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Endocrinology > Endo 3 - Neurohypophysial Disorders > Flashcards

Endo 3 - Neurohypophysial Disorders Flashcards

1
Q

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

A
  • Paraventricular

- Supraoptic

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2
Q

What two hormones are produced by the neurohypophysis?

A
  • Oxytocin

- Vasopressin

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3
Q

What does oxytocin stimulate?

A
  • Constriction of myometrium at parturition

- milk ejection

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4
Q

Is a lack of Oxytocin that important?

A

No

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5
Q

What is the principal action of vasopressin?

A

acts of V2 receptors in the renal cortical and medullary collecting ducts
stimulates the synthesis and assembly of aquaporin 2
this then increases water reasborption and so has an antidiuretic effect

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6
Q

Is vasopressin a diuretic or antidiuretic?

A

Antidiuretic - increases water REabsorption

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7
Q

What are the other actions of vasopressin?

A
  • vasoconstriction
  • corticotrophin release
  • vWf factor and Factor 8 release
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8
Q

Lack of vasopressin leads to?

A

Diabetes Insipidus

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9
Q

What are the two forms of diabetes insipidus?

A
  • Cranial (Central)

- Nephrogenic (Peripheral)

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10
Q

What is the difference between cranial and nephrogenic diabetes insipidus?

A 
cranial = lack of circulating vasopressin
nephrogenic = kidneys resistant to vasopressin
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11
Q

What are the causes of cranial diabetes insipidus?

A
  • injury to neurohypophysis system
  • surgery
  • tumours
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12
Q

What are the causes of nephrogenic diabetes insipidus?

A
  • drugs e.g. DMCT or lithium

- familial

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13
Q

What are the signs and symptoms of diabetes insipidus?

A
  • polyuria
  • polydipsia
  • nocturia
  • hypo-osmolar urine
  • dehydration if thirst not met
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14
Q

Explain the cycle in diabetes insipidus in terms of polyuria and polydipsia?

A
  • lack of vasopressin
  • increased urine excretion of hypotonic urine
  • plasma osmolarity increases
  • reduction in ECFV
  • polydipsia
  • expansion of ECFV
  • so increased urine
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15
Q

What is the normal range for plasma osmolarity?

A

270-290mOsm

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16
Q

State another cause of polydipsia which is not diabetes?

A

psychogenic polydipsia

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17
Q

What is psychogenic polydipsia?

A

central disturbance that increases the drive to drink

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18
Q

Describe the cycle in psychogenic polydipsia?

A
  • increased drinking due to central disturbance e.g. doctor telling them to drink loads of water
  • expansion of ECFV
  • reduced plasma osmolarity
  • less vasopressin secreted via posterior pituitary
  • large volumes of hypotonic urine excreted
  • reduction of ECFV
  • thirst triggered
19
Q

What test is used to diagnose and differentiate between Diabetes insipidus and psychogenic polydipsia?

A

Fluid Deprivation test

20
Q

Explain how a fluid deprivation test works?

A
  • normal person will be able to concentrate urine as vasopressin working, so less and less urine produced
  • pyschogenic - will be able to concentrate urine as vasopressin working so less and less urine produced
  • cranial and nephrogenic will NOT be able to concentrate urine as vasopressin not working - will produce excessive amounts of hypo-osmolar urine
21
Q

What test is used to differentiate between cranial and nephrogenic diabetes insipidus?

A

Desmopressin Administration

22
Q

How does the desmopressin administration test differentiate between the two forms of diabetes?

A
  • cranial = will be able to concentrate urine as desmopressin will work on the V2 receptors on kidneys to allow for aquaporin 2 to be made
  • nephrogenic - receptors resistant so will not be able to concentrate urine
23
Q

What is the treatment of cranial diabetes insipidus?

A
  • vasopresin or argipressin

- v1 stimulation causes vasoconstriction so give desmopressin

24
Q

What is the treatment of Nephrogenic DI?

A

thiazides which inhibit Na+/Cl- transport so reabsorption of water

25
Q

What is SIADH?

A

Syndrome of Inappropriate ADH - where the plasma vasopressin concentration is inappropriate for the existing plasma osmolality

26
Q

What hormone is in excess in SIADH?

A

Vasopressin

27
Q

What are the signs of SIADH?

A

decreased urine volume

increase urine osmolality

28
Q

What does increased vasopressin do?

A

increases water reabsorption

29
Q

What would SIADH do to plasma osmolality?

A

decreases plasma osmolarity

30
Q

What would SIADH do to Sodium levels?

A

reduced sodium concentration so Hyponatraemia

31
Q

What is the main consequence of SIADH?

A

Hyponatraemia

32
Q

When Na+ levels fall below 120mMol you get?

A
  • generalised weakness
  • poor mental function
  • nausea
33
Q

When Na+ levels fall below 110mM you get?

A

confusion, coma or deth

34
Q

What are the causes of SIADH?

A
  • Tumours
  • neurohypophysial malfunction
  • endocrine disease
  • drugs
35
Q

How is SIADH treated?

A
  • fluid restriction

- and then treat the cause e.g surgery

36
Q

What is the name given to exogenous vasopressin?

A

Argipressin

37
Q

Where are V1 receptors found?

A
  • vascular smooth muscle
  • anterior pituitary
  • liver
  • platelets
38
Q

Where are V2 receptors found?

A

Kidneys and endothelial cells

39
Q

Name the pharmacological actions of argipressin?

A
  • natriuresis
  • pressor action
  • contraction of vascular smooth muscle
  • increased ACTH secretion
40
Q

Name a v2 selective vasopressin agonist?

A

Desmopressin

41
Q

State some clinical uses of desmopressin?

A

treatment of diabetes insipidus

42
Q

Name a v1 vasopressin agonist and its use?

A

Terlipressin - oesophageal varices

43
Q

What are vaptans?

A

used to treat hyponatraemia in SIADH

Endocrinology (18 decks)

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