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Endocrinology > Neurohypophysial disorders > Flashcards

Neurohypophysial disorders Flashcards

1
Q

Aetiology of Cranial Diabetes Insipidus

A

Acquired (more common) or congenital (rare)
-Acquired causes involves damage to the neurohypophysial system

Examples of acquired causes include:

  • traumatic brain injury
  • pituitary surgery
  • pituitary tumours, craniopharyngioma
  • metastasis to the pituitary gland
  • granulomatous infiltration of the median eminence (eg: Tuberculosis, Sarcoidosis etc)
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2
Q

Aetiology of Nephrogenic Diabetes Insipidus

A

Acquired or congenital (rare)

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3
Q

Diabetes Insipidus presentation

A
  • Polyuria (large volumes of urine)
  • Hypo-osmolar urine (very dilute urine)
  • Polydipsia (excessive thirst and increased drinking)
  • Dehydration (and consequences) if fluid intake not maintained-> can result in death
  • Possible sleep disruption with associated problems
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4
Q

Psychogenic polydipsia

A
  • frequently seen in psychiatric patients (unclear aetiology but may reflect anti-cholinergic effects of medication)
  • can be in patients told to ‘drink plenty’ by healthcare professionals
  • presents with excess fluid intake (polydipsia) and excess urine output (polyuria)
  • differs from Diabets Insipidus as ability to secrete vasopressin in response to osmotic stimuli is preserved
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5
Q

Diabetes Insipidus biochemical features

A
  • Hypernatraemia
  • Raised urea
  • Increased plasma osmolality
  • Dilute (hypo-osmolar) urine
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6
Q

Psychogenic polydipsia biochemical features

A
  • Mild hyponatraemia (excess water intake)
  • Low plasma osmolality
  • Dilute (hypo-osmolar) urine
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7
Q

Desmopressin

A
  • Administered nasally, orally or subcutaneously

- reduces urine volume and concentration in Cranial Diabetes Insipidus

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8
Q

Selective vasopressin receptor peptidergic agonists

A
  • V1 receptors-> eg: Terlipressin

- V2 receptors-> eg: Desmopressin (DDAVP)

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9
Q

Nephrogenic diabetes insipidus treatment

A

THIAZIDES (EG: BENDROFLUMETHIAZIDE)

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10
Q

SIADH

A

SYNDROME OF INAPPROPRIATE ADH
-the plasma vasopressin concentration is inappropriately high for the existing plasma osmolality (excess ADH/Vasopressin)

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11
Q

SIADH signs

A
  • raised urine osmolality
  • decreased urine volume initially
  • hyponatraemia due largely to increased water reabsorption
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12
Q

SIADH symptoms

A
  • patient can be symptomless
  • however, if ……< 120mM, patient experiences generalised weakness, poor mental function and nausea
  • if ……< 110mM, patient experiences confusion which can lead to coma and ultimately death
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13
Q

SIADH causes

A
  • CNS (eg: subarachnoid haemorrhage, stroke, tumour, traumatic brain injury)
  • Pulmonary disease (eg: pneumonia, bronchiectasis)
  • Malignancy (eg: small cell lung cancer)
  • Drug-related (eg: Carbamazepine, SSRIs)
  • Idiopathic
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14
Q

SIADH treatment

A

/

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15
Q

Vaptans

A

NON-COMPETITIVE V2 RECEPTOR ANTAGONISTS

  • inhibits AQP2 synthesis and transport to collecting duct apical membrane, preventing renal water reabsorption
  • produce aquaresis (solute-sparing renal excretion of water)
  • Aquaresis contrasts with diuresis which produces simultaneous electrolyte loss
  • licensed in UK for hyponatraemia treatment associated with SIADH
  • very expensive (limits current use)
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16
Q

The effects of vasopressin

A
  • Principally, vasopressin (otherwise known as ADH) is an anti-diuretic
  • Anti-diuretics increase water reabsorption from renal cortical and medullary collecting ducts via V2 receptors
17
Q

Cranial (or Central) Diabetes Insipidus

A

-absence or lack of circulating Vasopressin

18
Q

Nephrogenic Diabetes Insipidus

A

-end-organ (kidneys) resistance to Vasopressin

19
Q

Diuresis

A

-increases urine production

20
Q

Regulation of vasopressin release

A

/

21
Q

The hypothalamo-neurohypophysial system

A

/

22
Q

The normal response to water deprivation

A

/

23
Q

Diabetes Insipidus

A

Insufficent ADH/ADH unable to work

24
Q

Normal hydrated range of plasma osmolality

A

270-290 mOsm/kg H20

25
Q

Diabetes Insipidus plasma osmolarity

A

> 290 mOsm/kg H20

26
Q

Psychogenic polydipsia plasma osmolarity

A

<270 mOsm/kg H20

27
Q

SIADH pathophysiology

A
  • increased vasopressin leads to increased water reabsorption from renal collecting ducts
  • results in ECF volume expansion
28
Q

Posterior pituitary gland

A
  • Otherwise known as the neurohypophysis

- ‘posterior bright spot’ on pituitary MRI (white and crescent shaped but not evident in every individual)

Endocrinology (18 decks)

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