LECTURE 2 DIABETE INSIPIDUS Flashcards by Ryan Al Hammad Ibrahim

WHAT IS Diabetes insipidus ? NUMBER OF CASES ?

Inability of the kidney to concentrate urine

🡺 copious amounts of very dilute urine

rare disease:1-2 cases/100.000 persons,

F:M = 1:1.

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Diabetes insipidus CAUSES ?

partial or total ADH deficit (central DI)

renal unresponsiveness to physiologic
actions of ADH (nephrogenic DI)

🡺!!! ADH levels are normal or elevated.

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Clinical features: HOW IT APPEARS ? WHAT AGE ?

onset – sudden

occurs at any age (rarely in suckling)

Polyuria:
may be > 10 liters/day
urine is dilute, discolored, inodorous, insipidus

Polydipsia
thirst has imperative character

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Polydipsia CHARACTERISTICS ?

ingestion of big amounts of liquid/24 hours,

Water is preferred

It exceeds polyuria :

due to an associated “potophillic index”

conditioned protective reflex (tendency to
over-satisfy the needs)

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WHAT Dehydration may occur ?

liquid loss > liquid ingestion

more frequent in:
older patients,
patients given anesthesia,
cerebro-vascular accidents,
children under 4 years of age.

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Dehydration results in ?

skin and mucosal dryness,

constipation,
weight loss,
confusion and
even death

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What Symptoms due to causal
agent ?

opto-chiasmatic compression syndrome – tumoral syndrome
●headache
●hypothalamic functional disorders :
●polyfagia,
●heat or cold intolerance,
●behavior modifications.

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What are Etio-pathogenic
mechanisms ?

Hypothalamic osmo-receptors destruction

ADH synthesis defect.
Absence of renal receptors

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What is Clinical forms of Central diabetes insipidus ?

Acquired
•Hereditary
•Idiopathic

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Clinical form of Nephrogenic diabetes insipidus ?

Hereditary
•Acquired

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Central diabetes insipidus acquired ?

Tumors
●Trauma
●Granulomatous infiltration
●Post-infectious status
●Vascular causes (trombosis, hemorrhage,
necrosis, cerebral aneurisms)

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Central diabetes insipidus Congenital?

Laurence-Moon-Bardet-Biedl syndrome (obesity, retinitis pigmentosa  blindness, polydactyly, hypogonadism)
● D.I.D.M.O.A.D. syndrome (diabetes insipidus, diabetes mellitus, optic atrophy, deafness)

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Central diabetes insipidus idiopathic ?

NOTHING

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Nephrogenic diabetes insipidus congénital ?

Nothing

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Nephrogenic diabetes insipidus acquired ?

drug-induced: lithium, colchicine, vinblastine
- renal diseases:
chronic renal failure,
hyperaldosteronism,
amiloidosis, sarcoidosis
- hypercalcemia:
hyperparathyroidism,
bone tumors,
Hodgkin disease,
sarcoidosis,
hypervitaminosis D.

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Particular clinical forms in Partial central diabetes insipidus ?

small amounts of ADH are secreted

●urinary volume - moderately increased,

●urinary specific gravity may reach 1010-1014.

Particular clinical forms in Diabetes insipidus with hypodipsia and essential hypernatremia – due to dehydration

severe form of diabetes insipidus,
●lesions that affect thirst mechanism,
●ADH secretion - delayed.
●diuresis - unchanged
●hypernatremia -160 mEq/l -mortality 75%.
●neuronal dehydration with convulsions and coma.

Particular clinical forms In Diabetes insipidus in children < 4 years old

growth deficit

●impared mental development

Particular clinical forms in Diabetes insipidus in pregnant women:

during the last trimester - vasopressinases occur

●needs in ADH doses are increased.

●risk to develop diabetes insipidus during the last months of pregnancy.

Investigations of ADH measurement by RIA:

low level,

●not a specific method.

Investigations of urine volume:

Very increased

Investigation in Urine specific gravity ?

very low - about 1000 (water-like).
- could be higher (in partial ADH deficit), but below normal values

Investigations in Seric and urinary ionogram?

hypernatremia in dehydration

●hyponatremia in dilution

Investigations in Urine and plasma osmolality

Plasma osmolality is high (depends upon the state of hydration)
-Urine osmolality is low

Investigations- dinamic tests in Water deprivation test

based on osmo-and volume-receptors stimulation •With mild polyuria, water deprivation can begin the night before the test. •With severe polyuria, water restriction is carried out during the day (to allow close observation) •The extent of deprivation is limited by the patient’s thirst, drop in BP, dehydration •urine - collected every hour (volume +density).

Water deprivation test results In normal persons ?

urinary volume- decreases and ● urinary density and osmolality increase.

Water deprivation test results In Diabetes insipidus ?

inability to concentrate urine. ●urine density may reach 1010 - partial forms.

Investigations- dinamic tests in adh test ?

useful in distinguishing central from nephrogenic DI -performed at the end of water deprivation test, - synthetic ADH is administered;

Investigations- dinamic tests in urine density

in normal persons – increment < 9% . - central diabetes insipidus – increment > 20 %. - nephrogenic diabetes insipidus- no response.

Investigations- dinamic tests in Endogenous ADH reserves - explored with ?

nicotine ●hypertonic saline solution ●clorpropamide.

Differential diagnosis in diabete mellitus

polyuria ●glycosuria ●increased urine specific gravity.

Differential diagnosis in hyperthyroidism

Polyuria - thyroxine effect on renal tubes, - effect accentuated by adrenergic stimulation. ●Betablockers improve the symptoms.

Differential diagnosis in hyper calcemia ?

Nothing

Differential diagnosis in Psychogenic polydipsia

with secondary polyuria - disappears with water restriction.

Differential diagnosis: in renal disease ?

chronic renal failure, ●congenital or acquired tubulopathy.

Treatment central di ?

desmopressin acetate – synthetic analogue of vasopressin: ●Intranasally/subcutaneously. ●No oxytocic effects

When adh must be taken ?

Only if needed

ADH overdose leads to water intoxication, what symptoms due to hyponatremia ?

weakness, ●loss of apetite, ●loss of thirst, ●nausea, ●vomiting, ●constipation, ●somnolence, ●convulsions/ even coma.

Treatment in Nephrogenic diabetes insipidus

Directed towards the underlying disorder ●In familial forms therapy must be given as soon as possible in infants due to particular susceptibility to neurologic damage due to dehydration. ●Diuretics (Amilorid;Triamteren) - with dietary salt restriction ●NSAIDs (Ibuprofen, Indomethacin): inhibit the PGs synthesis  reduce the delivery of solute to distal tubules  reduce urine volume and increase osmolality