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Year 2- ENDO mine > Neurohypophysial disorders > Flashcards

Neurohypophysial disorders Flashcards

1
Q

how can the posterior pituitary be identified on the MRI?

A

‘bright spot’ on pituitary MRI

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2
Q

what are the two nucleus associated with the hypothalamo-neurohypophysial system

A

paraventricular and supraoptic nucleus

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3
Q

what hormones does the neurohypophysis secrete?

A

oxytocin and vasopressin

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4
Q

what is the principal effect of vasopressin?

A

= ANTI-DIURETIC ie increases water reabsorption from renal cortical and medullary collecting ducts via V2 receptors

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5
Q

what is vasopressin also known as?

A

Vasopressin also known as ADH – Anti Diuretic Hormone

Diuresis = increase in urine production

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6
Q

describe the actions of vasopressin?

A
  • acts on the renal cortical and medullary collecting ducts (SPECIFICALLY: DCT + CT)
  • acts on V2 receptors
  • increases cAMP
  • activated PKA
  • stimulates synthesis and assembly of aquaporin 2
  • increased water transport
  • this has an antidiuretic effect
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7
Q

what does oxytocin do?

A

contraction of myometrium at parturition
milk ejection reflex
central effects
acts on oxytocin receptors

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8
Q

where are the osmoreceptors located?

A 
organum vasculosum (devoid of the BBB)
osmoreceptors then project to the hypothalamic PVN and SON
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9
Q

what are osmoreceptors very sensitive to?

A

changes in extracellular osmolality

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10
Q

what happens to the osmoreceptors when there is an increase in extracellular sodium?

A

Water moves out of the osmoreceptors when the extracellular sodium conc increases and the osmoreceptors shrink
this leads to increased osmoreceptor firing
VP is then released from hypothalamic PVN and SON neurones

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11
Q

what is the normal response to water deprivation?

A

lack of water leads to increased serum osmolality
this stimulates the osmoreceptors (leading to thirst)
this increases VP release
this increases water re-absorption from renal collecting ducts
this leads to a reduction in serum conc as well sa reduced urine volume and an increase in urine osmolality

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12
Q

what is diabetes insipidus?

A

Absence or lack of circulating vasopressin

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13
Q

what are the two types of diabetes insipidus and what is the difference between the two?

A

cranial diabetes insipidus: lack of VP being produced from the brain

nephrogeic diabetes insipidus: this is when the kidneys are resistant to the vasopressin, there is still vasopressin being produced but it cannot carry out its function

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14
Q

what are the acquired and congenital causes of cranial diabetes insipidus?

A

Acquired (more common)
Damage to Neurohypophysial system
Traumatic brain injury
Pituitary surgery
Pituitary tumours, craniopharyngioma
Metastasis to the pituitary gland eg breast
Granulomatous infiltration of median eminence eg TB, sarcoidosis

Congenital - rare

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15
Q

what are the acquired and congenital 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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16
Q

what are the signs and symptoms of diabetes insipidus?

A

Large volumes of urine (polyuria)
Urine very dilute (hypo-osmolar)
Thirst and increased drinking (polydipsia)
Dehydration (and consequences) if fluid intake not maintained - can lead to DEATH
Possible disruption to sleep with associated problems

17
Q

what is the process of diabetes insipidus?

A

inadequate production/response to VP
large volumes of dilute (hypotonic urine)
increase in plasma osmolality and sodium
reduction in EC fluid volume
thirst-polydipsia
EC fluid volume expansion
-HOWEVER-
if there is no access to water then it can lead to dehydration and death

18
Q

what is psychogenic polydipsia?

A

Excess fluid intake (polydipsia) and excess urine output (polyuria) – BUT unlike DI, ability to secrete vasopressin in response to osmotic stimuli is preserved

19
Q

what are the causes of psychogenic polydipsia?

A

Most frequently seen in psychiatric patients – aetiology unclear, may reflect anti-cholinergic effects of medication – ‘dry mouth’
Can be in patients told to ‘drink plenty’ by healthcare professionals

20
Q

what happens in psychogenic polydipsia?

A 
increases drinking 
expansion of EC fluid volume, reduction in plasma osmolality 
less VP secreted by posterior pituitary 
large volumes of dilute urine 
EC volume return to normal
21
Q

what is the difference in plasma osmolality in diabetes insipidus and psychogenic polydipsia?

A

diabetes insipidus= plasma osmolality too high

psychogenic polydipsia= plasma osmolality too low

22
Q

how would you test for diabetes insipidus?

A

-water deprivation test
no water allowed and the urine osmolality is measured
then administer DDAVP

23
Q

in a water deprivation test what happens in normal, p polydipsia, central DI and nephrogenic DI?

A
  • urine osmolality
    normal: increases (as more water is retained)- urine is more concentrated

p polydipsia: increases

central DI: v little change

nephrogenic DI: v little change

24
Q

in a water deprivation test what happens when you add DDAVP in normal, p polydipsia, central DI and nephrogenic DI?

A
  • urine osmolality
    normal: drops slightly

p polydipsia: drops slightly

central DI: urine osmolality increases

nephrogenic DI: stays the same

25
Q

what are the biochemical features of diabetes insipidus?

A

Hypernatraemia (inc sodium ion conc)
Raised urea
Increased plasma osmolality
Dilute (hypo-osmolar) urine - ie low urine osmolality

26
Q

what are the biochemical features of psychogenic polydipsia?

A

Mild hyponatraemia – excess water intake
Low plasma osmolality
Dilute (hypo-osmolar) urine - ie low urine osmolality

27
Q

what is the treatment for diabetes insipidus?

A

Vasopressin receptor agonists- V2 desmopressin

28
Q

how can desmopressin be administered?
what does it do?
what do you need to be careful of?

A

Administration
Nasally
Orally
SC
Reduction in urine volume and concentration in cranial DI
CARE – to tell patient starting this NOT to continue drinking large amounts of fluid – risk of hyponatraemia

29
Q

what is the treatment for nephrogenic diabetes insipidus?

A

thiazides

eg bendroflumethiazide

30
Q

what are the possible mechanism for thiazides?

A

Possible mechanism
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
Reduced urine volume

31
Q

what is SIADH?

A

the plasma vasopressin concentration is inappropriately high for the existing plasma osmolality

32
Q

what happens in SIADH?

A

increased vasopressin
leads to increased water reabsorption from renal collecting ducts
leads to expansion of ECF volume
this can lead to hyponatraemia (LOW sodium ions)

33
Q

what are the signs for SIADH?

A

raised urine osmolality, decreased urine volume (initially)

decreased p[Na+] (HYPONATRAEMIA) mainly due to increased water reabsorption

34
Q

what are the symptoms for SIADH?

A

can be symptomless
however if p[Na+] <120 mM: generalised weakness, poor mental function, nausea
if p[Na+] <110 mM: CONFUSION leading to COMA and ultimately DEATH

35
Q

what are the cuases of SIADH?

A 
-CNS
SAH, stroke, tumour, TBI
-Pulmonary disease
Pneumonia, bronchiectasis
-Malignancy
Lung (small cell)
-Drug-related
Carbamazepine, SSRI
-Idiopathic
36
Q

what is the treatment for SIADH?

A

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 DI ie reduce renal water reabsorption - demeclocyline
inhibit action of ADH - V2 receptor antagonists

37
Q

what are VAPTANS and how do they work?

A

VAPTANS
Non-competitive V2 receptor antagonists.
Used in the treatment of SIADH
Inhibit aquaporin2 synthesis and transport to collecting duct apical membrane, preventing renal water reabsorption
Aquaresis – solute-sparing renal excretion of water, contrast with diuretics (diuresis) which produce simultaneous electrolyte loss
Licensed in the UK for treatment of hyponatraemia associated with SIADH
Very expensive – limits their current use

Year 2- ENDO mine (19 decks)

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