originate in supraoptic and paraventricular neurons

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4
Q

What is the main physiological action of vasopression (or ADH)?

A

Stimulation of water reabsorption in the renal collecting duct (concentrating urine)

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5
Q

Where does vasopressin act?

A

the V2 receptor in the kidney

also the V1 receptor

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6
Q

What is the secondary actions of vasopressin?

A
  • vasoconstriction via the V1 receptor

- stimulates the release of ACTH from the anterior pituitary gland

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7
Q

How does vasopressin concentrate urine?

A
  • binds to the V2 receptor (on the basolateral membrane)
  • encourages the movement of water from the apical membrane to the basolateral membrane (into the blood) via aquaporin-2 and aquaporin-3
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8
Q

How does the posterior pituitary gland look in MRIs?

A

shows as a bright spot

not visualised in all healthy individuals

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9
Q

What can stimulate AVP release?

A

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

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10
Q

What are the 2 main osmorecepters involved in osmotic stimulation?

A
  • Organum vasculosum
  • Subfornical organ
    (nuclei that sit around the 3rd ventricle)
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11
Q

What are the properties of the 2 main osmoreceptors?

A
  • no blood brain barrier (can respond to changes in systemic circulation)
  • highly vascularised
  • project into the supraoptic nucleus
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12
Q

What is the supraoptic nucleus?

A

The site of vasopressinergic neurons

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13
Q

How do osmoreceptors regulate vasopressin?

A
  • increase in extracellular Na+
  • water moves out of osmoreceptor
  • osmoreceptor shrinks
  • increased osmoreceptor firing
  • AVP release from the hypothalamic neurons
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14
Q

Describe the process of non-osmotic stimulation of vasopressin release

A
  • atrial stretch receptors detect pressure in the RA
  • inhibit AVP release via the vagal afferents to the hypothalamus
  • reduction in circulating volume (eg by haemorrhage) means less stretch and therefore less inhibition.
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15
Q

Why is vasopressin released following a haemorrhage?

A
  • less stretch of the atrial stretch receptors, therefore less inhibition of AVP
  • AVP release results in increased water reabsorption in the kidney (via V2 receptors)
  • vasoconstriction (via V1 receptors)
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16
Q

What is the physiological response to water deprivation?

A
  • increased plasma osmolarity
  • stimulation of osmoreceptors
  • thirst
  • release of AVP
  • increased water reabsorption from renal collecting ducts
  • reduced urine volume, increased urine osmolarity
  • reduction in plasma osmolarity
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17
Q

What are the symptoms of diabetes insipidus?

A
  • polyuria
  • nocturia
  • thirst (often extreme)
  • polydipsia
18
Q

What is the difference between diabetes mellitus and diabetes insipidus?

A

In diabetes mellitus, the symptoms are caused by osmotic diuresis.
In diabetes insipidus, the symptoms are caused due to a problem with AVP

19
Q

What are the two different types of diabetes insipidus?

A
  • cranial diabetes insipidus
    (vasopressin insufficiency)
  • nephrogenic diabetes insipidus
    (vasopressin resistance)
20
Q

Describe cranial diabetes insipidus?

A

A problem with the hypothalamus and/or the posterior pituitary - unable to make AVP
(vasopressin insufficiency)

21
Q

Describe nephrogenic diabetes insipidus?

A

Normal AVP production (normal hypothalamus and posterior pituitary)
Abnormal kidney collecting duct (unable to respond)
(vasopressin resistance)

22
Q

What are the possible causes of cranial diabetes insipidus?

A 
Acquired
- brain injury
- pituitary surgery
- pituitary tumours
- metastasis to the pituitary gland
- granulomatous infiltration of the pituitary stalk
- autoimmune
Congenital (rare)
23
Q

What are the possible causes of nephrogenic diabetes insipidus?

A 
(much less common than cranial)
Congenital (rare)
- eg: mutation in gene encoding the V2 receptor, aquaporin-2 water channel
Acquired
- drugs (eg: lithium)
24
Q

Presentation of diabetes insipidus.

A 
Urine
- very dilute (hypo-osmolar)
- large volumes
Plasma
- increased concentration (hyper-osmolar)
- increases sodium (hypernatraemia)
- NORMAL GLUCOSE
25
Q

What causes the presentation of diabetes insipidus?

A
  • AVP problem
  • impaired concentration of urine in the renal collecting duct
  • large volumes of dilute (hypotonic) urine
  • increased plasma osmolarity (and sodium)
  • stimulation of osmoreceptors
  • thirst, polydipsia
  • this maintains circulating volume while there is access to water
26
Q

Can diabetes insipidus cause death?

A

Only if there is not a constant access to water, as it will lead to dehydration and death.

27
Q

What is psychogenic polydipsia?

A

Problem caused by overconsumption of water leading to large volumes of dilute urine

28
Q

How does psychogenic polydipsia present?

A 
same as diabetes insipidus
- nocturia
- polyuria
- polydipsia
(BUT no problem with AVP)
29
Q

What causes the symptoms of psychogenic polydipsia?

A
  • increased drinking (polydipsia)
  • plasma osmolarity falls
  • less AVP is secreted by the posterior pituitary
  • large volumes of dilute (hypotonic) urine
  • plasma osmolarity returns to normal
30
Q

How to distinguish between diabetes insipidus and psychogenic polydipsia?

A

A water deprivation test

31
Q

What is involved in a water deprivation test?

A 
no access to any drink 
over time, measure:
- urine volumes
- urine concentration
- plasma concentration
weigh regularly, if lose more than 3% of body weight (significant dehydration) stop.
32
Q

How to differentiate between diabetes insipidus and psychogenic polydipsia based on the results of the water deprivation test?

A

Psychogenic polydipsia:
urine osmolarity increases are time progresses, but not to the same extent as normal
Diabetes Insipidus:
no change in urine osmolarity over time (as problem with AVP)

33
Q

How to distinguish between cranial diabetes insipidus and nephrogenic diabetes insipidus during a water deprivation test?

A
  • give ddAVP (similar to AVP)
    if cranial:
    will respond to ddAVP, urine with concentrate as collecting duct is fine
    if nephrogenic:
    no response, and no change to urine concentration as collecting duct is resistant to AVP.
34
Q

What is the approximate plasma osmolarity with diabetes insipidus?

A

> 290 mOsm/kg

35
Q

What is the approximate osmolarity with psychogenic polydipsia?

A

<270 mOsm/kg

36
Q

What is the treatment of cranial diabetes insipidus?

A
  • replace AVP with desmopressin
  • selective for V2 receptor (V1 would be unhelpful)
  • available either in tablets or intranasal
37
Q

Hospital neglect and diabetes insipidus?

A
  • desmopressin nasal spray is often disregarded upon admission
  • fluid restriction is dangerous and can cause death
38
Q

What is the treatment for nephrogenic diabetes insipidus?

A

Difficult to treat successfully
- Thiazide diuretics
(eg: bendofluazide)
unknown mechanism

39
Q

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

A

The presence of too much AVP

40
Q

How does SIADH present?

A
  • reduced urine output
  • water retention
  • high urine osmolarity
  • low plasma osmolarity
  • dilutional hyponatraemia
41
Q

What are the causes of SIADH?

A 
CNS
- head injury
- stroke
- tumour
Pulmonary disease
- pneumonia
- bronchiectasis
Malignancy
- small cell lung cancer
Drug related
- Carbamazepine
- SSRIs
Idiopathic
42
Q

What is the management plan for SIADH?

A
  • fluid restriction
  • can use vasopressin antagonist (vaptan) that binds to V2 receptors in the kidney
    (£££)

BRS YR2 (70 decks)

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