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Z YEAR 2 BRS ENDO > Disorders of Vasporessin > Flashcards

Disorders of Vasporessin Flashcards

1
Q

What is the posterior pituitary anatomically continuous with?

A

hypothalamus

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2
Q

Where do the hypothalamic magnocellular neurons containing AVP or oxytocin originate?

A
  • in supraoptic and paraventricular hypothalamic nuclei

- nuclei to stalk to posterior pituitary

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3
Q

What is the other name for vasopressin?

A

ADH

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4
Q

What is diuresis?

A

Production of urine

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5
Q

How does vasopressin act in the kidney? What receptor does it work through?

A
  1. Stimulate water reabsorption in renal collecting duct (concentrates urine)
  2. Through V2 receptor in kidney
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6
Q

What else does vasopressin do? What receptor does it use?

A
  1. Vasoconstriction via V1 receptor

2. Stimulate ACTH release from anterior pituitary

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7
Q

How can you find the posterior pituitary on a MRI?

A

‘bright spot’ (not all do)

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8
Q

What causes vasopressin to be released is an osmotic way?

A

Rise in plasma osmolality sensed by osmoreceptors

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9
Q

What causes vasopressin to be released is a non-osmotic way?

A

Decrease in atrial pressure sensed by atrial stretch receptors

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10
Q

What is the organum vasculosum + subfornical organ?

A

nuclei which sit around the 3rd ventricle (‘circumventricular’)

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11
Q

Why can the neurons respond to changes in the systemic circulation?

A
  • no blood brain barrier
  • Highly vascularised
  • neurons project to the supraoptic nucleus - site of vasopressinergic neurons
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12
Q

What is the non-stimulation of vasopressin release?

A
  1. Atrial stretch receptors detect pressure in the right atrium
  2. Inhibit vasopressin release via vagal afferents to hypothalamus
  3. Reduction in circulating volume eg haemorrhage means less stretch of these atrial receptors, so less inhibition of vasopressin
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13
Q

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

A
  1. Vasopressin release (less inhibition) results in increased water reabsorption in the kidney (some restoration of circulating volume) V2 receptors
  2. vasoconstriction via V1 receptors
    • (NB renin-aldo system will also be important, sensed by JG apparatus)
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14
Q

What is the physiological response to water deprivation?

A
  1. Increased plasma osmolarity
  2. Stimulation of osmoreceptors
  3. Thirst / increased AVP release
  4. increase AVP release goes to increase water reabsorption from renal collecting duct
  5. Reduced urine volume, increase in urine osmolarity
  6. Reduction in plasma osmolarity
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15
Q

What are symptoms of diabetes insipidus/mellitus?

A
  • Polyuria
  • Nocturia
  • Thirst – often extreme
  • Polydispia
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16
Q

What are these symptoms due to in diabetes mellitus?

A

due to osmotic diuresis

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17
Q

What are these symptoms due to in diabetes insipidus?

A

due to a problem with arginine vasopressin

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18
Q

What are the two types of diabetes inspidus?

A
  • Cranial

- Nephrogenic

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19
Q

What happens in cranial diabetes insipidus?

A
  • Problem with hypothalamus + posterior pituitary

* Unable to make arginine vasopressin

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20
Q

What happens in nephrogenic diabetes insipidus?

A
  • Can make arginine vasopressin (normal hypothalamus + posterior pituitary)
  • Kidney (collecting duct) unable to respond to it
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21
Q

What are the acquired causes of cranial diabetes insipidus?

A
  1. Traumatic brain injury
  2. Pituitary surgery
  3. Pituitary tumours
  4. Metastasis to the pituitary gland eg breast
  5. Granulomatous infiltration of pituitary stalk eg TB, sarcoidosis
  6. Autoimmune
22
Q

What are the congenital causes of cranial diabetes insipidus?

A

rare

23
Q

What are the congenital causes of nephrogenic diabetes inspidus?

A

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

24
Q

What are the acquired causes of nephrogenic diabetes inspidus?

A

drugs e.g. lithium

25
Q

What is the urine like in diabetes insipidus?

A
  • Very dilute (hypo -osmolar)

* Large volumes

26
Q

What is the plasma like in diabetes insipidus?

A
  1. Increased concentration (hyper-osmolar) as patient becomes dehydrated
  2. Increased sodium (hypernatraemia)
  3. Glucose normal (make sure you ALWAYS check this in a patient with these symptoms)
27
Q

What is psychogentic polydipsia?

A
  • Mimic symptoms of diabetes inspidus
  • No problem with arginine vasopressin tho
  • Problem is that the patient drinks all the time, so passes large volumes of dilute urine
28
Q

How do you distinguish between diabetes insipidus and psychogenic polydipsia?

A

Water deprivation test

29
Q

What happens in a water deprivation test? What do you measure?

A
  • No access to anything to drink
  • Over time, measure
  • Urine volumes
  • Urine concentration (osmolality)
  • Plasma concentration (osmolality)
30
Q

Why do you need to weigh someone regularly during water deprivation test?

A

stop test if lose >3% body weight (a marker of significant dehydration which can occur in diabetes insipidus)

31
Q

How to distinguish between cranial and nephrogenic diabetes insipidus?

A
  • Give ddAVP

* This will work ‘like’ vasopressin

32
Q

Which one responds to ddAVP?

A
  1. Cranial diabetes insipidus – response to ddAVP – urine concentrates
  2. Nephrogenic diabetes insipidus – no increase in urine osmolality with ddAVP, as kidneys can’t respond
33
Q

How do you treat cranial DI?

A

-replace vasopressin
•Desmopressin
•Selective for V2 receptor (V1 receptor activation would be unhelpful)

34
Q

What are two forms of desmopressin?

A
  • Tablets

* Intranasal

35
Q

How do you treat nephrogenic DI?

A
  • very rare – difficult to treat successfully
  • Thiazide diuretics eg bendofluazide
  • Paradoxical! Mechanism unclear
36
Q

What happens in Syndrome of Inappropriate Anti-Diuretic Hormone (SIADH)?

A
  • Too much arginine vasopressin
  • Reduced urine output
  • Water retention
37
Q

What happens to levels in SIADH?

A
  • High urine osmolality
  • Low plasma osmolality
  • Dilutional hyponatraemia (low sodium_
38
Q

What is a CNS cause of SIADH?

A

Head injury, stroke, tumour,

39
Q

What is a pulmonary disease cause of SIADH?

A

Pneumonia, bronchiectasis

40
Q

What is a malignancy cause of SIADH?

A

Lung cancer (small cell)

41
Q

What is a drug related cause of SIADH? Or other causes?

A
  • Carbamazepine, Serotonin Reuptake Inhibitors (SSSRIs)

- Idiopathic

42
Q

How does vasopressin concentrate urine?

A
  1. AVP travels in blood supply to collecting duct and binds to V2 receptor
  2. This triggers intracellular signalling cascade
  3. Results in migration of aquaporin 2 to apical membrane of collecting duct 4. allow passage of water through aqauporin channel back across collecting duct cells, out through aquaporin-3 channels and into the plasma
43
Q

How do osmoreceptors regulate vasopressin?

A
  1. Osmo-receptors around 3rd ventricle are sensitive to change in systemic circulation
  2. Increase in extracellular Na+ ,senses this as water flows out of osomoreceptor, it shrinks
  3. By changing shape the osmoreceptor fires more AP and this stimulate AVP release from hypothalamic neurones in supraoptic nucleus and paraventicular nucleus
44
Q

Why do. the symptoms occur in diabetes insipidus?

A
  1. Increased plasma osmolarity
  2. Stimulation of osmoreceptors
  3. Thirst / increased AVP release
  4. increase AVP release goes to increase water reabsorption from renal collecting duct
  5. Reduced urine volume, increase in urine osmolarity
  6. Reduction in plasma osmolarity
45
Q

Why do the symptoms occur in diabetes insipidus?

A
  1. AVP problem (not enough in CDI) or (not responding NDI)
  2. Impaired concentration of urine in renal collecting duct
  3. Large volume of dilute (hypotonic) urine
  4. increase in plasma osmolarity (and sodium)
  5. Stimulation of osmorecpetors
  6. Thirst polydispsia
  7. Maintains circulating volume as long as patient has access to water
46
Q

How does diabetes a cause of death?

A
  1. AVP problem (not enough in CDI) or (not responding NDI)
  2. Impaired concentration of urine in renal collecting duct
  3. Large volume of dilute (hypotonic) urine
  4. increase in plasma osmolarity (and sodium)
  5. Stimulation of osmorecpetors
  6. Thirst polydispsia
  7. No accèss to water leads to dehydration and death
47
Q

What happens in psychogenic polydipsia?

A
  1. increased drinking (polydipsia)
  2. Plasma osmolality falls
  3. Less AVP secreted by posterior pituitary
  4. Large volumes of dilute (Hypotonic) urine
  5. plasma osmolarity returns to normal
48
Q

What happens to a patient with diabetes insipidus during a water deprivation test?

A

Progressive increase in plasma osmolality

49
Q

What is your plasma osmolality is diabetes insipidus?

A

Increase (290)

50
Q

What is your plasma osmolality is psychogenic polydipsia?

A

Decrease (270)

51
Q

What is the management of SIADH?

A
  1. Commonest cause of prolonged hospital stay
  2. Fluid restrict
  3. Can use vasopressin antagonist (captain) - binds. to V2 receptors. on kidney (££££)

Z YEAR 2 BRS ENDO (13 decks)

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