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LCRS Endocrinology > 3. Neurohypophyseal Disorders > Flashcards

3. Neurohypophyseal Disorders Flashcards

1
Q

Hypothalamo- Neurohypophysial system

A
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2
Q

Principle Actions of Vasopressin

A
  • Acts on the renal, cortical and medullary collecting ducts
  • Stimulates synthesis and assembly of aquaporin 2
  • Increased water transport and WATER REABSORPTION
  • This has an antidiuretic effect
  • This occurs by action on V2 RECEPTORS

Other Actions:

  • Vasoconstrictor activity- V1a
  • Corticotophin (ACTH) release- V1b
  • Factor VIII and von Willebrand Factor- V2
  • Central effects
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3
Q

Principle actions of Oxytocin

A
  • Constriction of myomentrium at parturition (uterine wall)
  • Milk ejection reflex
  • Acts via Oxytocin receptors
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4
Q

Effect of Oxytocin deficiency

A

Parturition and milk ejection effects are induced/ replaced by other means (not that dramatic)

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5
Q

Effect of vasopressin deficiency

A

DIABETES INSIPIDUS

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6
Q

Classification of diabetes insipidus

A

Can be one of TWO forms:

  1. CENTRAL (cranial)- abscence or lack of circulating vasopressin
  2. NEPHROGENIC- end organ (kidney) resistence to vasopressin
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7
Q

Causes of central diabetes insipidus

A

Damage to neurohypophysial system

  • surgery
  • cerebral thrombosis
  • tumours (intrasellar or suprasellar)
  • granulomatous infiltration of median eminence

Idiopathic

Familial (rare) usually receptor gene mutations

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8
Q

Causes of nephrogenic diabetes insipidus

A

Familial (rare)

Drugs- e.g lithium, DMCT

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9
Q

Signs and Symptoms of DIabetes Insipidus

A
  • Large volumes of urine (polyuria)
  • Very dilute urine (hypo-osmolar)
  • Thirst and increased drinking (polydipsia)
  • Dehydration (and consequences) if fluid intake is not maintained
  • Possible disruption of sleep with associated problems
  • Possible electrolyte imbalance
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10
Q

Cycle in diabetes insipidus

A

A lack of vasopressin causes an increase in urine excretion and a reduction in extracellular fluid volume

This leads to an increase in plasma osmolarity- osmoreceptors trigger vasopressin release triggering thirst

As a result the patient may present with normal plasma osmolarity if they are well hydrated

POLYDIPSIA- large volumes of urine and increased drinking

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11
Q

Plasma osmolarity in diabetes insipidus and polydipsia

A

DIABETES INSIPIDUS= 290 mOsm.kg H20-1

POLYDIPSIA= 270 mOsm.kg H20-1

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12
Q

Psychogenic Polydipsia

A

There is a central disturbance and this increases the drive to drink

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13
Q

Fluid deprivation test

A

This should stimulate the vasopressin system- a normal person will release AVP (arginine vasopressin) and concentrate the urine

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14
Q

Fluid deprivation test in psychogenic polydipsia

A

The vasopressin system is working fine so when they are dehydrated they will release vasopressin and concentrate the urine

  • The urine osmolarity is slightly lower than in a normal person because over a long period of time you will start to loose the osmotic gradient necessary for AVP to exert its antidiuretic effect
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15
Q

Fluid deprivation effects in central and nephrogenic diabetes insipidus

A

There will be little or no change in urine concentration

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16
Q

Desmopressin (DDAVP) (+ clinical uses)

A

An alternative (ANALOGUE) to vasopressin

Effective in a person with polydipsia and CENTRAL diabetes insipidus because the receptors can be stimulated by DDAVP

It will not be effective in patients with nephrogenic diabetes insipidus because they already have normal vasopressin levels

Can be adminitered nasally or orally

Clinical uses:

  • Cranial diabetes insipidus
  • Nocturnal eneuresis (bedwetting)
  • Haemophilia (need V2 stimulation)
17
Q

How does urine osmorality change with plasma osmolarity

A

As someone becomes more and more dehydrated, their plasma osmolarity AND urine osmolarity should both increase considerably

18
Q

Stimulation with hypertonic saline IV

A
  • Used where you can measure plasma vasopressin

You can give the patient hypertonic saline I.V and this quickly increases plasma osmolarity and should stimulate AVP release

  • Normal, polydipsics and patients with nephrogenic diabetes insipidus will show a rapid increase in plasma vasopressin
  • Patients with Central diabetes insipidus will show NO CHANGE in plasma vasopressin
19
Q

Characteristics, signs and symptoms of the Syndrome of Innapropriate ADH (SIADH)

A

The plasma vasopressin concentration is INNAPROPRIATE for the existing plasma osmolarity

Raised vasopressin despite normal or low plasma osmolarity leads to:

  • Decreased urine volume
  • Raised urine osmolarity
  • HYPONATRAEMIA- decrease in plasma sodium concentration due to increased water reabsorption

Symptoms of SIADH:

  • Can be asymptomatic
  • When Na+ conc. falls <120mM
    • Generalised weakness
    • Poor mental function
    • Nausea
  • <110mM
    • CONFUSION, DEATH, COMA
20
Q

Causes of SIADH

A
  • Tumours (ectopic secretion)
  • Neurohypophysial malfunction (e.g meningitis, cerebrovascular disease)
  • Thoracic disease (pneumonia)
  • Endocrine disease (e.g Addison’s disease)
  • Drugs
  • Idiopathic
  • Physiological
21
Q

Treatment of SIADH

A

Once the cause (e.g tumour) is identified, you can undergo surgery

HOWEVER, if someone is already hyponatreamic:

  • Immediate: fluid restriction
  • Longer term: use drugs that prevent vasopressin action in the kidneys (e.g) DMCT
22
Q

Pharmacological actions of argipressin

A

Argipressin is the term used for exogenous vasopressin (arginine vasopressin)

  1. Natriuresis (Na+ excretion)
  • An unexplained effect of large amounts of vasopressin
  • V2 mediated
  • Only occurs when given high doses
  1. Pressor Action
  • V1 mediated
  • Not all vascular beds are equally sensitive
  • The coronary vessels are particularly sensitive to vasopressin
  • can cause ischaemia or angina attacks
  1. Other Actions
  • V1a- gut motility
  • V1b- ACTH
  • V2- Von Willebrand factor production
23
Q

V1 selective vasopressin receptor agonist (peptidergic)

A

Terlipressin- analogue of vasopressin but essentially only has V1 effects

24
Q

V2 selective vasopressin receptor agonist (peptidergic)

A

Desmopressin

25
Q

Peptidergic definition

A

Nerve cells or fibres that use small peptide molecules as their neurotransmitters

26
Q

Clinical uses of Peptidergic V1 receptor agonists (Terlipressin+Felypressin)

A
  • Terlipressin- V1 agonist, useful for treating oesophageal varices (causes vasoconstriction)
  • Felypressin- prolongs the action of local anaesthetics- used by dentists
27
Q

Treatment of nephrogenic diabetes insipidus

A

THIAZIDES

Possible mechanism of action:

  • Inhibits NA+/Cl- transport in the distal convoluted tubule (leads to a diuretic effect)
  • Volume depletion
  • Compensatory Na+ reabsorption from the PCT
  • Increased PROXIMAL water reabsorption so it doesnt reach the CD
  • reduced urine volume
28
Q

Name given to non-peptide vasopressin analogues

A

VAPTANS

29
Q

Drugs which increase vasopressin secretion

A

Nicotine

30
Q

Drugs which decrease vasopressin secretion

A
  1. Alcohol
  2. Glucocorticoids

LCRS Endocrinology (18 decks)

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