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Yr 2 LCRS - Endo > 3 - Neurohypophysial Disorders > Flashcards

3 - Neurohypophysial Disorders Flashcards

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1
Q

How can the posterior pituitary be identified on an MRI?

A

It’s the bright spot on a pituitary MRI.

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2
Q

What is the other name for the Posterior Pituitary Gland?

A

Neurohypophysis

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3
Q

Which two hormones are released from the PPG?

A

ADH (Vasopressin)

Oxytocin

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4
Q

What is the principal effect of Vasopressin?

A
  • Anti-Diuretic
  • Increases water reabsorption from renal cortical and medullary collecting ducts
  • Via V2 receptors
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5
Q

What is diuresis?

A

Increase in urine production

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6
Q

Where are osmoreceptors located?

A

Osmoreceptors are neurones

  • located in Organum Vasculosum of the brain
  • project to hypothalamic PVN and SON
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7
Q

How do osmoreceptors sense hydration/dehydration?

A

Very sensitive to changes in EC osmolality

EXAMPLE

  • Dehydration
  • increase in EC Na+
  • Osmolality increases
  • Osmoreceptor loses water and shrinks
  • Increased Osmoreceptor firing
  • Vasopressin released from hypothalamic paraventricular nucleus and supra-optic nucleus neurones
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8
Q

Other than its principal effect, what are the other actions of vasopressin?

A
  • Vasoconstrictor Activity - V1a
  • Corticotrophin (ACTH) Release - V1b
  • Factor VIII and von Willebrand Factor - V2
  • Central Effects
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9
Q

What are the effects of Oxytocin in the body?

A
  • Constriction of myometrium at parturition
  • Milk ejection reflex
  • Central effects
    (Acts on oxytocin receptors)
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10
Q

What is parturition?

A

The action of giving birth to young; childbirth.

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11
Q

What happens in conditions of lack of the 2 neurohypophysial hormones?

A 
Oxytocin
- not that bad
- parturition and milk ejection effects are induced/replaced by other means
Vasopressin
- diabetes insipidus
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12
Q

What are the 2 forms of Diabetes Insipidus?

A

CENTRAL (CRANIAL) [absence or lack of vasopressin]
and
NEPHROGENIC [kidney resistance to vasopressin]

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13
Q

List the causes of the 2 forms of Diabetes Insipidus

A 
CENTRAL (CRANIAL)
Damage to neurohypophysial system
- Injury to neurohypophysis (TBI)
- Pituitary Surgery
- Cerebral Thrombosis
- Tumours (intrasellar and suprasellar)
- Granulomatous infiltration of median eminence
- Metastasis to pituitary gland (e.g. from breast)
Idiopathic
Familial/Congenital (Rare)

NEPHROGENIC
Familial/Congenital (Rare)
- e.g. mutation in gene encoding V2 receptor
Drugs/Acquired
- lithium
- dimethyl chlortetracycline (DMCT)
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14
Q

What are the signs and symptoms of Diabetes Insipidus?

A
  • Polyuria (large volumes of urine)
  • Hypo-osmolar urine (very dilute urine)
  • Polydipsia (thirst and increased drinking)
  • Dehydration and consequences if fluid intake is not maintained [can lead to death without access to fluid]
  • Disruption of sleep (possible)
  • Electrolyte imbalance
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15
Q

Explain the mechanism of how Diabetes Insipidus occurs

A
  • Inadequate production/response to VP
  • Can’t reabsorb water
  • Increase in urine excretion (polyuria). Large volumes of dilute (hypotonic) urine.
  • Reduction in extracellular fluid volume
  • Increase in plasma osmolarity (increased sodium)
  • Osmoreceptors trigger VP release
  • Triggers thirst (polydipsia)
  • Increased drinking
  • Decreased plasma osmolarity
  • Increased extracellular fluid volume
    CYCLE STARTS AGAIN

If patient does not have access to extra water, they become dehydrated and can die.

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16
Q

What is the normal range for plasma osmolarity?

A

Measure in mOsm.kg H20-1

280 - approximate normal hydrated range
290 - diabetes insipidus
270 - polydipsia

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17
Q

What condition presents in a similar way to Diabetes Insipidus and how can you differentiate between them?

A

Polydipsia

  • large volumes of urine
  • increased drinking
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18
Q

Explain the mechanism behind Psychogenic Polydipsia

A
  • Central disturbance
  • Increases the drive to drink
  • Fall in plasma osmolarity
  • Vasopressin is inhibited
  • Produce large volumes of dilute urine
  • This reduces extracellular fluid volume
  • Increase plasma osmolarity
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19
Q

What is a collection of cell bodies in the brain called?

A

A nucleus

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20
Q

What regulates Vasopressin release?

A

EC Osmolality detected by osmoreceptors

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21
Q

What happens to serum osmolality during water deprivation?

A

Serum osmolality increases

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22
Q

Where are VP and and Oxytocin produced?

A

Magnocellular nuclei in hypothalamus
= Paraventricular Nucleus
= Supraoptic Nucleus

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23
Q

Where are VP and and Oxytocin secreted from?

A

Posterior Pituitary Gland (Neurohypophysis)

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24
Q

Which form of Diabetes Insipidus is most common?

A

Cranial/Central Diabetes Insipidus

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25
What is most often the cause of Nephrogenic Diabetes Insipidus?
Lithium (drug)
26
What group of people most frequently present with Pyschogenic Polydipsia?
Psychiatric patients - e.g. medication gives dry mouth causing patients to want to drink more despite being told not to - they drink lots of water for many various reasons Aetiology is unclear
27
What are the similarities between Diabetes Insipidus and Pyschogenic Polydipsia?
BOTH HAVE EXCESS FLUID INTAKE (POLYDIPSIA) BOTH HAVE EXCESS URINE OUTPIT (POLYURIA)
28
What is the difference between Diabetes Insipidus and Pyschogenic Polydipsia?
Ability to secrete vasopressin in response to osmotic stimuli is preserved Nothing wrong with their vasopressin system.
29
How do you differentiate a diagnosis between Diabetes Insipidus and Pyschogenic Polydipsia as both have similar systems?
Diabetes Insipidus - person becomes dehydrated - may have high plasma osmolality above 290 most/kg H20 - unless person is drinking a lot more than the average person in which case they may not appear dehydrated Pyschogenic Polydipsia - will have low plasma osmolality - they are drinking a lot but they have a normal vasopressin system
30
What test is used clinically to distinguish between Diabetes Insipidus and Pyschogenic Polydipsia?
WATER DEPRIVATION TEST - put person in a room with absolutely no water - cannula in their arm - measure their urine output for a day (volume and concentration) - (urine osmolality) - taking blood samples (blood osmolality)
31
What happens in a normal individual during a water deprivation test?
Increase in urine osmolality - concentrated urine - reduced urine volumes - they have a normal VP response causing the collecting ducts to reabsorb more fluid
32
What happens in a patient with Pyschogenic Polydipsia during a water deprivation test?
Increase in urine osmolality - concentrated urine - reduced urine volumes - they're VP response in normal so they reabsorb more fluid - they may have a slightly lower osmolality than a normal individual but this is only because they may have drunk a lot more water than a normal person prior to the water deprivation test
33
What happens in a patient with Diabetes Insipidus during a water deprivation test?
Urine osmolality remains low - urine is not concentrated - still large volumes of urine - they do not have a normal VP response because they're not making enough VP - therefore they can't reabsorb more fluid in their collecting ducts when dehydrated
34
What happens when a patient with Cranial Diabetes Insipidus is given synthetic VP during a water deprivation test?
They are able to concentrate their urine because they are given VP which they previously lacked, and there is nothing wrong in their kidneys.
35
What happens when a patient with Nephrogenic Diabetes Insipidus is given synthetic VP during a water deprivation test?
They are still not able to concentrate their urine because it is their kidneys that are not functioning, they do not have a lack of VP.
36
What are the biochemical features of Diabetes Insipidus?
- Hypernatraemia [high sodium] - Raised urea - Increased plasma osmolality - Dilute (hypo-osmolar) urine [low urine osmolality]
37
What are the biochemical features of Pyschogenic Polydipsia?
- Mild hyponatraemia due to excess water intake - Low plasma osmolality - Dilute (hypo-osmolar) urine [low urine osmolality]
38
What is the problem with administering Exogenous Vasopressin as treatment for Cranial Diabetes Insipidus?
All vasopressin receptors would be activated (V1 and V2) You only want to act on the V2 receptors in the kidneys
39
Where are V1 Vasopressin Receptors found and what is the action of them?
VASOPRESSIN IS A CONSTRICTOR VIA V1 RECEPTORS - Vascular smooth muscle - Non-Vascular smooth muscle - Anterior Pituitary - Liver - Platelets - CNS
40
Where are V2 Vasopressin Receptors found?
- Kidney | - Endothelial Cells
41
What is a selective vasopressin receptor peptidergic agonist for V1 receptors and what is it used for?
Terlipressin - Vasoconstrictor action - Used for GI bleeds
42
What is a selective vasopressin receptor peptidergic agonist for V2 receptors and what is it used for?
Desmopressin (DDAVP) - synthetic AVP - a VP substitute for people with Cranial Diabetes Insipidus that acts specifically on V2 receptors in the kidneys
43
How is Desmopressin administered?
Nasally Orally Subcutaneous (injection)
44
What are the effects of Desmopresin in a patient with Cranial Diabetes Insipidus?
Reduction in urine volume Increase in urine concentration
45
Why must patients started on Desmopressin be warned to not continue drinking large amounts of fluid (polydipsia)?
Given them AVP V2 receptors will be working They will retain a lot more water than needed Risk of hyponatraemia [low sodium]
46
What treatment is used for Nephrogenic Diabetes Insipidus?
Thiazides e.g. bendroflumethiazide
47
What is the mechanism of action of Thiazides as treatment for Nephrogenic Diabetes Insipidus?
POSSIBLE MECHANISM (how they work as treatment is poorly understood) - inhibits Na+/Cl- transport in distal convoluted tubule - diuretic effect - volume depletion - compensatory increase in Na+ reabsorption from the proximal tubule (plus small decrease in GFR etc.) - increased proximal water reabsorption - decreased fluid reaches collecting duct
48
What does SIADH stand for?
Syndrome of Inappropriate ADH
49
What is SIADH?
The plasma vasopressin concentration is inappropriately high for the existing plasma osmolality. - you are retaining more water in the kidneys - diluting your plasma osmolality - therefore, diluting your serum sodium
50
What is the mechanism behind SIADH?
- Increased VP - Increased H20 reabsorption from renal collecting ducts - Expansion of ECF volume - Hyponatraemia OR Euvolaemia (due to ANP from right atrium causing natriuresis) - No swelling etc but do have low serum sodium
51
What is natriuresis?
Excretion of sodium in the urine.
52
What is euvolaemia?
A medical term implying that the individual described appears to have a normal circulatory or blood fluid volume within their body
53
What are the signs of SIADH?
- raised urine osmolality - decreased urine volume (initially) - decreased p[Na+] = hyponatraemia mainly due to increased water reabsorption
54
What are the symptoms of SIADH?
Can be symptomless However if p{Na+] <120mM - generalised weakness - poor mental function - nausea If p[Na+] <110 mM - confusion - leading to coma and death
55
What are the causes of SIADH?
CNS - Sub-Arachnoid Haemorrhage - Stroke - Tumour - TBI PULMONARY DISEASE (always do chest x-ray of patient with SIADH) - Pneumonia - Bronchiectasis MALIGNANCY - Lung (Small Cell Carcinoma) DRUG-RELATED - Carbamazepine - SSRI IDIOPATHIC
56
How do you treat someone with SIADH?
Appropriate Treatment (e.g. surgery for tumour) To Reduce Immediate Concern i.e. hyponatraemia 1. Immediate: fluid restriction 2. Longer-term: use drugs which prevent vasopressin action in kidneys - e.g. Induce nephrogenic diabetes insidious to reduce renal water reabsorption. This drug is demeclocyline - e.g. Inhibit action of ADH. V2 receptor antagonists (Vaptans)
57
What drugs are used as longer-term treatment for SIADH?
Dermeclocyline (induces nephrogenic diabetes insipidus) V2 Receptor Antagonists (inhibits action of ADH)
58
What is another name for drugs which are V2 Receptor Antagonists?
VAPTANS
59
What is Aquaresis?
Solute-sparing renal excretion of water
60
What is the contrast between aquaresis and diuresis?
Aquaresis spares solutes whilst excreting water Diuresis produces simultaneous loss of water and electrolytes
61
How do V2 Receptor Antagonists work to treat SIADH?
They inhibit aquaporin2 synthesis and transport to the collecting duct apical membrane This prevents renal water reabsorption
62
What limits the use of V2 Receptor Antagonists as SIADH treatment?
They are very expensive.

Yr 2 LCRS - Endo (28 decks)

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