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Endo yr 2 > disorders of vasipressin > Flashcards

disorders of vasipressin Flashcards

1
Q

how does anterior pituitary communicate with hypothalamus structurally?

A

not anatomically continuous, hormones sent through hypothalamic- pituitary portal system

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2
Q

how does hypothalamus communicate with posterior pituitary?

A

they are anatomically continuous
long neurons originate in supraoptic and paraventricular hypothalamic nuclei, go through stalk and terminate in posterior pit

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3
Q

other name for arginine vasioressin

A

anti diuretic hormone

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4
Q

Main physiological action of vasopressin

A

stimulation of water reabsorption in the renal collecting duct when dehydrated

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5
Q

does vasopressin make urine more or less concentrated?

A

more

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6
Q

what receptor does vasopressin mainly bind to in which organ?

A

V2 receptor in kidney

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7
Q

what other functions does vasopressin have?

A

responce to stress:
vasoconstriciton by binding to V1 receptor

stimulates ACTH release from anterior pituitary

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8
Q

describe mechanism of water reabsorption stimulated by avp in renal tubule cell (also see slide 5 image)

A

1) avp binds to V2 receptor in basolateral membrane
2) g protein links to V2 receptor and activates adenylate cyclase
3)- activates cAMP - activates protein kinase A-> leads to aquaporins binding on both apical and basolateral membranes

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9
Q

what does posterior pit look like on MRI?

A

bright spot (little white - comma shaped lol) look at image ipad

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10
Q

what is the stimulus for AVP release?

A

increase in plasma osmolarity (happens when ur dehydrated) sensed by osmoreceptors

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11
Q

what are osmoreceptors and where?

A

special sensory receptors in hypothalamus

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12
Q

How do osmoreceptors communicate the need for AVP to hypothalamus?

A

when increased osmolarity in blood, osmoreceptor cells loose water, they shrink

the shrinking leads to increased osmoreceptor firing to hypothalamus leading to AVP release

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13
Q

what is the end goal of the body in its physiological responce to water deprivaion?

A

reducing the plasma osmolarity so that you dont get even more dehydrated by your cells losing fluids in your blood

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14
Q

problem in what areas can cause AVP deficiency? (AVP-D)

A

hypothalamus or posterior pituitary

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15
Q

what is the old name for AVP-D

A

Cranial (central) diabetes insipidus

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16
Q

what is the pathology in AVP-R

A

KIDNEY is unable to respond to AVP but hypothalamus and posterior pituitary are wokring fine

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17
Q

what is the other name for arginine vassopressin resistance

A

nephrogenic diabetes insipidus

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18
Q

why do we not call them diabetes insipidus any more

A

huge confusion in doctors with diabetes melitus and ppl have died

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19
Q

what happens to urine volume and concentration during AVP defeciency and resistance ?

A

increased volume and decreased osmolarity (more dilute)

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20
Q

what happens to plasma osmolarity during AVP - D and R ?

A

increases

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21
Q

what do we feel as a response in increased plasma osmolarity and how is it detected?

A

the response is thirst and the detection method is stimulation of osmoreceptors

22
Q

can avp resistant/ deficient patients be ok without medication?

A

yes as long as they have access to water

23
Q

what happens if AVP resistant/ deficient patients don’t have access to water?

A

it can lead to dehydration and death

24
Q

what are the sympotms of AVP- and R

A

Polyuria
Nocturia
Thirst – often extreme
Polydipsia

25
Q

what is the most common diagnosis for the symptoms of polyuria, nocturia, thirst (often extreme) and polydipsia and what causes them? what is alternative diagnosis

A

diabetes melitus due to osmotic diuresis
alt: AVP - D OR R

26
Q

HOW to distinguish between diabetes melitus and AVP - D R

A

in avp r and d
in blood

glucose normal
hypernatraemia
hyperosmolar blood

and
very dilute urine
large volumes

27
Q

is congenital or acquired AVP-D more common?

A

acquired

28
Q

what are some acquired causes of AVP-D

A

Traumatic brain injury
Pituitary surgery
Pituitary tumours
Metastasis to the pituitary gland eg breast
Granulomatous infiltration of pituitary stalk eg TB, sarcoidosis
Autoimmune

29
Q

is AVP resistance or deficiency more common?

A

AVP deficiency

30
Q

is congenital AVP resistance common? what is the cause

A

no, : mutation in gene encoding V2 receptor (aquaporin 2 type water channel)

31
Q

example of acquired cause of AVP R

A

drugs : lithium (lithium carbonate taken for manic depression and mental stuff )

32
Q

what is a differential diagnosis other than diabetes melitus and AVP -D or R for polydipsia, polyuria and nocturia?

A

psychogenic polydipsia

33
Q

what happens in psychogenic polydipsia?

A

no problem with arginine vasopressin
problem is patient drinks too much water because they think they have some issue/ think they need to and they pass large volumes of dilute urine

34
Q

explain exact mechanism (with avp) of how drinking too much water makes you pee large volumes of dilute urine

A

1) increased drinking 2) plasma osmolarity decreases 3) less AVP released 4) more volume of dilute urine excreted 5) plasma osmolarity back to normal

35
Q

what is done to distinguish between AVP def resistance and psychogenic polydipsia?

A

water deprivation test,
1) no access to anything to drink
2) measure:
-urine osmolarity
-urine volumes
-plasma osmolarity
-weight regularly
3) over 8 hours

(see ipad for graphs)- urine osmolarity over time increases for normal, increases but LESS than normal for psychogenic bc some concentrating ability lost
for defeciencies osmolarity remains super low

36
Q

what is a marker that should interupt the test?

A

if loss of > 3% of body weight its a sign of significant dehydration which can occure in AVP resistance/ deficiency

37
Q

what is done to distinguish between avp d and r?

A

desmopressin is given which will act as AVP. In deficiency there will be a change (increase in urine osmolarity over few hours whereas there will be no change in avp r as the kidneys cant respond.

38
Q

what is the treatment for AVP-d

A

-need to replace vasopressin
-give desmopressin

39
Q

why is chemically prepared: desmopressin given as medication to avp d instead of arginine vasopressin?

A

1) desmopressin is selective to V2 receptor (doesnt act on V1 receptor, this would aimlessly raise BP)
2) chemically prepared is not biodegradable so it lasts way more: whole day

40
Q

different preparaitons of desmopressin

A

tablets
intranasal

41
Q

AVP resistance treatment

A

thankfully its very rare bc its difficult to treat successfully

42
Q

what is syndrome of inappropriate Anti-Diuretic Hormone? (SIADH)

A

too much AVP

43
Q

What are the symptoms of SIADH

A

REDUCED URINE OUTPUT: water retention
increased urine osmolarity
reduced plasma osmolarity
dilutional hyponatraemia

44
Q

what is dilutional hyponatraemia

A

when you get confused because of too much water/ little sodium in the brain

45
Q

categories of causes of SIADH

A

CNS related,
lung related
drug related
idiopathic (we don’t know why)

46
Q

CNS causes of SIADH

A

head injury
stroke
tumour

47
Q

lung related causes of SIADH

A

PNEUMONIA,
BRONHIECTASIS,
small cell lung cancer (cells retain a lot if water in this condition)

why are lungs so relevant:
(in general sometimes lung cells release adh ans hang on to water, maybe evolutionary for when you are septic to have water but now we have antibiotics so its actually more harm than good)

48
Q

drug related causes od SIADH

A

Carbamazepine, Serotonin Reuptake Inhibitors (SSSRIs)

49
Q

what does SIADH commonly lead toin hospital ?

A

common to cause a prolonged hospital stay

50
Q

how do you treat SIADH ?

A

restrict fluids
can use a vasopressin receptor antagonist (vaptan) binds to v2 receptor in kidney (very expensive) (also not good long term solution)

51
Q

what should you be careful with in SIADH patients when in hospital?

A

how many fluids you give them, in normal patients for sepsis for ex ud give so many fluids in these patients sodium conc in blood drops and theres confusion

Endo yr 2 (11 decks)

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