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Y2 BRS (Haroop) > Disorders of vasopressin > Flashcards

Disorders of vasopressin Flashcards

1
Q

Which hypothalamic neurones secrete AVP and oxytocin?

A

Hypothalamic magnocellular neurones

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2
Q

Which part of the pituitary gland secretes AVP and oxytocin?

A

Posterior pituitary gland

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3
Q

Which pituitary gland is anatomically continuous with the hypothalamus?

A

Posterior pituitary gland

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4
Q

Which hormones are secreted by the neurohypophysis?

A

Vasopressin

Oxytocin

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5
Q

Which hypothalamic nuclei contain the magnocellular neurone cell bodies?

A

Supraoptic and paraventricular nuclei

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6
Q

What is the main physiological action of vasopressin?

A

Stimulation of water reabsorption in the renal collecting duct.
-Concentrates urine

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7
Q

Which renal receptors are responsive to vasopressin?

A

V2 receptor

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8
Q

Which receptors are responsive to vasopressin induced vasocontriction?

A

V1 receptors

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9
Q

Stimulation of V1 receptors results in what action?

A

Vasoconstriction

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10
Q

Which hormone is released in response to vasopressin from the pituitary gland?

A

ACTH

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11
Q

Which protein channels are embedded on the apical membrane of renal tubule cells, facilitating the movement of water molecules?

A

Aquaporin-2

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12
Q

What response is induced by AVP-V2 stimulation?

A

G-protein coupled response, formation of a secondary messenger.

  • Adenylate cyclase activity elevates cAMP concentration and protein kinase A.
  • Migration and synthesis of aquaporin-2 channels to apical membrane.
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13
Q

Which aquaporin channels are embedded on the basolateral membrane?

A

Aquaporin-3

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14
Q

How is the posterior pituitary gland identified on a pituitary MRI?

A

Bright spot

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15
Q

What are two main stimuli that stimulates vasopressin release?

A

Osmotic: Rise in plasma osmolarity sensed by osmoreceptors.

Non-osmotic: Decreases atrial pressure sensed by atrial stretch receptors

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16
Q

Which receptors respond to non-osmotic changes?

A

Atrial stretch receptors

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17
Q

Which circumventricular nuclei respond to changes in systemic circulation and thus stimulate vasopressin release?

A

Organ vasculosum

Subfornical organ

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18
Q

Where are the organ vasculosum and subfornical organs located?

A

Reside around the 3rd ventricle (circumventricular)

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19
Q

How can the circumventricular nuclei detect immediate changes to systemic circulation?

A

There is no blood-brain barrier and are highly vascularised structures

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20
Q

Which hypothalamic structure communicates with projections of the organum vasculosum and subfornical organ?

A

Supraoptic nucleus

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21
Q

Which hypothalamic nucleus contains vasopressinergic neurones?

A

Supraoptic nucleus

22
Q

What type of receptors are sensitive to plasma osmolarity?

A

Osmoreceptors

23
Q

How do osmoreceptors detect changes in plasma osmolarity?

A

There is an increase in extracellular sodium

  • This alters the water potential of the plasma
  • Water flows from the osmoreceptor to the plasma
  • Osmoreceptor shrinks
  • Increased osmoreceptor firing
  • AVP release from magnocellular hypothalamic neurones of the supraoptic nucleus
24
Q

What happens to the structural shape of osmoreceptors in response to an increase plasma osmolarity?

A

Osmoreceptors shrink

25
Q

Where are atrial stretch receptors predominantly fonud?

A

Within the right atrium

26
Q

Stimulation of atrial stretch receptors result in what?

A

Inhibit vasopressin release

Vagal afferents to the hypothalamus

27
Q

How does a haemorrhage result in vasopressin release?

A

The circulating volume decreases, leading to hypovolemia, this subsequently leads to less stretch and stimulation of atrial receptors, therefore this reduces inhibition of vasopressin - leading to vasopressin release (Increased water reabsorption) and vasoconstriction via v1 receptors.

28
Q

What is the impact on plasma osmolarity in individuals with water deprivation?

A

Increased plasma osmolarity

29
Q

What are the physiological responses to water deprivation?

A

Increased thirst and released AVP (Reduces plasma osmolarity through increased water reabsorption.

30
Q

What are the osmotic symptoms associated with diabetes?

A

Polyuria
Nocturia
Thirst- often extreme
Polydypsia

31
Q

What is osmotic diuresis?

A

Hyperglycaemia increases water retention within the urine, leading to decreased water reabsorption

32
Q

What pathology is associated with diabetes insipidus?

A

Issue with arginine vasopressin.

33
Q

What are the two types of of diabetes insipidus?

A
  • Cranial (central) diabetes insipidus

- Nephrogenic diabetes insipidus

34
Q

What is central diabetes insipidus?

A

Problem concerned with hypothalamus/posterior pituitary gland
There is an insufficient secretion of arginine vasopressin.

35
Q

What is nephrogenic diabetes inspidus?

A

Arginine vasopressin production is normal from the posterior pituitary gland and hypothalamus

The collecting duct is unable to respond to AVP.

36
Q

What are the common causes of cranial diabetes inspidus?

A

Acquired:

  • Traumatic brain injury
  • Pituitary surgery
  • Pituitary tumours
  • Metastasis to the pituitary gland (breast)
  • Granulomatous infiltration of pituitary stalk: TB, sarcoidosis (Accumulation of inflammatory cells)
  • Autoimmune
37
Q

What are the common causes of nephrogenic diabetes?

A

Mutation encoding V2 receptor, aquaporin 2 type water channel.

Lithium drugs

38
Q

Which types of drugs are concerned with causing nephrogenic diabetes inspidus?

A

Lithium

39
Q

What are the symptoms of diabetes insipidus?

A 
Polyuria
Nocturia
Thirst
Polydypsia 
Hypo-osmolar urine (and in large volumes)

Hyper-osmolar plasma
-Hypernatremia

Glucose is normal (HbA1c)

40
Q

What is psychogenic polydypsia?

A

Polydipsia is excessive or abnormal thirst, accompanied by intake of excessive quantities of water or fluid. Psychogenic polydipsia (PPD), or primary polydipsia, is characterised by excessive volitional water intake and is often seen in patients with severe mental illness and/or developmental disability.

41
Q

What test can be conducted to distinguish between diabetes insipidus and psychogenic polydipsia?

A

Water deprivation test

42
Q

In patients with diabetes insipidus, what are the likely results of the water deprivation test?

A

There is no increase in urine osmolarity (AVP is suppressed)

43
Q

At what parameter should the water deprivation test be stopped?

A

If there is a loss of 3% body weight (marker of dehydration)

44
Q

How is central diabetes insipidus distinguished from nephrogenic diabetes?

A 
Administer ddAVP (behaving like vasopressin)
-in central diabetes, ddAVP will interact with V2 receptors facilitating water reabsorption and leading to a significant increase in urine osmolarity

This is unresponsive in nephrogenic diabetes

45
Q

What is the treatment for diabetes insipidus?

A

Desmopressin to replace vasopressin
Selective v2 receptor
(Tablets, intranasal)

46
Q

What is the available treatment for nephrogenic diabetes insipidus?

A

Thiazide diuretics

47
Q

Which disorder is associated with an increase in AVP?

A

Syndrome of inappropriate ADH

48
Q

What are the features of SIADH?

A 
Reduced urine output
Water retention 
high urine osmolarity 
Low plasma osmolarity 
Dilutional hyponatremia
49
Q

What are the causes of SIADH?

A

CNS
-Head injury, stroke, tumour

Pulmonary disease
-Pneumonia, bronchiectasis

Malignancy
-Lung cancer

Drug related
-Carbazepine, serotonin reuptake inhibitors

Idiopathic

50
Q

What is the available management for SIADH?

A

Vaptan (Vasopressin antagonist), binds to V2 renal receptors.

Fluid restrict

Y2 BRS (Haroop) (62 decks)

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