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Year 2 - ENDO > 3 - Neurohypophysial disorders > Flashcards

3 - Neurohypophysial disorders Flashcards

1
Q

What are nuclei in the NS?

A

groups of neuronal cell bodies

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2
Q

Name the two main nuclei within which neurones of the neurohypophysis have their cell bodies.

A

Paraventricular Nucleus

Supraoptic Nucleus

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3
Q

What two hormones are produced by the neurohypophysis?

A

Vasopressin

Oxytocin

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4
Q

What is the principal action of vasopressin and how does it carry out this action?

A

main action is on the V2 receptors in the renal cortical and medullary collecting ducts
It stimulates the synthesis and assembly of aquaporin 2, which then increases water reabsorption and has an antidiuretic effect

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5
Q

What is meant by antidiuresis?

A

decreased production of urine by increasing water reabsorption

(Diuresis = increase in urine production)

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6
Q

Where are osmoreceptors found?

A

in the organum vasculosum which project to the PVN (paraventricular nuclei) and SON (supraoptic nuclei)

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7
Q

What are the main actions of oxytocin?

A

contraction of the myometrium during parturition

involved in milk ejection

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8
Q

Describe how osmoreceptors detect a change a osmolality of an extracellular environment

A
  • in a high osmolality ectracelflulaer environment, water moves out the osmoreceptors, causing them to shrink
  • as it shrinks, the cells increase firing, which stimulates vasopressin release from hypothalamic PVN and SON
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9
Q

What are the consequences of a lack of the neurohypophysial hormones?

A

Lack of Oxytocin – not clinically significant

Lack of Vasopressin – Diabetes Insipidus

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10
Q

What are the two forms of diabetes insipidus?

A

Central (cranial) and Nephrogenic Diabetes Insipidus

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11
Q

What can cause central diabetes insipidus?

A

ACQUIRED:
Damage to Neurohypophysial system:
- Traumatic brain injury
- Pituitary surgery
- Pituitary tumours, craniopharyngioma
- Metastasis to the pituitary gland eg breast
- Granulomatous infiltration of median eminence eg TB, sarcoidosis

CONGENITAL - rare

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12
Q

What can cause nephrogenic diabetes insipidus?

A

Acquired - Drugs (e.g. lithium - used for bipolar disorder)

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

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13
Q

State some signs and symptoms of diabetes insipidus.

A 
Polyuria
Polydipsia
Hypo-osmolar (dilute) urine
Dehydration (if fluid intake is not maintained)
Possible disruption of sleep (nocturia)
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14
Q

What is the normal range for plasma osmolality?

A

275–295 mosm/kg

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15
Q

State a cause of polydipsia that isn’t diabetes.

Define it

A

Psychogenic polydipsia
This is a central disturbance that increases the drive to drink
(can be caused by ‘dry mouth’ from meds or being told to drink lots by healthcare professionals)

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16
Q

How are the symptoms of psychogenic polydipsia similar to that of diabetes insipidous?

A

POLYDIPSIA (excess fluid intake - thirst)

POLYURIA (excess urine output)

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17
Q

How is psychogenic polydipsia different to diabetes insipidous?

A

in PP, the body’s ability to secrete vasopressin in response to osmotic stimuli is preserved

18
Q

What test can be used to distinguish between normal, psychogenic polydipsia, central DI and nephrogenic DI? Describe the results you would expect.

A

Fluid deprivation with administration of DDAVP (Desmopressin)
• Central diabetes insipidus will show a rise in urine osmolality
• Nephrogenic DI will still have a low urine osmolality (because of end-organ resistance)

19
Q

What test can be used to distinguish between normal, psychogenic polydipsia and diabetes insipidous?
Describe the results you would expect.

A

Fluid deprivation test
• Normal and psychogenic polydipsia will show a rise in urine osmolality
• the urine osmolality of someone with psychogenic polydipsia will be slightly lower than a normal person
• DI will show little/no change in urine osmolality (don’t have the ability to concentrate the urine)

20
Q

What test can be used further to distinguish between central DI and nephrogenic DI?
Describe the results you would expect.

A

Fluid deprivation with administration of DDAVP (Desmopressin)
• Central diabetes insipidus will show a rise in urine osmolality
• Nephrogenic DI will still have a low urine osmolality (because of resistance to VP)

21
Q

What are the biochemical features of DI?

A

Hypernatraemia
Raised urea
Increased plasma osmolality
hypo-osmolar (dilute ) urine - ie low urine osmolality

22
Q

What are the biochemical features of psychogenic polydipsia?

A

Mild hyponatraemia – excess water intake
Low plasma osmolality
Hypo-osmolar (dilute) urine - ie low urine osmolality

23
Q

Why is the urine osmolality of someone with psychogenic polydipsia lower (in the fluid deprivation test) than a normal subject?

A

Over time, the constant passage of large volumes of water through the kidneys will wash out the osmotic gradient that is necessary for AVP to exert its diuretic effect

24
Q

Describe the normal change in urine osmolality as plasma osmolality increases.
Describe the changes for someone with DI

A

Normally, urine osmolality will increase as plasma osmolality increases (in a graph of urine osmolality against plasma osmolality it will show a sigmoid shape)
In DI, there is little change in urine osmolality as plasma osmolality increases

25
Q

What is the treatment of cranial DI?

A
  • give selective vasopressin receptor peptidergic agonists (desmopressin)
  • give exogenous vasopressin (this will activate all vasopressin receptors, but most importantly the ones in the kidney)
26
Q

What are the (non-intentional effects) of treating someone with DI with exogenous vasopressin (argipressin)?

A

there will be V1 action as well as V2

this includes vasoconstriction

27
Q

Name the selective vasopressin receptor peptidergic agonists and which vasopressin receptors they act on

Which one would be used to treat DI?

A

TERLIPRESSIN - V1 receptors

DESMOPRESSIN (DDAVP) - V2 receptors

use DDAVP to treat DI, since it acts on V2 receptors

28
Q

How is desmopressin administered?

A

Nasally
Orally
Subcutaneously

29
Q

What is desmopressin used to treat? What is the result of administering it?

A

cranial diabetes insipidous

results in a reduction in urine volume and concentration

30
Q

What is the treatment for nephrogenic DI?

A

THIAZIDE DIURETICS

31
Q

What is SIADH?

A

Syndrome of Inappropriate ADH = when the plasma vasopressin concentration is inappropriate (excessive) for the existing plasma osmolality

32
Q

State some signs of SIADH.

A 
Decreased urine volume 
Increased urine osmolality 
HYPONATRAEMIA
natriuresis (excretion of sodium)
Euvolaemia (normal amount of body fluids)
33
Q

Why does SIADH cause you to become hyponatraemic?

A

increased water reabsorption, so the ions in plasma become diluted

34
Q

What are the symptoms of SIADH?

A
  • can be symptomless
  • if [Na+] <120 mM: generalised weakness, poor mental function, nausea
  • if [Na+] <110 mM: CONFUSION leading to COMA and ultimately DEATH
35
Q

State some causes of SIADH

A
  • CNS
  • —-> SAH, stroke, tumour, TBI
  • Pulmonary disease
  • —-> Pneumonia, bronchiectasis
  • Malignancy
  • —-> Lung (small cell)
  • Drug-related
  • —-> Carbamazepine, SSRI
  • Idiopathic
36
Q

How is SIADH treated?

A

Appropriate treatment (e.g. surgery for tumour)

To reduce immediate concern, i.e. hyponatraemia

  1. Immediate: fluid restriction
  2. Longer-term: use drugs which prevent vasopressin action in kidneys
37
Q

How do the drugs used to treat SIADH work (i.e. how do they prevent the action of ADH in the kidney)?

A
  • induce nephrogenic DI ie reduce renal water reabsorption - demeclocyline
  • inhibit action of ADH - V2 receptor antagonists (VAPTANS)
38
Q

What are vaptans?

What do they do?

A
  • Non-competitive V2 receptor antagonists

- Inhibit aquaporin2 synthesis and transport to collecting duct apical membrane, preventing renal water reabsorption

39
Q

What are vaptans used to treat?

A

hyponatraemia associated with SIADH

40
Q

Why is the use of VAPTANS currently limited in the UK?

A

very expensive

41
Q

What is aquaresis?

A

solute-sparing renal excretion of water

contrast with diuretics (diuresis) which produce simultaneous electrolyte loss

42
Q

Explain the differences in plasma osmolality in a patients with DI and a patient with PP

A

DI - high plasma osmolality - lots of water excretion (low urine osmolality)
PP - low plasma osmolality - increased water intake with low urine osmolality (hypoosmolar urine)

Year 2 - ENDO (20 decks)

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