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Year 2 Collin > Endo 3 - Neurohypophysial Disorders > Flashcards

Endo 3 - Neurohypophysial Disorders Flashcards

1
Q

On an MRI, how does the PPG look?

A

Bright spot

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2
Q

What are the 2 nuclei in relation to the PPG?

A

Supraoptic nuclei and paraventricular nuclei

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3
Q

What 2 hormones does the PPG secrete?

A

Oxytocin and ADH/Vasopressin

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4
Q

What does ADH do?

A

Increases water reabsorption from renal cortical and medullary collecting ducts, via V2 receptors

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5
Q

Where are osmoreceptors located?

What do the osmoreceptors project onto?

A

Located in organum vasculosum

Project onto hypothalamic supraoptic and paraventricular nuclei

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6
Q

How is VP release brought about by osmoreceptors?

A
  1. Increased extracellular Na conc
  2. Causes osmoreceptor to lose water and osmoreceptor shrinks
  3. Causes increased osmoreceptor firing
  4. VP release from PVN and SON neurones
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7
Q

How does increased water reabsorption from Renal CD impact urine osmolality (and volume) and serum osmolality?

A

Urine Volume = decreases

Urine osmolality = increases

Serum osmolality = decreases

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8
Q

What is diabetes insidious caused by?

A

Insufficient ADH or ADH unable to work

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9
Q

What are the 2 types of Diabetes insipidus and explain their characteristics

A
  1. Cranial / central (absence/lack of circulating VP)

2. Nephrogenic (kidneys resistant to VP)

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10
Q

Which is the more common form of diabetes insidious, cranial or nephrogenic?

A

Cranial is more common

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11
Q

Name 5 causes of acquired cranial diabetes insipidus

A
  1. Traumatic brain injury
  2. Pituitary surgery
  3. Pituitary tumours, craniopharyngima
  4. Metastasis to pituitary gland (e.g. breast)
  5. Infiltrative disease of median eminence (e.g. TB / sarcoidosis)
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12
Q

What is more common, acquired cranial diabetes insipidus or congenital cranial diabetes insipidus

A

Acquired cranial diabetes insipidus

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13
Q

What drug is given to treat bipolar disorder?

A

Lithium

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14
Q

What are congenital causes of nephrogenic diabetes insipidus?

A

Mutation in gene encoding V2 receptor / AQP2 water channel

RARE

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15
Q

What are acquired cause of nephrogenic diabetes insipidus?

A

Lithium

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16
Q

What are the signs and symptoms of diabetes insipidus?

A
  1. Polyuria
  2. Hypo-osmolar urine
  3. Polydipsia
  4. Dehydration if fluid intake not maintained - can cause death
  5. Disruption to sleep
17
Q

Give an example of medications that can cause a dry mouth

A

Anti-cholinergic medications

18
Q

What is the difference between psychogenic polydipsia and DI?

A

Psychogenic polydipsia does not involve a problem in secreting VP.

IE psychogenic polydipsia they drink and urinate a lot and have a higher urine osmolality than DI

19
Q

What is the normal hydrated plasma osmolality range?

A

270 - 290 most/kg H2O

20
Q

Above the reference range for plasma osmolality indicates?

A

Diabetes insipidus

21
Q

Below the reference range for plasma osmolality indicates?

A

Psychogenic polydipsia

22
Q

Why do patients with psychogenic polydipsia have a reasonable, but slightly lower urine osmolality when fluid deprived compared to normal?

A

Because they are drinking so much, the concentration gradient in the medulla is decreased

23
Q

4 biochemical features of Diabetes insipidus? (sodium, urea, plasma osmolality, urine osmolality)

A
  1. Hypernatraemia
  2. Increased urea
  3. Increased plasma osmolality
  4. Low urine osmolality (hypo-osmolar urine / dilute)
24
Q

Describe biochemical features of psychogenic polydipsia (sodium, plasma osmolality, urine osmolality)

A
  1. Mild hyponatraemia (excess water intake)
  2. Low plasma osmolality
  3. Low urine osmolality
25
Q

How is cranial diabetes insipidus treated?

A

V2 agonist given - Desmopressin (DDAVP). Works in central diabetes insipidus

26
Q

Why is normal VP not given?

A

V1 agonists would have other effects on vasculature which are not wanted

27
Q

How is desmopressin administered?

A
  1. Nasally
  2. Orally
  3. SC
28
Q

How does desmopressin affect urine?

A

Reduces urine volume

Increases urine concentration

29
Q

Why must patients not be drinking large amounts of fluid when giving DDAVP?

A

Risk of hyponatraemia

30
Q

Nephrogenic diabetes is a rare form of DI. How is it treated?

A

Thiazide diuretic

31
Q

What is SIADH

A

Syndrome of Inappropriate ADH.

Plasma VP conc is inappropriately high for plasma osmolality

32
Q

What are the plasma sodium levels and blood circulating volume in SIADH patients?

A
  1. Hyponatraemic

2. Euvolaemia

33
Q

How is ANP involved in hyponatraemia and euvolaemia?

A

ANP secreted from Right atrium, causing natriuresis

This contributes to euvolaemia and hyponatraemia

34
Q

What are the signs of SIADH?

A
  1. Raised urine osmolality, decreased urine volume (initially)
  2. Decreased plasma sodium conc mainly due to increased water reabsorption
35
Q

What are the symptoms of SIADH?

A

Can be symptomless

If plasma sodium < 120mM, generalised weakness, poor mental function, nausea

If plasma sodium < 110mM, confusion leading to coma leading to death

36
Q

What are the causes of SIADH?

A
  1. CNS - subarachnoid haemorrhage, stroke, tumour, TBI
  2. Pulmonary disease - pneumonia, bronchiectasis
  3. Malignancy - small cell lung carcinoma
  4. Drug related - carbamazepine, SSRI
  5. Idiopathic
37
Q

How is SIADH treated

A
  1. Appropriate treatment, e.g. surgery if tumour
  2. Reduce immediate concern (e.g. hyponatraemia).

Immediate: fluid restriction

Long term: drugs preventing VP action in kidneys - e.g. demeclocycline / drugs to inhibit action of ADH - V2 receptor antagonists

38
Q

What are vaptans?

A

Non competitive V2 receptor antagonists that promote aquaresis - renal water loss (as opposed to diuresis which involves electrolyte loss also)

VERY EXPENSIVE

39
Q

How do vaptans work?

A

Inhibit AQP2 synthesis and transport to CD apical membrane - prevents renal water absorption

Year 2 Collin (114 decks)

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