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Endocrinology (Sahil Notion) > Disorders of Vasopressin > Flashcards

Disorders of Vasopressin Flashcards

1
Q

What is the main physiological action of ADH?

A

Stimulation of water reabsorption in the renal collecting duct

This concentrates urine

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2
Q

What receptor does ADH act through in the kidney?

A

V2 Recptor

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3
Q

What receptor does ADH act through as a vasoconstrictor?

A

V1 Recptor

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4
Q

Which hormone does ADH stimulate the release of?

A

ACTH from the anterior pituitary

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5
Q

What is the definition of osmolality?

A

Concentration of particles dissolved within a fluid

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6
Q

What are the names of the nuclei involved in the osmotic stimulation of vasopressin release?

A

Organum vasculosum and subfornical organ

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7
Q

Where are these nuclei (Organum vasculosum and subfornical organ) in the brain?

A

Both sit around the 3rd ventricle (‘circumventricular’)

So they are highly vascularised

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8
Q

What enables the neurons to be able to respond to changes in the systemic circulation?

A

There is no blood brain barrier

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9
Q

Where do these neurons project to?

A

Hypothalamic Supraoptic nucleus - site of vasopressinergic neurons

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10
Q

Supraoptic nucleus - site of vasopressinergic neurons

A

Increase in plasma osmolality leading to loss of H20 via osmosis in the osmoreceptors

Osmoreceptor shrinks leading to increased osmoreceptor firing and AVP is released from the hypothalamic neurons in the supraoptic nucleus

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11
Q

Describe the non-osmotic stimulation of vasopressin release

A

Atrial stretch receptors detect pressure in the right atrium

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

This increases vasoconstriction

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12
Q

Why is ADH released following a haemorrhage (reduction in circulating volume)?

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 as sensed by the JG apparatus

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13
Q

Describe the physiological response pathway to water deprivation

A

Increased plasma osmolality → Stimulation of osmoreceptors → Thirst as well as Increased AVP release → Increased water reabsorption from renal collecting ducts → Reduced urine volume, Increased urine osmolality → Reduction in plasma osmolality

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14
Q

What are the 4 clinical symptoms of diabetes insipidus?

A

Polyuria

Nocturia

Thirst - often extreme

Polydipsia

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15
Q

Is the most common cause of polyuria, nocturia and polydipsia diabetes mellitus or diabetes insipidus?

A

Mellitus

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16
Q

What is cranial diabetes insipidus?

A

Problem with hypothalamus and/or posterior pituitary

Unable to make ADH

17
Q

What is nephrogenic diabetes insipidus?

A

Can make ADH (normal hypothalamus and posterior pituitary)

Kidney collecting duct unable to respond to it

18
Q

What are the acquired causes of cranial diabetes insipidus?

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

19
Q

What are some of the acquired causes of nephrogenic diabetes insipidus?

A

Drugs - Lithium

20
Q

What are possible congenital causes of nephrogenic diabetes insipidus?

A

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

21
Q

What presentations would be seen in the urine of someone with diabetes insipidus?

A

Very dilute (hypo-osmolar)

Large volumes

22
Q

What presentations would be seen in the plasma of someone with diabetes insipidus?

A

Increased concentration (hyper-osmolar) as patient becomes dehydrated

Increased sodium (hypernatraemia) due to excess free water losses

Glucose normal (make sure you always check this in a patient with these symptoms)

23
Q

Why do these symptoms occur in diabetes insipidus?

A

AVP insufficiency (CDI) or resistance (NDI) → Impaired concentration of urine in renal collecting duct → Large volumes of hypotonic urine → Increase in plasma osmolality and sodium → Stimulation of osmoreceptors → Polydipsia due to thirst → Maintains circulating volume as long as patient has access to water

24
Q

What happens if a patient with diabetes insipidus does not quench their thirst?

A

They dehydrate and die

25
Q

What is psychogenic polydipsia

A

Similar presentation to diabetes insipidus with polydipsia, polyuria and nocturia however there is no issue with AVP, it is just that the patient drinks all the time so they pass large volumes of dilute urine

26
Q

Describe the pathophysiology of psychogenic polydipsia

A

Increased drinking (polydipsia) → Plasma osmolality falls → less AVP secreted by posterior pituitary → Large volumes of hypotonic urine → Plasma osmolality returns to normal

27
Q

What tests do we do to distinguish between diabetes insipidus and psychogenic polydipsia?

A

Water deprivation test

No access to anything to drink

Measure over time:

Urine volumes

Urine concentration (osmolality)

Plasma concentration (osmolality)

Weigh regularly

Stop test if lose >3% of body weight as this is a marker of significant dehydration which can occur in diabetes insipidus

28
Q

What are the results from this test that distinguish between psychogenic polydipsia and diabetes insipidus?

A

Psychogenic polydipsia - Slight decrease in max urine osmolality relative to normal, however it still increases ( and fairly significantly relative to pts with Diabetes Insipidus)

Diabetes insipidus - No increase in urine osmolality from start as there is an issue with AVP so there is no way of removing the water from urine and so it is hypotonic (very dilute)

29
Q

Do you expect to see a progressive increase in urine osmolality in a patient with diabetes insipidus during a water deprivation test?

A

No you would see a progressive increase in plasma osmolality as there is no way for them to concentrate their urine so the water leaves the plasma making the plasma more concentrated

30
Q

How do we distinguish between cranial and nephrogenic diabetes insipidus?

A

Give ddAVP which is a synthetic analogue to vasopressin

Cranial diabetes insipidus - Response to ddAVP is the urine will become concentrated (increased urine osmolality)

Nephrogenic diabetes insipidus - No increase in urine osmolality with ddAVP as kidneys cannot respond (no change to urine osmolality)

31
Q

How do you treat cranial diabetes insipidus?

A

Replace ADH by giving ddAVP (desmopressin)

Selective for V2 receptor (V1 receptor activation would be unhelpful)

Different preparations:

Tablets

Intranasal

32
Q

How do you treat nephrogenic diabetes insipidus?

A

Thiazide diuretics e.g. bendofluazide (Mechanism unclear)

33
Q

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

A

Too much ADH

34
Q

What are the symptoms in SIADH?

A

Reduced urine output

Water retention

35
Q

How would you describe the urine and plasma osmolality and sodium concentrations in SIADH?

A

High urine osmolality

Low plasma osmolality

Dilutional hyponatraemia

36
Q

What are the CNS related causes of SIADH?

A

Head injury, stroke and tumour

37
Q

What are the other causes of SIADH?

A

Pulmonary disease - Pneumonia, bronchiectasis

Malignancy - Lung cancer

Drug related - Carbamazepine, Serotonin Reuptake Inhibitors (SSRIs)

Idiopathic

38
Q

How would you manage a patient with SIADH?

A

Fluid restriction

Can use a vasopressin antagonist (vaptan) to bind to the V2 receptors in the kidney

Endocrinology (Sahil Notion) (3 decks)

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