Diabetes Insipidus

Andrew E. Uloko,
BM BCh, MD, FMCP, FACE, FRCP (Lond.).
Professor of Medicine (Endocrinology)
Consultant Physician & Endocrinologist
Bayero University Kano & Aminu Kano
Teaching Hospital
Kano, Nigeria
*CORRESPONDENCE: andyuloko@yahoo.com

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 Learning objectives
Upon completion of this lecture, the student should
be able to:
1. Give a brief overview of anatomy & physiology
of the neurohypophysis
2. Define Diabetes Insipidus (DI)
3. Describe the pathophysiology of DI
4. Identify the symptoms and signs of DI
5. Discuss the diagnostic approach to DI
6. Describe the treatment of DI
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 Outline
• Brief anatomy & physiology of the
neurohypophysis
• Definition & types of DI
• Pathophysiology of DI
• Causes
• Presentation
• Diagnosis & investigations
• Treatment
• Take Homes
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 Anatomy

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 Neurohypophysis

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 Posterior pituitary - anatomy

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 Neurohypophysis blood supply

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 Vasopressin- ‘Neural hormone’

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 Regulation of Vasopressin Secretion

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 Osmoregulation

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 Other modes of regulation

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 How Vasopressin acts

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 Feedback control

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 AE Uloko. NPMCN General Medicine
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 Diabetes Insipidus

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 Definition of DI

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 Types

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 Causes

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 Causes

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 Incidence

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 Incidence in craniopharingioma

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 Pathophysiology of DI
A. Central DI
• Loss of vasopressin-producing cells
• Causing deficiency in ADH synthesis or release
• Deficiency in ADH, resulting in an inability to
conserve water
• Leading to extreme polyuria and polydipsia

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 Pathophysiology of DI

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 Pathophysiology of DI
B. Nephrogenic DI
• Depression of aldosterone release or inability
of the nephrons to respond to ADH.
• Causing extreme polyuria and polydipsia

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 Pathophysiology of DI

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 Symptoms and signs

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 Diagnosis of post-operative DI

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 Differential Diagnoses of Polyuria

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 Water Deprivation Test

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 Water Deprivation Test

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 Differentiation of central and
nephrogenic DI

• Can be made by measuring plasma AVP levels

after water deprivation or spontaneous
development of mild hypernatraemia

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 Differentiation of central and
nephrogenic DI

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 Results interpretation

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 Summary of lab findings in DI

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 Variations in Clinical Course

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 Variations - Transient DI

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 Variations - Permanent DI

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 Variations - Permanent DI

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 Triphasic DI

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 Triphasic DI

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 Triphasic DI

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 Complications

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 TREATMENT

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 ‘Expectant’ monitoring

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 Maintain fluid balance

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 Maintain fluid balance
• The establish water deficit = premorbid weight
x [1 – 140/serum Na (mmol/L)]

• Ongoing losses decrease the efficacy of this

formula

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 Maintain fluid balance
• Even slow correction of the volume deficit
may necessitate a high rate of hypotonic fluid
administration if there is ongoing polyuria.

• Overhydration water diuresis medullary

washout sustaining the polyuria even if the
DI resolves

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 Monitor for resolution of transient
DI or triphasic response

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 Manage anterior pituitary
insufficiency

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 Preparations

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 Antidiuretic hormone therapy

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 Desmopressin: side effects
• Headache, nausea, nasal congestion, flushing
and abdominal cramping.
• No pressor effects because it selectively binds
to the AVP V2 receptors
• Safe in patients with coronary or hypertensive
cardiovascular disease

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Patients with DI coming for surgery

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 Treatment of Nephrogenic DI

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 Treatment of Nephrogenic DI

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 Treatment of Nephrogenic DI

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 References

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 Thank You

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