Diabetes insipidus ( DI ) is a condition characterized by a large amount of dilute urine and an increase in thirst. The amount of urine produced can be nearly 20 liters per day. Fluid reduction has little effect on urine concentration. Complications may include dehydration or seizures.
There are four types of DI, each with a different set of causes. In Middle (CDI) is due to lack of vasopressin hormone (antidiuretic hormone). This could be due to damage to the hypothalamus or pituitary gland or genetics. Nephrogenic diabetes insipidus (NDI) occurs when the kidneys do not respond well to vasopressin. DI Dipsogenic is due to the abnormal thirst mechanism in the hypothalamus while DI pregnancy occurs only during pregnancy. Diagnosis is often based on urine tests, blood tests, and fluid deprivation tests. Diabetes mellitus is a separate condition with an unrelated mechanism, although both can produce large amounts of urine production.
Treatment involves drinking enough fluids to prevent dehydration. Other treatments depend on the type. In the treatment of central and gestational DI is by desmopressin. IN nephrogenic can be treated by overcoming the underlying cause or use of thiazide, aspirin, or ibuprofen. The number of new cases of diabetes insipidus each year is 3 out of 100,000. In Central it usually starts between the ages of 10 and 20 and occurs in men and women alike. IN nephrogenic can start at any age. The term "diabetes" comes from the Greek word meaning siphon.
Video Diabetes insipidus
Signs and symptoms
Excessive urination and extreme thirst and increased fluid intake (especially for cold water and sometimes ice or ice water) are typical for DI. The symptoms of excessive urination and extreme thirst are similar to those seen in untreated diabetes mellitus, with the difference that urine does not contain glucose. Blurred vision is a rare thing. Signs of dehydration can also appear in some individuals, because the body can not save much (if any) water enters.
Extreme urination continues throughout the day and night. In children, DI can interfere with appetite, eat, weight, and growth, as well. They may come with fever, vomiting, or diarrhea. Adults with untreated DI can stay healthy for decades as long as enough water is consumed to compensate for the loss of urine. However, there is a continuous risk of dehydration and potassium loss that can lead to hypokalemia.
Maps Diabetes insipidus
Cause
Some DI forms are:
Center
DI Central has many possible causes. According to the literature, the main causes of central DI and their frequent forecast frequencies are as follows:
- Idiopathic - 30%
- Malignant or benign tumors in the brain or pituitary - 25%
- Cranial surgery - 20%
- Head trauma - 16%
Sumber: www.ncbi.nlm.nih.gov
Nefrogenik
Nephrogenic diabetic insipidus is due to the inability of the kidneys to respond normally to vasopressin.
Dipsogenic
Dipsogenic DI or primary polydipsia results from excessive fluid intake compared with arginine vasopressin deficiency. This may be due to defects or damage to thirst mechanisms, located in the hypothalamus; or because of mental illness. Treatment with DDAVP can cause water poisoning.
Gestational
Gestational DI occurs only during pregnancy and the postpartum period. During pregnancy, women produce vasopressinase in the placenta, which breaks down the antidiuretic hormone (ADH). DI Gestational suspected to occur with excessive production and/or vasopressinase cleansing disorders.
Most cases of DI pregnancy can be treated with desmopressin (ddAVP), but not vasopressin. In rare cases, however, abnormalities in the thirst mechanism cause DI pregnancy, and desmopressin should not be used.
Diabetes insipidus is also associated with several serious diseases of pregnancy, including pre-eclampsia, HELLP syndrome and acute fatty liver pregnancy. This causes DI by damaging the cleansing of the liver from circulating vasopressinase. It is important to consider these diseases if a woman comes with diabetes insipidus in pregnancy, because their care requires the birth of a baby before the disease improves. Failure to treat this disease can immediately lead to maternal or perinatal death.
Pathophysiology
Electrolytes and volume homeostasis are complex mechanisms that balance the body's need for blood pressure and sodium and potassium main electrolytes. In general, the electrolyte setting precedes the volume setting. When the volume is greatly reduced, however, the body will retain water at the expense of destructive electrolyte levels.
The regulation of urine production occurs in the hypothalamus, which produces ADH in the supraoptic and paraventricular nuclei. After synthesis, the hormone is transported in the neurosecretory granule under the axon of the hypothalamus neuron to the posterior lobe of the pituitary gland, where it is stored for later release. In addition, the hypothalamus regulates thirst sensation in the ventromedial nucleus by sensing an increase in serum osmolarity and conveying this information to the cortex.
Neurogenic/central DI results from lack of ADH; sometimes may present with diminished thirst due to thirst regulation and the production of ADH occurs near the hypothalamus. It is encountered as a result of hypoxic encephalopathy, neurosurgery, autoimmunity or cancer, or sometimes without a cause (idiopathic).
The main effector organ for fluid homeostasis is the kidney. ADH acts by increasing the permeability of water in the collecting ducts and the distal tubules that are convoluted; specifically, it acts on a protein called aquaporins and more specifically aquaporin 2 in the following cascade. When released, ADH binds to a receptor in pairs of V2 G-proteins in the distal convoluted tubule, increasing the cyclic AMP, which is paired with protein kinase A, stimulating the translocation of the 2 aquaporin channels stored in the cytoplasm of the distal convoluted tubule and collecting the ducts into the apical membrane. These transcribed channels allow water to enter the collecting duct cells. Increased permeability allows reabsorption of water into the bloodstream, resulting in urine concentration.
IN nefrogenic results from a lack of aquaporin channels in the distal collecting channel (decreased surface expression and transcription). This is seen in lithium toxicity, hypercalcemia, hypokalemia, or ureteral discharge. Therefore, ADH deficiency prevents water reabsorption and increased blood osmolarity. As osmolarity increases, the osmoreceptors in the hypothalamus detect these changes and stimulate thirst. With increased thirst, patients now experience a cycle of polydipsia and polyuria.
Hereditary forms of diabetes insipidus account for less than 10% of cases of diabetes insipidus seen in clinical practice.
Diagnosis
To differentiate DI from other causes of excessive urination, blood glucose levels, bicarbonate levels, and calcium levels need to be tested. Blood electrolyte measurements can reveal high levels of sodium (hypernatremia as dehydration development). Urinalysis shows a dilute urine with a low specific gravity. Urine osmolarity and electrolyte levels are usually low.
Liquid deprivation test is another way to distinguish DI from other causes of excessive urination. If there is no change in fluid loss, the administration of desmopressin can determine whether DI is caused by:
- defects in ADH production
- defective kidney response to ADH
This test measures changes in body weight, urine output, and urine composition when fluid is retained to induce dehydration. The body's normal response to dehydration is to conserve water by concentrating urine. Those with DI continue to urinate much diluted urine despite the lack of water. In primary polydipsia, urine osmolality should be increased and stable above 280 Osm/kg with fluid restriction, while stabilization at lower levels indicates diabetes insipidus. Stabilization in this test means, more specifically, when the increase in urine osmolality is less than 30 Osm/kg per hour for at least three hours. Sometimes measuring ADH blood levels near the end of this test is also necessary, but more time consuming to do.
To distinguish between major forms, desmopressin stimulation is also used; desmopressin may be taken by injections, nasal sprays, or tablets. When taking desmopresin, a patient should drink fluids or water only when thirsty and not at other times, as this may cause sudden fluid accumulation in the central nervous system. If desmopresin reduces urine output and increases urine osmolarity, hypothalamus production of ADH becomes less, and the kidneys respond normally to exogenous vasopressin (desmopresin). If DI is caused by renal pathology, desmopresin does not alter urine output or osmolarity (since endogenous vasopressin levels are high).
While diabetes insipidus usually occurs with polydipsia, it can also be rare not only in the absence of polydipsia but in the opposite view, adipsia (or hypodipsia). "Adipic diabetes insipidus" is recognized as the absence of a real thirst even in response to hyperosmolality. In some cases of adipsic DI, the patient may also fail to respond to desmopressin.
If central DI is suspected, other pituitary hormonal tests, as well as magnetic resonance imaging, particularly pituitary MRI, are needed to determine whether a disease process (such as prolactinoma, or histiocytosis, syphilis, tuberculosis or other tumors or granulomas) affects pituitary function. Most people with this form have experienced head trauma or stopped production of ADH for unknown reasons.
The drinking habit (in its most severe form called psychogenic polidipsia) is the most common type of diabetic insipidus imitator at all ages. While many adult cases in medical literature are associated with mental disorders, most patients with habit polydipsia have no other detectable disease. The difference is made during the water deprivation test, because some level of urine concentration above the isoosmolar is usually obtained before the patient becomes dehydrated.
Treatment
Middle
In Central and DI gestational responds to desmopresin given as an intranasal or oral tablet. Carbamazepine, an anticonvulsive drug, also has some success in this type of DI. In addition, DI gestational tends to decline at four to six weeks after delivery, although some women may develop it again in subsequent pregnancies. In dipsogenic DI, desmopressin is usually not an option.
Nefrogenik
Desmopressin will not be effective in treated nephrogenic DI by reversing the underlying cause (if possible) and replacing the free water deficit. Hydrochlorothiazide diuretics (thiazide diuretics) or indomethacin may be used to create mild hypovolemia that encourages the taking of salt and water in the proximal tubule and thus increases nephrogenic diabetes insipidus. Amyloride has the added benefit of blocking Na uptake. Thiazide diuretics are sometimes combined with amiloride to prevent hypokalemia. It seems paradoxical to treat extreme diuresis with diuretics, and the exact mechanism of action is unknown but thiazide diuretics will decrease tubular reabsorption of sodium and turbulent water, thereby causing diuresis. This reduces plasma volume, thereby lowering glomerular filtration rate and increasing sodium and water absorption in the proximal nephron. Less fluid reaches the distal nephron, so overall fluid conservation is obtained.
IN lithium-induced nephrogenic can be effectively administered with amiloride, a potassium-sparing diuretic often used in conjunction with thiazide or loop diuretics. Doctors have been aware of lithium toxicity for many years, and have traditionally been given thiazide diuretics for polyuria induced by lithium and nephrogenic diabetic insipidus. However, amiloride has recently proven to be a successful treatment for this condition.
Etymology
The word "diabetes" ( or ) comes from the Latin diab? T? S , which in turn comes from the Ancient Greek ????? ??? ( diab? t? s ) which literally means "a pedestrian; siphon". Ancient Greek physician Aretaeus of Cappadocia (Fl. In the first century AD) used the word, with the meaning meant "excessive urine drain", as the name for the disease. In the end, the word comes from the Greek word ?????????? ( diabainein ), meaning "passes", which consists of ??? - ( he -), which means "through" and ??????? ( bainein ), meaning "to go". The word "diabetes" was first recorded in English, in the form of "diabete", in medical texts written around 1425.
"Insipidus" comes from the Latin insipidus (bland), from the Latin: di - "not" sapidus "delicious" from sapere "has taste" - its full meaning is "lack of taste or spirit, bad taste". The application of this name to DI arises from the fact that diabetes insipidus does not cause glycosuria (excretion of glucose into the urine).
References
External links
- Diabetes insipidus in Curlie (based on DMOZ)
Source of the article : Wikipedia
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