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BRS YR2 > Disorders of Vasopressin > Flashcards

Disorders of Vasopressin Flashcards

(42 cards)

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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?

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

What is the difference between diabetes mellitus and diabetes insipidus?

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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?

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

Describe cranial diabetes insipidus?

Study These Flashcards
A

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

21
Q

Describe nephrogenic diabetes insipidus?

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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?

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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?

Study These Flashcards
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.

Study These Flashcards
A 
Urine
- very dilute (hypo-osmolar)
- large volumes
Plasma
- increased concentration (hyper-osmolar)
- increases sodium (hypernatraemia)
- NORMAL GLUCOSE
25
What causes the presentation of diabetes insipidus?
- 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
Can diabetes insipidus cause death?
Only if there is not a constant access to water, as it will lead to dehydration and death.
27
What is psychogenic polydipsia?
Problem caused by overconsumption of water leading to large volumes of dilute urine
28
How does psychogenic polydipsia present?
``` same as diabetes insipidus - nocturia - polyuria - polydipsia (BUT no problem with AVP) ```
29
What causes the symptoms of psychogenic polydipsia?
- 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
How to distinguish between diabetes insipidus and psychogenic polydipsia?
A water deprivation test
31
What is involved in a water deprivation test?
``` 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
How to differentiate between diabetes insipidus and psychogenic polydipsia based on the results of the water deprivation test?
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
How to distinguish between cranial diabetes insipidus and nephrogenic diabetes insipidus during a water deprivation test?
- 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
What is the approximate plasma osmolarity with diabetes insipidus?
>290 mOsm/kg
35
What is the approximate osmolarity with psychogenic polydipsia?
<270 mOsm/kg
36
What is the treatment of cranial diabetes insipidus?
- replace AVP with desmopressin - selective for V2 receptor (V1 would be unhelpful) - available either in tablets or intranasal
37
Hospital neglect and diabetes insipidus?
- desmopressin nasal spray is often disregarded upon admission - fluid restriction is dangerous and can cause death
38
What is the treatment for nephrogenic diabetes insipidus?
Difficult to treat successfully - Thiazide diuretics (eg: bendofluazide) unknown mechanism
39
What is the Syndrome of Inappropriate Anti-Diuretic Hormone (SIADH)?
The presence of too much AVP
40
How does SIADH present?
- reduced urine output - water retention - high urine osmolarity - low plasma osmolarity - dilutional hyponatraemia
41
What are the causes of SIADH?
``` CNS - head injury - stroke - tumour Pulmonary disease - pneumonia - bronchiectasis Malignancy - small cell lung cancer Drug related - Carbamazepine - SSRIs Idiopathic ```
42
What is the management plan for SIADH?
- fluid restriction - can use vasopressin antagonist (vaptan) that binds to V2 receptors in the kidney (£££)

BRS YR2 (70 decks)

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