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Endocrine and Metabolic Y3 > Diabetes Insipidus > Flashcards

Diabetes Insipidus Flashcards

1
Q

What is diabetes insipidus?

A

A disorder of inadequate secretion or of insensitivity to vasopressin (ADH) leading to dilute (hypotonic) polyuria.  

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2
Q

What is the main physiological action of vasopressin?

A

Stimulation of water reabsorption in the renal collecting duct
- Concentrates urine (reduces urine volume)
- Acts through the V2 receptor in the kidney
- Also acts as a vasoconstrictor (via V1 receptor) to increase b.p
- Also stimulates ACTH release from the anterior pituitary

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3
Q

Describe the mechanism by which vasopressin stimulates water reabsorption

A
  1. AVP in the blood travels to the renal collecting duct and binds to V2 receptors on the basolateral membrane of the duct
  2. Binding stimulates cascade
  3. Cascade stimulates the formation of aquaporin-2 channels on the apical membrane
  4. More H2O molecules taken into the lumen and out of the basolateral membrane into the blood
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4
Q

How does the posterior pituitary appear on an MRI?

A
  • “bright spot”
  • Not visulaised in all healthy individuals, so absence may be normal variant
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5
Q

What 2 factors stimulate vasopressin release?

A
  1. OSMOTIC:
    Rise in plasma osmolality sensed by osmoreceptors
  2. NON-OSMOTIC: (stretch)
    Decrease in atrial pressure sensed by atrial stretch receptors
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6
Q

How do osmoreceptors regulate vasopressin?

A
  1. There is an increase in extracellular Na+
  2. Water flows out of the osmoreceptors
  3. Osmoreceptors change in shape (shrink)
  4. Leads to osmoreceptor firing
  5. Stimulates vasopressin release from hypothalamic neurons (AVP will increase the water to decrease the Na+ conc)
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7
Q

Describe the mechanism by which Non- osmotic stimulation of vasopressin release?

A
  1. Atrial stretch receptors detect pressure in the right atrium
  2. Inhibit vasopressin release via vagal afferents to hypothalamus
  3. Reduction in circulating volume (e.g. haemorrhage) means less stretch of these atrial receptors, so less inhibition of vasopressin (vasopressin can increase Na+ conc/ b.p)
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8
Q

Why is vasopressin released following a haemorrhage (ie reduction in circulating volume)

A
  • Vasopressin release results in increased water reabsorption in the kidney (some restoration of circulating volume) V2 receptors (INCREASES BLOOD VOL)
  • Vasoconstriction via V1 receptors (INCREASES BP)
  • Renin-aldo system also activated
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9
Q

Describe the physiological response to water deprivation

A
  1. Increased plasma osmolality (conc of plasma)
  2. Simulates osmoreceptors
  3. Can lead to thirst OR increased AVP release
  4. Increased AVP= increased water rebasoption from renal collecting ducts
  5. Leads to reduced urine volume, increase in urine osmolality (conc)
  6. Leads to reduction in plasma osmolaltiy (more water reabsorbed from the blood)
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10
Q

What are the 2 types of diabetes insipidus?

A
  1. Central/ Cranial DI:
    - More common 
    - Lack of ADH/vasopressin production/secretion from the posterior pituitary  
  2. Nephrogenic DI:
    - Very rare 
    - Kidney resistance/insensitivity of the collecting duct to ADH/vasopressin
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11
Q

What are the causes of cranial diabetes insipidus?

A
  • Congenital (rare) 
  • Acquired (more common) - related to damage to posterior pituitary: pituitary surgery
  • Pituitary tumour or metastases 
  • Brain trauma 
  • Infiltrative (e.g. sarcoidosis) 
  • Infection (e.g. meningitis) 
  • Vascular (e.g. aneurysms, Sheehan syndrome) 
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12
Q

What causes nephrogenic DI?

A
  • Congenital (mutation in gene encoded for V2/AQP2 receptor 
  • Drugs (e.g. lithium) 
  • Post-obstructive uropathy 
  • Pyelonephritis 
  • Pregnancy 
  • Osmotic diuresis (e.g. diabetes mellitus)  
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13
Q

Summarise the epidemiology of diabetes insipidus

A

● Median onset is 24 yrs
● Depends on cause

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14
Q

What are the presenting symptoms of diabetes insipidus?

A

● Polyuria
● Nocturia
● Polydipsia
● In children:
*Enuresis (bed-wetting)
*Sleep disturbance
● Other symptoms depend on aetiology

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15
Q

What signs of diabetes insipidus can be found on physical examination?

A

● Central DI has few signs if the patient drinks sufficiently to maintain adequate fluid levels
● Urine output > 3 L/day
● If fluid intake < fluid output, signs of dehydration will be present (e.g. tachycardia, reduced tissue turgor, postural hypotension, dry mucous membranes)
● Signs related to the cause (e.g. visual defect due to pituitary tumour)

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16
Q

What investigations are used to diagnose/ monitor diabetes insipidus?

A
  1. Low urine osmolality + High serum osmolality
  2. Water Deprivation Test → confirmatory test. If osmolality corrects itself then may be psychogenic polydipsia. If not (if osmolality is low it is likely diabetes insipidus), after 8 hours administer desmopressin to differentiate between CDI and NDI. Urine osmolality will rise in CDI but remain low in NDI.
  3. MRI → look for brain/pituitary tumour
  4. Hypernatremia and Hypokalaemia
  5. If Low Sodium → psychogenic polydipsia (in context of low urine osmolality)
  6. Normal blood glucose → exclude DM
17
Q

How is diabetes insipidus managed?

A
  1. Hypernatremia → manage with oral or IV fluids (prevent dehydration)
    - Correction of chronic hypernatremia too fast predisposes to cerebral oedema
  2. Central DI → intranasal Desmopressin
  3. Nephrogenic DI →
    - Nephrogenic diabetes insipidus is managed by correcting any underlying metabolic abnormalities and discontinuing any offending drugs.
    - High dose desmopressin has been used with variable results.
    - Other potential treatments include using a thiazide diuretic (counter-intuitive, we know) and a non-steroidal anti-inflammatory drug to reduce urine volume.
18
Q

What complications may arise from diabetes insipidus?

A
  • Hyponatraemic dehydration 
  • Excess desmopressin –> hyponatraemia 
19
Q

Describe the prognosis of diabetes insipidus

A
  • Depends on CAUSE 
  • Cranial DI may be transient following head trauma 
  • It may be cured by removing the cause (e.g. drug discontinuation, tumour resection) 

Endocrine and Metabolic Y3 (22 decks)

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