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eLCRS - 엔도 > Endo 3: Neurohypophysial Disorders > Flashcards

Endo 3: Neurohypophysial Disorders Flashcards

1
Q

describe how posterior pituitary would be describe on pituitary MRI

A
  • bright spot
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2
Q

What is the principal effect of vasopressin?

A

Vasopressin =
- anti diuretic

  • increases water reabsorption from renal cortical + medullary collecting ducts (via V2 receptors)
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3
Q

What is vasopressin also known as?

A
  • ADH
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4
Q

How is vasopressin release regulated?

A
  • regulated via osmoreceptors
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5
Q

Describe the process of VP release.

starting from the stimulus

A

Stimulus = increase in EC Na+ conc

  • detected by osmoreceptor
  • increase in water outflow from osmoreceptors
  • osmoreceptor shrinks
  • causes increased osmoreceptor firing
  • causes release from hypothalamic PVN + SON neurons
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6
Q

Describe the normal response to water deprivation.

A
  1. water deprivation
  2. causes increase serum osmolality
  3. stimulates osmoreceptors
    - causes sensation of thirst
  4. then causes increase in VP release
  5. which increases water reabsorption from renal Collecting ducts
  6. results in REDUCED URINE VOLUME + INCREASE URINE OSMOLALITY
  7. and also REDUCTION IN SERUM OSMOLALITY
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7
Q

Describe the aetiology of cranial diabetes insipidus.

A
  • Damage to neurohypophysial system
    (injury to neurohypophysis, surgery, cerebral thrombosis)
  • idiopathic
  • familial

NOTE: usually acquired

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8
Q

Describe the aetiology of nephrogenic diabetes insipidus.

A
  • congenital = rare
  • usually acquired
    ( e.g drugs - lithium)
    –> bipolar disorder medication
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9
Q

What are signs and symptoms of diabetes insipidus

A
  • polyuria (large volumes)
  • hypo-osmolar urine (dilute)
  • polydipsia (thirst + inc. drinking)
  • dehydration
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10
Q

Describe the onset of diabetes inspidus

A
  1. inadequate production of VP
  2. large vol of dilute urine produced
  3. causes increase in plasma osmolality
  4. causes reduction in EC fluid volume
  5. leads to polydipsia (thirst)
  6. re-expansion of EC fluid volume

Note: if no access to water –> causes dehydration + death

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11
Q

State a difference between Diabetes Insipidus and psychogenic polydipsia.

A

UNLIKE Diabetes Insipidus:

- ability to secrete VP in response to osmotic stimuli = preserved

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12
Q

Describe the onset of psychogenic polydipsia

A
  • there is central disturbance
  • increases drive to drink
  • leads to fall in plasma osmolarity
  • so VP is inhibited
  • and you produce large vol of urine
  • this increase in urine excretion –> reduces ECFV + increases plasma osmolarity
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13
Q

What are biochemical features of DI ?

A
  • hypernatraemia
  • raised urea
  • increased plasma osmolarity
  • dilute urine
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14
Q

What are biochemical features of Psychogenic polydipsia ?

A
  • mild hyponatraemia
  • low plasma osmolarity
  • dilute urine
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15
Q

List methods of administrating desmopressin

A
  • nasally
  • orally
  • SC
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16
Q

What is the effect of Desmopressin (DDAVP) on person with CENTRAL DI?

A

effect:
- allows concentration of urine
- (because their VP receptors are working properly + can be stimulated by DDAVP

17
Q

What is the effect of DDAVP on a person with NEPHROGENIC DI ?

A
  • no effect

- no response

18
Q

Give a main method of treatment of nephrogenic diabetes insipidus.

A
  • thiazides

e. g bendroflumethiazide

19
Q

Explain the mechanism of thiazides as a method of treating nephrogenic DI.

EXTRA STUDY

A

mechanism - thiazide:

  • inhibits Na+/Cl- transport in DCT
  • causes volume depletion
  • causes compensatory increase in Na+ reabsorption from PCT
  • which increases proximal water reabsorption
  • decreased fluid reaches CD
  • causes reduced urine volume

e.g bendroflumethiazide

20
Q

Define Syndrome of Inappropriate ADH (SIADH)

A

SIADH

- the plasma vasopressin concentration = inappropriately high for the existing plasma osmolality .

21
Q

Describe the mechanism of SIADH

A
  • excess Vasopressin in plasma
  • causes increase in water reabsorption form renal collectiong ducts
  • which causes an increase in ECF volume
  • and leads to HYPONATRAEMIA
  • and ANP (atrial natriuretic peptide) = produce from the right atrium
    which causes natriuresis
  • which also causes hypo natraemia
  • as well as euvolaemia.
22
Q

What are some signs of SIADH?

A
  • raised urine osmolality
  • decreased urine volume
  • decreased p{na+] (HYPONATRAEMIA)
    due to increased water reabsorption.
23
Q

What are some symptoms of SIADH?

A
  • SIADH can be symptomless
  • if p[na+] < 120 mM
  • -> causes generalized weakness, poor mental function, nausea
  • if p[na+] <110 mM
  • -> causes CONFUSION
  • leading to coma –> death
24
Q

What are some causes of SIADH?

A
  • CNS (stroke, SAH, tumor)
  • PULMONARY DISEASE (pneumonia, bronchiectasis)
  • MALIGNANCY (lung - small cell)
  • DRUG RELATED (carbamazepine, SSRI)
  • IDIOPATHIC
25
Q

What are some treatments of SIADH?

A
  • e.g surgery for tumor

if hyponatraemia:

  • immediate = fluid restriction
  • long term = drugs to prevent VP action in kidneys (e.g DMCT, V2 receptor antagonists- inhibits action of ADH)
26
Q

What is VAPTANS?

A

VAPTANS:

- Non competitive V2 receptor antagonists

27
Q

How do VAPTANS work?

What is its effect?

A

VAPTANS:

  • inhibits AQP2 synthesis + transport
  • prevents renal water resorption
  • causes aquaresis
  • used for treatment of hyponatraemia associated with SIADH
28
Q

What are osmorecptors

A
  • they project to the PVN + SON
29
Q

Where are osmoreceptors located in ?

A

the organum vasculosum

30
Q

what is diabetes insipidus?

A
  • ADH problem

- large volumes of insipid urine

31
Q

Whats the ranger or normal plasma osmolality?

how does this differ in diabetes insipidus patients?

how does this differ in psychogenic polydipsia patients?

A

270-290 mOsm/kg H2O

DI: higher than 290

Psychogenic polydipsia: Lower than 270

32
Q

give central DI patients high dose of vasopressin –>

A

responds well to DDAVP

33
Q

What is DDAVP?

A
  • synthetic AVP
  • vasopressin receptor peptidergic agonists
  • desmopressin
34
Q

how does desmopressin work?

A
  • nasally/ orally/ SC administrated

–> causes reduction in urine value + conc in CRANIAL DI only

35
Q

What should you warn patients who have started on desmopressin?

A
  • tell patient starting this NOT to continue drinking large amounts of fluid
  • -> due risk of hyponatraemia
36
Q

give 3 actions of vasopressin

and the respective receptors for each action.

A
  1. antidiuretic effect –> inserts AQP2 (V2 receptors)
  2. Vasoconstrictor activity (V1a)
  3. ACTH release (V1b)
37
Q

what are 2 conditions vasopressin agonist is used for?

A
  • cranial DI (desmopressin)

- Oesophageal varices (terlipressin)

eLCRS - 엔도 (20 decks)

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