• DIABETES INSIPIDUS

    This condition is characterized by relative or absolute deficiency of ADH or inability of kidney to respond to normal ADH resulting in polyuria of very dilute urine with polydipsia.

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    ETIOLOGY (Causes of Diabetes Insipidus)

    Central (neurogenic) diabetes insipidus (CDI)

    Familial

    Manifested as autosomal dominant
    Associated with

    • Diabetes mellitus
    • Optic atrophy
    • Nerve deafness
    • Bladder atony
    • Acquired
    • Idiopathic
    • Tumor, e.g  craniopharyngioma
    • Inflammatory e.g basal meningitis
    • Head  trauma
    • Surgery causing disruption of pituitary
    • stalk
    • Irradiation
    • Sheehan s syndrome

    Nephrogenic diabetes insipidus (NDI)

    Familial

    • Manifested as sex-linked recessive
    • Acquired
    • Iatrogenic e.g lithium demeclocycline meth oxyflurane colchicine
    • After pyelonephritis
    • Polycystic kidney  disease
    • Obstructive uropathy
    • Hypokalaemia
    • Hypercalcaemia
    • Sickie cell anaemia

    PATHOLOGY
    ADH regulatory mechanism

    – Inappropriate ADH Secretion implies

    • Persistent release of ADH unrelated to plasma osmolarity.

    – AS a conseqence, there is

    • Excessive reabsorption of water kidneys
    • Expansion of extracellular fluid volume

    – These lead to

    • Haemodilution
    • Hyponatraemia
    • Inability to excrete dilute urine

     
    Central (neurogenic) diabetes insipidus (CDI)

    Complete or partial ADH deficiency
    Results in polyuric state in which
    –         Kidney is unable to concentrate urine
    –         Large amounts of dilute urine are excreted
    Nephrogenic diabetes insipidus (NDI)
    ADH is produced normally
    There is ineffectual response of ADH on distal tubule or Collecting tubule
    ADH levels are elevated in face of
    –         Hypertonic plasma.
    –         Dilute urine.

    CLINICAL FEATURES

    Symptoms
    Onset: Sudden or insidious
    Polyuria
    –         Increased frequency, day and night
    –         May pass 15-20 liters of urine in 24 hours
    Polydipsia
    –         Compensatory mechanism to prevent dehydration
    –         excessive incessant thirst
    –         Craving for ice- cold water
    –         Disturbs night sleep
    –         patient may consume in excess of 10 litres of fluid per day
    –         Attempts to limit fluid intake may lead to se vere dehydration
    Other features
    –         Weakness
    –         Fatigue
    –         Irritability
    –         Muscular pains
    –         Headache
    –         Constipation
    In  prolonged cases
    –         Weight loss
    –         Exhaustion
    –         If intracranial tumor associated features of
    –         Increased intracranial tension
    –         Endocrine disturbances

    Signs

    –         Drowsiness
    –         Sunken eyes
    –         Dry skin
    –         Dry tongue
    –         Temperature subnormal
    –         Pulse fast
    –         Blood pressure low
    –         Emaciation in prolonged cases

    COMPLICATIONS

    –         Severe dehydration
    –         Shock
    –         Coma with or without convulsions

    INVESTIGATIONS

    –         Diagnosis of DI requires assessment of ADH Secretion
    –         Random measurement of ADH is of little use
    –         Any ADH measurement must take into account serum and urine osmolarity.

    Tests used are:
    –         Indirect test.
    –         Direct test.
    Indirect or water deprivation test:

    • It is done by measuring effect of dehydration on serum and osmolarity.
    • It is called indirect because it measures effect of ADH, not level itself.
    • Patient is dehydrated until serum becomes hypertonic.

    If the patient has DI

    • Specific gravity is not in creases by 50% in CDI.
    • Specific gravity is not increased in NDI.

    After decompressing:

    • Produced anti –diuresis in CDI.
    • Failure of response indicates NDI.

    Direct or hypertonic saline test:

    • It is done by measuring ADH after dehydration.
    • Patient is made hypertonic by saline infusion.
    • ADH levels are then measured.

    In normal parsons

    • Serum ADH increases in relatively Linear Fashion with serum osmolarity .

    In DI, this linearity is lost

    • If ADH levels are decreased, patient has CDI.
    • If ADH levels are elevated, patient has NDI.

    Urinalysis :

    • Increased daily output.
    • Specific gravity low.
    • No sugar.

    X-ray skull

    • Deformed or enlarged sella.

    IVP shows :

    • Enlargement of ureters, kidneys, bladder.

    PROGNOSIS

    – Variable according to cause

    • If caused by tumor, it is reversible with surgery.
    • If caused by head trauma spontaneous recovery is likely within one year.
    • If caused by brain infection symptoms may persist indefinitely.

    – Acute cases have better prognosis than those which start insidiously
    – Patients who have an intact thirst mechanism

    • Do not require medication to live as long as they have free access to water.
    • However this can be very disruptive to their life style.
    • In due course of time can result in renal damage.

    PREDOMINAT MIASM
    –         Sycotic disorder

     
    THERAPEUTIC AIM
    –         To treat underlying cause, if possible.
    –         To replace hormone deficiency.
    –         To maintain baseline hormonal levels.
    –         To prevent/control complications.

    GENERAL MANAGEMENT
    –  Maintain fluid, electrolyte balance.
    –  Monitor for signs of dehydration.
    –  Well balanced nutritious  diet.

     

    HOMEOPATHIC MEDICINE FOR DIABETES

    Hormone replacement therapy.
    Complimentary homeopathic drugs for symptomatic treatment

    •  Arnica Montana (Head Trauma)
    •  Arsenicum Album
    •  Conium Maculatum (Tumor)
    •  Gelsemium
    •  Lachesis (sheehan’s syndrome)
    •  Natrium Sulphuricum (head trauma)
    •  Phosporus
    •  Phosphoric Acid
    •  Pituitary Extract
    •  Lycopodium
    •  Thuja Occidentalis (anti-miasmatic)
    •  Tuberculinum (basal meninggitis).

    }

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