Disorders of Vasopressin Flashcards

1
Q

What is the role of ADH?

A

Stimulate water reabsorption in the renal collecting duct

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2
Q

Distinguish between V1 & V2 receptors

A

V1 receptors have a role in vasoconstriction
V2 receptors are present on the basolateral membrane of the CD to concentrate the urine and promote water reabsorption

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3
Q

What are the 2 stimuli fro vasopressin release?

A

Osmotic - osmoreceptors detect rise in plasma osmolarity
Non-osmotic - atrial stretch receptors sense a decrease in atrial pressure

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4
Q

Describe the osmotic release of vasopressin

A

Organum vasculosum and subfornical organ sit around the 3rd ventricle; the axons project into the supraoptic nuclei, where vasopressinergic neurones are found; there is no blood brain barrier so neurones can respond to changes in systemic circulation.

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5
Q

Explain the functioning of osmoreceptors

A

Osmosreceptors detect a rise in extracellular Na+, thus water leaves the osmoreceptors causing shrinking and AVP is released stimulating water reabsorption

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6
Q

How do atrial stretch receptors work?

A

They detect pressure changes in the right atrium. When circulating blood volume decreases e.g. in haemorrhage, there is less stretch of the receptors so less inhibition of AVP and so it’s released

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7
Q

What are the main symptoms of diabetes inspidus?

A

Polydispia
Nocturia
Polyuria
Thirst

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8
Q

Distinguish between the 2 types of diabetes insipidus

A

Cranial/Central/Vasopressin Insufficiency - where there is an absence of AVP due to issues with the hypothalamus or posterior pituitary gland
Nephrogenic - when there is resistance to AVP, it’s produced but V2 receptors are not responsive

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9
Q

Causes of cranial DI

A

Metastasis from another organ i.e. breast
Pituitary tumour
Pituitary surgery
Autoimmune
Brain trauma
Granulomatous infiltration of infundibulum
Congential - rarer

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10
Q

Causes of Nephrogenic DI

A

Congenital - mutations in V2 receptor gene or aquaporin 2 channel
Acquired - drugs like lithium

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11
Q

What are some presentations of DI?

A

Hypernatraemia
Very dilute urine
Hyper-osmolar blood thus dehydrated
Glucose is normal

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12
Q

What is psychogenic polydipsia

A

Similar presentations to DI but there are no issues with AVP
The issue is that the patient drinks excessive water
It’s psychological

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13
Q

How to distinguish between psychogenic polydipsia and DI?

A

Water deprivation test - measure urine volume and conc. of urine and plasma
Weigh regularly and if body weight drops by more than 3% it indicates DI
In DI the patient is also unable to concentrate their urine

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14
Q

What is ddAVP?

A

Desmopressin - synthetic AVP

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15
Q

How to distinguish between cranial and nephrogenic DI?

A

Following administration of desmopressin:
Cranial - urine concentrates
Nephrogenic - urine doesn’t concentrate as kidneys cannot respond

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16
Q

Outline the treatment of cranial DI

A

Desmopressin administered - selective for V2
Given orally or intranasally
Patients should be kept hydrated or they can die

17
Q

Outline the treatment of nephrogenic DI

A

Difficult to treat but can give thiazide diuretics e.g. bendofluazide

18
Q

What is SIADH & what are the presentations?

A

Syndrome of inappropriate ADH
Presents with low volume and high conc. urine
Low osmolality plasma
Hyponatraemia
Increased water retention

19
Q

Causes of SIADH?

A

Malignancy - lung cancer
CNS - brain trauma, tumour, stroke
Pulmonary - pneumonia
Drug related - SSRI & epilepsy medication
Idiopathic

20
Q

Treatment of SIADH?

A

Vaptan - a vasopressin antagonist, binds to V2 receptors
Restrict Fluid