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Year 2 Endo > Disorders of Vasopressin > Flashcards

Disorders of Vasopressin Flashcards

1
Q

What two hormones does the posterior pituitary produce?

A

AVP and Oxytocin

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2
Q

What is the relationship between the hypothalamus and p. pituitary?

A

Anatomically continuous with the hypothalamus

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3
Q

What connects the hypothalamus and p. pituitary?

A

supraoptic and paraventricular hypothalamic nuclei that stalk (long axons)

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4
Q

What does diuresis means?

A

Production of urine

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5
Q

What is the main physiological action of Vasopressin?

A

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

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6
Q

What does Vasopressin act via?

A

V2 receptor

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7
Q

How does AVP concentrate urine?

A

AVP binds to V2 receptor
Triggers intracellular signalling cascade
Results in migration of aquaporin 2 to the apical membrane of the collecting duct
Allows passage of water from tubular lumen (aquaporin 2) back to bloodstream via aquaporin 3

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8
Q

How does the posterior pituitary look on a MRI?

A

‘bright spot’

not visualised in all healthy individuals

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9
Q

What does AVP stimulate?

A

ACTH stimulation

We don’t really know why

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10
Q

What 2 things stimulate vasopressin release?

A

Osmotic
- rise in plasm osmolality sensed by osmoreceptors
Non-Osmotic
- decrease in atrial pressure sensed by atrial sense receptors

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11
Q

What are the special types of nuclei that sit around the 3rd ventricle?

A

Organum vasculosum & subfornical organ

both nuclei which sit around the 3rd ventricle (‘circumventricular’)
no blood brain barrier – so neurons can respond to changes in the systemic circulation
highly vascularised

neurons project to the supraoptic nucleus - site of vasopressinergic neurons

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12
Q

How do osmoreceptors regulate vasporessoin?

A

Increase in extracellular sodium

Osmoreceptor around 3rd ventricle senses this change

Senses this because of the change in conc. gradient water flows out of the osmoreceptor causing it to change shape

The change in shape results in increased osmoreceptor firing

Causes AVP release from hypothalamic neurones

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13
Q

How is vasopressin stimulates non-osmotically?

A

Detect pressure in right atrium

Inhibit vasopressin release via vagal afferents to hypothalamus

Reduction in circulating volume e.g. haemorrhage

Less stretch of the atrial receptors so less inhibition of vasopressin

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14
Q

Why is AVP important following haemorrhage?

A

Via V2 receptor increased water reabsorption increased circulating volume

Via V1 receptor AVP is a vasoconstrictor

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15
Q

What is the physiological response to water deprivation?

A

Increased plasma osmolality

Stimulation of osmoreceptors

Causes thirst and increased AVP release

AVP causes increased water reabsorption from renal collecting ducts

Reduces urine volume, increase in urine osmolality

Reduction of plasma osmolality

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16
Q

What are symptoms of diabetes insipidus?

A

Polyuria
Nocturia
Thirst- often extreme
Polydipsia

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17
Q

What causes diabetes insipidus?

A

A problem with arginine vasopressin

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18
Q

What causes these symptoms in diabetes mellitus?

A

Osmotic diuresis

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19
Q

Which form of diabetes is more common?

A

Diabetes mellitus

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20
Q

What are the two forms of diabetes insipidus?

A

Cranial (central) diabetes

Nephrogenic diabetes insipidus

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21
Q

What is cranial diabetes insipidus?

A

Problem with hypothalamus and or posterior pituitary

Unable to make AVP

22
Q

What are the causes of cranial diabetes insidious?

A 
Traumatic brain injury
Pituitary surgery
Pituitary tumours
Metastasis
Granulomatous infiltration of pituitary stalk e.g. TB, sarcoidosis 
Autoimmune
23
Q

What are the causes of nephrogenic diabetes insipidus?

A

Congenital
rare (e.g. mutation in gene encoding V2 receptor)

Acquired
Drugs (e.g. lithium)

24
Q

What happens to urine in D.I?

A 
Very dilute (hypo-osmolar)
Large volumes
25
Q

What happens to plasma in D.I?

A

Increased concentration (hyper-osmolar) as patient becomes dehydrated

Increased sodium (hypernatraemia)

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

26
Q

Why do these symptoms occur in D.I?

A

Not enough/Not responding AVP

Impaired conc. of urine in renal collecting duct

Large volumes of dilute urine

Increase in plasma osmolality (and sodium)

Stimulation of osmoreceptors

Thirst

Maintains circulating volume as long as patient has access to water

27
Q

What causes nephrogenic diabetes insipidus?

A

Can make AVP

Collecting duct unable to respond to it

28
Q

How can D.I cause death?

A

No access to water
Dehydration
Death

29
Q

What is psychogenic poludipsia?

A

Similar presentation to diabetes insipidus

Polyuria
Nocturia

No problem with arginine vasopressin

Problem is that they drink too much

Dilute plasma conc.

Less AVP secreted

Large volumes of dilute urine

Plasma osmolality returns to normal

30
Q

How do you distinguish between D.I and psychogenic polydipsia?

A

Water deprecation test

No access to anything to drink

31
Q

What do you measure during a water deprivation test?

A

Urine volumes
Urine concentration
Plasma concentration

Weigh regularly stop test if they loose more than 3% of body weight

32
Q

How would someone with psychogenic polydipsia perform on a water deprivation test?

A

With time you can increase your urine osmolality (making it more concentrated)

33
Q

How would someone with D.I perform on a water deprivation test?

A

Not matter how long they are in the room they cannot concentrate their urine

34
Q

How do we distinguish between cranial and nephrogenic diabetes insipidus?

A

At end of water deprivation test

Give ddAVP (synthetic AVP)

Cranial D.I will respond to this and urin concentrates

Nephrogenic D.I there will be no increase in urine osmolality

35
Q

How do you treat Cranial DI?

A

Replace

Desmopressin

Selective for V2 receptor

Nasal spray or tablet

36
Q

How do you treat Nephrogenic DI?

A

Luckily very rare

Thiazide diuretic e.g. bendofluazide

or NSAIDS

Paradoxical, mechanism nuclear

37
Q

What is SIADH?

A

Syndrome of Inappropriate Anti-Diuretic Hormone

More common than DI

38
Q

What happens in SIADH?

A

Too much vasopressin

Reduces urin output

Water retention

High urine osmolality

Low plasma osmolality

Dilutional hyponatraemia

39
Q

What causes SIADH?

A 
CNS: head injury, stoke, tumour
Pulmonary disease: pneumonia, bronchiectasis
Malignancy: Lung cancer (small cell)
Drug-related: Carbamazepine, serotonin
Idiopathic
40
Q

How is SIADH managed?

A

Common cause prolonged hospital stay

Fluid restrict

Can uses vasopressin antagonist (vaptan)
Prevent binding to V2 receptors in the kidney
Very Expensive ££££
Not prescribed often

41
Q

Why do we monitor weight during the water deprivation test?

A

If they do have DI it is important to allow them to drink water or else they can become extremely dehydrated as they have no way to concentrate their urine and will continue to pass large volumes, loosing a great deal of water.

42
Q

What would be the response to water deprivation in a healthy person?

A

Urine volumes will decrease with time

Osmolality will increase with time and urine will become more concentrated

AVP preserves plasma osmolality

43
Q

Why is desmopressin nasal spray potentially better than a tablet?

A

Acid in stomach reduces biological effect of peptides

Nose is highly vascularised

44
Q

What are signs of hypovolaemia?

A 
Tachycardia
Reduced skin turgor
Low urine sodium
Low BP
Dry membranes
45
Q

How do you treat hyponatraemia?

A

Fluid restrict

46
Q

What causes hypervolaemia?

A

HF
Cirrhosis
Nephrotic sydnrome

47
Q

What are signs of hypervolaemia?

A

Peripheral oedema
Lung crackles
Raised JVP

48
Q

What happens if you give too much saline too quickly?

A

Central pontine myelionylysis

Quadruplegia, pseudobulbar palsy

49
Q

What do give in severe hyponatraemia? Reduced GCS

A

IV Saline 3%

50
Q

What causes hypernatremia?

A 
Cushing's
Conn's
Iatrogenic
Sweating
GI loses

Year 2 Endo (15 decks)

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