Review of literature on gestational diabetes mellitus Posted on September 16, Poetry explication essay
Dipsogenic[ edit ] Dipsogenic DI or primary polydipsia results from excessive intake of fluids as opposed to deficiency of arginine vasopressin.
It may be due to a defect or damage to the thirst mechanism, located in the hypothalamus;  or due to mental illness.
Gestational[ edit ] Gestational DI occurs only during pregnancy and the postpartum period. During pregnancy, women produce vasopressinase in the placentawhich breaks down antidiuretic hormone ADH.
In rare cases, however, an abnormality in the thirst mechanism causes gestational DI, and desmopressin should not be used. Diabetes insipidus is also associated with some serious diseases of pregnancy, including pre-eclampsiaHELLP syndrome and acute fatty liver of pregnancy.
These cause DI by impairing hepatic clearance of circulating vasopressinase. It is important to consider these diseases if a woman presents with diabetes insipidus in pregnancy, because their treatments require delivery of the baby before the disease will improve.
Failure to treat these diseases promptly can lead to maternal or perinatal mortality. Pathophysiology[ edit ] Electrolyte and volume homeostasis is a complex mechanism that balances the body's requirements for blood pressure and the main electrolytes sodium and potassium.
In general, electrolyte regulation precedes volume regulation. When the volume is severely depleted, however, the body will retain water at the expense of deranging electrolyte levels. The regulation of urine production occurs in the hypothalamuswhich produces ADH in the supraoptic and paraventricular nuclei.
After synthesis, the hormone is transported in neurosecretory granules down the axon of the hypothalamic neuron to the posterior lobe of the pituitary glandwhere it is stored for later release.
In addition, the hypothalamus regulates the sensation of thirst in the ventromedial nucleus by sensing increases in serum osmolarity and relaying this information to the cortex.
It is encountered as a result of hypoxic encephalopathy, neurosurgery, autoimmunity or cancer, or sometimes without an underlying cause idiopathic. The main effector organ for fluid homeostasis is the kidney. ADH acts by increasing water permeability in the collecting ducts and distal convoluted tubules; specifically, it acts on proteins called aquaporins and more specifically aquaporin 2 in the following cascade.
When released, ADH binds to V2 G-protein coupled receptors within the distal convoluted tubules, increasing cyclic AMPwhich couples with protein kinase Astimulating translocation of the aquaporin 2 channel stored in the cytoplasm of the distal convoluted tubules and collecting ducts into the apical membrane.
These transcribed channels allow water into the collecting duct cells. The increase in permeability allows for reabsorption of water into the bloodstream, thus concentrating the urine. Nephrogenic DI results from lack of aquaporin channels in the distal collecting duct decreased surface expression and transcription.
It is seen in lithium toxicityhypercalcemia, hypokalemia, or release of ureteral obstruction. Therefore, a lack of ADH prevents water reabsorption and the osmolarity of the blood increases.
With increased osmolarity, the osmoreceptors in the hypothalamus detect this change and stimulate thirst. With increased thirst, the patient now experiences a polydipsia and polyuria cycle. Measurement of blood electrolytes can reveal a high sodium level hypernatremia as dehydration develops.
Urinalysis demonstrates a dilute urine with a low specific gravity. Urine osmolarity and electrolyte levels are typically low.
A fluid deprivation test is another way of distinguishing DI from other causes of excessive urination. If there is no change in fluid loss, giving desmopressin can determine if DI is caused by: The body's normal response to dehydration is to conserve water by concentrating the urine.
Those with DI continue to urinate large amounts of dilute urine in spite of water deprivation.Doctor answers on Symptoms, Diagnosis, Treatment, and More: Dr. Fisher on literature review on diabetes mellitus: Mild effect of stimulating peristalsis and decreasing nausea. It has minimal place in any standard therapy for any form of diabetes.
for topic: Literature Review On Diabetes Mellitus. Gestational diabetes risk factors and long-term consequences for both mother and offspring: a literature review Salar Farahvar Department of Obstetrics and Gynecology, Faculty of Health, Sciences, Soroka University Medical Center, Ben-Gurion, University of the Negev, Beer Sheva, Israel Correspondence [email protected] Review of literature on gestational diabetes mellitus.
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