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endo - yr2 > neurohypophysial disorders > Flashcards

neurohypophysial disorders Flashcards

1
Q

summarise the neurohypophysial system

A

the paraventricular nucleus and the supraoptic nucleus are in the hypothalamus
the neurons from these project through the stalk into the posterior pituitary
oxytocin and vasopressin are released from these neurons

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2
Q

what is the principle effect of vasopressin

A

Anti-diuretic hormone - increases water reabsorption from renal cortical and medullary collecting ducts by binding to V2 receptors and reduce urine production

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3
Q

define diuresis

A

increase in urine production and loss of electrolytes

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4
Q

what are the posterior pituitary hormones *

A

oxytocin and vasopressin

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5
Q

describe the how vasopressin causes water reabsorption

A

VP binds to V2 receptors
causes an intracellular signalling cascade
stimulate AC
elevate cAMP
activate PKA
which results in the synthesis of aquaporin 2
the aggraphores migrate towards the apical membrane
AQP2 inserts into the wall
provides a water channel and allow water down the osmotic gradient into the collecting duct cell
water then continues down the conc grad into the plasm through AQP 3 and 4

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6
Q

where are the osmoreceptors and what are they near

A

organum vasculosum, near the hypothalamus

the neurons project to the paraventricular nucleus and supraoptic nucleus which release VP

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7
Q

describe how osmoreceptors are involved in VP release

A

they are v sensitive to changes in EC osmolarity
if there is an increase in EC Na conc - ie osmolarity of the blood
this causes water to leave the osmoreceptor down the osmotic gradient
the osmoreceptor then shrinks - this irritates the osmoreceptor and causes increased osmoreceptor firing
this results in VP release for the hypothalamic PVN and SON neurons that are in the hypothalamus

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8
Q

describe the normal response to water deprivation

A

increased plasma osmolarity
this stimulates osmoreceptors (induces thirst)
increase VP release
increase water reabsorption from the renal collecting ducts - body retain as much as impossible
therefore the serum osmolarity is reduced and there is reduced urine vol, increase in urine osmolarity

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9
Q

what is the problem with diabetes insipidus *

A

cant absorb water properly = dehydration

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10
Q

what are the 2 subtypes of DI *

A

cranial/central (CNS) - absence or lack of circulating VP - problem with VP production
nephrogenic - end organs (kidneys) are resistant to VP - the intracellular cascade is abnormal, kidney cant respond to VP

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11
Q

what is the cause of cranial DI *

A

acquired more common than congenital
damage to the neurohypophysial system - mess with the pituitary of the stalk
traumatic brain injury
pit surgery - transiently
pituitary tumours eg craniopharyngioma (tumour derived from pit embryonic tissue)
metastasis to the pituitary gland eg breast
granulomatous infiltration of median eminence eg TB, sarcoidosis, hypophysitis - if inflamed the VP cant get into the posterior pit - VP travel down stalk from hypothalamus

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12
Q

what is the cause of nephrogenic DI *

A

congenital - mutation anywhere in the cascade eg mutation in gene encoding V2 receptor, AQP2 type water channel.
acquired - drug eg lithium - toxicity/long term lithium can also cause primary hypoparathyroidism
high Ca

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13
Q

signs and symptoms of DI *

A

polyuria (cant absorb the water
very dilute urine - hypo-osmolar
polydipsia and thirst - to replace the lost water
because large vol
dehydration and death if the fluid intake is not maintained because a large volume of fluid is lost in the urine.
possible disruption to sleep - getting up in the night to pass urine

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14
Q

what is the osmolarity of urine for people with DM and why

A

hyperosmolar - there is a lot of glucose in the urine

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15
Q

describe the process of fluid control in DI *

A

there is inadequate production of or response to ADH
therefore large vol of dilute (hypotonic) urine is produced (no water reabsorbed)
become dehydrated so there is an increase in the plasma osmolarity and Na and a reduction in EC fluid vol
this causes thirst - polydipsia - have to drink all the time to stay alive
EC fluid vol expands as you drink more

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16
Q

what happens in DI when you have no access to water *

A

you have the reduction in EC vol, increase in plasma os and Na
you cant maintain plasma osmolarity by large intake of water -> dehydration and death

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17
Q

why would you have no access to water

A

stroke

post-op so under general anaesthetic (GA)

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18
Q

describe the overall concept of psychogenic/primary polydipsia *

A

they have excess fluid intake - polydipsia and therefore pass a lot of hypotonic urine - natural process

ability to produce VP in response to osmotic stimuli is preserved.

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19
Q

what kind of people get psychogenic polydipsia *

A

psychiatric patients

people told to drink plenty

20
Q

aetiology of psychogenic/primary polydipsia *

A

unclear

may be because of anti-cholinergic effects of medication in psychiatric patients - dry mouth so drink more

21
Q

describe the pathway of psychogenic polydipsia *

A

increased drinking
expansion of EC fluid vol, reduce in plasma osmolarity
therefore less VP secreted by posterior pituitary gland
therefore large vol of hypotonic urine is produced
EC vol returns to normal

22
Q

what is the difference in the plasma osmolarity of someone with DI and someone with psychogenic polydipsia *

A

plasma osmolarity high in DI because intake cant keep up with the water leaving as urine

polydipsia - plasma osmolarity is lower - plasma is diluted by the excess intake of water

23
Q

what is the process of a water stress test *

A

place the person in a room with no water and measure the conc of the urine, vol of urine and plasma osmolarity
it is used to test for DI and psychogenic polydipsia
measure body weight every hour, if lose 3% weight - stop experiment it shows clinical dehydration and is dangerous. also shows it is DI, because the person cant conc urine even when there is no fluid intake so are losing a lot of fluid

24
Q

describe what the normal response should be to a water stress test when fluid deprived and when you have DDAVP administration (analogue of VP) *

A

urine osmolarity increases when fluid deprived - VP produced and reabsorb more water from the urine - produce little/no urine - maintain plasma osmolarity
when DDAVP is added - there is no further change to urine osmolarity as VP was already present and worked

25
Q

describe what the psychogenic polydipsia response should be to a water stress test when fluid deprived and when you have DDAVP administration (analogue of VP) *

A

when fluid deprived still have the VP system so can concentrate urine - urine osmolarity increases
when DDAVP is added - no change - VP system is already working normally

ie the response is the same as a normal person. Urine osmolarity might be slightly lower than normal if they have been drinking excess long term because they have overcome the water concentration gradient in the kidney

26
Q

describe what the central DI response should be to a water stress test when fluid deprived and when you have DDAVP administration (analogue of VP) *

A

fluid deprivation - cant conc urine as not producing any VP so still produce large vol of hypotonic urine so urine osmolarity stays the same
when given DDAVP - VP system now work, because the body can respond to vasopressin so urine osmolarity increases

27
Q

describe what the nephrogenic DI response should be to a water stress test when fluid deprived and when you have DDAVP administration (analogue of VP) *

A

fluid deprivation - cant conc urine as not responding to VP so still produce large vol of hypotonic urine so urine osmolarity stays the same
when given DDAVP - kidney still can’t respond to VP so the urine is not concentrated

28
Q

what are the biochemical features of DI *

A

hypernatremia, raised urea and increased plasma osmolarity - markers in the bloodstream that show you’re dehydrated
dilute hypo-osmolar urine - low urine osmolarity

29
Q

what is the first condition you thing of when presented with osmotic symptoms - polyuria, nocturia and polydipsia

A

DM

30
Q

biochemical features of psychogenic polydipsia *

A

mild hyponatraemia and low plasma osmolarity - because excess water intake dilutes everything
dilute hypoosmolar urine - this is appropriate considering the excess intake

31
Q

why do we need selective VP receptor agonists and what is the V2 peptidergic agonist *

A

lots of VP all over body - we specifically want to activate V2 - desmopressin

32
Q

how is desmopressin administered and issues with this *

A

nasally - people think nasal spray is a less important medication so it gets pushed to the sid e
orally
buckle tablet
SC injection eg after pituitary operation injection

give at niught to prevent nocturia

33
Q

how does desmopressin work, what does it treat, warning you need to give patients *

A

works like VP
casues a reduction in urine vol and conc
treats CRANIAL DI
need to tell patients not to drink large amounts of fluid - now they can reabsorb water they would be at risk hyponatraemia

34
Q

how would you treat nephrogenic DI *

A

thiazide diuretics
complex mechanism

prostaglandin inhibitors
high dose of desmopressin

35
Q

what is syndrome of inappropriate ADH *

A

the plasma VP conc is inappropriately high for the existing plasma osmolarity
so produce very conc urine

36
Q

pathophysiology of SIADH *

A

increased VP
therefore increased water reabsorption
expansion of ECF vol
hyponatraemia and atrial natriuretic peptide which causes natriuresis and further hyponatraemia and returns EC fluid vol to normal

37
Q

causes of SIADH *

A

CNS or lung problem so do brain CT and chest x-ray
CNS - subarachnoid haemorrhage, tumour, stroke, traumatic brain injury
pul disease - pneumonia, bronchiectasis - chest infection
malignancy - lung (small cell), ectopic tumour
drug related - carbamazepine for epilepsy or SSRI (antidepressants)
idiopathic

38
Q

signs of SIADH *

A

raised urine osmolarity and decreased vol

hyponatraemia - due to water reabsorption diluting plasma Na - plasma osmolarity has reduced

39
Q

symptoms of SIADH *

A

can be symptomless
p[Na+] <120mM - generalised poor mental function and nausea
if p[Na+] <110 mM confusion leading to coma and death

low Na cause neuron instability because you get oedema in the brain

40
Q

treatment of SIADH *

A

appropriate treatment - eg remove lung cancer
then reduce immediate concern eg the hyponatraemia
- short term: fluid restriction - reduce the vol of intake because they’re reabsorbing it all
- long term: use drugs which prevent vasopressin action in kidneys eg induce nephrogenic DI to reduce renal absorption using lithium or V2 receptor antagonists eg demeclocycline - inhibit action of ADH

41
Q

describe VAPTANS *

A

non-comp V2 receptor antagonists
inhibit ACP2 synthesis, transport to membrane abd renal absorption
aquaresis - solute sparing renal excretion of water - don’t want to lose Na because already hyponatraemic
very expensive so limits the current use.

42
Q

why do we look at Na to measure plasma osmolarity

A

it is the predominant anion in the blood so expresses the most osmotic pressure:
osmotic pressure= 2xNa+K+urea +glucose k is 5 ur 4 glu 5

43
Q

how can you treat cranial DI fro peole who pass <4L of water a day *

A

get them to drink plenty

44
Q

role of oxytocin

A

parturition and milk ejection effects easily induced/replaced by other means

45
Q

can lithium cause DI *

A

yes - nephrogenic DI

46
Q

is SIADH associated with fluid overload *

A

no- this is psychogenic DI

endo - yr2 (24 decks)

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