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brs (phase 1b) > (endo) disorders of vasopressin > Flashcards

(endo) disorders of vasopressin Flashcards

1
Q

what type of hypothalamic neurones release AVP and oxytocin?

A

magnocellular hypothalamic neurones

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2
Q

what type of hypothalamic neurones release TSH/LH/FSH/prolactin/GH/ACTH?

A

parvocellular hypothalamic neurones

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3
Q

what are magnocellular neurones?

A

hypothalamic neurones that release AVP and oxytocin into the posterior pituitary

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4
Q

what are parvocellular neurones?

A

hypothalamic neurones that release LH/FHS/TSH/ACTH/GH/prolactin into the anterior pituitary

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5
Q

which hypothalamic nuclei do the magnocellular neurones originate in?

A

paraventricular AND supraoptic hypothalamic nuclei

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6
Q

what are the two types of nuclei in the hypothalamus?

A

paraventricular and supraoptic nucleus

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7
Q

which hypothalamic nuclei do the parvocellular neurones originate in?

A

paraventricular hypothalamic nucleus

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8
Q

what is AVP alternatively called?

A

anti-diuretic hormone (ADH)

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9
Q

define diuresis

A

production of urine

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10
Q

describe the main physiological action of vasopressin

A

stimulates water reabsorption in the renal collecting duct = concentrates urine

(maximising water reabsorption back into the bloodstream)

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11
Q

through what does vasopressin act to stimulate water reabsoprtion?

A

via the V2 receptor

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12
Q

what is the physiological effect of vasopressin acting on the V1 receptor?

A

vasoconstriction

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13
Q

what is the physiological effect of vasopressin acting on the V2 receptor?

A

stimulates water reabsoprtion in the renal collecting duct to concentrate urine

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14
Q

what is the physiological effect of vasopressin acting on the V3 receptor?

A

stimulates the release of ACTH from the anterior pituitary gland

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15
Q

what impact does vasopressin release have on the pituitary gland?

A

stimulates ACTH release from the APG, via the V3 receptor

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16
Q

explain, in detail, how vasopressin acts to concentrate urine

A

AVP in the bloodstream binds to V2 receptors on the surface of renal collecting duct cells

binding stimulates an intracellular signalling cascade

cascade causes the insertion of aquaporin-2 channels into the apical membrane of the collecting duct cells

water molecules enter the CD cells via aquaporin-2 channels from the tubular lumen

molecules travel down a concentration gradient and enter the bloodstream via aquaporin-3 channels on the basolateral membrane

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17
Q

how is the posterior pituitary visualised usually on an MRI?

A

posterior pituitary ‘bright spot’

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18
Q

is the posterior pituitary ‘bright spot’ present in all MRIs?

A

no, absense of the bright spot is normal - not visualised in all healthy individuals

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19
Q

what are the stimuli for vasopressin release?

A

osmotic stimuli and non-osmotic stimuli

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20
Q

describe the osmotic stimulus for vasopressin release

A

increase in plasma osmolality (concentration) detected by osmoreceptors

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21
Q

describe the non-osmotic stimulus for vasopressin release

A

decrease in atrial pressure sensed by atrial stretch receptors

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22
Q

what is plasma osmolality?

A

measure of the plasma electrolyte conenctration

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23
Q

when does plasma osmolality increase?

A

dehydration

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24
Q

what detects plasma osmolality?

A

osmoreceptors in the organum vasculosum and the subfornical organ (nuclei found around the third ventricle)

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25
Q

what are the subfornical organ and the organum vasculosum?

A

nuclei around the third ventricle that contain osmoreceptors that detect plasma osmolality

collection of neuronal cell bodies

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26
Q

where are the subfornical organ and the organum vasculosum located?

A

around the third ventricle

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27
Q

what feature of the subfornical organ and the organum vasculosum enables neuronal response?

A

no blood-brain barrier so the neurones can respond to changes in the systemic circulation

(+ highly vascularised)

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28
Q

where do the neurones from the subfornical organ and the organum vasculosum project to?

A

supraoptic nucleus in the hypothalamus where vasopressinergic neurones lie

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29
Q

explain, in detail, the process by which osmoreceptors control vasopressin release

A

plasma sodium osmolality increases

stimulates water to move out of the osmoreceptor into the surrounding plasma causing the osmoreceptor to shrink

osmoreceptor shrinkage causes increased osmoreceptor firing

increased firing rate causes AVP release from the PPG

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30
Q

what stimulates osmoreceptor action?

A

increase plasma sodium osmolality

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31
Q

what impact does osmoreceptor shrinkage have on the firing rate?

A

increases osmoreceptor firing rate

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32
Q

what is the function of atrial stretch receptors?

A

detect atrial pressure in the right atrium

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33
Q

explain, in detial, the non-osmotic stimulation of vasopressin release

A

reduction in circulating volume = reduction in pressure

reduction in pressure detected by atrial stretch receptors that stretch less

reduced stretching = less inhibition of vasopressin release (i.e. more AVP released)

more vasopressin released = more vasoconstriction AND water reabsorption so pressure can normalise

(i.e less stretching = more vasopressin)

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34
Q

explain, in detail, the osmotic stimulation of vasopressin release

A

osmoreceptors shrink due to the stimulus of increased plasma sodium osmolality, increasing firing rate causing increased AVP release from the PPG

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35
Q

what impact does stretching have on vasopressin release?

A

less stretching = more vasopressin = more vasoconstriction AND water reabsorption

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36
Q

through what is vasopressin release inhibited?

A

via vagal afferents to hypothalamus

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37
Q

give two reasons why vasopressin is released following a haemorrhage

A

haemorrhage = reduction in circulating volume

1 – more vasoconstriction via V1 receptors to increase vascular pressure and prevent blood loss (!!)
2 – to stimulate more water reabsorption via the renal collecting duct via V2 receptors to restore some of the circulating volume

(less volume = less pressure = less stretch of atrial stretch receptors = more vasopressin)

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38
Q

why is vasopressin release important during a haemorrhage?

A

so vasoconstriction can take place to prevent further blood loss and to increase pressure in the circulatory system again

++

so concentrated urine can be produced and as much water as possible can be retained within the systemic circulation (to maintain circulating volume)

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39
Q

what is the physiological response to water deprivation?

A

plasma osmolality increases

stimulate osmoreceptors to shrink

osmoreceptor firing rate increases and stimulates vasopressin release from the PPG

vasopressin increases water reabsorption from the renal collecting duct via the V2 receptors

urine volume reduces while the urine osmolality increases

plasma osmolality reduces and eventually returns to normal

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40
Q

what symptoms can be seen in a patient with diabetes insipidus?

A

polyuria
nocturia
polydipsia (extreme thirst)

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41
Q

how common is diabetes insipidus?

A

extremely rare

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42
Q

what is the most common cause of polyuria, polydipsia and nocturia?

A

diabetes MELLITUS, not diabetes insipidus

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43
Q

what causes polyuria, polydipsia and nocturia in diabetes mellitus?

A

osmotic diuresis - increased plasma glucose osmolality causes spillage into urine

44
Q

what causes polyuria, polydipsia and nocturia in diabetes insipidus?

A

inefficient function of vasopressin

45
Q

what are the two types of diabetes insipidus?

A

cranial (central) diabetes insipidus OR nephrogenic diabetes insipidus

46
Q

what is cranial (central) diabetes insipidus?

A

occurs due to a dysfunctional hypothalamus or posterior pituitary gland
(i.e. cannot make sufficient vasopressin)

47
Q

what is nephrogenic diabetes insipidus?

A

occurs due to a dysfunctional renal collecting duct

i.e. cannot respond to the vasopressin made

48
Q

differentiate between cranial (central) and nephrogenic diabetes insipidus

A

while cranial diabetes insipidus occurs due to a problem with the hypothalamus/PPG so sufficient vasopressin isn’t released, nephrogenic diabetes insipidus occurs due to the inability of the renal collecting duct to respond to the vasopressin released

49
Q

what is cranial diabetes insipidus alternatively known as?

A

vasopressin insufficiency

50
Q

what is nephrogenic diabetes insipidus alternatively known as?

A

vasopressin resistance

51
Q

what are the acquired causes of cranial diabetes insipidus?

A

(acquired = most common)

traumatic brain injury
pituitary surgery
pituitary tumours
metastasis (from other cancers to pituitary gland e.g. breast)
autoimmunity
granulomatous infiltration/inflammation of pituitary stalk (e.g. TB, sarcoidosis)

52
Q

what are the two types of causes of any disease?

A

congenital (present from birth) OR acquired (develops during life)

53
Q

how does granulomatous inflammation/infiltration of the pituitary stalk result in cranial diabetes insipidus?

A

inflammation and infiltration causes thickening of the pituitary stalk, impairing the transport of vasopressin from the hypothalamus into the posterior pituitary gland

54
Q

what are the congenital causes of nephrogenic diabetes insipidus?

A

congenital = rare

mutation in the gene encoding the V2 receptor

mutation in the gene encoding the aquaporin-2 channels

55
Q

which type of diabetes insipidus is more common?

A

cranial DI > nephrogenic DI

56
Q

what are the acquired causes of nephrogenic diabetes insipidus?

A

use of drugs (e.g. lithium)

57
Q

how do patients with diabetes insipidus present?

A

most commonly with polyuria, polydipsia and nocturia

58
Q

describe the urine production of individuals with diabetes insipidus

A

inefficient vasopressin function results in the production of large volumes of hypo-osmolar (very dilute) urine

= dehydrated

59
Q

describe the plasma status of individuals with diabetes insipidus

A

inefficient vasopressin function results in plasma with an increased osmolality (hyperosmolar)

specifically hypernatraemia (increased sodium)

60
Q

what plasma level must you always check in patients that present with polyuria, nocturia and polydipsia?

A

plasma glucose

to either confirm or rule out diabetes mellitus as the cause

61
Q

what will occur in DI as a result of losing large volumes of dilute urine?

A

dehydration

62
Q

explain why osmotic symptoms occur in diabetes insipidus and how they are responded to

A

in CDI, insufficient vasopressin while in NDI, no response to vasopressin so lack of binding to renal collecting duct V2 receptors

subsequently unable to stimulate insertion of aquaporin-2 channels into apical membrane and so water is not reabsorbed into systemic circulation

production of large volumes of very dilute (hypotonic) urine

causes dehydration and increase in plasma osmolality (hypernatraemia specifically)

hypernatraemia stimulates osmoreceptors to shrink and osmoreceptor firing rate increases

stimulates feeling of thirst (polydipsia)

if water available, water consumed and plasma osmolality decreases

63
Q

how can diabetes insipidus lead to death?

A

when feelings of thirst are stimulated by increased osmoreceptor firing rate, if there is no access to water, it cannot be consumed

= plasma osmolality cannot be decreased
= remains high causing dehydration (as large amounts of water are lost) and death

64
Q

how is diabetes insipidus managed if there is no access to water or if water cannot be given to the patient?

A

give IV fluids to regulate their osmotic balance if they are unable to do so themselves

65
Q

which condition can mimic diabetes insipidus?

A

psychogenic polydipsia

66
Q

what is psychogenic polydipsia?

A

a condition wherein there is excessive volitional water intake usually due to severe mental illness/developmental disability

67
Q

what symptoms does psychogenic polydipsia present with?

A

polyuria, polydipsia, nocturia

similar presentation to diabetes insipidus

68
Q

why is psychogenic polydipsia confused with diabetes insipidus?

A

both present with the same symptoms of polyuria, polydipsia and nocturia

69
Q

differentiate between psychogenic polydipsia and diabetes insipidus

A

both present with the same symptoms of polyuria, polydipsia and nocturia however in PPD, the excessive water intake causes the osmotic symptoms whereas in DI, the inefficient vasopressin function (insufficiency/resistance) causes the osmotic symptoms

70
Q

why do patients with psychogenic polydipsia present with polyuria and nocturia?

A

due to excessive volitional water intake

71
Q

explain how symptoms arise in psychogenic polydipsia

A

increased water intake due to polydipsia

plasma osmolality falls

reduced stimulation of osmoreceptors so they do not shrink

osmoreceptor firing rate does not fall and so vasopressin release from the PPG is not stimulated

with less vasopressin, there is less stimulation of water reabsorption so large volumes of dilute urine (hypotonic) are produced

plasma osmolality increases back to normal levels

72
Q

why is vasopressin release reduced in psychogenic polydipsia?

A

no stimulus for vasopressin release as plasma osmolality is low due to excessive water intake

73
Q

how can we distinguish between diabetes insipidus and psychogenic polydipsia?

A

using the water deprivation test and testing how the urine osmolality changes over time

74
Q

how is a water deprivation test carried out?

A

patient has no access to water at all for a given number of hours and their urine osmolality, plasma osmolality and their urine volume is measured regularly (alongside their weight as as well)

75
Q

what is measured in a water deprivation test?

A

urine volume, urine osmolality, plasma osmolality

76
Q

why must weight be regularly tested in a water deprivation test?

A

as if >3% of the body weight is lost = marker of significant dehydration (sign of diabetes insipidus)

77
Q

what would the results of a water deprivation test be for a normal individual?

A

expected rapid and then gradual increase in urine osmolality

78
Q

what would the results of a water deprivation test be for a patient with psychogenic polydipsia?

A

gradual increase in urine osmolality (less of an increase compared to an individual with diabetes insipidus)

  • will drink water in anyway possible (e.g. from a flower vase, toilet) as they are desperate
79
Q

what would the results of a water deprivation test be for a patient with diabetes insipidus?

A

no increase in urine osmolality at all

80
Q

why does urine osmolality not increase in diabetes insipidus?

A

in DI, the function of vasopressin is not effectively carried out so water reabsorption cannot take place

so large amounts of dilute urine is being excreted instead of small amounts of concentrated urine

81
Q

what are patients with diabetes insipidus unable to do?

A

unable to concentrate their urine and therefore the only thing preventing dehydration and death is regular intake of water

82
Q

how do we distinguish between cranial and nephrogenic diabetes insipidus?

A

give the patient ddAVP (desmopressin) after a period of water deprivation

measure urine osmolality regularly

if CDI = urine osmolality will increase after ddAVP is administered

if NDI = if CDI = urine osmolality will NOT increase even after ddAVP is administered

83
Q

what is ddAVP and why is it used?

A

ddAVP = desmopressin

synthetic vasopressin that stimulates specifically the V2 receptors

used to differentiate between vasopressin insufficiency (CDI) and vasopressin resistance (NDI)

84
Q

what does ddAVP mimic?

A

mimics vasopressin

85
Q

how does a patient with cranial diabetes insipidus react to ddAVP?

A

desmopressin (ddAVP) will bind to the collecting duct V2 receptors and stimulate water reabsorption so urine osmolality increases

86
Q

how does a patient with nephrogenic diabetes insipidus react to ddAVP?

A

desmopressin (ddAVP) cannot properly bind to the V2 receptors due to vasopressin resistance

= cannot stimulate water reabsorption

= urine osmolality remains low

87
Q

what is the approximate normal plasma osmolality range for a well-hydrated person?

A

280 mOsm/kg H20

88
Q

what is the approximate normal plasma osmolality range for a patient with diabetes insipidus?

A

290 mOsm/kg H20

89
Q

what is the approximate normal plasma osmolality range for a patient with psychogenic polydipsia?

A

270 mOsm/kg H20

90
Q

how is cranial diabetes insipidus treated?

A

using synthetic vasopressin (desmopressin) to replace missing vasopressin

acts on the V2 receptors to stimulate water reabsorption

intranasal spray OR tablets

91
Q

what are the different preparations of desmopressin?

A

intranasal spray

tablets

92
Q

what happens if you prevent a person with diabetes insipidus from drinking water or do not give him IV fluids if he cannot drink?

A

can cause death due to dehydration

don’t assume every diabetes is mellitus, could be insipidus

93
Q

how is nephrogenic diabetes insipidus treated?

A

luckily very rare because difficult to treat successfully BUT
can use thiazide diuretics (e.g. bendofluazide) = paradoxical mechanism unclear

94
Q

which drug is used to treat cranial diabetes insipidus?

A

desmopressin

95
Q

which drug is used to treat nephrogenic diabetes insipidus?

A

thiazide diuretics (paradoxical mechanism unclear)

96
Q

how is a diuretic used to treat nephrogenic diabetes insipidus?

A

paradoxical mechanism unclear

97
Q

what is SIADH?

A

syndrome of inappropriate anti-diuretic hormone (ADH)

too much vasopressin released causing water retention and reduced urine output

98
Q

what happens in SIADH?

A 
too much vasopressin released causing reduced urine output and water retention
SO
- high urine osmolality
- low plasma osmolality
- dilutional hyponatraemia
99
Q

how does SIADH lead to dilutional hyponatraemia?

A

excess vasopressin concentrates the urine so there is high urine osmolality and low plasma osmolality as more water is reabsorbed back into the blood, reducing plasma sodium osmolality

100
Q

list the possible causes of SIADH

A

CNS - injury, stroke, tumour

pulmonary disease - bronchiectasis, pneumonia

malignancy - lung cancer

drug-related - carbamazepine, selective serotonin reuptake inhibitors (SSRIs)

IDIOPATHIC (most common cause - ‘unknown’)

101
Q

why is hyponatraemia harmful and who is it particularly harmful to?

A

causes CNS effects (e.g. dizziness)

particulalry harmful for the elderly (increased risk of falls)

102
Q

how is SIADH managed?

A

fluid restriction of 500ml per day in an attempt to normalise plasma sodium levels

103
Q

why is SIADH particularly dangerous for the elderly?

A

can cause dizziness (due to dilutional hyponatraemia)
AND
common cause of prolonged stay in hospital

104
Q

which drug can be used to manage SIADH?

A

vaptan (V2 receptor antagonist) which counteracts the effects of vasopressin

105
Q

why is fluid restriction used preferentially over the drug vaptan?

A

with fluid restriction = takes longer to normalise plasma sodium levels BUT cheap

with drug vaptan = quicker normalising of plasma sodium levels BUT extremely EXPENSIVE

brs (phase 1b) (71 decks)

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