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BRS 1b > 3.3 Disorders of Vasopressin > Flashcards

3.3 Disorders of Vasopressin Flashcards

1
Q

Why do you get polyuria, nocturia, and polydipsia in diabetes mellitus?

A
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2
Q

What is vasopressin also known as?

A

Anti-diuretic hormone

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3
Q

What is diuresis?

A

production of urine

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4
Q

What are the main physiological actions of vasopressin?

A

Stimulation of water reabsorption in the renal collecting duct via the V2 receptors in the kidney (this concentrates urine)

Vasoconstriction via the V1 receptor

Stimulates ACTH release from anterior pituitary (* main stimulus of ACTH release from anterior pituitary is CRH, which is hypothalamic factor)

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5
Q

What organ is the posterior pituitary anatomically continuous with?

A

Hypothalamus

*Neuronal cell bodies cluster together in the hypothalamus forming the nuclei, the stalk of these neurones flow down the hypothalamus into the posterior pituitary.

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6
Q

How does the posterior pituitary differentiate from the anterior pituitary?

A

The posterior pituitary is made up of neural tissue

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7
Q

What hormones are released from the posterior pituitary?

A

Arginine Vasopressin - AVP

Oxytocin

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8
Q

How does vasopressin concentrate urine?

A

Vasopressin in the plasma
Crosses the basolateral membrane
Binds to V2 receptor
Results in intracellular signalling cascade (G protein, Adenylate cyclase, cAMP, protein kinase A)
which results in the insertion of aquaporin-2 (water channels) on the tubular luminal membrane .
This results in increased water uptake from the tubular lumen across the concentration gradient, then out aquaporin 3 channels into the plasma.

NET = more reabsorption of water from the urine into the blood stream

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9
Q

How can we spot the posterior pituitary on MRI?

A

Posterior pituitary bright spot (on sagittal section MRI)

Not visualised in all healthy individuals

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10
Q

What are the two types of stimuli for vasopressin release?

A

osmotic and non osmotic

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11
Q

What is the osmotic stimulus which results in vasopressin release, and how is it detected?

A

Increase in concentration of plasma (increase in plasma osmolarity)
This is detected by osmoreceptors

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12
Q

What is the non - osmotic stimulus which results in vasopressin release, and how is it detected?

A

Decrease in atrial pressure

Detected by atrial stretch receptors

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13
Q

What two tissues sense plasma osmolarity?

A

Organum vasculosum

Subfornical organ

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14
Q

What are the organum vasculosum and the subfornical organ?

A

nuclei which sit around the 3rd ventricle (circumventricular)
neurons project to the supraoptic nucleus - site of vassopressinergic neurons
sense and respond to changes in plasma osmolarity

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15
Q

What is the systemic circulation?

A

The circuit of vessels which provides functional blood supply to all body tissue.

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16
Q

Why can the organum vasculosum and subfornical organ responsed to changes in the systemic circulation?

A

Because they don’t have a blood brain barrier and are highly vascular.
- can talk directly to vasopressinergic neurons

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17
Q

How do osmoreceptors regulate vasopressin

A

e.g an increase in extracellular Na+
This would cause water to exit the osmoreceptor cell
The osmoreceptor would therefore shrink
Which increases osmoreceptor firing
Resulting in AVP release from hypothalamic neurones and supraoptic nucleus

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18
Q

What do atrial stretch receptors do?

A

Detect pressure in the right atrium

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19
Q

How do atrial stretch receptors affect vasopressin release?

A

Inhibit vasopressin release via vagal afferents to hypothalamus

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20
Q

Why is vasopressin released following a haemorrhage?

A

Reduction in circulating volume means less stretch of the atrial receptors, so less inhibition of vasopressin.

Vasopressin release results in increased water in the kidneys via V2 receptors (some restoration of blood volume)

Vasoconstriction caused via V1 receptors (tightening up of vasculature helps increase blood pressure)

*renin-aldo system will also be important, sensed by JG apparatus and other hormones also released

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21
Q

What is the physiological response to water deprivation? (6)

A
  1. Increased plasma omsolarity (concentration inc.)
  2. Stimulation of osmoreceptors
  3. Increased AVP release (+thirst)
  4. Increased water reabsorption from collecting duct
  5. Reduced urine volume, increase in urine osmolarity
  6. Reduction in plasma osmolarity
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22
Q

What are the clinical symptoms are diabetes insipidus?

A

Polyuria - excessive peeing
Nocturia - having to wake up in the night to pee
Thirst - often extreme
Polydipsia - thirst

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23
Q

What is the most common cause of polyuria, nocturia, and polydipsia?

A

Diabetes mellitus - diabetes insipidus is much more rare

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24
Q

Why do you get polyuria, nocturia, and polydipsia in diabetes insipidus?

A

due to problems with arginine vasopressin

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25
Q

Why do you get polyuria, nocturia, and polydipsia in diabetes mellitus?

A

due to osmotic diuresis
hyperglycaemia (>10mmol/L)
kidneys cannot reabsorb any more glucose
glucose spill out into urine dragging water with it

26
Q

What are the two types of diabetes insipidus?

A

cranial (central) diabetes insipidus

nephrogenic diabetes insipidus

27
Q

What is the difference between the two types of diabetes insipidus?

A

cranial diabetes insipidus - vasopressin insufficiency

nephrogenic diabetes insipidus - vasopressin resistance

28
Q

What is crainial diabetes insipidus?

A

Problems with hypothalamus and/or posterior pituitary –> unable to make arginine vasopressin

29
Q

What is nephrogenic diabetes insipidus?

A

Kidney (collecting duct) unable to respond to arginine vasopressin

However normal hypothalamus and posterior pituitary - can make arginine vasopressin

30
Q

What are some acquired causes of cranial diabetes insipidus?

A

traumatic brain injury
pituitary surgery
pituitary tumours
metastasis to the pituitary from other cancer
granulomatous infiltration of pituitary stalk e.g. TB, sarcoidosis (thickened stalk)
autoimmune

31
Q

Which type of diabetes insipidus is more common?

A

Cranial diabetes insipidus

32
Q

What type of cause is more common, in both cranial and nephrogenic diabetes insipidus?

33
Q

What is an acquired cause of nephrogenic diabetes insipidus?

A

drugs (e.g. lithium)

34
Q

What is a mutation that can result in congenital nephrogenic diabetes insipidus?

A

mutation in gene encoding V2 receptor, aquaporin 2 type water channel

35
Q

How does does diabetes insipidus affect urine?

A 
very dilute (hypo-osmolar)
large volumes
36
Q

How does diabetes insipidus affect plasma?

A 
increased concentration (hyper-osmolar) as patient becomes dehydrated
Increased sodium (hypernatraemia)
Glucose normal (if not would be DM)
37
Q

How does diabetes insipidus affect plasma?

A 
increased concentration (hyper-osmolar) as patient becomes dehydrated
Increased sodium (hypernatraemia)
Glucose normal (if not would be DM)
38
Q

Why do patients with diabetes insipidus present with these symptoms? (6)

A
  1. arginine vasopressin problem
  2. impaired concentration of urine in renal collecting duct
  3. large volumes of dilute (hypotonic) urine –> POLYURIA, NOCTURIA
  4. increase plasma osmolarity (and Na)
  5. stimulation of osmoreceptors
  6. thirst –> POLYDIPSIA
39
Q

Why is thirst important in diabetes insipidus?

A

As long as patient has access to water, they can maintain circulating volume

40
Q

What if a patient with diabetes insipidus has not got enough access to water?

A

dehydration which could lead to death

41
Q

What is a non-diabetes related cause of nocturia, polyuria, and polydipsia?

A

Psychogenic polydipsia

42
Q

What is the difference between psychogenic polydipsia and diabetes insipidus?

A

psychogenic polydipsia - no problem with arginine vasopressin

43
Q

What is psychogenic polydipsia caused by?

A

drinking too much water

44
Q

How does drinking too much water causes similar symptoms to diabetes insipidus? (5)

A
  1. increased drinking –> POLYDIPSIA
  2. plasma osmolarity falls
  3. less AVP secreted by posterior pituitary
  4. large volumes of dilute (hypotonic) urine –> POLYURIA, NOCTURIA
  5. plasma osmolarity falls
45
Q

How do we distinguish between diabetes insipidus and psychogenic polydipsia?

A

Water deprivation test

46
Q

What does a water deprivation test involve?

A 
no access to anything to drink
over time measure:
- urine volume
- urine conc. (osmolarity)
- plasma conc. (osmolarity)
47
Q

What does urine osmolarity again hours of water deprivation look like in a normal patient?

A

urine osmolality increases over time y=x

48
Q

What does urine osmolarity again hours of water deprivation look like in a patient with psychogenic polydipsia?

A

urine osmolality increases over time (although can be slightly less than normal patient)
y=2/3x

49
Q

What does urine osmolarity again hours of water deprivation look like in a patient with diabetes insipidus?

A

Flat line

y=50 mOsm/kgH2O

50
Q

Why is it important to weigh a patient regularly during a water deprivation test?

A

stop test if lose >3% of body weight

  • marker of significant dehydration
  • this can occur in patients with diabetes insipidus
51
Q

How do we distinguish between cranial and nephrogenic diabetes insipidus?

A

give ddAVP
cranial diabetes insipidus - urine concentrates, and passes smaller volumes of urine
nephrogenic diabetes insipidus - no increase in urine osmolarity with ddAVP, as kidneys can’t respond

52
Q

What would you expect to see in a patient with diabetes insipidus in a water deprivation test?

A

urine volume: same throughout
urine osmolarity: same throughout
plasma osmolarity: progressively increase

53
Q

What is ddAVP?

A

V2 receptor agonist

54
Q

What does plasma osmolarity look like in a patient with diabetes insipidus compared to patient with psychogenic polydipsia?

A

diabetes insipidus - plasma osmolality higher than normal hydrated range
psychogenic polydipsia - plasma osmolality lower than normal hydrated range

55
Q

What is the treatment for cranial diabetes insipidus?

A

replace vasopressin with drug –> desmopressin
selective for V2 receptor (V1 receptor activation would be unhelpful)
tablets or transnasal spray

56
Q

How has the desmopressin nasal spray contribute to death from diabetes insipidus?

A
  • desmopressin nasal spray can be disregarded an not important and not included on drug chart
  • preventing a diabetes insipidus patient from drinking or not giving fluids can cause death
57
Q

What is the treatment for nephrogenic diabetes insipidus?

A
  • difficult to treat successfully

- Thiazide diuretics –> no clue why, paradoxical, mechanism unclear

58
Q

What does SIADH stand for?

A

Syndrome of Inappropriate Anti-Diuretic Hormone

59
Q

What is SIADH?

A 
too much arginine vasopressin
reduced urine output
water retention
high urine osmolarity
low plasma osmolarity
dilutional hyponatremia - because reabsorbing water all the time
60
Q

What are some causes of SIADH

A

commonly idiopathic
CNS - head injury, stroke, tumour
Pulmonary - pneumonia, lung cancer, bronchiectasis
Drug related - Serotonin reuptake inhibitors (SSRIs), carbamazepine

61
Q

Why is it management of SIADH important?

A

commonest cause of prolonged hospital stay

62
Q

How is SIADH treated?

A 
fluid restriction - until sodium levels inc.
vasopressin antagonist (vaptan) - binds to V2 receptors in kidney PROHIBITIVLY EXPENSIVE

BRS 1b (25 decks)

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