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LCRS Year 2 - Endocrinology > Neurohypophysial (Posterior Pituitary) Disorders > Flashcards

Neurohypophysial (Posterior Pituitary) Disorders Flashcards

1
Q

What is the term for a group of neuronal cell bodies?

A

Nucleus

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2
Q

What are the names of the two hypothalamic nuclei that supply the neurohypophysis?

A

Supraoptic

Paraventricular

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3
Q

What are the two main hormones produced by the neurohypophysis?

A

Vasopressin (ADH)

Oxytocin

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4
Q

What is the principal effect of vasopressin/ADH and how does it do this?

A

Anti-diuretic

  • Increases water reabsorption from renal cortical and medullary collecting ducts via V2 receptors
  • Decreases urine production
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5
Q

What is the name of the small region of the brain which regulates vasopressin release?

A

Organum Vasculosum

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6
Q

What is located in the Organum Vasculosum which allows regulation of vasopressin release and what do they project to/communicate with?

A

Osmoreceptors (neurones)
- Project to hypothalamic paraventricular and supraoptic nuclei which then control posterior pituitary action and thus vasopressin release

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7
Q

Osmoreceptors are very sensitive to extracellular osmolality. What sequence of events takes place when there is an increase in extracellular sodium?

A

Osmoreceptor shrinks as water flows out of them

  • Increased osmoreceptor firing
  • Stimulates vasopressin release from hypothalamic paraventricular and supraoptic neurones
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8
Q

What is the normal response to water deprivation?

A
  • No water is drank
  • Serum osmolality is increased
  • Osmoreceptors are stimulated
  • Thirst is stimulated as well as increased vasopressin release
  • More water is reabsorbed from renal collecting ducts
  • Reduced urine volume, increased urine osmolality, reduced serum osmolality
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9
Q

What is the name of the disorder where you have insufficient vasopressin or vasopressin unable to work?

A

Diabetes Insipidus

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10
Q

What are the two types of diabetes insipidus?

A

Cranial (or central)

Nephrogenic (much less common)

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11
Q

Where does the problem lie in cranial and nephrogenic diabetes insipidus?

A

Cranial - absence of lack of circulating vasopressin

Nephrogenic - end-organ (kidneys) resistant to vasopressin, vasopressin unable to work

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12
Q

What are the acquired (more common than congenital) causes of cranial diabetes insipidus?

A

Damage to neurohypophysial system

  • Traumatic brain injury
  • Pituitary surgery
  • Pituitary tumours, craniopharyngioma
  • Metastasis to the pituitary gland e.g. breast
  • Granulomatous infiltration of median eminence e.g. TB, sarcoidosis
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13
Q

What are the congenital and acquired causes of nephrogenic diabetes insipidus?

A

Congenital - rare, e.g. mutation in gene encoding V2 receptor, aquaporin 2 type water channel
Acquired - drugs, e.g. lithium

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14
Q

What are the signs and symptoms of diabetes insipidus?

A
  • Large volumes of urine (polyuria)
  • Urine very dilute (hypo-osmolar0
  • Urinating in the night (nocturia) (disrupted sleep as presenting complaint)
  • Thirst and increased drinking (polydipsia)
  • Dehydration (and its consequences) if fluid intake not maintained - can lead to DEATH
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15
Q

What is the physiological sequence of events in diabetes insipidus starting with inadequate production of/response to vasopressin leading to symptoms when the patient has access to water?

A
  • Inadequate response to/production of vasopressin
  • Large volumes of dilute (hypotonic) urine
  • Increase in plasma osmolality (and sodium)
  • Reduction in extracellular fluid volume
  • Thirst and then polydipsia (drinking a lot)
  • Extracellular fluid volume expands, sort of keeping up with the diabetes insipidus when access to water is provided
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16
Q

What is the difference in physiological events when the patient does NOT have access to water?

A

All the steps up to reduction in extracellular fluid volume occur the same way.

  • Thirst is stimulated but patient has no access to water.
  • Sodium goes up and up and patient becomes dehydrated and possibly dies
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17
Q

What is the other cause of polydipsia in patients with healthy vasopressin release and kidneys?

A

Psychogenic polydipsia

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18
Q

Who is psychogenic polydipsia most frequently seen in, what is the cause, how do health professionals end up making it worse, and what are the two main symptoms despite what?

A
  • Most frequently seen in psychiatric patients
  • Causes are unclear, may be due to anti-cholinergic drug side effects e.g. dry mouth
  • Healthcare professionals tell patients to drink plenty
  • Excess fluid intake (polydipsia) and excess urine output (polyuria)
  • DESPITE ability to secrete vasopressin in response to osmotic stimuli is normal
19
Q

What is the physiological sequence of events in psychogenic polydipsia?

A

Normal response to drinking, no thirst stimulus except mental stimulus to drink

  • Increased drinking (polydipsia)
  • Expansion of extracellular fluid, reduction in plasma osmolality
  • Less vasopressin secreted by neurohypophysis
  • Large volumes of dilute (hypotonic) urine
  • Extracellular fluid volume returns to normal, starts again with excessive drinking
20
Q

How tightly is plasma osmolality controlled, what are the boundaries of the normal range and what conditions cause movement outside these boundaries?

A
  • Very tightly controlled
  • 270-290 mOsm/kg H2O
  • Diabetes insipidus >290
  • Psychogenic polydipsia <270
21
Q

How is diabetes insipidus diagnosed and differentiated from psychogenic polydipsia? (since signs/symptoms are the same)

A

Water deprivation test

  • Patient is asked to not drink water at all and take samples of urine throughout the day when they go to the toilet
  • Results are plotted on a graph of urine osmolality when normally hydrated, fluid deprived, and after DDAVP (vasopressin drug) administration)
22
Q

How does the osmolality and volume of urine change in a normal person after fluid deprivation?

A
  • Osmolality increases

- Volume decreases

23
Q

How does the osmolality of urine change in a psychogenic polydipsia patient after fluid deprivation?

A
  • Osmolality increases but not as concentrated as normal person (due to polydipsia reducing the gradient in the kidney thus less water moves out)
  • Volume decreases
24
Q

How does the concentration and volume of urine change in a diabetes insipidus patient after fluid deprivation?

A
  • Osmolality doesn’t increase as unable to (no VP/VP response)
  • Central and nephrogenic DI around the same osmolality after deprivation as they were hydrated
25
Q

How is central and nephrogenic DI distinguished?

A

Urine osmolality test after injection of synthetic ADH (DDAVP)

  • Central - urine osmolality will increase
  • Nephrogenic - urine osmolality will remain low
26
Q

Draw a diagram of a urine osmolality graph showing the general states (no specific numbers needed) of normal, psychogenic polydipsia, central DI, nephrogenic DI people when normally hydrated, fluid deprived, after DDAVP administered (on paper)

A

Graph in notes

  • Normal goes low, high, slightly less high
  • PP goes low, slightly less high than normal, slightly less high than normal
  • Central DI goes low, low, slightly lower than PP
  • Nephrogenic DI goes low, low, low
27
Q

What are the biochemical features of diabetes insipidus?

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

All due to dehydration due to inability to concentrate urine

28
Q

What are the biochemical features of psychogenic polydipsia?

A
  • Mild hyponatraemia (excess water intake)
  • Low plasma osmolality
  • Dilute urine (hypo-osmolar)
29
Q

Why can just vasopressin not be used to treat diabetes insipidus?

A

Non-selective for V1/2 receptors

  • V1 receptors on lots of organs and smooth muscle types including vasculature, generally won’t have the effect desired as it stimulates all vasopressor effects
  • V2 found on kidney and endothelial cells, selective agent required
30
Q

What is the V2-selective vasopressin receptor agonist drug used?

A

Desmopressin (DDAVP)

31
Q

What are the different routes of desmopressin administration?

A

Nasally
Orally
Subcutaneous

32
Q

What effects does desmopressin cause?

A

Reduction in urine volume

Reduction in concentration in cranial DI (not nephrogenic)

33
Q

What is the caution that needs to be made clear to the patient who is beginning desmopressin?

A

Must tell patient NOT to continue to drink large amounts of fluid once they’ve started on desmopressin
- Risk of hyponataemia now that water is correctly being reabsorbed

34
Q

How is nephrogenic diabetes insipidus treated and how does it work?

A

Using Thiazide Diuretics

  • Mechanism not fully known but can possibly cause increased Na+ reabsorption in proximal tubule and therefore increased water reabsorption in proximal tubule as well
  • Point is it’s very difficult to treat but these go someway to helping
35
Q

What is SIADH and what is its definition?

A

Syndrome of Inappropriate ADH

- by definition “the plasma vasopressin concentration is inappropriately high for the existing plasma osmolality”

36
Q

What is the physiological development of the disease starting with increased vasopressin release?

A
  • Increased VP
  • Increased H2O reabsorption from renal collecting ducts
  • Expansion of extracellular fluid volume
  • Atrial natriuretic peptide from right atrium
  • Natriuresis (sodium being removed with water being retained leads to…)
  • HYPONATRAEMIA
  • Euvolaemia (normal amount of fluid in blood so increased water content is being balanced out by removal of sodium)
37
Q

What are signs of SIADH?

A

Opposite of DI

  • Raised urine osmolality, decreased urine volume (initially)
  • Decreased plasma Na+ concentration (hyponatraemia) mainly due to increased water reabsorption
38
Q

What are the symptoms of SIADH?

A
  • Can be symptomless
  • However, if p[Na+] <120mM, generalised weakness, poor mental function, nausea
  • If p[Na+] <110mM, confusion leading to coma and death
39
Q

What are the causes of SIADH?

A 
CNS - SAH, stroke, tumour, TBI
Pulmonary disease - pneumonia, bronchiectasis
Malignancy - Lung (small cell tumour)
Drug-related - Carbamazepine, SSRI
Idiopathic
40
Q

What is the treatment for SIADH?

A
  • Appropriate treatment for the case (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 DI i.e. reduce renal water reabsorption - demeclocycline
    e. g. inhibit action of ADH - V2 receptor antagonists
41
Q

What are Vaptans?

A

Non-competitive V2 receptor antagonists

42
Q

What do Vaptans do?

A

Inhibit aquaporin2 synthesis and transport to collecting duct apical membrane, preventing insertion into the membrane and therefore preventing renal collecting duct water reabsorption

43
Q

What is meant by the term “Aquaresis” and why is relevant?

A

Solute-sparing renal excretion of water, contrasted with diuresis which produce electrolyte loss with the water loss

This is how Vaptans work in treating SIADH, removes the water but doesn’t disrupt the electrolytes

44
Q

What are Vaptans licensed for use for in the UK and why are they not used more?

A

Licensed in the UK for treatment of hyponatraemia associated with SIADH
- Very (very) expensive

LCRS Year 2 - Endocrinology (21 decks)

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