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Year 2 - Endocrinology > Neurohypophysial Disorders > Flashcards

Neurohypophysial Disorders Flashcards

1
Q

Supraoptic nucleus?

A
  • Magnocellular Neurones
  • Terminate in neurohypophysis
  • Release neurosecretions into neurohypophysis
  • Herring Bodies - sites of storage of the NS/hormone
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2
Q

2 hormones of the neurohypophysis?

A

Vasopressin (ADH)

Oxytocin

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3
Q

Principal effect of vasopressin?

A

Anti-diuretic

i.e. increases water reabsorption from renal cortical & collecting duct via V2 receptors

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4
Q

Diuresis?

A

Increase in urine production
SO
anti-diuretic - decreases urine production

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5
Q

Vasopressin action?

A
  1. VP binds to V2 receptors (Gs receptors)
  2. AQP2 created which more to apical membrane in aggraphores
  3. AQP2 insert into apical membrane = water reabsorption
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6
Q

What regulates vasopressin release?

A

Osmoreceptors in the Organum Vasculosum

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7
Q

How do these osmoreceptors work?

A

Project axons into the hypothalamic PVN and SON

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8
Q

When do osmoreceptors fire the most?

A

Increased blood plasma osmolality

Send more signals as they shrink to release VP

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9
Q

2 types of diabetes insipidus?

A

Cranial (central)

Nephrogenic

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10
Q

Definition of the 2 types of diabetes insipidus?

A

Cranial - ABSENCE/LACK of circulating VP

Nephrogenic - End-organ (kidneys) RESISTANCE to VP

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11
Q

2 subtypes of cranial DI - which is more rare?

A

Acquired (more common)

Congenital (rare)

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12
Q

Aetiology of acquired cranial DI?

A 
Damage to Neurohypophysial system
x Traumatic brain injury
x Pituitary surgery
x Pituitary tumours, craniopharyngioma
x Metastasis to the pituitary gland
x Granulomatous infiltration of median eminence e.g. TB (pituitary stalk issue!)
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13
Q

2 subtypes of nephrogenic DI - which is more rare?

A

Cogenital (rare)

Acquired

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14
Q

Aetiology of nephrogenic diabetes?

A

Cogenital - mutation in V2 receptor/AQP2

Acquired - drugs e.g. lithium (used in depression medication)

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15
Q

Signs/symptoms of DI?

A

x Polyuria
x Hypo-osmolar urine (very dilute)
x Polydipsia (increased thirst & drinking)
x Dehydration - if fluid intake not maintained could lead to death
x Possible sleep disruption & fatigue

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16
Q

What keeps patients with DI from dying?

A

Access to water - keeps them just about hydrated

If remove access to water = dehydration & death

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17
Q

What is psychogenic polydipsia?

A

Polydipsia & Polyuria as excess fluid intake
BUT
unlike DI, ability to secrete VP is preserved

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18
Q

When can you get psychogenic polydipsia?

A

x Psychiatric patients - anti-cholinergic effects of mediaition (‘dry-mouth)

x Can also be seen in patients told to ‘drink plenty’ by healthcare progessionals

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19
Q

Difference in plasma osmolality between DI and PP patients? Why?

A

DI - HIGH plasma osmolality

PP - LOW plasma osmolality

Even though both drink LOTS of water, difference lies in VP

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20
Q

How can you diagnose if a patient has DI or PP?

A

Water deprivation test

cannula inserted to take regular readings

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21
Q

What can be seen in the water deprivation test when the patient is deprived of fluid?

A

Normal - urine osmolality increases

PP - urine osmolality increases

DI - urine osmolality does NOT increase (as cannot reabsorb water!)

*pay attention its URINE osmolality NOT plasma!

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22
Q

What is a limitation of the water deprivation test and how can it be overcome?

A

Cannot differentiate between central & nephrogenic DI if just deprive fluid

Need to administer DDAVP

23
Q

DDAVP?

A

Synthetic AVP - analogue of VP

24
Q

Why does a PP patient have a slightly lower urine osmolality than a normal patient?

A

The polydipsia has ‘washed away’ the [graidnet] in the medulla slightly

25
Q

Difference between Central & Nephrogenic DI when DDAVP is administered?

A

Central - urine osmolality INCREASES (as issue is they can’t MAKE VP so can respond to it!)

Nephrogenic - urine osmolality STAYS THE SAME (as cannot respond to VP at all!)

26
Q

DI biochemical features?

A
  • Hypernatraemia
  • Raised urea
  • Increased plasma osmolality
  • Hypo-osmolar urine
27
Q

PP biochemical features?

A
  • Mild HYPOnatraemia - as excess water intake
  • Low plasma osmolality
  • Hypo-osmolar urine
28
Q

What is an issue with exogenous VP treatment?

A

ALL VP receptors will be activated (V1 & V2) - when just want V2

29
Q

How do we overcome the issue with exogenous VP treatment?

A

Use SELECTIVE VP receptors - they are PEPTIDERGIC AGONISTS

30
Q

Selective VP receptor agonists ?

A

V1 - Terlipressin

V2 - DDAVP (Desmopressin!)

31
Q

How can Desmopressin (DDAVP) be administered?

A

Nasally
Orally
Sub-cutaneous (e.g. if after PG surgery as went up nose for that)

32
Q

What results can be seen after Desmopressin (DDAVP) use?

A

Reduction in:
x urine volune & concentration

(in cranial DI)

33
Q

Desmopressin?

A

DDAVP

34
Q

What do you need to ensure in patients who take Desmopressin (DDAVP)?

A

Tell patient to NOT continue drinking large amounts of fluid - risk of hyponatraemia

35
Q

What is a potential treatment of nephrogenic DI?

A

Thiazides - don’t really know mechanism & hard to treat nephrogenic DI

(a bit odd because this actually makes you pass MORE urine in other cases!)

36
Q

Possible mechanism of thiazides in use as treatment for nephrogenic DI?

A
  1. Inhibits Na+/Cl- transport in DCT (promotes dieresis)
  2. Volume depletion
  3. Compensatory increase in Na+ reabsorption from PCT
  4. Increased PCT water reabsorption
  5. Decreases fluid reaching collecting duct
  6. Reduced urine volume
37
Q

SIADH?

A

Syndrome of Inappropriate ADH

38
Q

Definition of SIADH?

A

Plasma [VP] is INAPPROPRIATELY HIGH for exisiting plasma osmolality

39
Q

What can an expansion of ECF volume lead to?

A

x Hyponatraemia

x Atrial Natriuretic Peptide (ANP) release from right atrium = natriuresis = hyponateamia & euvolaemia

40
Q

Natriuresis?

A

Excretion of Na+ in the urine

41
Q

Euvolaemia?

A

State of normal body fluid volume

42
Q

Sign of SIADH?

A

x raised urine osmolality
x decreased urine volume (initally)
x decreased p[Na+] (nyponatraemia) mainly due to increased water reabsorption

43
Q

Symptoms of SIADH?

A

Can be symptomless!

BUT can lead to issues if p[Na+] is below threshold

44
Q

p[Na+] < 120mM?

A

x Generalised weakness
x Poor mental function
x Nausea

45
Q

p[Na+] < 110mM?

A

Confusion = Coma = Death

46
Q

5 potential causes of SIADH?

A
  • Normally idiopathic
  • CNS - SAH, stroke, tumour, TBI
  • Pulmonary disease - pneumonia, bronchiectasis
  • Malignancy - lung (small cell)
  • Drug-related - carbamazepine (epilepsy), SSRI
47
Q

Most appropriate treatment for SIADH?

A

Cannot turn off VP production so either:
- treat UNDERLYING cause (e.g. tumour surgery)
OR
- manage the p[Na+] levels

48
Q

What is the immediate concern of SIADH?

A

Hyponatraemia

49
Q

How can you reduce the immediate concern of SIADH?

A
  1. Immediate = fluid restriction

2. Longer-term = use drugs which prevent VP action in kidneys

50
Q

How does the longer-term treatment for SIADH work?

A

Induces nephrogenic DI i.e. reduced renal water reabsorption - demeclocyline

51
Q

Vaptans?

A

Non-competitive V2 receptor antagonists

52
Q

Mechanism of vaptans?

A
  • Inhibit AQP2 synthesis and transport to apical membrane

- Aquaresis

53
Q

Issues with vaptans use?

A

VERY expensive

54
Q

Aquaresis?

A

Solute-sparing renal exrection of water

In contrast w. diuretics (diuresis) which produces simultaneous electrolyte loss

Year 2 - Endocrinology (19 decks)

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