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Y2 ENDOCRINOLOGY > Disorders of Vasopressin > Flashcards

Disorders of Vasopressin Flashcards

1
Q

The posterior pituitary is composed of what type of tissue and is anatomically continuous with what structure?

A

neural tissue, anatomically continuous with the hypothalamus

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2
Q

What type of neurons are found in the posterior pituitary and what do they contain?

A

Hypothalamic magnocellular neurons containing either oxytocin or AVP

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3
Q

describe the structure of the neurones in the posterior pituitary

A

long, originating in supraoptic and paraventricular nuclei. nuclei-stalk-posterior pituitary

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4
Q

What is the other name for vasopressin?

A

Anti-diuretic hormone (ADH)

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5
Q

What are the physiological actions of ADH/ vasopressin?

A

Stimulation of water reabsorption in the renal collecting duct to concentrate urine through the V2 receptor in the kidney. vasoconstrictor through V1 receptors, stimulates ACTH release from anterior pituitary.

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6
Q

How does Vasopressin concentrate urine?

A

AVP binds to V2 receptor in the collecting duct. this stimulates an intracellular cascade, promoting the movement of aquaporin-2 into the apical membrane. Water moves out of cell via aquaporin-3 on basolateral membrane into plasma creating more concentrated urine.

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7
Q

What happens when AVP binds to V2 receptors to promote aquaporin-2 movement into the apical membrane?

A

AVP binds to V2, a G-coupled receptor. the G protein unit binds with adenylate cyclase producing c-AMP which activates protein kinase A, protein kinase a causes transcription and insertion of aquaporin-2 into membrane.

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8
Q

How is the posterior pituitary visualised on an MRI?

A

visualized as a bright spot however not visualized in all healthy individuals so absence could be normal variation

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9
Q

what are the two types of stimulus for vasopressin release?

A

osmotic and non-osmotic

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10
Q

what is the osmotic stimuli for the release of vasopressin?

A

rise in plasma osmolality sensed by osmoreceptors

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11
Q

What structures are involved in the osmotic stimulation of vasopressin release?

A

Organum vasculosum and subfornical organ. both nuclei which sit around the 3rd ventricle.

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12
Q

what features of the organum vasculosum and subfornical organ aid them in the stimulation of vasopressin release?

A

are circumventricular, have no blood brain barrier so neurons can respond to changes in the systemic circulation. are highly vascularised. nuerones project to the supraoptic nucleus, the site of vasopressinergic neurons

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13
Q

Describe the process of the osmotic stimulation of vasopressin release

A

increase in extracellular Na+, causes water to move out of osmoreceptors. this causes osmoreceptor shrinkage resulting in increased osmoreceptor firing to supraoptic nuclei. AVP is released from hypothalamic neurons

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14
Q

what is the non-osmotic stimuli for vasopressin release?

A

decrease in atrial pressure sensed by stretch receptors

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15
Q

outline the process of non-osmotic stimulation of vasopressin release

A

atrial stretch receptors detect pressure in right atrium and act to inhibit vasopressin release via vagal afferents to hypothalamus causing a reduction in circulating volume. A lower pressure results in less inhibition of vasopressin release resulting in increased water resorption and vasoconstriction

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16
Q

why is vasopressin released following a haemorrhage? what other system will play an important role in control of BP?

A

to increase water reabsorption in the kidney and vasoconstriction. the renin-angiotensin system will also be important through detection via the juxtaglomerular apparatus.

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17
Q

Outline the physiological response to water deprivation

A

plasma osmolality increases causing stimulation of osmoreceptors. This causes the feeling of thirst and increases AVP release. Water reabsorption from the renal collecting ducts increases reducing the volume of urine but increasing the urine osmolality. This results in a reduction in plasma osmolality

18
Q

What is the foundational difference between diabetes insipidus and diabetes mellitus?

A

diabetes insipidus is due to an issue with vasopressin not insulin/glucose

19
Q

what is the cause of diabetes insipidus?

A

a problem with the hypothalamus and/or posterior pituitary resulting in the inability to make AVP

20
Q

what are the two types of diabetes insipidus?

A

Cranial diabetes insipidus - Vasopressin insufficiency. a problem with the hypothalamus or posterior pituitary so that AVP isnt produced. Nephrogenic diabetes insipidus - Vasopressin resistance. the kidneys are unable to respond to vasopressin

21
Q

what are the hallmark symptoms of diabetes insipidus?

A

polyuria, nocturia, polydipsia, thirst.

22
Q

is diabetes insipidus or diabetes mellitus more common?

A

diabetes mellitus

23
Q

is CDI or NDI more common?

A

CDI

24
Q

What are the causes of cranial diabetes insipidus?

A

Acquired: traumatic brain injury, pituitary surgery, pituitary tumours, metastasis to the pituitary gland, granulomatous inflammation of pituitary stalk, autoimmune.
congenital

25
Q

Is congenital or acquired CDI more common?

A

acquired, congenital causes are rare

26
Q

what are the causes of nephrogenic diabetes insipidus?

A

Congenital: mutation in gene encoding V2 receptors or aquaporin-2 channels. Acquired: drugs such as lithium

27
Q

How does diabetes insipidus present?

A

4 hallmark symptoms plus very dilute urine in large volumes. increased plasma concentration as patient becomes dehydrated. hypernatraemia, normal glucose

28
Q

what causes the symptoms of diabetes insipidus?

A

Problem with AVP impairs concentration of urine in renal collecting duct producing large volumes of hypotonic urine. This causes an increase in plasma osmolality resulting in stimulation of osmoreceptors, the feeling of thirst and polydipsia but circulation volume is maintained aslong as the patient has access to water

29
Q

how much water does a patient with diabetes insipidus need per day to maintain circulation volume?

A

Around 6-8 hours per day

30
Q

Why is it important in clinical practice to distinguish between DM and DI?

A

if diabetes insipidus patients are given nil by mouth they could become dehydrated and die

31
Q

What is psychogenic polydipsia?

A

similar presentation to diabetes insipidus however no problem with AVP, problem is that the patient drinks too much so passes large volumes of dilute urine

32
Q

What tests can be done to differentiate between DM and DI?

A

Blood tests such as random glucose test (11.1< and symptoms is DM), fasting glucose test (7< is a DM), HbA1c - taken over three months however if has SCA may be inaccurate. serum sodium test to show blood osmolality, sodium will be high in DI.

33
Q

How do we distinguish between DI and psychogenic polydipsia?

A

Water deprivation test - measures urine osmolality over hours of water deprivation

34
Q

What is seen in the water deprivation test of a healthy person/ psychogenic polydipsia compared to someone with DI?

A

when deprived of water the urine volume of a healthy individual would decrease and urine osmolality would increase. In someone with DI urine osmolality will increase but not to the standard reference range

35
Q

Why is weight monitored in the water deprivation test?

A

if the test patient loses more than 3% body weight the test must be stopped as this can be a marker of significant dehydration which can occur during diabetes insipidus

36
Q

How do we use the water deprivation test to distinguish between CDI and NDI?

A

Give ddAVP, this will work like vasopressin therefore if there is an increase in urine osmolality this confirms cranial diabetes insipidus as the kidneys are able to respond and increase urine concentration

37
Q

What happens to plasma osmolality during the water deprivation test in someone with DI compared to psychogenic polydipsia?

A

plasma osmolality increases in someone with DI, but decreases in a patient with psychogenic polydipsia

38
Q

How is CDI (vasopressin insufficiency) treated?

A

desmopressin, selective for V2 receptors

39
Q

How is NDI (vasopressin resistance) treated?

A

Difficult to treat, prescribe thiazide diuretics

40
Q

What is Syndrome of Inappropriate ADH (SIADH)?

A

Too much vasopressin reducing urine output and retaining water. this results in high urine osmolality, low plasma osmolality and dilutional hyponatraemia

41
Q

What are the causes of SIADH?

A

head injury, stroke, tumour, pneumonia, lung cancer, SSSRIs or idiopathic

42
Q

How is SIADH managed?

A

Fluid restriction, vasopressin antagonists - vaptan, binds to V2 receptors

Y2 ENDOCRINOLOGY (13 decks)

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