Anti-diuretic hormone Flashcards

1
Q

anti-diuretic hormone

A

synthesised by the supra-optic nucleus of the hypothalamus and stored in the posterior pituitary

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2
Q

anti-diuretic hormone is secreted in response to

A
  • hypotension which causes production of angiotensin II, hypothalamus has angiotensin II receptors so when angiotensin II production increases the hypothalamus increases its production and secretion of anti-diuretic hormone
  • increased serum osmolarity= when the plasma is hypertonic the hypothalamus has osmoreceptors which are stimulated to release anti-diuretic hormone
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3
Q

anti-diuretic hormone is also known as

A

vasopressin

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4
Q

ADH is released into the circulation in respsone to hypotension or increased serum osmolarity and it

A

binds to vasopressin-2-receptors on the base-lateral membrane of the principal cells, this activates G-stimulatory protein which activates adenylate cyclase which converts ATP to cAMP which activates protein Kinase A

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5
Q

protein Kinase A then

A

simulates the formation of vesicles which contain aquapoin type 2 and also causes the vesicles it has created to fuse with the apical membrane of the principal cells which allows water to be re-absorbed into the cell from the tubule

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6
Q

once water is within the cell

A

it passes into the blood through type 3 and type 4 aquaporins on the baso-lateral membrane

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7
Q

anti-diuretic hormone also binds to

A

vasopressin type 1 receptos (V1) which are present on any systemic blood vessel this causes the smooth muscle of the blood vessel to contract causing vasoconstriction which increases total peripheral resistance which increases systemic blood pressure

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8
Q

so what would happen if you don’t make enough ADH (i.e. vasopressin)

A

known as central diabetes insidious where the hypothalamus does not create or release vasopressin

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9
Q

causes of central diabetes insidious

A

head trauma, iatrogenic, wolfram syndrome

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10
Q

in central diabetes insipidus

A

because vasopressin is not present in the circulation there is not formation of aquaporin type 2 receptor on the apical membrane of the principal cells therefore, no water is re-absorbed so excessive amounts of water are excreted which reduces the urine osmolarity and causing polyuria and increases the plasma osmolarity causing excessive thirst

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11
Q

treatment of central diabetes insipidus

A

desmopressin (synthetic anti-diuretic hormone)

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12
Q

nephrogenic diabetes insipidus

A

inability of the nephron to respond to the vasopressin that has been produced by the hypothalamus

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13
Q

causes of nephrogenic diabetes insipidus

A
  • X-linked recessive mutation in the V2 receptor gene (AVPR-2)
  • LITHIUM
  • DEMELOCYCLINE which is an antibiotic used to block the excessive release of vasopressin by tumours
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14
Q

examples of vasopressin analogues

A

desmopressin and terlipressin

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15
Q

vasopressin analogues are used in

A

central diabetes insipidus, bedwetting/ nocturnal enuresis in children over 10, to control vatical bleeding in portal hypertension

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16
Q

aquaretics mechanism of action

A

act as competitive antagonists of vasopressin receptors of the V1 and V2 subtype

17
Q

V1 receptors mediate

A

VASOCONSTRICTION

18
Q

V2 receptos mediate

A

h20 re-absorption

19
Q

so aquatics cause

A

inhibition of vasoconstriction, water excretion without causing loss of sodium in the plasma so causes an increase in plasma sodium concentration

20
Q

main clinical indications for use of aquaretics

A

in condition where there is excess anti-diuretic hormone to correct hyponatraemia

  • ie SIADH
  • Congestive heart failure
  • Cirrhosis
21
Q

examples of aquatics

A
  • Conivaptan (non-selective blocker of V1 and V2) IV FORMULATION ONLY
  • Tolvaptan= oral and V2 selective
22
Q

main side affects of aquatics

A

increased thirst