Neurohypophysial disorders Flashcards

1
Q

What two types of diabetes inspipdus are there?

How do they differ?

A

Cranial (central) DI

  • No adequate secretion of VP

Nephrogenic

  • kidneys can’t response to secreted ADH
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2
Q

What are possible causes of cranial Diabetes insipidus?

A

Most of the: aquired

Damage to the neurohyophysal system

  • traumatic brain injury
  • pituitary surgery
  • pituitary tumors, metastisis spreading to pituitary
  • Granulomatous infiltration of median eminence (i.e. inflammation)

Can be congenital (very rare)

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3
Q

What are possible causes of nephrogenic diabetis inspidus?

A

Congenital causes

  • rare e.g. mutation in V2 receptors or aquaporin channels

Aquired

  • drugs (e.g. lithium used in treatment of depression etc.)
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4
Q

What are the biochemical signs and symptoms of Diabetis inspidus?

A

Symptoms/Signs

  • Polydipsia
  • Polyuria
  • Hypoosmolar urine
  • Dehydration

Biochemical markers

  • Hypernatraemia
  • raised urea
    • –> Both signs for dehydration
  • High plasma osmolarity
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5
Q

Which tests would you do with someone you suspect to have diabetis insipidus?

A

Next to biochemical markers (HIgh NA+. high plasma osmolarity, high urea)

Water deprivation test

  • Deprive people from water and regularly measure urine production, concentration, plasma osmolality, and body weight
  • In the end: Administer ADH analogue (DDAVP)
  • When loosind >3% of body weight : end of test (dehydreation)

Findings:

  • When water deprived: DI patients no concentration of urine, in other patients (normal, psychogenic polydipsia) urine will be concentrated
  • Administering DDAVP: nephrogenic and cranial can be differentiated
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6
Q

What is psychogenic polydipsia?

What are the consequences?

A
  • Seen in psychiatric patients (might be due to anti-cholinergic drugs causing dry mouth)
  • People who are told to “drink plenty”

–> Nothing wrong with body function, people just drink to much (–> pee a lot)

Leading to:

  • Low plasma osmololity
  • Low NA+
  • Dilute urine
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7
Q

Which conditions could you suspect when a patient comes to you with polyuria and polydipsia?

What are the differential diagnosis

A
  1. Most common: Diabetis Mellitus
    • rule out by test, glucose etc
  2. If not DM:
    • Diabetis insipidus
    • Psychogenic polydipsia
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8
Q

How could you treat cranial Diabetis inspipdus?

What is important after treatment?

A

Selective V2 agonst: Desmopressin (DDAVP) (ADH analogue)

  • nasal administration (majority) (–> might be considered less important medication in hospital –> easity forgotton –> might cause death)
  • Can also be orally or subcutaneous

Important:

  • Tell patients to not drink that much anymore! Otherwise risk of hyponatraemia!
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9
Q

How could you treat nephrogenic diabetis inspidus?

A

Rhiazide diuretics

–> noone knows how and why this works

Possible mechanism:

High plasma osmolarity

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10
Q

How do you call a disease that casues too much ADH secretion?

What is its definition/characteristic?

A

Syndrome of Inappropriate ADH (SIADH)

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

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11
Q

What are the symptoms and characteristics of SIADH?

A
  • •can be symptomless
  • •however if p[Na+] <120 mM: generalised weakness, poor mental function, nausea –> Na+ essential to maintain depolerisation etc. in neurones
  • •if p[Na+] <110 mM: CONFUSION leading to COMA and ultimately DEATH

Biochemical characteristics:

  • Hyerosmolar urine
  • Hypoosmolar plasma
  • Hyponatraemia
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12
Q

What are causes of SIADH?

A

CNS causes:

  • stroke, tumor, trauma, sub-arrachnoid haemorrhage

Pulmonary disease

  • Pneumonia, bronchiectasis

Malignancy

  • ectopic ADH e.g. by small cell lung carcinoma

Drug-related

  • Carbamazepine (seizure control) , SSRI (Selective Serotonin Reuptake Inhibitor)

Ideopathic

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13
Q

How would you treat SIADH?

A
  1. Appropriate treatment (e.g. surgery for tumour)
  2. To reduce immediate concern, i.e. hyponatraemia
  3. Immediate: fluid restriction
  4. 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 (VAPTANS)
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14
Q

Explain the use of Vaptans in SIADH

A

Non-competitive V2 antagonist

  • inhibts AQP2 production and transport
  • causing aquaresis: electrolyte sparing diuretic (only water)

–> very expensive is limiting current use

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15
Q

Which test should you always perform after diagnosing a patient with Diabetis insipidus?

Why?

A

Always perform imaging:

About 1/2 of cases: metastasis of systemic tumor spreading to neurohypophysis)

to rule out cancer cause

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