For example, there's a psychiatric condition called psychogenic polydipsia, which can lead to compulsive water drinking.
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We know that polydipsia tends to be associated with other psychiatric conditions such as depression, bipolar disorder, and schizophrenia.
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Sometimes that process isn't as straightforward as it should be: People with a syndrome called polydipsia feel excessive thirst and drink enormous quantities of water.
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Primary polydipsia, or psychogenic polydipsia, is a form of polydipsia characterised by excessive fluid intake in the absence of physiological stimuli to drink. Psychogenic polydipsia which is caused by psychiatric disorders, often schizophrenia, is often accompanied by the sensation of dry mouth. Some forms of polydipsia are explicitly non-psychogenic. Primary polydipsia is a diagnosis of exclusion.
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Polydipsia can be the result of a bird having ingested a toxin, or overconsumption of natural substances. For example, in pet birds, crackers, snack items, chips, fast foods, and canned vegetables (unrinsed) if eaten in sufficient quantities may cause a mild salt toxicity (5-10 times requirement) and subsequent polydipsia. Polydipsia can result from zinc poisoning to which caged birds may be particularly susceptible because of the zinc coating often used on birdcage bars. Polydipsia has been experimentally induced in pigeons, budgerigars and ducks, by the administration of lithium chloride (LiCl).
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Psychogenic polydipsia is also observed in some non-human patients, such as in rats and cats.
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Primary polydipsia describes excessive thirst and water intake caused in the absence of physiological stimuli to drink. This includes both psychogenic primary polydipsia and non- psychogenic primary polydipsia, such as in patients with autoimmune chronic hepatitis with severely elevated globulin levels. Psychogenic polydipsia is an excessive water intake seen in some patients with mental illnesses such as schizophrenia, and/or the developmentally disabled. It should be taken very seriously, as the amount of water ingested exceeds the amount that can be excreted by the kidneys, and can on rare occasions be life-threatening as the body's serum sodium level is diluted to an extent that seizures and cardiac arrest can occur.
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Polydipsia can be characteristic of diabetes mellitus, often as an initial symptom. It is observed in cases of poorly controlled diabetes, which is sometimes the result of low patient adherence to anti-diabetic medication. Diabetes insipidus ("tasteless" diabetes, as opposed to diabetes mellitus) can also cause polydipsia.
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Although primary polydipsia is usually categorised as psychogenic, there are some rare non- psychogenic causes. An example is polydipsia found in patients with autoimmune chronic hepatitis with severely elevated globulin levels. Evidence for the thirst being non-psychogenic is gained from the fact that it disappears after treatment of the underlying disease.
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Symptoms of hypercalcemia include anorexia, nausea, vomiting, constipation, abdominal pain, lethargy, depression, confusion, polyuria, polydipsia and generalized aches and pains.
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Polydipsia is excessive thirst or excess drinking.Porth, C. M. (1990). Pathophysiology: Concepts of altered health states. Philadelphia: J.B. Lippincott Company.
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Polydipsia is an excessively large water intake. Its occurrence in captive birds has been recorded, although it is a relatively rare abnormal behaviour.
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In many respects, the diagnosis of central diabetes insipidus begins as a diagnosis of exclusion. Specifically, other more common causes of polyuria and polydipsia are ruled out. Common rule outs include: diabetes mellitus, chronic kidney disease, hypokalemia, hypercalcemia, and psychogenic polydipsia. Once these conditions have been ruled out a water deprivation test is employed to confirm the diagnosis of CDI.
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Polyuria () is excessive or an abnormally large production or passage of urine (greater than 2.5 L or 3 L over 24 hours in adults). Increased production and passage of urine may also be termed diuresis. Polyuria often appears in conjunction with polydipsia (increased thirst), though it is possible to have one without the other, and the latter may be a cause or an effect. Primary polydipsia may lead to polyuria.
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Habit drinking (in its severest form termed psychogenic polydipsia) is the most common imitator of diabetes insipidus at all ages. While many adult cases in the medical literature are associated with mental disorders, most people with habit polydipsia have no other detectable disease. The distinction is made during the water deprivation test, as some degree of urinary concentration above isoosmolar is usually obtained before the person becomes dehydrated.
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Is there a role for corticosterone in expression of abnormal behaviour in restricted-fed fowls? Physiology & Behavior, 62: 7-13 Under experimental conditions where birds receive reinforcements on a strict schedule, for example receiving one pellet of food each minute often indicated by a tone or other stimulus, the birds may develop polydipsia. Under these conditions it is called schedule induced polydipsia or sometimes, adjunctive drinking.Hamm, R.J., Porter, J.H. and Kaempf, G.L. 1981.
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Sodium, chloride and potassium are excreted in osmotic diuresis, originating from diabetes mellitus (DM). Osmotic diuresis results in dehydration from polyuria and the classic polydipsia (excessive thirst) associated with DM.
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Typically, the signs and symptoms of juvenile nephronophthisis are limited to the kidneys. They include polyuria, polydipsia, weakness, and fatigue. Anemia, growth retardation, no hypertension. Proteinuria and hematuria are usually absent.
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Speech disorder and/or developmental delay 2\. Ophthalmic abnormalities other than rod-cone dystrophy (strabismus, cataract, astigmatism etc) 3\. Brachydactyly or Syndactyly 4\. Polyuria and/or polydipsia (nephrogenic diabetes insipidus) 5\.
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The combination of polydipsia and (nocturnal) polyuria is also seen in (primary) hyperaldosteronism (which often goes with hypokalemia). Antipsychotics can have side effects such as dry mouth that may make the patient feel thirsty.
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As a diagnosis of exclusion, a diagnosis of primary polydipsia may be the result of elimination of the possibility of diseases causing similar signs and symptoms, such as diabetes insipidus. Diagnosis may be complicated by the fact that chronic and extreme compulsive drinking may impair the response of the kidneys to vasopressin, thus reducing the kidney's ability to concentrate the urine. This means that psychogenic polydipsia may lead to test results (e.g. in a water restriction test) consistent with diabetes insipidus or SIADH, leading to misdiagnosis.
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The following conditions should also be excluded: DI, cerebral salt wasting, pseudohyponatraemia caused by hyperlipidemia or hyperparaproteinemia, SIADH, mineralcorticoid deficiency, salt-wasting nephropathy, nephrotic syndrome, chronic heart failure and cirrhosis. Tobacco smoking is an often overlooked factor linked to hyponatremia, due to the ADH-releasing effect of nicotine, although this is usually limited to heavy smokers. One study suggested that around 70% of patients with self-induced polydipsia were tobacco smokers. Diagnostic tests for primary polydipsia usually involves the fluid deprivation test to exclude ADH problems.
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Psychogenic polydipsia is found in patients with mental illnesses, most commonly schizophrenia, but also anxiety disorders and rarely affective disorders, anorexia nervosa and personality disorders. PPD occurs in between 6% and 20% of psychiatric inpatients. It may also be found in people with developmental disorders, such as those with autism. While psychogenic polydipsia is usually not seen outside the population of those with serious mental disorders, it may occasionally be found among others in the absence of psychosis, although there is no existent research to document this other than anecdotal observations.
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It can also be caused by a change in the osmolality of the extracellular fluids of the body, hypokalemia, decreased blood volume (as occurs during major hemorrhage), and other conditions that create a water deficit. This is usually a result of osmotic diuresis. Polydipsia is also a symptom of anticholinergic poisoning. Zinc is also known to reduce symptoms of polydipsia by causing the body to absorb fluids more efficiently (reduction of diarrhea, induces constipation) and it causes the body to retain more sodium; thus a zinc deficiency can be a possible cause.
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Furthermore, enalapril is an emerging treatment for psychogenic polydipsia. A double-blind, placebo-controlled trial showed that when used for this purpose, enalapril led to decreased water consumption (determined by urine output and osmolality) in 60% of patients.
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If the patient presents with acute hyponatraemia (overhydration) caused by psychogenic polydipsia, treatment usually involves administration of intravenous hypertonic (3%) saline until the serum sodium levels stabilise to within a normal range, even if the patient becomes asymptomatic.
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The word derives from the Greek () "very thirsty", which is derived from (, "much, many") + (, "thirst"). Polydipsia is a nonspecific symptom in various medical disorders. It also occurs as an abnormal behaviour in some non-human animals, such as in birds.
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In the kidney, HNF4A is expressed in the proximal tubules specifically. Deletion of Hnf4a in the developing mouse kidney caused Fanconi syndrome phenotypes including polyruia, polydipsia, glycosuria, and phosphaturia. The Hnf4a mutant kidney showed a defect in the formation of proximal tubules.
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Psychogenic polydipsia often leads to institutionalisation of mentally ill patients, since it is difficult to manage in the community. Most studies of behavioural treatments occur in institutional settings and require close monitoring of the patient and a large degree of time commitment from staff.
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While taking desmopressin, a person should drink fluids or water only when thirsty and not at other times, as this can lead to sudden fluid accumulation in the central nervous system. If desmopressin reduces urine output and increases urine osmolarity, the hypothalamic production of ADH is deficient, and the kidney responds normally to exogenous vasopressin (desmopressin). If the DI is due to kidney pathology, desmopressin does not change either urine output or osmolarity (since the endogenous vasopressin levels are already high). Whilst diabetes insipidus usually occurs with polydipsia, it can also rarely occur not only in the absence of polydipsia but in the presence of its opposite, adipsia (or hypodipsia).
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With increased osmolarity, the osmoreceptors in the hypothalamus detect this change and stimulate thirst. With increased thirst, the person now experiences a polydipsia and polyuria cycle. Hereditary forms of diabetes insipidus account for less than 10% of the cases of diabetes insipidus seen in clinical practice.
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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. Treatment with desmopressin may lead to water intoxication.
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The symptoms of latent autoimmune diabetes in adults are similar to those of other forms of diabetes: polydipsia (excessive thirst and drinking), polyuria (excessive urination), and often blurred vision. Compared to juvenile type 1 diabetes, the symptoms develop comparatively slowly, over a period of at least six months.
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Additionally, ingestion of household plants is a cause of hypercalcemia. Plants such as Cestrum diurnum, and Solanum malacoxylon contain ergocalciferol or cholecalciferol which cause the onset of hypercalcemia. Consuming small amounts of these plants can be fatal to pets. Observable symptoms may develop such as polydipsia, polyuria, extreme fatigue, or constipation.
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Differential diagnosis includes nephrogenic diabetes insipidus, neurogenic/central diabetes insipidus and psychogenic polydipsia. They may be differentiated by using the water deprivation test. Recently, lab assays for ADH are available and can aid in diagnosis.If able to rehydrate properly, sodium concentration should be nearer to the maximum of the normal range.
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The cornerstone of therapy for SIADH is reduction of water intake. If hyponatremia persists, then demeclocycline (an antibiotic with the side effect of inhibiting ADH) can be used. SIADH can also be treated with specific antagonists of the ADH receptors, such as conivaptan or tolvaptan. Another cause is psychogenic polydipsia.
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Polyuria is also a common symptom – which results in very dilute urine, as well as polydipsia which means having extreme thirst. Another symptom is hyperprolactinemia, which is when there are abnormally high prolactin levels in the blood. Usually, a mass will be found located on the sella turcica and loss of hormonal function.
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Psychogenic polydipsia is the psychiatric condition in which patients feel compelled to drink large quantities of water, thus putting them at risk of water intoxication. This condition can be especially dangerous if the patient also exhibits other psychiatric indications (as is often the case), as the care-takers might misinterpret the hyponatremic symptoms.
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Overview of the most significant symptoms of diabetes. The classic symptoms of diabetes are frequent urination (polyuria), increased thirst (polydipsia), increased hunger (polyphagia), and weight loss. Other symptoms that are commonly present at diagnosis include a history of blurred vision, itchiness, peripheral neuropathy, recurrent vaginal infections, and fatigue. Other symptoms may include loss of taste.
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Symptoms directly due to hypercalcemia are relatively rare, being more common in patients with malignant hypercalcemia. If present, common manifestations of hypercalcemia include weakness and fatigue, depression, bone pain, muscle soreness (myalgias), decreased appetite, feelings of nausea and vomiting, constipation, polyuria, polydipsia, cognitive impairment, kidney stones () and osteopenia or osteoporosis.Hyperparathyroidism . National Endocrine and Metabolic Diseases Information Service.
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Side effects of osaterone acetate include diminished sperm quality (for up to 6 weeks post-treatment), transient elevation of liver enzymes (caution should be observed with known liver disease), vomiting, diarrhea, polyuria/polydipsia, lethargy, and hyperplasia of the mammary glands. It can also decrease cortisol levels, interfere with adrenocorticotropic hormone response, induce or exacerbate adrenal insufficiency, and exacerbate diabetes mellitus.
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The most common presenting symptoms are: rapid weight loss, tachycardia (rapid heart rate), vomiting, diarrhea, increased consumption of fluids (polydipsia), polyphasia, and increased urine production (polyuria). Other symptoms include hyperactivity, possible aggression, an unkempt appearance, and large, thick claws. Heart murmurs and a gallop rhythm can develop due to secondary hypertrophic cardiomyopathy. About 70% of afflicted cats also have enlarged thyroid glands (goiter).
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Loss of blood volume and water from nausea, vomiting, diarrhea, and bleeding causes blood pressure to drop and organ damage to begin, which can be seen as the person begins to have somnolence/drowsiness, hematuria (blood in the urine), stupor, convulsions, polydipsia (excessive thirst), and oliguria (low urine production). This ultimately results in multi-system organ failure, hypovolemic shock, vascular collapse, and death.
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The clinical manifestation is similar to neurogenic diabetes insipidus, presenting with polydipsia (excessive thirst) and polyuria (excretion of a large amount of dilute urine). Dehydration is common, and incontinence can occur secondary to chronic bladder distension. On investigation, there will be an increased plasma osmolarity and decreased urine osmolarity. As pituitary function is normal, ADH levels are likely to be abnormal or raised.
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Thiazide diuretics are used in treatment because diabetes insipidus causes the excretion of more water than sodium (i.e., dilute urine). This condition results in a net concentrating effect on the serum (increasing its osmolarity). This high serum osmolarity stimulates polydipsia in an attempt to dilute the serum back to normal and provide free water for excreting the excess serum solutes.
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American Association of Avian Pathologists, Inc. Web. 15 Apr. 2017. Symptoms of avian spirochetosis include drop in egg production, depression, polydipsia (increased thirst), drowsiness, anorexia, loss of appetite, green diarrhea, ruffled feathers, pale combs, weight loss, paralysis of the legs and wings (flaccid paralysis), and abrupt death. Before death, the bird tends to become recumbent or begins to lie down stretched out.
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The size and half-life of copeptin permit an easier immunological testing, compared to vasopressin, and hence copeptin is proposed as a reliable AVP surrogate. The clinical interest in copeptin testing is closely linked to the pathophysiological pathways in which vasopressin is involved: polydipsia- polyuria syndrome, hyponatremia, syndrome of inappropriate antidiuretic hormone secretion (SIADH) as well as heart failure and acute coronary syndrome.
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In 1683, a surgical experiment by Johann Conrad Brunner almost led to a medical breakthrough. He excised the pancreas of a neighbour's hunting dog, causing polyuria and polydipsia. Brunner very clearly described these classic symptoms in pancreatectomized dogs, but made no association with diabetes. In 1788, Thomas Cawley published a case study in the London Medical Journal based on an autopsy of a diabetic patient.
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It is often accompanied by pronounced diarrhoea, dehydration, oedema, polydipsia, anaemia, listlessness and weight loss. In sheep profuse diarrhoea usually develops two to four weeks after initial infection. If infection is not properly attended death can ensue within 20 days, and in a farm mortality can be very high. In fact there are intermittent reports of mortality as high as 80% among sheep and cattle.
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Besipirdine was originally suggested as a treatment for OCD due to its effects on the adrenergic and serotonergic systems. "In vitro" studies of besipirdine indicated its potency in inhibiting serotonin reuptake in addition to norepinephrine reuptake. "In vivo", besipirdine showed efficacy in reducing schedule-induced polydipsia (SIP) in rats. The drug's anticonvulsant properties ultimately led Hoechst AG to pursue it as a treatment for Alzheimer's disease.
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Pituitary gland tumors are very common in the canine. A productive form arising from the anterior pituitary is the primary cause of Cushing's disease of dogs. This tumor causes excessive production of cortisol from the adrenal cortex which leads to the classic signs of alopecia (hair loss), polyuria (excessive urination), polydipsia (excessive water drinking), and a pot-bellied appearance of the abdomen due to muscle break down. See picture here.
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Global polyuria is the continuous overproduction of urine that is not only limited to sleep hours. Global polyuria occurs in response to increased fluid intake and is defined as urine outputs of greater than 40 mL/kg/24 hours. The common causes of global polyuria are primary thirst disorders such as diabetes mellitus and diabetes insipidus (DI). Urination imbalance may lead to polydipsia or excessive thirst to prevent circulatory collapse.
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Haemorrhage causes bloody feces (melena) and vomiting blood (hematemesis). The low blood volume (hypovolemia) caused by gastrointestinal fluid loss can lead to organ failure in the pancreas, kidney, liver, and GI tract and progress to shock. Shock and organ failure are indicated by disorientation, stupor, weakness, drowsiness, excessive thirst (polydipsia), low urine production (oliguria), and bloody urine (hematuria). Symptoms of ricin inhalation are different from those caused by ingestion.
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Polydipsia sometimes occurs under housing or experimental conditions which purportedly lead to stress or frustration. Growing parent stock of meat-type chickens (broilers), subjected routinely to chronic food restriction, show increased drinking after a single daily meal along with other oral stereotypies. Expression of these activities is correlated positively with the level of restriction imposed, and is thought to be controlled mainly by central dopaminergic mechanisms.Savory, C.J. and Mann, J.S., 1997.
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Symptoms of PST deficiency are mainly resulted from the disruptions in multiple metabolic processes due to the accumulation of phenols in the body. Common symptoms include polydipsia, flushing, tachycardia, night sweats, and gastrointestinal problems such as diarrhoea. Neurological and psychiatric disorders such as depression may also occur when regulation of phenolic neurotransmitters is disrupted. PST deficiency is also a risk factor for various diseases including autism, migraine, and cancers.
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Antidiuretic hormone (ADH) is released from the posterior pituitary for a number of physiologic reasons. The majority of people with hyponatremia, other than those with excessive water intake (polydipsia) or renal salt wasting, will have elevated ADH as the cause of their hyponatremia. However, not every person with hyponatremia and elevated ADH has SIADH. One approach to a diagnosis is to divide ADH release into appropriate (not SIADH) or inappropriate (SIADH).
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An overconsumption of water can lead to water intoxication, which can dangerously dilute the concentration of salts in the body. Overhydration sometimes occurs among athletes and outdoor laborers, but it can also be a sign of disease or damage to the hypothalamus. A persistent desire to drink inordinate quantities of water is a psychological condition termed polydipsia. It is often accompanied by polyuria and may itself be a symptom of Diabetes mellitus or Diabetes insipidus.
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Polydipsia is a symptom (evidence of a disease state), not a disease in itself. As it is often accompanied by polyuria, investigations directed at diagnosing diabetes insipidus and diabetes mellitus can be useful. Blood serum tests can also provide useful information about the osmolality of the body's extracellular fluids. A decrease in osmolality caused by excess water intake will decrease the serum concentration of red blood cells, blood urea nitrogen (BUN), and sodium.
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By the 18th century, many such pathologic observations were being published in textbooks and journals. This work lay important foundations for advances in medical treatment and intervention. Historically, various notions of present- day "diabetes" have described some general mix of excessive urine (polyuria), excessive thirst (polydipsia), and weight loss (see: History of diabetes#Early accounts). Over the past few centuries, these symptoms have been linked to updated understandings of how the disease works, and how it manifests differently across cases.
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Many consumed three to four times their normal daily water intake during a three-hour session, and some drank nearly half of their body weight in water during this time.Falk, J.L., (1961). Production of polydipsia in normal rats by an intermittent food schedule. Science 133: 195–196 Further research has revealed that intermittent food presentation to a variety of organisms results in an inordinately excessive consumption of water as well as other behaviours including attack, pica, escape, and alcohol consumption.
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The most common clinical manifestations are related to mental status and gastrointestinal function; they include lethargy, anorexia, vomiting, weight loss, and weakness. Additional findings may include dehydration, bradycardia, weak femoral pulses, abdominal pain, lack of appetite, tremors or shaking, muscle weakness, low body temperature, collapse, and pain in the hindquarters. Polyuria and polydipsia, diarrhea, and shivering are occasionally reported. Hypoglycemia can also be present, and initially may be confused with a seizure disorder or an insulin-secreting pancreatic tumor (insulinoma).
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Diabetic ketoacidosis arises because of a lack of insulin in the body. The lack of insulin and corresponding elevation of glucagon leads to increased release of glucose by the liver (a process that is normally suppressed by insulin) from glycogen via glycogenolysis and also through gluconeogenesis. High glucose levels spill over into the urine, taking water and solutes (such as sodium and potassium) along with it in a process known as osmotic diuresis. This leads to polyuria, dehydration, and polydipsia.
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Symptoms and signs include abdominal discomfort, polyuria, polydipsia, incidental discovery of hypertension, abdominal mass. The classic presentation for ARPKD is systemic hypertension with progression to end-stage kidney disease (ESKD) by the age of 15. In a typical presentation, a small number of ARPKD sufferers live to adulthood with some kidney function; but with significant deterioration in liver function. This outcome is postulated to result from expression of the polycystic kidney and hepatic disease gene PKHD1, which is located on chromosome 6p.
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The following outline is provided as an overview of and topical guide to diabetes mellitus (diabetes insipidus not included below) : Diabetes mellitus - group of metabolic diseases in which a person has high blood sugar, either because the pancreas does not produce enough insulin, or because cells do not respond properly to the insulin that is produced, a condition called insulin resistance. The resultant high blood sugar produces the classical symptoms of polyuria (frequent urination), polydipsia (increased thirst) and polyphagia (increased hunger).
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Continuous dehydration can cause acute and chronic diseases, but is most often associated with renal and neurological disorders. Excessive thirst, called polydipsia, along with excessive urination, known as polyuria, may be an indication of diabetes mellitus or diabetes insipidus. There are receptors and other systems in the body that detect a decreased volume or an increased osmolite concentration. Some sources distinguish "extracellular thirst" from "intracellular thirst", where extracellular thirst is thirst generated by decreased volume and intracellular thirst is thirst generated by increased osmolite concentration.
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Vitamin D overdose causes hypercalcemia, which is a strong indication of vitamin D toxicity – this can be noted with an increase in urination and thirst. If hypercalcemia is not treated, it results in excess deposits of calcium in soft tissues and organs such as the kidneys, liver, and heart, resulting in pain and organ damage. The main symptoms of vitamin D overdose which are those of hypercalcemia including anorexia, nausea, and vomiting. These may be followed by polyuria, polydipsia, weakness, insomnia, nervousness, pruritus and ultimately kidney failure.
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Hashitoxicosis, which can be abbreviated "Htx", is a transient hyperthyroidism caused by inflammation associated with Hashimoto's thyroiditis disturbing the thyroid follicles, resulting in excess release of thyroid hormone.Robins Basic Pathology Major clinical signs include weight loss (often accompanied by an increased appetite), anxiety, intolerance to heat, fatigue, hair loss, weakness, hyperactivity, irritability, apathy, depression, polyuria, polydipsia, delirium, and sweating. Additionally, patients may present with a variety of symptoms such as palpitations and arrhythmias (notably atrial fibrillation), shortness of breath (dyspnea), loss of libido, nausea, vomiting, and diarrhea. Long term untreated hyperthyroidism can lead to osteoporosis.
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Antidiuretic hormone (ADH) deficiency leads to the syndrome of diabetes insipidus (unrelated to diabetes mellitus): inability to concentrate the urine, leading to polyuria (production of large amounts of clear urine) that is low in solutes, dehydration and—in compensation—extreme thirst and constant need to drink (polydipsia), as well as hypernatremia (high sodium levels in the blood). ADH deficiency may be masked if there is ACTH deficiency, with symptoms only appearing when cortisol has been replaced. Oxytocin (OXT) deficiency generally causes few symptoms, as it is only required at the time of childbirth and breastfeeding.
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The most common cause of polyuria in both adults and children is uncontrolled diabetes mellitus, which causes osmotic diuresis, when glucose levels are so high that glucose is excreted in the urine. Water follows the glucose concentration passively, leading to abnormally high urine output. In the absence of diabetes mellitus, the most common causes are decreased secretion of aldosterone due to adrenal cortical tumor, primary polydipsia (excessive fluid drinking), central diabetes insipidus and nephrogenic diabetes insipidus. Polyuria may also be due to various chemical substances, such as diuretics, caffeine, and ethanol.
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A fluid or water deprivation test is a medical test which can be used to determine whether the patient has diabetes insipidus as opposed to other causes of polydipsia (a condition of excessive thirst that causes an excessive intake of water). The patient is required, for a prolonged period, to forgo intake of water completely, to determine the cause of the thirst. This test measures changes in body weight, urine output, and urine composition when fluids are withheld. Sometimes measuring blood levels of ADH (a synonym for vasopressin) during this test is also necessary.
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Overview of the most significant symptoms of diabetes A posterior subcapsular cataract is an uncommon symptom in those with type 1 DM The classical symptoms of type 1 diabetes include: polyuria (increased urination), polydipsia (increased thirst), dry mouth, polyphagia (increased hunger), fatigue, and weight loss. Type 1 diabetes is often diagnosed when diabetic ketoacidosis occurs. The signs and symptoms of diabetic ketoacidosis include dry skin, rapid deep breathing, drowsiness, increased thirst, frequent urination, abdominal pain, and vomiting. About 12 percent of people with type 1 diabetes have clinical depression.
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Hyponatremia has many causes including heart failure, chronic kidney disease, liver disease, treatment with thiazide diuretics, psychogenic polydipsia, syndrome of inappropriate antidiuretic hormone secretion. It can also be found in the postoperative state, and in the setting of accidental water intoxication as can be seen with intense exercise. Common causes in pediatric patients may be diarrheal illness, frequent feedings with dilute formula, water intoxication via excessive consumption, and enemas. pseudohyponatremia is a false low sodium reading that can be caused by high levels of fats or proteins in the blood.
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Infantile, juvenile, and adolescent forms of nephronophthisis have been identified. Although the range of characterizations is broad, people affected by nephronophthisis typically present with polyuria (production of a large volume of urine), polydipsia (excessive liquid intake), and after several months to years, end-stage kidney disease, a condition necessitating either dialysis or a kidney transplant in order to survive. Some individuals that suffer from nephronophthisis also have so-called "extra-renal symptoms" which can include tapetoretinal degeneration, liver problems, ocularmotor apraxia, and cone-shaped epiphysis (Saldino-Mainzer syndrome).
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The addition of weight loss, appetite loss, vomiting, polyuria, and polydipsia to the aforementioned symptoms may indicate that OFC is the result of parathyroid carcinoma. Parathyroid carcinoma, an uncommon cancer of the parathyroid glands, is generally indicated by serum calcium levels higher than usual, even in comparison to the high serum calcium levels that OFC generally presents with. Symptoms are also often more severe. Generally, the presence of a palpable neck mass is also indicative of the cancer, occurring in approximately 50% of sufferers, but virtually nonexistent in individuals with OFC with a different origin.
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In primary polydipsia, the urine osmolality should increase and stabilize at above 280 mOsm/kg with fluid restriction, while a stabilization at a lower level 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 blood levels of ADH toward the end of this test is also necessary, but is more time consuming to perform. To distinguish between the main forms, desmopressin stimulation is also used; desmopressin can be taken by injection, a nasal spray, or a tablet.
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The acute stage of the disease, occurring most often in the spring and summer, begins one to three weeks after infection and lasts for two to four weeks. Clinical signs include a fever, petechiae, bleeding disorders, vasculitis, lymphadenopathy, discharge from the nose and eyes, and edema of the legs and scrotum. There are no outward signs of the subclinical phase. Clinical signs of the chronic phase include weight loss, pale gums due to anemia, bleeding due to thrombocytopenia, vasculitis, lymphadenopathy, dyspnea, coughing, polyuria, polydipsia, lameness, ophthalmic diseases such as retinal hemorrhage and anterior uveitis, and neurological disease.
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ACE inhibitors may also be used to help decrease excessive water consumption in people with schizophrenia resulting in psychogenic polydipsia. A double-blind, placebo-controlled trial showed that when used for this purpose, enalapril led to decreased consumption (determined by urine output and osmolality) in 60% of people; the same effect has been demonstrated in other ACE inhibitors. Additionally ACEi are commonly used after renal transplant to manage post-transplant erythrocytosis, a condition characterised by a persistently high hematocrit greater than 51% which often develops 8-24 months after successful transplantation, as ACEi have been shown to decrease erythropoietin production.
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Similarly to progesterone, 19-norprogesterone is a potent progestogen and possesses high affinity for the mineralocorticoid receptor (MR). However, unlike progesterone, which is an antagonist of the MR, 19-norprogesterone acts as a partial agonist of the MR and produces mineralocorticoid effects such as sodium retention, polydipsia, and hypertension in animals. Like progesterone, 19-norprogesterone is very active as a progestogen parenterally but is only minimally active orally. A study found that 19-norprogesterone had 47% of the affinity of aldosterone for the rat MR and that 17α-hydroxylation (17α-hydroxy-19-norprogesterone, or gestronol) decreased it to 13%.
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Since the glucose that normally enters the cells is unable to do so without insulin, it begins to build up in the blood where it can be seen as hyperglycemia or high blood glucose levels. The tubules of the kidneys are normally able to re-absorb glucose, but they are unable to handle and process the amount of glucose they are being presented with. At this point, which is called the renal threshold, the excess glucose spills into the urine (glycosuria), where it can be seen in urine glucose testing. It is the polyuria, or over-frequent urination, which causes polydipsia, or excessive water consumption, through an osmotic process.
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Rodents are somewhat more susceptible to high doses than other species, and cholecalciferol has been used in poison bait for the control of these pests. The mechanism of high dose cholecalciferol is that it can produce "hypercalcemia, which results in systemic calcification of soft tissue, leading to kidney failure, cardiac abnormalities, hypertension, CNS depression, and GI upset. Signs generally develop within 18-36 hr of ingestion and can include depression, loss of appetite, polyuria, and polydipsia." High- dose cholecalciferol will tend to rapidly accumulate in adipose tissue yet release more slowly which will tend to delay time of death for several days from the time that high-dose bait is introduced.
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Psychogenic disease (or psychogenic illness) is a name given to physical illnesses that are believed to arise from emotional or mental stressors, or from psychological or psychiatric disorders. It is most commonly applied to illnesses where a physical abnormality or other biomarker has not yet been identified. In the absence of such biological evidence of an underlying disease process, it is often assumed that the illness must have a psychological cause, even if the patient shows no indications of being under stress or of having a psychological or psychiatric disorder. Examples of diseases that are believed by many to be psychogenic include psychogenic seizures, psychogenic polydipsia, psychogenic tremor, and psychogenic pain.
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In their 1995 paper, Metcalf and Allen maintained that they uncovered in animal behavior a pattern of period doubling leading to chaos. The authors examined a well-known response called schedule-induced polydipsia, by which an animal deprived of food for certain lengths of time will drink unusual amounts of water when the food is at last presented. The control parameter (r) operating here was the length of the interval between feedings, once resumed. The authors were careful to test a large number of animals and to include many replications, and they designed their experiment so as to rule out the likelihood that changes in response patterns were caused by different starting places for r.
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By looking at the timing of different behaviors within the interval, Staddon and Simmelhag were able to distinguish two classes of behavior: the terminal response, which occurred in anticipation of food, and interim responses, that occurred earlier in the interfood interval and were rarely contiguous with food. Terminal responses seem to reflect classical (as opposed to operant) conditioning, rather than adventitious reinforcement, guided by a process like that observed in 1968 by Brown and Jenkins in their "autoshaping" procedures. The causation of interim activities (such as the schedule-induced polydipsia seen in a similar situation with rats) also cannot be traced to adventitious reinforcement and its details are still obscure (Staddon, 1977).
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Signs and symptoms of CSWS include large amounts of urination (polyuria, defined as over three liters of urine output over 24 hours in an adult), high amounts of sodium in the urine, low blood sodium concentration, excessive thirst (polydipsia), extreme salt cravings, dysfunction of the autonomic nervous system (dysautonomia), and dehydration. Patients often self-medicate by consuming high amounts of sodium and by dramatically increasing their water intake. Advanced symptoms include muscle cramps, lightheadedness, dizziness or vertigo, feelings of anxiety or panic, increased heart rate or slowed heart rate, low blood pressure and orthostatic hypotension which can result in fainting. Other symptoms frequently associated with dysautonomia include headaches, pallor, malaise, facial flushing, constipation or diarrhea, nausea, acid reflux, visual disturbances, numbness, nerve pain, trouble breathing, chest pain, loss of consciousness, and seizures.
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These drugs help the body rid itself of extra water via the extra urine. The concentrations of electrolytes in the blood are closely linked to fluid balance, so any action or problem involving fluid intake or output (such as polydipsia, polyuria, diarrhea, heat exhaustion, starting or changing doses of diuretics, and others) can require management of electrolytes, whether through self-care in mild cases or with help from health professionals in moderate or severe cases. Sometimes a connotative difference is felt between diuresis in the sense of appropriate increase (as in successful diuretic therapy that is controlling symptoms well) and polyuria in the sense of inappropriate increase, that is, excess (as in failed oral antihyperglycemic therapy that must be stepped up to achieve control). However, sometimes the words are simply synonymous.
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