What Are The 3 P's Of Diabetes?
The 3 classic symptoms of diabetes mellitus are polyuria, polydipsia and polyphagia -- also known as the 3 P's. Polyuria, polydipsia and polyphagia are defined as an increase in urination, thirst and hunger, respectively. The presence of the 3 P’s is a good indication that your blood sugar may be too high. With type 1 diabetes (T1DM), these symptoms typically develop relatively quickly and are more obvious, often leading to diagnosis of the condition. With type 2 diabetes (T2DM), the 3 P's are often more subtle and develop more gradually. As a result, people with type 2 diabetes may overlook these symptoms, leading to a delay in diagnosis. Video of the Day The 3 P’s of diabetes are typically among the first symptoms to occur in T1DM, but they can occur with other conditions. Polyuria, or excessive urine production, can be identified by needing to urinate during the night, frequent bathroom trips or accidents in potty-trained children. Polydipsia, a consequence of polyuria, is characterized by excessive thirst. An increase in fluid intake due to polydipsia can also contribute to increased urination. Polyphagia is the term for excessive or increased hunger. It occurs with diabetes because blood sugar is fails to enter body tissues normally, leaving them short of fuel to produce energy. To compensate, fat and muscle are broken down and used for energy resulting in weight loss, lack of energy and fatigue, which are most often seen with T1DM. Signs of long-term high blood sugar, such as blurred vision and tingling or numbness in hands and feet, are more common at diagnosis with T2DM. High Blood Sugar and the 3 P's The 3 P's of diabetes all stem from high blood sugar levels. Blood sugar is normally filtered by the kidneys but then reabsorbed into the blood. When blood sug Continue reading >>
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Diabetes Insipidus – Diagnosis And Management
Abstract Central diabetes insipidus (CDI) is the end result of a number of conditions that affect the hypothalamic-neurohypophyseal system. The known causes include germinoma/craniopharyngioma, Langerhans cell histiocytosis (LCH), local inflammatory, autoimmune or vascular diseases, trauma resulting from surgery or an accident, sarcoidosis, metastases and midline cerebral and cranial malformations. In rare cases, the underlying cause can be genetic defects in vasopressin synthesis that are inherited as autosomal dominant, autosomal recessive or X-linked recessive traits. The diagnosis of the underlying condition is challenging and raises several concerns for patients and parents as it requires long-term follow-up. Proper etiological diagnosis can be achieved via a series of steps that start with clinical observations and then progress to more sophisticated tools. Specifically, MRI identification of pituitary hyperintensity in the posterior part of the sella, now considered a clear marker of neurohypophyseal functional integrity, together with the careful analysis of pituitary stalk shape and size, have provided the most striking findings contributing to the diagnosis and understanding of some forms of ‘idiopathic’ CDI. MRI STIR (short-inversion-time inversion recovery sequencing) is a promising technology for the early identification of LCH-dependent CDI. © 2012 S. Karger AG, Basel Definition/Classification Diabetes insipidus is a disease in which large volumes of dilute urine (polyuria) are excreted due to vasopressin (AVP) deficiency [central diabetes insipidus (CDI)], AVP resistance [nephrogenic diabetes insipidus (NDI)], or excessive water intake (primary polydipsia). Polyuria is characterized by a urine volume in excess of 2 l/m2/24 h or approximately 150 ml/k Continue reading >>
Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find the Diabetes Insipidus article more useful, or one of our other health articles. Diabetes insipidus (DI) is a condition caused by hyposecretion of, or insensitivity to the effects of, antidiuretic hormone (ADH), also known as arginine vasopressin (AVP). ADH is synthesised in the hypothalamus and transported as neurosecretory vesicles to the posterior pituitary. There it is released into the circulation, governed by plasma osmolality. Its deficiency or failure to act causes an inability to concentrate urine in the distal renal tubules, leading to the passage of copious volumes of dilute urine. Usually the person with this condition passes >3 litres/24 hours of low osmolality (<300 mOsmol/kg) urine. There are two major forms of DI: Cranial DI: decreased secretion of ADH. Decreased secretion of ADH reduces the ability to concentrate urine and so causes polyuria and polydipsia. Nephrogenic DI: decreased ability to concentrate urine because of resistance to ADH in the kidney. There are two other forms of DI (both caused by deficiencies in ADH; however, the deficiencies do not result from a defect in the neurohypophysis or kidneys): Gestational DI: results from degradation of vasopressin by a placental vasopressinase. Gestational DI may be associated with increased complications of pregnancy, including pre-eclampsia. Primary polydipsia (dipsogenic DI): caused by a primary defect in osmoregulation of thirst. Dipsogenic DI has been reported in tuberculous meningitis, multiple sclerosis and neurosarcoidosis. The combined prevalence of cranial DI and nephrogenic D Continue reading >>
Signs & Symptoms Of Diabetes: Type 2. The 3 P’s!
Type 2 diabetes is a slow developing condition and can often go unnoticed for a very long time. We can have pre-diabetes/insulin resistance for 5-10 years before an ‘official' diagnosis and for this reason diabetes often gets overlooked, meaning many people are walking around not knowing they are prediabetic or diabetic. It's good to get regular fasting blood sugar tests but also ask your doctor to test for insulin resistance, because if you catch it early you can prevent an ‘official' diagnosis from ever occuring. Having the insulin test is VERY important because you can have a normal blood glucose level but have high insulin and this can be an indicator that you need to take some positive healthy action. Signs and Symptoms of Diabetes: Type 2 As suggested above, signs and symptoms can be unobvious so for this reason just be sure to get regular health checks. The 3 P's: Most Common Symptoms There are 3 P's that are the most common symptoms of type 2 diabetes to look out for: Polyuria – having high blood glucose makes your blood thick, sticky, and syrupy, so the body draws more fluid into the bloodstream but at the same time has to eliminate that. The result is frequent urination (polyuria – means more urine), increased thirst, feeling dehydrated or having a dry mouth. Polydipsia – means increased thirst. But don't reach for the sugary drinks because it only makes things worse. The polyuria and polydipsia are closely related. Polyphagia – you feel hungry because the glucose is not moving into the cells like it should be, instead it's staying in the blood stream and sending the wrong hunger signals to the body. You may have just eaten but you're still hungry. So remember the 3 P's as the most common signs: Polyuria – increased urination Polydipsia – incre Continue reading >>
Practice Essentials Diabetes insipidus (DI) is defined as the passage of large volumes (>3 L/24 hr) of dilute urine (< 300 mOsm/kg). It has the following 2 major forms: Two other forms are gestational DI and primary polydipsia (dipsogenic DI); both are caused by deficiencies in AVP, but the deficiencies do not result from a defect in the neurohypophysis or kidneys. Signs and symptoms The predominant manifestations of DI are as follows: The most common form is central DI after trauma or surgery to the region of the pituitary and hypothalamus, which may exhibit 1 of the following 3 patterns: In infants with DI, the most apparent signs may be the following: In children, the following manifestations typically predominate: If the condition that caused DI also damaged the anterior pituitary or hypothalamic centers that produce releasing factors, patients may present with the following: Physical findings vary with the severity and chronicity of DI; they may be entirely normal or may include the following: See Clinical Presentation for more detail. If the clinical presentation suggests DI, laboratory tests must be performed to confirm the diagnosis, as follows: Additional studies that may be indicated include the following: See Workup for more detail. Management Most patients with DI can drink enough fluid to replace their urine losses. When oral intake is inadequate and hypernatremia is present, provide fluid replacement as follows: Give dextrose and water or an intravenous fluid that is hypo-osmolar with respect to the patient’s serum; do not administer sterile water without dextrose IV Administer fluids at a rate no greater than 500-750 mL/hr; aim at reducing serum sodium by approximately 0.5 mmol/L (0.5 mEq/L) every hour Pharmacologic therapeutic options include the follo Continue reading >>
Diabetes Insipidus: Causes & Symptoms + 5 Natural Treatments
Diabetes insipidus, is a debilitating and rare disease, with a prevalence of 1 out of 25,000 people. Often referred to as “water diabetes,” it is a condition characterized by frequent and heavy urination, excessive thirst and an overall feeling of weakness. It’s caused by a defect in the pituitary gland or in the kidneys. (1) The term insipidus means “without taste” in Latin, while diabetes mellitus involves the excretion of “sweet” urine. People with diabetes insipidus pass urine that is diluted, odorless and relatively low in sodium content. Diabetes insipidus and diabetes mellitus (which includes both type 1 and type 2 diabetes) are unrelated. Both conditions do cause frequent urination and constant thirst. People with diabetes insipidus have normal blood sugar levels, but their kidneys cannot balance fluid in the body. Although the symptoms of diabetes insipidus can be bothersome and sometimes even life-changing, the condition doesn’t increase future health risks when it is managed properly. It’s important to find the right treatment plan, which typically involves taking measures to avoid dehydration. What is Diabetes Insipidus? Diabetes insipidus is a condition that disrupts normal life due to increased thirst and passing of large volumes or urine, even at night. It is a part of a group of hereditary or acquired polyuria (when large amounts of urine is produced) and polydipsia (excessive thirst) diseases. It’s associated with inadequate vasopressin or antidiuretic hormone secretion. Vasopressin, which includes arginine vasopressin (AVP) and antidiuretic hormone (ADH), is a peptide hormone formed in the hypothalamus. It then travels to the posterior pituitary where it releases into the blood. In order to fully understand the cause of diabetes ins Continue reading >>
Diabetes Insipidus - Endotext - Ncbi Bookshelf
Honorary Professor of Medicine and Endocrinology, Central Manchester University Hospitals Foundation Trust and Manchester Academic Health Science Centre, Manchester, UK. Diabetes Insipidus (DI) is the excess production of dilute urine. Diagnosis requires a targeted history, examination and confirmation through appropriate laboratory and radiological investigations. DI presents with polyuria and polydipsia. Urine output is more than 40 ml/kg /24 hours in adults and more than 100 ml/kg/24 hours in children. DI reflects either the lack of production or action of the posterior pituitary hormone vasopressin (AVP). There are three subtypes. Cranial or hypothalamic DI (HDI): due to relative or absolute lack of AVP. Nephrogenic DI (NDI): due to partial or total resistance to the renal antidiuretic effects of AVP. Dipsogenic DI (DDI, primary polydipsia): where polyuria is secondary to excessive, inappropriate fluid intake. All forms of DI are rare. HDI has an estimated prevalence of 1/25,000. While presentation is more common in adults, familial forms of both HDI and NDI characteristically present in childhood. AVP is a nine-amino acid peptide made within magnocellular neurones of the paraventricular (PVN) and supraoptic (SON) nuclei of the hypothalamus that project through the hypophyseal portal tract to terminate in the posterior pituitary, where AVP is released into the circulation. Together, the PVN, SON and posterior pituitary form an anatomical and functional unit- the neurohypophysis ( figure 1 ). The neurohypophysis. Vasopressinergic magnocellular neurones originating in the supraoptic (SON) and paraventrical (PVN) nucleii terminate in the posterior pituitary (arrow). Together, the 3 structures form a functional and anatomical unit: the neurohypophysis. AVP is produced Continue reading >>
Diagnosis Of Polyuria And Diabetes Insipidus
DEFINITION Polyuria has generally been defined as a urine output exceeding 3 L/day in adults and 2 L/m2 in children. It must be differentiated from the more common complaints of frequency or nocturia, which are not associated with an increase in the total urine output. The following is an overview of the diagnosis of polyuria and diabetes insipidus (DI). The causes and treatment of polyuria due to central or nephrogenic DI are presented separately. (See "Clinical manifestations and causes of central diabetes insipidus" and "Clinical manifestations and causes of nephrogenic diabetes insipidus" and "Treatment of central diabetes insipidus" and "Treatment of nephrogenic diabetes insipidus".) CAUSES In the absence of a glucose-induced osmotic diuresis in uncontrolled diabetes mellitus, there are three major causes of polyuria in the outpatient setting, each of which is due to a defect in water balance leading to the excretion of large volumes of dilute urine (urine osmolality usually below 250 mosmol/kg): primary polydipsia, which is primarily seen in adults and adolescents; central DI; and nephrogenic DI . Primary polydipsia — Primary polydipsia (sometimes called psychogenic polydipsia) is characterized by a primary increase in water intake. This disorder is most often seen in middle-aged women and in patients with psychiatric illnesses, including those taking a phenothiazine, which can lead to the sensation of a dry mouth. Primary polydipsia can also be induced by hypothalamic lesions that directly affect the thirst center, as may occur with an infiltrative disease such as sarcoidosis . (See "Causes of hyponatremia in adults".) Central DI — Central DI (also called neurohypophyseal or neurogenic DI) is associated with deficient secretion of antidiuretic hormone ( Continue reading >>
Diabetes Insipidus: Causes, Symptoms And Treatment
Diabetes insipidus is a condition where the body loses too much fluid through urination, causing a significant risk of dangerous dehydration as well as a range of illnesses and conditions. There are two forms of the disease: nephrogenic diabetes insipidus and central diabetes insipidus (also known as neurogenic diabetes insipidus). A number of factors have been linked to the development of diabetes insipidus, which may also occur in pregnancy or with the use of certain medications. Establishing the cause of the problem can help determine the most appropriate treatment to support the regulation of water balance in the body. Diabetes insipidus is a condition that can be managed successfully. Contents of this article: What is diabetes insipidus? An uncommon condition, diabetes insipidus is a disorder affecting the regulation of body fluid levels. Two key symptoms resemble those of the more common forms of diabetes that affect blood sugar levels (diabetes mellitus types 1 and 2).1-5 People with diabetes insipidus produce excessive amounts of urine (polyuria), resulting in frequent urination and, in turn, thirst (polydipsia). However, the underlying cause of these two symptoms is quite different from the causes in types 1 and 2 diabetes. In diabetes mellitus, elevated blood sugar prompts the production of large volumes of urine to help remove the excess sugar from the body. In diabetes insipidus, it is the body's water balance system itself that is not working properly. Here are some key points about diabetes insipidus. More detail and supporting information is in the body of this article. Diabetes insipidus is a condition where the body fails to properly control water balance, resulting in excessive urination. Diabetes insipidus can be caused by low or absent secretion of t Continue reading >>
Diabetes Insipidus - Statpearls - Ncbi Bookshelf
Diabetes insipidus (DI) is a disease process that results in either decreased release of or response to antidiuretic hormone (ADH, also known as vasopressin or AVP), which can cause electrolyte imbalances. There are two types of diabetes insipidus, central and nephrogenic, and each has congenital and acquired causes. Idiopathic central diabetes insipidusis the most common cause, in which no identifiable cause was determined. The congenital form of central diabetes insipidusis rare and is associated with hypothalamus malformations, defects in ADH precursor synthesis, or deficiency in ADH. Acquired forms of central diabetes insipidusinclude autoimmune and vascular diseases, sarcoidosis, craniopharyngioma, Langerhans Cell Histiocytosis, surgery, trauma, structural malformations, metastasis, hypoxic brain injury, or ischemia. The congenital form of nephrogenic diabetes insipidusis associated with mutations in either the AVPR2 or AQP2 gene. AVPR2 receptor defects are the source of 90% of congenital nephrogenic diabetes insipidusforms of nephrogenicdiabetes insipidusare more common and can stem from multiple drug treatments including lithium, antibiotics, antifungals, and antineoplastic agents. Other acquired causes include renal disease, sickle cell disease, obstructive uropathy, pregnancy, craniopharyngioma surgery, and electrolyte disturbances such as hypokalemia and hypercalcemia. Diabetes insipidusis an uncommon disease process with a low prevalence of 1:25,0000. In clinical practice, congenital forms of diabetes insipidusconstitute less than 10% of patient cases. Water balance is regulated by ADH, thirst, and kidney function. ADH is produced by the posterior pituitary and released into the blood supply via the inferior hypophyseal arteries. Subsequently, ADH targets th Continue reading >>
What Are The 3 P’s Of Diabetes & Their Characteristics?
Diabetes is a dreaded and serious illness affecting large number of people worldwide. In diabetes, there is increased blood glucose level, which can lead to several health complications and may prove to be fatal at times. The most common symptoms to identify this condition are the 3 P's of diabetes, namely polyuria, polydipsia and polyphagia, which is increase in urination, thirst and hunger or appetite, respectively. Diagnosing the condition at an early stage can save lives and also reduce the burden of the patients suffering from diabetes. Diagnosing can help in early treatment and hence the advancement of complications and diseases can be prevented. Presence of these 3 P's of diabetes is an early indication that the person is having higher blood sugar level and diabetes. However, in type 1 diabetes, all these three symptoms usually develop quickly and are obvious, making the diagnosis easier. But, in type 2 diabetes these 3 Ps are always subtle and it develops slowly, which makes it difficult to diagnose. Patients with type 2 diabetes often overlook the symptoms and hence they delay their diagnosis which may worsen the condition. Well, all the 3 P's of diabetes usually shoot from high blood glucose levels. The glucose in blood is usually filtered by the kidneys and it is then absorbed back into the blood. If the blood glucose level is higher, the kidneys can't function efficiently to reabsorb all the sugar and hence it ends up in urine. Polyuria - If there is high content of sugar in urine, excessive water from body is lost through urination and hence polyuria develops. Polydipsia - The loss of excessive body water causes dehydration and this increases thirst, thus polydipsia develops. Polyphagia - When there is lack of insulin production in body, which occurs in dia Continue reading >>
Management Of Diabetes Insipidus In Children
Go to: Abstract Diabetes Insipidus (DI) is a heterogeneous clinical syndrome of disturbance in water balance, characterized by polyuria (urine output > 4 ml/kg/hr), polydypsia (water intake > 2 L/m2/d) and failure to thrive. In children, Nephrogenic DI (NDI) is more common than Central DI (CDI), and is often acquired. The signs and symptoms vary with etiology, age at presentation and mode of onset. Neonates and infants with NDI are severely affected and difficult to treat. Diagnosis is based on the presence of high plasma osmolality and low urinary osmolality with significant water diuresis. Water deprivation test with vasopressin challenge, though has limitations, is done to differentiate NDI and CDI and diagnose their partial forms. Measurement of urinary aquaporin 2 and serum copeptin levels are being studied and show promising diagnostic potential. Magnetic Resonance Imaging (MRI) pituitary helps in the etiological diagnosis of CDI, absence of posterior pituitary bright signal being the pathognomic sign. If pituitary stalk thickening of < 2 mm is present, these children need to be monitored for evolving lesion. Neonates and young infants are better managed with fluids alone. Older children with CDI are treated with desmopressin. The oral form is safe, highly effective, with more flexibility of dosing and has largely replaced the intranasal form. In NDI besides treatment of the underlying cause, use of high calorie low solute diet and drugs to ameliorate water excretion (thiazide, amelioride, indomethacin) are useful. Children with NDI however well treated, remain short and have mental retardation on follow up. Continue reading >>
Diabetes insipidus (DI) is a condition characterized by large amounts of dilute urine and increased thirst. The amount of urine produced can be nearly 20 liters per day. Reduction of fluid has little effect on the concentration of the urine. Complications may include dehydration or seizures. There are four types of DI, each with a different set of causes. Central DI (CDI) is due to a lack of the hormone vasopressin (antidiuretic hormone). This can be due to damage to the hypothalamus or pituitary gland or genetics. Nephrogenic diabetes insipidus (NDI) occurs when the kidneys do not respond properly to vasopressin. Dipsogenic DI is due to abnormal thirst mechanisms in the hypothalamus while gestational DI occurs only during pregnancy. Diagnosis is often based on urine tests, blood tests, and the fluid deprivation test. Diabetes mellitus is a separate condition with an unrelated mechanism, though both can result in the production of large amounts of urine. Treatment involves drinking sufficient fluids to prevent dehydration. Other treatments depend on the type. In central and gestational disease treated is with desmopressin. Nephrogenic disease may be treated by addressing the underlying cause or the use of a thiazide, aspirin, or ibuprofen. The number of new cases of diabetes insipidus each year is 3 in 100,000. Central DI usually starts between the ages of 10 and 20 and occurs in males and females equally. Nephrogenic DI can begin at any age. The term "diabetes" is derived from the Greek word meaning siphon. 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 Continue reading >>
Diabetes Insipidus: The Other Diabetes Kalra S, Zargar Ah, Jain Sm, Sethi B, Chowdhury S, Singh Ak, Thomas N, Unnikrishnan A G, Thakkar Pb, Malve H - Indian J Endocr Metab
Diabetes insipidus (DI) is part of a group of hereditary or acquired polyuria and polydipsia diseases. It is associated with inadequate arginine vasopressin (AVP) or antidiuretic hormone (ADH) secretion or renal response to AVP, resulting in hypotonic polyuria and a compensatory/underlying polydipsia.  Polyuria (>50mL/kg), dilute urine (osmolality <300 mOsm/L), and increased thirst (water intake of up to 20 L/day) are characteristic of DI.  The kidneys pass large amounts of water irrespective of the body's hydration state.  Untreated DI can cause hypovolemia, dehydration, and electrolyte imbalances.  This article reviews the physiology, causes, and treatment of DI. A search of literature on the causes, physiology, and treatment options for DI was carried out using the PubMed database. Only English language articles were included in this review. DI can be caused by two fundamentally different defects: Inadequate/impaired secretion of AVP from the posterior pituitary gland and impaired/insufficient renal response to ADH.  AVP, a neurohypophyseal nonapeptide, regulates body water and osmotic homeostasis.  ,  The AVP-neurophysin II gene (AVP-NPII) encodes AVP, which is synthesized in the supraoptic and paraventricular nuclei of the hypothalamus as a precursor complex of AVP, NPII, and glycopeptides copeptin and is released as AVP from neurons in the posterior pituitary. AVP and its protein carrier, NPII, are released by calcium-dependent exocytosis.  AVP release may occur due to nonosmotic stimuli also including orthostatic hypotension or emetic reflexes (manifested in nausea and vomiting).  The AVP system [Figure 1] maintains water balance based on serum osmolality and arterial blood volume via the vasopressin-2-receptor (V2R).  ,  ,  A Continue reading >>
Over the past two decades our understanding of the mechanisms that control water balance in health and disease has increased substantially. Following the establishment of reliable assay techniques to measure circulating vasopressin, the application of molecular biological methods to define hormonal and receptor abnormalities, and a greater knowledge of intracellular events within the renal tubular cells, it is now possible to characterise disorders of water balance more accurately. The physiology of water homeostasis is briefly discussed before the pathophysiology, diagnosis, and treatment of diabetes insipidus are described in detail. Physiology of water homeostasis It is essential that body water, both intracellular and extracellular, remains stable to allow normal cellular functions to take place. In humans, the maintenance of normal water balance is achieved principally by three interrelated determinants: vasopressin, thirst, and the kidneys. The secretion of vasopressin from the posterior pituitary is under very precise control. Small changes in blood solute concentration (plasma osmolality) regulate vasopressin release.1 An increase in plasma osmolality, usually indicating a loss of extracellular water, stimulates vasopressin secretion and, conversely, a decrease in plasma osmolality inhibits its release into the systemic circulation (fig 1). Vasopressin then acts on its major target organ, the kidneys. The hormone binds to its V2 receptor (the antidiuretic receptor) on the basal aspect of the renal collecting tubular cell to activate an adenyl cyclase system that stimulates intracellular protein kinases. These, in turn, control the arrangement and insertion of “water channel” proteins (aquaporin 2) into the cell membrane to allow water to pass from the lumen Continue reading >>