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Endocrinology > 3. Neurohypophysial disorders > Flashcards

3. Neurohypophysial disorders Flashcards

1
Q

How does vasopressin have an antidiuretic effect?

A
  • Acts on the renal (cortical and medullary) collecting ducts
  • Stimulates synthesis and assembly of Aquaporin 2
  • Increased water transport
  • Increased water reabsorption
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2
Q

Apart from being an antidiuretic, what are the other actions of vasopressin?

A
  • Vasoconstriction - V1a
  • Corticotrophin (ACTH) release - V1b
  • Factor VIII and von Willebrand Factor release - V2
  • Central effects
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3
Q

What are actions of oxytocin?

A
  • Constriction of myometrium (middle layer of uterine wall) at parturition
  • Milk ejection reflex
  • Central effects
  • Acts on oxytocin receptors
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4
Q

What does a lack of oxytocin cause?

A
  • Not that bad

* Parturition and milk effects are induced/replaced by other means

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5
Q

What does a lack of vasopressin lead to?

A

Diabetes insipidus
• Central/cranial - absence or lack of circulating vasopressin
• Nephrogenic - kidneys resistant to vasopressin
• Water isn’t reabsorbed

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6
Q

What can cause central diabetes insipidus?

A

• Damage to neurohypophysial system:
- injury to neurohypophysis
- surgery
- cerebral thrombosis
- tumours (intrasellar and suprasellar)
- granulomatous infiltration of median eminence
• Idiopathic (unknown cause/spontaneous origin)
• Familial (rare) - usually receptor gene mutations

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7
Q

What can cause nephrogenic diabetes insipidus?

A
  • Drugs e.g. lithium, DMCT

* Familial (rare)

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8
Q

What are the signs and symptoms of diabetes insipidus?

A
  • Polyuria (lot of urine)
  • Very dilute urine (hypo-osmolar)
  • Thirst and increased drinking (polydipsia)
  • Dehydration
  • Disruption of sleep
  • Electrolyte imbalance
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9
Q

Outline how a lack of vasopressin leads to the effects this has on the body

A
  • Can’t reabsorb water => increased urine excretion and reduced ECF volume
  • This leads to increased plasma osmolarity => osmoreceptors trigger vasopressin release and thirst
  • Increased drinking, decreased pOsm, expansion of ECF volume
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10
Q

What is psychogenic polydipsia?

A
  • Vasopressin system works fine
  • Central disturbance - increased drive to drink
  • Fall in plasma osmolarity => vasopressin inhibited
  • Polyuria => reduced ECF volume, increased plasma osmolariy
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11
Q

Describe the tests used to compare polydipsia, central DI and nephrogenic DI in a person?

A

• Initially all have similar urine osmolarities when hydrated
• Fluid deprivation test:
- normal person releases vasopressin and concentrates urine => increased urine osmolarity (pOsm remains)
- in polydipsia, urine osmolarity is slightly lower due to washed out osmotic gradient (polyuria has already removed some ions in the patient previously)
- no/little change in central and nephrogenic diabetes insipidus
• DDAVP administration:
- central DI urine osmolarity increases - vasopressin receptors work
- nephrogenic DI doesn’t respond

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12
Q

When a diabetes insipidus patient is dehydrated, how does their urine and plasma osmolarity change?

A
  • Normally, urine and plasma osmolarity increase when dehydrated
  • In DI, plasma osmolarity increases but urine osmolarity barely increases
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13
Q

How can you test if someone has central DI without dehydration?

A
  • Give patient hypertonic saline IV
  • Quick increase in pOsm
  • Stimulates vasopressin release
  • Rapid increase in plasma vasopressin in normal people, polydipsics and nephrogenic DI patients
  • Central DI - no change in vasopressin
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14
Q

What is SIADH and what does it lead to?

A

• Syndrome of inappropriate ADH

  • increased ADH
  • increased water reabsorption
  • decreased plasma osmolarity (hyponatraemia)
  • decreased urine volume
  • natriuresis - more sodium excreted in urine
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15
Q

What are the symptoms of SIADH, referring to responses to changing [Na+]?

A 
• Can be asymptomatic
• When [Na+] falls <120 mM
- generalised weakness
- poor mental function
- nausea
• When [Na+] falls <110 mM
- confusion
- coma
- death
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16
Q

What are the different causes of SIADH?

A
  • Tumours (ectopic secretion)
  • Neurohypophysial malfunction e.g. meningitis
  • Thoracic disease e.g. pneumonia
  • Endocrine disease e.g. Addison’s disease
  • Physiological - normal circumstances where vasopressin release is stimulated by non-osmotic stimuli e.g. hypovolaemia, pain, surgery
  • Drugs e.g. chlorpropamide
  • Idiopathic
17
Q

How is SIADH treated?

A

• Treatment depends on cause e.g. surgery for tumour
• If hyponatraemic
- immediate: fluid restriction
- longer-term: drugs that prevent vasopressin action in kidneys e.g. lithium, DMCT, V2 receptor antagonists

18
Q

What is the response in the body to exogenous vasopressin (argipressin)?

A
  • V1 actions as well as V2
  • V1: vasoconstriction on VSMCs, affects non-vascular smooth muscle in intestines, liver, platelets and CNS
  • V2: effect on kidneys
19
Q

What effect does Argipressin have on sodium?

A
  • Natriuresis
  • Unexplained side effect
  • V2 mediated
  • Only when given in high doses
  • Contributes to hyponatraemia
20
Q

What effect does Argipressin have on the CVS?

A
  • Pressor action (elevated arterial BP)
  • V1 mediated
  • Coronary vessels are particularly sensitive to vasopressin
  • Can cause cardiac ischaemia or angina attacks
21
Q

What effect does Argipressin have on ACTH and Factor VIII + von Willebrand factor?

A
  • Increased ACTH secretion (V1b)

* Increased Factor VIII and von Willebrand factor production (V2)

22
Q

Give 2 examples of selective vasopressin receptor peptidergic agonists

A

• Terlipressin
- analogue of vasopressin
- only V1 effects
• Desmopressin (DDAVP)
- larger dose than argipressin needed for contraction effects (∴ little effect on vasculature)
- lower dose needed for osmolarity effects (∴ higher effect in the kidneys)

23
Q

What are the clinical uses of desmopressin?

A
  • Cranial diabetes insipidus
  • Nocturnal eneuresis (bedwetting)
  • Haemophilia - for V2 receptor stimulation
24
Q

How can desmopressin be administered?

A
  • Nasally

* Orally

25
Q

What is the immediate effect of oral desmopressin?

A
  • Prompt sustained decrease in urine volume

* Increase in urine osmolarity

26
Q

Outline the distribution, metabolism and half-life of desmopressin?

A
  • Retained in ECF
  • Hepatic/renal metabolism
  • Half-life = 5 hours
27
Q

What are the negative side-effects of desmopressin?

A
  • Fluid retention and hyponatraemia
  • Abdominal pain
  • Headaches
  • Nausea
28
Q

What does ‘peptidergic’ mean?

A

Describes nerve cells or fibres that use small peptide molecules as their neurotransmitters

29
Q

What is terlipressin used for?

A

• Treating oesophageal varices

  • causes vasoconstriction
  • V1 agonist
30
Q

What is felypressin used for?

A

• Added to anaesthetics that dentists use
• Prolongs action of local anaesthetics
- causes vasoconstriction in injected area, keeping it more local ∴ lasts longer

31
Q

What can be used to treat nephrogenic diabetes insipidus and how does it work?

A

Thiazides
• Inhibits Na+/Cl- transport in distal convoluted tubule (leads to diuretic effect)
• Volume depletion
• Compensatory increase in Na+ reabsorption from PCT (+ small decrease in GFR)
• Increased proximal water reabsorption
• Decreased fluid reaching the collecting duct
• Reduced urine volume

32
Q

What are Vaptans and what are they used for?

A

• Non-peptide vasopressin analogues
• e.g. Tolvaptan - V2 receptor ANTAGONIST
- treatment of hyponatraemia associated with SIADH
- treatment of congestive heart failure

33
Q

What drugs affect vasopressin secretion?

A 
Increase
• nicotine
Decrease
• alcohol
• glucocorticoids

Endocrinology (17 decks)

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