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Phase 1b - Endocrinology > Disorders of Vasopressin > Flashcards

Disorders of Vasopressin Flashcards

-> Function of endocrine glands: Summarise the function of the key endocrine glands, including the synthesis, regulation and physiological effects of their hormones. -> Endocrine disorders: Describe the clinical features and treatment options of endocrine disorders.

1
Q

Which mutation is concerned with congenital hypopituitarism?

A
  • PROP1 mutation (transcription factor required for anterior pituitary development)
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2
Q

Which part of the pituitary gland is anatomically continuous with the hypothalamus?

A
  • Posterior pituitary gland
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3
Q

Which hormones are secreted by the neurohypophysis / posterior pituitary gland (2)?

A
  • Vasopressin / AVP / ADH
  • Oxytocin
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4
Q

Which hypothalamic neurones secrete vasopressin / AVP / ADH & oxytocin?

A
  • Hypothalamic magnocellular neurones
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5
Q

Which hypothalamic nuclei contain the magnocellular neurone cell bodies?

A
  • Supraoptic and paraventricular nuclei
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6
Q

How can one radiologically visualise the posterior pituitary gland?

A

Posterior pituitary ‘bright spot’ on MRI

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7
Q

What is the main physiological action of vasopressin?

A
  • Stimulation of water reabsorption in the renal collecting duct → concentrates urine
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8
Q

Which renal receptors are responsive to vasopressin?

A
  • V2 receptor
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9
Q

Which receptors are responsive to vasopressin induced vasocontriction?

A
  • V1 receptors
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10
Q

Stimulation of V1 receptors results in what action?

A
  • Vasoconstriction
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11
Q

Which hormone is released in response to vasopressin from the pituitary gland?

A
  • ACTH
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12
Q

Which protein channels are embedded on the apical membrane of renal tubule cells, facilitating the movement of water molecules?

A
  • Aquaporin-2
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13
Q

What response is induced by AVP-V2 stimulation (3 steps)?

A
  1. G-protein coupled response, formation of a secondary messenger
  2. Adenylate cyclase activity elevates cAMP concentration and protein kinase A
  3. Migration and synthesis of aquaporin-2 channels to apical membrane
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14
Q

Which aquaporin channels are embedded on the basolateral membrane?

A
  • Aquaporin-3
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15
Q

What are two main stimuli that stimulates vasopressin release?

A
  • Osmotic
  • Non-osmotic
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16
Q

Outline the osmotic stimulus of vasopresin (6 steps).

A
  1. Increase in plasma osmolarity
  2. Increase in extracellular Na+
  3. H2O escapes from osmoreceptors
  4. Osmoreceptor shrinks
  5. Increase in osmoreceptor firing
  6. AVP release from hypothalamic neurones
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17
Q

What type of receptors are sensitive to plasma osmolarity?

A
  • Osmoreceptors
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18
Q

What happens to the structural shape of osmoreceptors in response to an increase plasma osmolarity?

A
  • Osmoreceptors shrink
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19
Q

What is the impact on plasma osmolarity in individuals with water deprivation?

A
  • Increased plasma osmolarity
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20
Q

Which circumventricular nuclei respond to changes in systemic circulation and thus stimulate vasopressin release (2)?

A
  • Organ vasculosum
  • Subfornical organ
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21
Q

Where are the vasculosum and subfornical organs located?

A
  • Reside around the 3rd ventricle (circumventricular)
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22
Q

How can the circumventricular nuclei detect immediate changes to systemic circulation?

A
  • There is no blood-brain barrier and are highly vascularised structures
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23
Q

Which hypothalamic structure communicates with projections of the organum vasculosum and subfornical organ?

A
  • Supraoptic nucleus
24
Q

Which hypothalamic nucleus contains vasopressinergic neurones?

A
  • Supraoptic nucleus
25
Q

Outline the non-osmotic stimulus of vasopresin (3 steps).

A
  1. Decrease in blood volume in body
  2. Decrease in atrial pressure (sensed by atrial stretch receptors)
  3. Stimulate in vasopressin release, via vagal afferents to hypothalamus
26
Q

Which receptors respond to non-osmotic changes?

A
  • Atrial stretch receptors
27
Q

Where are atrial stretch receptors predominantly fonud?

A
  • Within the right atrium
28
Q

Stimulation of atrial stretch receptors result in what?

A
  • Inhibit vasopressin release
  • Vagal afferents to the hypothalamus
29
Q

How does a haemorrhage result in vasopressin release?

A
  • The circulating volume decreases, leading to hypovolemia, this subsequently leads to less stretch and stimulation of atrial receptors, therefore this reduces inhibition of vasopressin - leading to vasopressin release (Increased water reabsorption) and vasoconstriction via V1 receptors.
30
Q

What are the physiological responses to water deprivation (3)?

A

Increase AVP release:
* Reduced plasma osmolarity
* Reduce urine volume
* Increase urine osmolarity

31
Q

What is the physical response to water deprivation?

A

Thirst

32
Q

What is osmotic diuresis?

A
  • Hyperglycaemia increases water retention within the urine, leading to decreased water reabsorption
33
Q

What pathology is associated with diabetes insipidus?

A
  • Issue with vasopressin
34
Q

What are the osmotic symptoms associated with diabetes insipidus (3)?

A
  • Polyuria
  • Nocturia
  • Polydypsia
35
Q

What are the two types of of diabetes insipidus?

A
  • Cranial (central) diabetes insipidus
  • Nephrogenic diabetes insipidus
36
Q

What is central diabetes insipidus?

A
  • Problem concerned with hypothalamus / posterior pituitary gland
    • There is an insufficient secretion of arginine vasopressin

Potential new name of disease: Vasopressin insufficiency

37
Q

What is nephrogenic diabetes inspidus?

A
  • Arginine vasopressin production is normal from the posterior pituitary gland and hypothalamus
    • The collecting duct is unable to respond to AVP

Potential new name of the disease: Vasopressin resistance

38
Q

What are the common causes of cranial diabetes inspidus (7)?

A
  • Congenital
  • Acquired:
    • Traumatic brain injury
    • Pituitary surgery
    • Pituitary tumours
    • Metastasis to the pituitary gland (breast)
    • Granulomatous infiltration of pituitary stalk: TB, sarcoidosis (Accumulation of inflammatory cells)
    • Autoimmune
39
Q

What are the common causes of nephrogenic diabetes (2)?

A
  • Congenital: mutation encoding V2 receptor, aquaporin 2 type water channel
  • Acquired: Lithium drugs
40
Q

Which types of drugs are concerned with causing nephrogenic diabetes inspidus?

A
  • Lithium
41
Q

What are the symptoms of diabetes insipidus (5)?

A
  • Polyuria
  • Nocturia
  • Polydypsia
  • Hypoosmolar urine (and in large volumes)
  • Hyperosmolar plasma
    • Hypernatremia
  • Glucose is normal (HbA1c)
42
Q

How do the symptoms of diabetes inspipidus arise?

A
43
Q

How can diabetes inspidus lead to death?

A
44
Q

What is psychogenic polydypsia?

A
  • Psychogenic polydipsia (PPD), or primary polydipsia, is characterised by excessive volitional water intake and is often seen in patients with severe mental illness and / or developmental disability
45
Q

What are the symptoms of psychogenic polydipsia (3)?

A
  • Polydipsia
  • Polyuria
  • Nocturia

Unlike diabetes insipidus - No problem with arginine vasopressin

46
Q

How do the symptoms of psychogenic polydipsia arise?

A
47
Q

What test can be conducted to distinguish between diabetes insipidus and psychogenic polydipsia?

A
  • Water deprivation test
  • If urine osmolarity increases -> psychogenic polydipsia (similar to normal)
  • If urine osmolarity is not affected -> Diabetes Insipidus
48
Q

In patients with diabetes insipidus, what are the likely results of the water deprivation test?

A
  • There is no increase in urine osmolarity (AVP is suppressed)
49
Q

At what parameter should the water deprivation test be stopped?

A
  • If there is a loss of > 3% body weight

A marker of significant dehydration which can occur in diabetes insipidus

50
Q

How is central diabetes insipidus distinguished from nephrogenic diabetes?

A
  • Administer ddAVP (behaving like vasopressin)
    • In central diabetes incipitus, ddAVP will interact with V2 receptors facilitating water reabsorption and leading to a significant increase in urine osmolarity
    • This is unresponsive in nephrogenic diabetes
51
Q

What is the available treatment for cranial diabetes insipidus (2)?

A
  • Desmopressin to replace vasopressin
  • Selective V2 receptor (V1 receptor activation would be unhelpful)
    • Tablets / Intranasal
52
Q

What are the effects of a poorly managed cranial diabetes insipidus?

A

Preventing a patient with diabetes insipidus from drinking or not giving fluids if unable to drink can cause death

53
Q

What is the available treatment for nephrogenic diabetes insipidus?

A
  • Thiazide diuretics

Paradoxical - Mecahnism unclear

54
Q

Which disorder is associated with an increase in AVP?

A
  • Syndrome of inappropriate ADH (SIADH)
55
Q

What are the features of syndrome of inappropriate ADH (SIADH) (5)?

A
  • Reduced urine output
  • Water retention
  • High urine osmolarity
  • Low plasma osmolarity
  • Dilutional hyponatremia
56
Q

What are the causes of syndrome of inappropriate ADH (SIADH) (8)?

A
  • CNS
    • Head injury
    • Stroke
    • Tumour
  • Pulmonary disease
    • Pneumonia
    • Bronchiectasis
  • Malignancy
    • Lung cancer
  • Drug related
    • Carbazepine
    • Serotonin reuptake inhibitors
  • Idiopathic
57
Q

What is the available management for syndrome of inappropriate ADH (SIADH) (2)?

A
  • Vaptan (Vasopressin antagonist), binds to V2 renal receptors
  • Fluid restriction

Vaptan is quite expensive

Phase 1b - Endocrinology (19 decks)

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