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Year 2 - LCRS - Endocrinology > Neurohypophyseal disorders > Flashcards

Neurohypophyseal disorders Flashcards

09.10.2019

1
Q

What are the 2 posterior pituitary hormones?

A

Vasopressin (=anti diuretic hormone)

Oxytocin

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2
Q

What radiological method is used to visualise the PP?

A

MRI

-> PP bright spot on the MRI

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3
Q

What are the actions of VP? What receptors does it act on?

A

a) V1 receptors: arterial SM -> vasoconstriction -> increased BP and also ACTH production
b) V2 receptors in principal collecting duct cells: increases water reabsorption by inserting AQP2 into cell membrane

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4
Q

Diuresis

A

Increase in urine production

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5
Q

What is the main action of VP?

A

Principal effect of vasopressin = ANTI-DIURETIC ie increases water reabsorption from renal cortical and medullary collecting ducts via V2 receptors

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6
Q

What happened once VP binds to a V? receptor?

A

1) G-protein activares adenyl cyclase
2) ATP is transformed into cAMP through AC
3) cAMP activates PKA
4) PKA activates other cellular mediators
5) AQP2 synthesis occurs
6) aggraphores migrate to the apical membrane
7) insertion of AQP2 in apical membrane
8) water enters the cell along osmotic gradient
9) water is reabsorbed on the basolateral side via AQP3 and AQP4

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7
Q

Organum vasculosum

A
  • deviod of a BBB
  • communicates with systemic circulation, can sense changes in plasma osmolarity
  • one of the 4 circumventricular organs of the brain
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8
Q

Which osmoreceptors act on the release of VP?

A
  • osmoreceptors located in the organum vasculosum
  • project into hypothalamic paraventricular and supraopticc nuclei
  • osmoreceptors = neurones
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9
Q

How do osmoreceptors sense changes in osmolarity and cause VP release?

A
  • osmoreceptors located in the organum vasculosum sense changes in osmolarity and shrink (due to water release) when it rises
  • this shrinking leads to increased firing of osmoreceptors
  • firing -> VP release
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10
Q

What are the 2 types of Diabetes Insipidus?

A
  • Cranial/central - absence or lack of circulating VP
  • Nephrogenic - end organ (kidney) resistance to VP
    - > very rare!!!
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11
Q

Aetiology of cranial DI

A

Acquired (generally)

  • traumatic brain injury
  • pituitary surgery
  • pituitary tumors (craniopharyngioma)
  • metastasis to the pituitary (e.g. breast)
  • granulomatous infiltration of median eminence eg TB, sarcoidosis

Congenital - rare

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12
Q

Aetiology of nephrogenic DI

A

Congenital
- rare (e.g. mutation in gene encoding V2 receptor, aquaporin 2 type water channel)

Acquired
- Drugs (e.g. lithium)

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13
Q

Signs and Symptoms of DI

A
  • Polydipsia
  • Polyuria
  • Nocturia
  • Hypoosmolar urine
  • Dehydration (and consequences) if fluid intake is not maintained - can lead to death
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14
Q

Psychogenic polydipsia

A
  • most frequently seen in psychiatric patients, aetiology unclear, may reflect anti-cholinergic effects of medication
  • can be in patients told to drink plenty

-> excess fluid intake (polydipsia) and therefore excess urination (polyuria). However, in contrast to DI patients the ability to secrete VP in response to osmotic stimuli is preserved.

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15
Q

What are biochemical features of DI?

A
  • hypernatraemia
  • raised urea
  • increased plasma osmolarity
  • hypo-osmolar urine
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16
Q

biochemical features of psychogenic polydipsia

A
  • mild hyponatraemia
  • low plasma osmolarity
  • hypo-osmolar urine
17
Q

How does the body respond to exogenous VP?

A

Response at V1 AND V2 receptors!!

18
Q

Where are V1 receptors located?

A 
Vascular smooth muscle
Non-vascular smooth muscle
Anterior pituitary
Liver 
Platelets
CNS
19
Q

Where are V2 receptors located?

A
  • Kidney (principal collecting duct cells)

- endothelial cells

20
Q

Selective V1 Receptor VP agonist exampled

A

TERLIPRESSIN

21
Q

VP agonist that acts selectively on V2 receptors

A

Desmopressin (DDAVP)

22
Q

Desmopressin administration

A
  • nasally
  • tablets
  • subcutaneous
23
Q

Desmopressin

A

SELECTIVE VASOPRESSIN RECEPTOR PEPTIDERGIC AGONIST for V2 receptors

-> reduces urine volume in cranial DI + concentration

24
Q

How do you treat cranial DI?

A
  • Desmopressin

- care to tell patients not to continue drinking massive amounts of fluid - risk of hyponatraemia

25
Q

How do you treat nephroggenic DI?

A
  • thiazides (e.g. bendoflumethiazide)
26
Q

Possible mechanism of thiazides in treatment of nephrogenic DI

A
  • Inhibits Na+/Cl- transport in distal convoluted tubule (→ diuretic effect)
  • Volume depletion
  • Compensatory increase in Na+ reabsorption from the proximal tubule (plus small decrease in GFR, etc.)
  • Increased proximal water reabsorption
  • Decreased fluid reaches collecting duct
  • Reduced urine volume
27
Q

SIADH

A

Syndrome of inaproppraite Anti-Diuretic Hormone

the plasma vasopressin concentration is inappropriately high for the existing plasma osmolality

28
Q

Signs of SIADH

A
  • raised urine osmolality
  • decreased urine volume (initially)
  • decreased p[Na+] (HYPONATRAEMIA) mainly due to increased water reabsorption
29
Q

Symptoms of SIADH

A
  • can be symptomless
  • however if p[Na+] <120 mM: generalised weakness, poor mental function, nausea
  • if p[Na+] <110 mM: CONFUSION leading to COMA and ultimately DEATH
30
Q

Causes of SIADH

A
  • idiopathic
  • CNS (stroke, tumor, TBI, Sub arachnoid haemorrhage)
  • malignancy (lung, small cell ca)
  • pulmonary (pneumonia, bronchiectasis)
  • drug related (SSRI, carbamazepine)
31
Q

Vaptans

A
  • Non-competitive V2 receptor antagonists
  • Inhibit AQP2 synthesis and transport to collecting duct apical membrane, preventing renal water reabsorption
  • Aquaresis – solute-sparing renal excretion of water, contrast with diuretics (diuresis) which produce simultaneous electrolyte loss
  • Licensed in the UK for treatment of hyponatraemia associated with SIADH
  • Very expensive – limits their current use
32
Q

Treatment of SIADH

A
  • Appropriate treatment (e.g. surgery for tumour)

To reduce immediate concern, i.e. hyponatraemia
1. Immediate: fluid restriction
2. Longer-term: use drugs which prevent vasopressin action in kidneys
e.g. induce nephrogenic DI ie reduce renal water reabsorption - demeclocyline
inhibit action of ADH - V2 receptor antagonists

33
Q

Give an example of what causes ANP release

A
  • high extra cellular fluid (ECF) volume
  • right atrium releases atrial natriuretic peptide
  • this causes natriuresis which
    a) restores euvolaemia
    b) may cause or contribute to hyponatraemia
34
Q

Aquaresis

A
  • solute sparing renal excretion of water (contrast with diuretic which cause diuresis and therefore produce simultaneous electrolyte loss
  • can be induced by vaptans (V2 receptor antagonists, used in SIADH)

Year 2 - LCRS - Endocrinology (18 decks)

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