neurohypophysial disorders Flashcards

1
Q

what are magnocellular neurones?

A

neurones that project into neurohypophysis (with herring bodies)

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2
Q

what are the 2 neurohypophysis hormones?

A

oxytocin

vasopressin

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3
Q

where does VP act?

A

by increasing water reabsoprtion from renal cortical and medullary collecting ducts via V2 receptors

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4
Q

describe the VP action

A
  1. VP binds to V2 receptors (Gs receptors)
  2. aquaporin 2 molecules are created which move to apical membrane in aggraphores
  3. AQA2 insert in apical membrane to allow water reabsorption
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5
Q

where do osmoreceptor neurones located? where do they project?

A

in organum vasculosum (no BBB)

neurones project axons into hypothalamic paraventricular and supraoptic nuclei

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6
Q

what happens when blood osmolarity goes up?

A
  • water moves out of osmoreceptor cells
  • osmoreceptors shrink
  • triggers them to send more signals to hypothalamus to release VP
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7
Q

describe what happens in water deprivation

A
  • inc. blood osmolarity
  • stimulation of osmoreceptors (thirst)
  • inc. VP release
  • inc. water reabsorption from renal collecting ducts
  • reduction in blood plasma osmolarity
  • reduced urine volume
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8
Q

what are the 2 forms of DI?

A
  • central/cranial: not making enough VP

- nephrogenic: target organ (kidneys) have resistance

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9
Q

what are the acquired and congenital causes of cranial DI?

A
Acquired:
- TBI
- pituitary surgery
- pituitary tumours
- metastasis to pituitary gland
- granulomatous infiltration of median eminence
Congenital: rare
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10
Q

what are the acquired and congenital causes of nephrogenic DI?

A

acquired: drugs
congenital: rare

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11
Q

what are the signs and symptoms of DI?

A
  • polyuria
  • very dilate urine
  • polydipsia
  • dehydration
  • disruption to sleep and fatigue
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12
Q

what is psychogenic polydipsia?

A
  • excess fluid intake and polyuria

- but VP secretion ability preserved

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13
Q

what is psychogenic polydispia seen in?

A
  • psychiatric patients
  • anti-cholinergic effects of medication stimulating dry mouth
  • seen in patients told to drink plenty
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14
Q

what is the differene between the plasma osmolarity in people with DI and PP?

A
DI = HIGH plasma osmolarity
PP = LOW plasma osmolarity
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15
Q

what is DDAVP?

A

synthetic AVP

differentiates cranial and central

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16
Q

what are the biochemical features of DI?

A
  • hypernatraemia
  • raised urea
  • inc. plasma osmolarity
  • hypo-osmolar urine
17
Q

what are the biochemical features of PP?

A
  • mild hyponatraemia
  • low plasma osmolarity
  • hypo-osmolar urine
18
Q

where are V1 receptors?

A
  • VSM
  • NVSM
  • anterior pituitary
  • liver
  • platelets
  • CNS
19
Q

where are V2 receptors?

A
  • kidney

- endothelial cells

20
Q

how do you treat DI?

A

remember ALL vasopressin receptors will be activated
but want to target just V2 receptors
to treat cranial use selective VP receptive agonists
V1: Terlipressin
V2: Desmopressin (DDAVP)

21
Q

what will DDAVP do? what must a patient be told not to do?

A
  • reduces urine conc and volume in cranial DI
  • patient must be told not to continue drinking large volumes of water
  • could lead to hyponatraemia
22
Q

what is the possible mechanism for thiazides in the treatment of nephrogenic DI?

A
  • inhibits Na/Cl transport in DCT in kidneys
  • volume depletion
  • inc. in Na reabsorption in PCT
  • inc. water reabsorption in PCT
  • reduced urine volume
23
Q

what is SIADH?

A

excessively high ADH

24
Q

what is natriuresis?

A

excretion of sodium in urine

25
Q

what is evolaemia?

A

state of normal body fluid volume

26
Q

what are the signs and symptoms of SIADH?

A
  • small volumes of concentrated urine, hyponatraemia

- if hyponatraemic, then weak, poor mental function and nausea or then coma and death

27
Q

what are the causes of SIADH?

A
CNS - SAH, stroke, tumour, TI
Pulmonary disease - penumonia, bronciesctasis
Malignancy - lung (small cell)
drug-related 
idiopathic
28
Q

how do you reduce the immediate concern in SIADH?

A

immediate - fluid restriction

long term - demeclocycline (prevent VP action in kidneys)

29
Q

what are VAPTANS?

A
  • non-competitive V2 receptor antagonists
  • inhibit AQA2 synthesis and transport
  • aquaresis: solute-sparing renal excretion of water