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TAS Endocrinology > Posterior Pituitary Gland ✅ > Flashcards

Posterior Pituitary Gland ✅ Flashcards

1
Q

What is the posterior pituitary also known as?

A

The neurohypophysis

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2
Q

What is the posterior pituitary derived from?

A

Neural ectoderm

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3
Q

What is the posterior pituitary formed from?

A

Neuronal projections (axons) of magnocellular neurosecretory cells

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4
Q

Where do the neuronal projections forming the posterior pituitary extend from?

A

The supraoptic and paraventricular nuclei of the hypothalamus

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5
Q

What bridges the hypothalamic and hypophyseal systems?

A

The infundibular or pituitary stalk

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6
Q

What hormone is synthesised in the posterior pituitary?

A

Arginine vasopressin (AVP)

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7
Q

What is AVP also known as?

A

Anti-diuretic hormone (ADH), or vasopressin

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8
Q

Where in the pituitary is ADH synthesised?

A

In neurons which originate in the supraoptic and paraventricular nuclei

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9
Q

Where do some paraventricular neurons end?

A

At the median eminence

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10
Q

What happens where paraventricular neurons end at the median eminence?

A

ADH is released into the hypophyseal circulation

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11
Q

Where do magnocellular neurons of the supraoptic and paraventricular nuclei end?

A

In the posterior pituitary

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12
Q

What happens where the magnocellular neurons of the supraoptic and paraventricular nuclei end in the posterior pituitary?

A

ADH is released into the systemic circulation

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13
Q

In what form is ADH synthesised?

A

In preprohormone formant

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14
Q

Where is ADH preprohormone synthesised?

A

In magnocellular neurones

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15
Q

What happens to ADH preprohormone after synthesis?

A

A signal peptide is cleaved, to form a prohormone

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16
Q

What happens to the prohormone of ADH after formation?

A

It folds and places ADH into a binding pocket of neurophysin

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17
Q

What does placing ADH into a binding pocket facilitate?

A

The production of high density neurosecretory granules

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18
Q

What happens to the neurosecretory granules of ADH?

A

They are transported to the posterior pituitary

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19
Q

What happens to the granules after they are transported to the posterior pituitary?

A

Vasopressin and neurophysin are released from the granules into the circulation after stimulation of vasopressinergic neurons

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20
Q

What is vasopressin secretion determined by?

A
  • Plasma osmotic status
  • Blood pressure
  • Circulating volume
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21
Q

How does vasopressin act?

A

By binding to 3 GPCRs

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22
Q

How are pressor effects of vasopressin mediated?

A

By binding of vasopressin to V1 receptors in vascular smooth muscle

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23
Q

What is the main action of vasopressin?

A

Regulate blood volume control by regulating clearance of free water

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24
Q

How does vasopressin regulate clearance of free water?

A

Through binding to V2 receptors in the kidney

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25
Q

What is the result of vasopressin binding to V2 receptors in the kidney?

A

It stimulates expression of aquaporin 2

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26
Q

What does aquaporin 2 allow?

A

Reabsorption of water from the collecting duct along an osmotic gradient

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27
Q

What is another action of vasopressin?

A

Facilitates ACTH release from corticotrophs

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28
Q

How does vasopressin facilitate ACTH release from corticotrophs?

A

By binding to V3 receptors in the anterior pituitary gland

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29
Q

What is the most common disturbance of posterior pituitary function?

A

Diabetes insipidus

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30
Q

What are the types of diabetes insipidus?

A
  • Cranial

- Nephrogenic

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31
Q

What is the problem in cranial diabetes insipidus?

A

Insufficient vasopressin release

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32
Q

What can cause insufficient vasopressin release?

A

Congenital or acquired defects of posterior pituitary anatomy

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33
Q

What is the problem in nephrogenic diabetes insipidus?

A

Renal resistance to vasopressin action

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34
Q

What needs to be determined from history in a child presenting with polyuria and a potential diagnosis of diabetes insipidus?

A
  • Timing of onset of symptoms
  • Details of mode of delivery
  • Family history, particularly of diabetes mellitus
  • Estimate of daily fluid intake
  • What fluids they are drinking
  • Details of symptoms suggestive of wider pituitary defects, and if there is past history of head injury or other brain insults e.g. surgery
  • Presence of headaches or disturbance to vision
  • History of renal disease
  • Presence of other disorders
  • Medication
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35
Q

Why is it important to know what fluids the child is drinking in suspected diabetes insipidus?

A

If only flavoured fluids, suggests habitual preference rather than defect in water homeostasis
If drinking usual fluids such as shampoo, or from unusual sources such as toilet bowls or flower pots, suggests extreme thirst, as occurs in diabetes insipidus

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36
Q

What other disorders should be enquired about in suspected diabetes insipidus?

A
  • Impaired vision
  • Hearing defects
  • Symptoms suggestive of hypercalcaemia
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37
Q

What symptoms might be suggestive of hypercalcaemia?

A
  • Anorexia
  • Abdominal pain
  • Constipation
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38
Q

What should clinical examination include in suspected diabetes insipidus?

A
  • Hydration state
  • Blood pressure
  • Check for wider defects associated with abnormal pituitary function, e.g. growth and pubertal staging
  • Craniofacial skeleton for midline defects
  • Presence of enlarged kidneys
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39
Q

What is the most common cause of referral for assessment of fluid balance abnormalities?

A

Habitual excess drinking

40
Q

How can habitual excess drinking be excluded?

A

Ask family to document fluid intake and output diary, with free access to water between meals and flavoured fluids only allowed at mealtimes

41
Q

What should be done if excess fluid losses persist when the child is only allowed water between meals?

A
  • Fasting serum sample for measurement of sodium, potassium, creatinine, osmolality, glucose, and calcium
  • Paired fasting urine sample for glycosuria, proteinuria, sodium, and osmolality
42
Q

How can paired urine/plasma testing confirm the presence of diabetes insipidus?

A

If inappropriately dilute urine (<759mOsm/kg) in presence of hyperosmolar state (serum osmolality >295mOsm/kg)

43
Q

What should be done if paired urine/plasma testing does not confirm diabetes insipidus?

A

Further tests should be performed in a specialist centre

44
Q

Why should further tests for diabetes insipidus be performed in a specialist centre?

A

As some of them are potentially dangerous

45
Q

What further testing is done to when diabetes insipidus is suspected?

A

Child should be admitted for initial monitoring of fluid balance, then if indicated, water deprivation test

46
Q

What happens in water deprivation test?

A

Fluids are withheld (usually for around 8 hours), until thirst cannot be tolerated anymore, weight loss exceeds 5%, or serum osmolality exceeds 295mOsm/kg. Once this is achieved and a urine sample obtained, test dose of desmopressin (DDVAP) given to monitor serum and urine osmolality over next few hours

47
Q

What is the purpose of giving desmopressin following a water deprivation test?

A

Distinguish cranial from nephrogenic diabetes insipidus

48
Q

How does giving desmopressin following a water deprivation test distinguish cranial from nephrogenic diabetes insipidus?

A

The presence of a urinary concentrating response confirms cranial

49
Q

What is an alternative to the water deprivation test?

A

Hypertonic saline infusion test

50
Q

What happens in the hypertonic saline infusion test?

A

5% saline is given IV until plasma osmolality exceeds 300mOsm/kg, following which plasma osmolality and plasma AVP are measured

51
Q

What results of the hypertonic saline infusion test would suggest cranial diabetes insipidus?

A

Low levels of AVP when hyperosmolar

52
Q

What results of the hypertonic saline infusion test would suggest nephrogenic diabetes insipidus?

A

High levels of AVP

53
Q

What further investigations should be done if cranial diabetes insipidus is suggested by testing?

A
  • Measurement of serum tumour markers ß-human chorionic gonadotrophin and α-fetoprotein
  • MRI scanning of hypothalamo-pituitary axis
54
Q

What are the categories of cranial DI?

A
  • Triphasic pattern
  • With intact thirst
  • Anatomical defects
55
Q

When does cranial DI with a triphasic pattern occur?

A

Following neurosurgery

56
Q

What kind of neurosurgery in particular might cranial DI with triphasic pattern occur after?

A

For craniopharyngioma

57
Q

What happens in triphasic pattern cranial DI?

A

DI may occur for up to 24 hours, followed by period of vasopressin excess for 2-4 days, then development of more permanent DI

58
Q

Why is there a period of vasopressin excess in triphasic cranial DI?

A

Thought to be due to a necrotic posterior pituitary releasing vasopressin

59
Q

When does cranial DI with intact thirst occur?

A

Inherited forms of DI, or where underlying pathology is confined to posterior pituitary and does not affect hypothalamic functioning

60
Q

What is the most common inherited cause of DI?

A

Familial autosomal dominant neurohypophyseal DI

61
Q

What is familial autosomal dominant neurohypophyseal DI usually due to?

A

Mutations in the neurophysin coding region or signal peptide, which impairs processing, folding, or dimerisation

62
Q

What do the mutations causing familial autosomal dominant neurohypophyseal DI cause?

A

Accumulation of abnormal prohormone and degeneration of the magnocellular neurons

63
Q

What does accumulation of abnormal prohormone and degeneration of the magnocellular neurons in familial autosomal dominant neurohypophyseal DI lead to?

A

Gradual but variable decline in vasopressin secretion in the first decade of life

64
Q

Give another cause of inherited DI?

A

Wolfram syndrome

65
Q

What is the inheritance pattern of Wolfram syndrome?

A

Autosomal dominant

66
Q

What is Wolfram syndrome?

A

Association of diabetes insipidus with;

  • Insulin dependant diabetes mellitus
  • Optic atrophy
  • Sensorineural deafness
67
Q

What can cause inherited anatomical defects in posterior pituitary function?

A
  • Congenital defects, e.g. septo-optic dysplasia

- In associated with other intracranial or midline abnormalities

68
Q

What might MRI scanning show in inherited anatomical defects in posterior pituitary function?

A

Absent posterior pituitary signal, in addition to other cranial abnormalitites

69
Q

What are the acquired causes of anatomical defects in posterior pituitary function?

A
  • Tumours
  • Infiltration
  • Trauma
  • Neurosurgery
  • Autoimmune disease
  • Hypoxia
  • Idiopathic
70
Q

What is the treatment for DI?

A

Desmopressin (DDAVP)

71
Q

What routes can desmopressin be given?

A
  • Orally
  • Nasally
  • Parenterally
72
Q

How should desmopressin be started?

A

At low doses, and slowly increased

73
Q

Why is it important desmopressin is started at low doses and slowly increased?

A

To avoid excess fluid retention

74
Q

Should free access to fluids be allowed when starting desmopressin?

A

Yes

75
Q

Why should free access to fluids be allowed when starting desmopressin?

A

To patient can correct inadequate therapy by increased fluid intake

76
Q

Why does great care need to be taken when administering IV fluids to patients on desmopressin?

A

To avoid overhydration, as following desmopressin administration, patients cannot excrete an excess water load

77
Q

Which type of DI is extremely difficult to manage?

A

Cranial DI with impaired thirst

78
Q

What might cause cranial DI with impaired thirst?

A
  • Impaired osmoreceptor function associated with neurodisability
  • Following tumours or surgery
79
Q

What does the management of cranial DI with impaired thirst require?

A

Careful balancing of desmopressin dose and fluid intake

80
Q

Why does management of cranial DI with impaired thirst require careful balancing of fluid intake and desmopressin administration?

A

These patients cannot correct abnormal fluid balance through perceived effects of thirst

81
Q

What is nephrogenic DI due to?

A

Renal resistance to AVP action

82
Q

What can cause renal resistance to AVP action?

A
  • Congenital abnormalities
  • Drug induced
  • Metabolic
  • Aquaporin-mediated effects of renal disease associated with acute or chronic renal failure
83
Q

Give an example of a drug induced cause of nephrogenic DI?

A

Lithium

84
Q

What does lithium act on to cause nephrogenic DI?

A

Aquaporin 2

85
Q

Give 3 metabolic causes of nephrogenic DI?

A
  • Hyperglycaemia-associated osmotic diuresis
  • Hypokalaemia
  • Hypercalcaemia
86
Q

What do the metabolic causes of nephrogenic DI act on?

A

Aquaporin 2 function

87
Q

Why is nephrogenic DI difficult to treat?

A
  • Free access to extra fluid is required

- Need attention to calorie intake

88
Q

How can some relief of symptoms be provided in nephrogenic DI?

A

Thiazide diuretics in combination with amiloride or indomethacin

89
Q

How do thiazides help in nephrogenic DI?

A

Thought to inhibit the NaCl cotransporter in the DCT, thereby increasing proximal tubular sodium and water reabsorption

90
Q

What are the causes of SIADH?

A
  • CNS system disorders
  • Haemorrhage
  • VP shunt obstruction
  • Guillain-Barre syndrome
  • Certain tumours
  • Drugs
91
Q

What CNS system disorders can cause SIADH?

A
  • Meningitis
  • Encephalitis
  • Trauma
  • Hypoxia
92
Q

What respiratory conditions can cause SIADH?

A
  • Pneumonia

- TB

93
Q

What tumours can cause SIADH?

A
  • Thymoma
  • Lymphoma
  • Ewing’s sarcoma
94
Q

What does SIADH result in?

A
  • Impaired free water clearance
  • Total body water excess
  • Hyponatraemia
95
Q

How is SIADH managed?

A
  • Treatment of underlying cause
  • Fluid restriction when mild and asymptomatic
  • When more severe, use of democycline
96
Q

How does democycline work in SIADH?

A

It inhibits the action of vasopressin on its receptor

97
Q

What is the limitation of the use of democycline in paediatrics?

A

It has yet to be tested and licensed for use in children

TAS Endocrinology (6 decks)

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