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Diabetes Mellitus

Diabetes mellitus

Diabetes mellitus is a medical disorder characterized by varying or persistent hyperglycemia (elevated blood sugar levels), especially after eating. All types of diabetes mellitus share similar symptoms and complications at advanced stages. Hyperglycemia itself can lead to dehydration and ketoacidosis. Longer-term complications include cardiovascular disease (doubled risk), chronic renal failure (it is the main cause for dialysis), retinal damage which can lead to blindness, nerve damage which can lead to erectile dysfunction (impotence), gangrene with risk of amputation of toes, feet, and even legs. The more serious complications are more common in people who have a difficult time controlling their blood sugars with medications (glycemic control). The most important forms of diabetes are due to decreased production of insulin (diabetes mellitus type 1, the first recognized form), or decreased sensitivity of body tissues to insulin (diabetes mellitus type 2, the more common form). The former requires insulin injections, while the latter is generally managed with oral medication and only requires insulin if the tablets are ineffective. Patient understanding and participation is vital as blood glucose levels change continuously. Treatments which return the blood sugar to normal levels can reduce or prevent development of some of the complications of diabetes. Other health problems that accelerate the damaging effects of diabetes are smoking, elevated cholesterol levels, obesity, high blood pressure, and lack of regular exercise.

History

Although diabetes has been recognized since antiquity, and treatments were known since the Middle Ages, the elucidation of the pathogenesis of diabetes occurred mainly in the 20th century⁶. Until 1922, when insulin was first discovered and made clinically available, a clinical diagnosis of diabetes was an invariable death sentence, more or less quickly. Non-progressing type 2 diabetics almost certainly often went undiagnosed then; many still do. The discovery of the role of the pancreas in diabetes is generally credited to Joseph Von Mering and Oskar Minkowski, two European researchers who, in 1889, found that when they completely removed the pancreas of dogs, the dogs developed all the signs and symptoms of diabetes and died shortly afterward. In 1910, Sir Edward Albert Sharpey-Schafer of Edinburgh in Scotland suggested diabetics were deficient in a single chemical that was normally produced by the pancreas - he proposed calling this substance insulin. The endocrine role of the pancreas in metabolism, and indeed the existence of insulin, was not fully clarified until 1921, when Sir Frederick Grant Banting and Charles Herbert Best repeated the work of Von Mering and Minkowski but went a step further and managed to show that they could reverse the induced diabetes in dogs by giving them an extract from the pancreatic islets of Langerhans of healthy dogs⁷. They went on to isolate the hormone insulin from bovine pancreases at the University of Toronto in Canada. This led to the availability of an effective treatment - insulin injections - and the first clinical patient was treated in 1922. For this, Banting et al received the Nobel Prize in Physiology or Medicine in 1923. The two researchers did not patent their discovery and insulin therapy rapidly spread around the world. The distinction between what is now known as type 1 and type 2 diabetes was made by Sir Harold Percival (Harry) Himsworth in 1935; he published his findings in January 1936 in The Lancet⁸. Other landmark discoveries⁶ include:
- identification of sulfonylureas in 1942
- the radioimmunoassay for insulin, as discovered by Rosalyn Yalow and Solomon Berson (gaining Yalow the 1977 Nobel Prize in Physiology or Medicine);
- Reaven's introduction of the metabolic syndrome in 1988
- identification of thiazolidinediones as effective antidiabetics in the 1990s.

Causes and types

The role of insulin

1990s Since insulin is the principal hormone that regulates uptake of glucose into cells (primarily muscle and fat cells) from the blood, deficiency of insulin or its action plays a central role in all forms of diabetes. Most of the carbohydrates in food are rapidly converted to glucose, the principal sugar in blood. Insulin is produced by beta cells in the pancreas in response to rising levels of glucose in the blood, as occurs after a meal. Insulin makes it possible for most body tissues to remove glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Insulin is also the principal control signal for conversion of glucose (the basic sugar unit) to glycogen for storage in liver and muscle cells. Lowered insulin levels result in the reverse conversion of glycogen to glucose when glucose levels fall — though only in the liver not muscle tissue. Higher insulin levels increase many anabolic ("building up") processes such as cell growth, cellular protein synthesis, and fat storage. Insulin is the principal signal in converting many of the bidirectional processes of metabolism from a catabolic to an anabolic direction. If the amount of insulin produced is insufficient, if cells respond poorly to the effects of insulin (insulin insensitivity or resistance), or if the insulin itself is defective, glucose is not handled properly by body cells (about 2/3 require it) nor stored appropriately in the liver and muscles. The net effect is persistent high levels of blood glucose, poor protein synthesis, and other metabolic derangements.

Types

Type 1

Main article: Diabetes mellitus type 1 Type 1 diabetes (formerly known as type I diabetes, insulin-dependent diabetes, childhood diabetes, or juvenile onset diabetes) is most commonly diagnosed in children and adolescents, but can occur in adults as well. It is characterized by β-cell destruction, which usually leads to an absolute deficiency of insulin. Most cases of type 1 diabetes are immune-mediated characterized by autoimmune destruction of the body's β-cells in the Islets of Langerhans of the pancreas, destroying them or damaging them sufficiently to reduce insulin production. However, some forms of type 1 diabetes are characterized by loss of the body's β-cells without evidence of autoimmunity. Currently, type 1 diabetes is treated with insulin injections, lifestyle adjustments, and careful monitoring of blood glucose levels using blood test kits. Insulin delivery is also available by an insulin pump, which allows the infusion of insulin 24 hours a day at preset levels, and the ability to program push doses (bolus) of insulin as needed at meal times. The treatment must be continued indefinitely.

Type 2

Main article: Diabetes mellitus type 2 Type 2 diabetes is characterized by "insulin resistance" as body cells do not respond appropriately when insulin is present. This is a more complex problem than type 1, but is often easier to treat, since insulin is still produced, especially in the initial years. Type 2 may go unnoticed for years in a patient before diagnosis, since the symptoms are typically milder (no ketoacidosis) and can be sporadic. However, severe complications can result from unnoticed type 2 diabetes, including renal failure, and coronary artery disease. Type 2 is initially treated by changes in diet and through weight loss. This can restore insulin sensitivity, even when the weight lost is modest e.g. around 5 kg (10 to 15 lb). The next step, if necessary, is treatment with oral antidiabetic drugs: the sulphonylureas, metformin, or (if these are insufficient) thiazolidinediones. If these fail, insulin therapy may be necessary to maintain normal glucose levels.

Gestational diabetes

Main article: Gestational diabetes Gestational diabetes mellitus appears in about 2-5% of all pregnancies. It is temporary and fully treatable, but if untreated it may cause problems with the pregnancy, including macrosomia (high birth weight) of the child. It requires careful medical supervision during the pregnancy. In addition, about 20-50% of these women go on to develop type 2 diabetes.

Other types

There are several causes of diabetes which do not fit into type 1, type 2, or gestational diabetes
- Genetic defects in beta cells.
- Genetically related insulin resistance.
- Diseases of the pancreas.
- Caused by hormonal defects.
- Caused by chemicals or drugs. "Malnutrition-related diabetes mellitus" (MRDM or MMDM) was introduced by the WHO as the [http://www3.who.int/icd/vol1htm2003/fr-icd.htm?ge10.htm+e12 third major category] of diabetes in the 1980s. However, in 1999 a WHO working group recommended that [http://www.staff.ncl.ac.uk/philip.home/who_dmc.htm#Terminol MRDM be deprecated], and proposed a [http://www.staff.ncl.ac.uk/philip.home/who_dmc.htm#OtherSpecDes new taxonomy] for alternative forms of diabetes. Classification of non-type 1, non-type 2, non-gestational diabetes remains controversial.

Genetics

Both type 1 and type 2 diabetes are at least partly inherited. Type 1 diabetes appears to be triggered by infection, stress, or environmental factors (e.g. exposure to a causative agent). There is a genetic element in the susceptibility of individuals to some of these triggers which has been traced to particular HLA genotypes (i.e. genetic "self" identifiers used by the immune system). However, even in those who have inherited the susceptibility, type 1 diabetes mellitus seems to require an environmental trigger. A small proportion of type 1 diabetics carry a mutation that causes maturity onset diabetes of the young (MODY). There is an even stronger inheritance pattern for Type 2 diabetes; those with type 2 ancestors or relatives have very much higher chances of developing Type 2. Concordance among monozygotic twins is close to 100%, and 25% of those with the disease have a family history of diabetes. It is also often connected to obesity, which is found in approximately 85% of (North American) patients diagnosed with that form of the disease, so some experts beleive that inheriting a tendency toward obesity seems also to contribute. However, working in concert with genetic predisposition, many experts believe that lifestyle factors (lack of exercise, poor diet, etc.) are the greatest contributors to the pathogenesis of type 2 diabetes and that stringent weight control in persons with a genetic predisposition will effectively prevent and ameliorate the pathology of the disease in most cases. Age is also thought to be a contributing factor, as most type 2 patients in the past were older. The exact reasons for these connections are unknown.

Diagnosis

Signs and symptoms

Type 2 diabetes almost always has a slow onset (often years), but in type 1, particularly in children, onset may be quite fast (weeks or months). Early symptoms of type 1 diabetes are often polyuria (frequent urination) and polydipsia (increased thirst, and consequent increased fluid intake). There may also be weight loss (despite normal or increased eating), increased appetite, and irreducible fatigue. These symptoms may also manifest in Type 2 diabetes in patients who present with frank poorly controlled diabetes. Thirst develops because of osmotic effects — sufficiently high glucose (above the 'renal threshold') in the blood is excreted by the kidneys but this requires water to carry it and causes increased fluid loss, which must be replaced. The lost blood volume will be replaced from water held inside body cells, causing dehydration. Another common presenting symptom is altered vision. Prolonged high blood glucose causes changes in the shape of the lens in the eye, leading to blurred vision and, perhaps, a visit to an optometrist. All unexplained quick changes in eyesight should force a fasting blood glucose test. These are now quick (less than 5 minutes total), inexpensive (materials less than USD $1), and can be safely performed by almost anyone with trivial training. Especially dangerous symptoms in diabetics include the smell of acetone on the patient's breath (a sign of ketoacidosis), Kussmaul breathing (a rapid, deep breathing), and any altered state of consciousness or arousal (hostility and mania are both possible, as is confusion and lethargy). The most dangerous form of altered consciousness is the so-called "diabetic coma" which produces unconsciousness. Early symptoms of impending diabetic coma include polyuria, nausea, vomiting and abdominal pain, with lethargy and somnolence a later development, progressing to unconsciousness and death if untreated.

Diagnostic approach

The diagnosis of type 1 diabetes and many cases of type 2 is usually prompted by recent-onset symptoms of excessive urination (polyuria) and excessive thirst (polydipsia), often accompanied by weight loss. These symptoms typically worsen over days to weeks; about 25% of people with new type 1 diabetes have developed a degree of diabetic ketoacidosis by the time the diabetes is recognized. The diagnosis of other types of diabetes is made in many other ways. The most common are (1) health screening, (2) detection of hyperglycemia when a doctor is investigating a complication of longstanding, unrecognized diabetes, and less commonly (3) new signs and symptoms attributable to the diabetes. # Diabetes screening is recommended for many types of people at various stages of life or with several different risk factors. The screening test varies according to circumstances and local policy and may be a random glucose, a fasting glucose and insulin, a glucose 2 hours after 75 g of glucose, or a formal glucose tolerance test. Many health care recommendations for adults recommend universal screening at age 40 or 50 years, and sometimes occasionally thereafter. Earlier screening is recommended for those with risk factors such as obesity, family history of diabetes, high-risk ethnicity (Hispanic [Latin American], American Indian, African American, Pacific Island, and South Asian ancestry). # Many medical conditions are associated with a higher risk of various types of diabetes and warrant screening. A partial list includes: high blood pressure, elevated cholesterol levels, coronary artery disease, past gestational diabetes, polycystic ovary syndrome, chronic pancreatitis, hepatic steatosis (fatty liver), cystic fibrosis, several mitochondrial neuropathies and myopathies, myotonic dystrophy, Friedreich's ataxia, some of the inherited forms of neonatal hyperinsulinism and many others. Risk of diabetes is higher with chronic use of several medications, including high dose glucocorticoids, some chemotherapy agents (especially L-asparaginase), and some of the antipsychotics and mood stabilizers (especially phenothiazines and some atypical antipsychotics). # Diabetes is often detected when a person suffers a problem frequently caused by diabetes, such as a heart attack, stroke, neuropathy, poor wound healing or a foot ulcer, certain eye problems, certain fungal infections, or delivering a baby with macrosomia or hypoglycemia.

Criteria for diagnosis

Diabetes mellitus is characterized by recurrent or persistent hyperglycemia, and is diagnosed by demonstrating any one of # fasting plasma glucose level above 7 mmol/L (125 mg/dL); # plasma glucose above 11.1 mmol/L (200 mg/dL) two hours after a 75 g glucose load; or # symptoms of diabetes and a random plasma glucose above 11.1 mmol/L (200 mg/dL). A positive result should be confirmed by any of the above methods on a different day, unless there is not doubt as to the presence of significantly elevated glucose levels. While not used for diagnosis, an elevated glucose bound to hemoglobin, HbA1c, of 6.0% or higher (2003 revised US standard); is a screening and treatment-tracking test reflecting average blood glucose levels over the preceding 90 days (approximately).

Diabetic ketoacidosis and coma

See more detail in the articles diabetic ketoacidosis and diabetic coma Diabetic ketoacidosis (DKA) is an acute, dangerous complication and is always a medical emergency. Prompt proper treatment usually results in full recovery, though death can result from inadequate treatment or a variety of complications. Hyperosmotic diabetic coma is another acute problem associated with improper management of diabetes mellitus. It has some symptoms in common with DKA, but a different cause, and requires different treatment. In anyone with very high blood glucose levels (usually considered to be above 16.6 mmol/l (300 mg/dl)) water will be osmotically driven out of cells into the blood. The kidneys will also be "dumping" glucose into the urine, resulting in concomitant loss of water, causing an increase in blood osmolality. The osmotic effect of high glucose levels combined with the loss of water will eventually result in such a high serum osmolality that the body's cells may become directly affected as water is drawn out from them. Electrolyte imbalances are also common. This combination of changes, especially if prolonged, will result in symptoms similar to ketoacidosis, including loss of consciousness. As with DKA, urgent medical treatment is necessary. This is the diabetic coma to which type 2 diabetics are prone; it is less common in type 1 diabetics.

Hypoglycemia

Hypoglycemia in patients with diabetes almost always arises as a result of poor management of the disease either from too much or poorly timed insulin or oral hypoglycemics or too much exercise, not enough food, or poor timing of either. If blood glucose levels are low enough, the patient may become agitated, sweaty, and have many symptoms of sympathetic activation of the autonomic nervous system - they may experience feelings similar to dread and immobilized panic. Consciousness can be altered, or even lost, in extreme cases, leading to coma and/or seizures or even death and brain damage. Experienced diabetics can often recognize the symptoms early on - all diabetics should always carry something sugary to eat or drink as these symptoms can be rapidly reduced if treated early enough. In the case of children, this can be a type of candy disliked by the patient, to prevent concerns about unnecessary use. Other ways of treating hypoglycemia include an injection of glucagon which causes the liver to convert its internal stores of glycogen to be released as glucose into the blood. Oral or intravenous dextrose can also be given. In most cases, recovery is rapid and troublefree. Longstanding hypoglycemia may require hospital admission to allow supervised recovery and adjustment of diabetic medications.

Long-term complications

Among the major risks of the disorder are chronic problems affecting multiple organ systems which will eventually arise in patients with poor glycemic control. Many of these arise from damage to the blood vessels. These illnesses can be divided into those arising from large blood vessel diseases, macroangiopathy, and those arising from small blood vessel disease, microangiopathy. Interestingly, small vessel disease is minimized by tight blood glucose control, but large vessel disease is unaffected by tight blood glucose control.
- Small vessel disease complications:
- Proliferative retinopathy and macular edema which can lead to severe vision loss or blindness;
- Peripheral neuropathy which, particularly when combined with damaged blood vessels, can lead to foot ulcers, and possibly progressing to necrosis, infection and gangrene, sometimes requiring limb amputation, see below
- Diabetic nephropathy (due to microangiopathy) which can lead to renal failure
- Large vessel disease complications:
- Ischemic heart disease caused by both large and small vessel disease
- Stroke
- Peripheral vascular disease which contributes to foot ulcers and the risk of amputation Diabetes mellitus is the most common cause of adult kidney failure worldwide. It also the most common cause of amputation in the US, usually toes and feet, often as a result of gangrene, and almost always as a result of peripheral vascular disease. Retinal damage (from microangiopathy) makes it the most common cause of blindness among non-elderly adults in the US. A number of studies have found that those with diabetes are more at risk for dry eye syndrome.

Management of the disease

See also: Diabetes management Diabetes is a chronic disease with no cure (except experimentally in type 1 diabetics) as of 2005. Management of this disease may include lifestyle modifications such as achieving and maintaining proper weight, diet, exercise and foot care. Additionally it may involve the use of oral medications or insulin therapy. In the case of Type 1, insulin therapy is pretty much a given. In addition, self-monitoring via self-administered glucose testing using a glucose monitor is an essential element of any diabetes management program.

Curing diabetes

A disease consisting of the failure of a single organ (type 1 diabetes, the Islets of Langerhans) with a relatively simple function should admit of a cure. Type 2 diabetes is more complex and difficult but to the extent it is regarded as an excursion by the organism from the control envelope of the metabolic functions around glucose metabolism, correcting body mass to reverse that excursion approaches a cure. Unfortunately this rarely occurs, and failure of the Islets also occurs in Type 2 diabetes. At present cures for islet cell failure are experimental or theoretical, however recent developments strongly suggest they should be achievable. Political and religious complications may arise in some states.

Biological

The most obvious approach is to replace the failed organ with more islet cells. A transplant of exogenous cells will provoke an immune reaction unless they are either perfectly tissue matched to the recipient or enclosed to isolate them from the immune system. Stem cell techniques and possibly genetic engineering offer the former, but as of 2005 this is not yet a working set of techniques. The latter has been experimentally demonstrated in humans, with membrane encapsulated clumps of islet cells injected in to the peritoneal cavity. The membrane must allow oxygen and sugar in, and insulin out, but not permit immunoglobulin molecules to get in. Since the cells have not lasted for prolonged periods, this technique may become merely part of the mechanism of use of a stem cell/cell culture source. An alternative is placement of loose - unencapsulated - cells into the liver, via the hepatic blood supply. Work at Kings College Hospital in London, UK, has demonstrated cells can settle and perform in that milieu.

Mechanical

A microsocopic or nanotechnological approach, with implanted stores of insulin metered out by a rapidly sensitive glucose measure would approach a cure, but is currently beyond available technology.

Public health, policy and health economics

The Declaration of St Vincent was the result of international efforts to improve the care accorded to diabetics. Doing so is important if only economically. Diabetes is enormously expensive for healthcare systems and governments. In North America, it is the largest single non-traumatic cause in adults of amputation, blindness, and dialysis, all extremely expensive events. Work in the Puget Sound area of North America (by the health organization Group Health) shows that, over its large and varied patient population, specially retaining medical information on diabetic patients, keeping it up to date, and basing their continuing care on that data reduced total healthcare costs for those patients by US$1000 per year per patient for the rest of life. Recognition of this reality drove the Hawkes Bay initiative which established such a system, and resulted in various activities throughout the world including the Black Sea Telediab project which produced elements of a distributed diabetic record and management system as an open source computer program. Some researchers believe breast-feeding may protect children from developing diabetes. Research published in the Journal of the American Medical Association in November 2005 also suggests that breast-feed might also be correlated with the prevention of the disease in mothers. The study found that the women's risk of developing diabetes was reduced the longer they nursed.

Statistics

In 2004, according to the World Health Organization, more than 150 million people worldwide suffered from diabetes. Its incidence is increasing rapidly, and it is estimated that by the year 2025 this number will double. Diabetes mellitus occurs throughout the world, but is more common (especially type 2) in the more developed countries. The greatest increase in prevalence is, however, expected to occur in Asia and Africa, where most of the diabetic patients will be seen by 2025. The increase in incidence of diabetes in the developing countries follows the trend of urbanization and life style changes. Diabetes is in the top 10, and perhaps the top 5, of the most significant diseases in the developed world, and is gaining in significance (see big killers). For at least 20 years, diabetes rates in North America have been increasing substantially. In 2005 there are about 20.8 million people with diabetes in the United States alone. According to the American Diabetes Association there are about 6.2 million people undiagnosed and about 41 million people that would be considered pre-diabetic. The Centers for Disease Control has termed the change an epidemic. The National Diabetes Information Clearinghouse estimates that diabetes costs $132 billion in the United States alone every year. About 5–10% of these cases of diabetes are type 1 diabetics. The fraction of type 1 diabetics in other parts of the world differs; this is likely due to both differences in the rate of type 1 and differences in the rate of other types, most prominently type 2. Most of this difference is not currently understood.

Etymology

"Diabetes" is a Greek word meaning "a passer through; a siphon". "Mellitus" comes from the Greek word "sweet". Apparently, the Greeks named it thus because the excessive amounts of urine diabetics produce (when blood glucose is too high) attracted flies and bees because of the glucose content. The ancient Chinese tested for diabetes by observing whether ants were attracted to a person's urine, and called the ailment "sweet urine disease"; medieval European doctors tested for it by tasting the urine themselves, a scene occasionally depicted in Gothic reliefs. It is probably important to note that passing abnormal amounts of urine is a symptom shared by several diseases (most commonly of the kidneys), and the single word diabetes is applied to many of them. The most common of them are diabetes insipidus and the subject of this article, diabetes mellitus.

References

# Diabetes Control and Complications Trial Research Group. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl J Med 1993;329:977-86. [http://content.nejm.org/cgi/content/full/329/14/977 Fulltext]. PMID 8366922. # World Health Organisation, Department of Noncommunicable Disease Surveillance. Definition, Diagnosis and Classification of Diabetes Mellitus and its Complications. Geneva: WHO, 1999 ([http://whqlibdoc.who.int/hq/1999/WHO_NCD_NCS_99.2.pdf PDF]) # UK Prospective Diabetes Study Group. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet 1998;352:837-53. PMID 9742976. #Conditions in Occupational Therapy: effect on occupational performance. Edited by Ruth A. Hansen and Ben Atchison. Baltimore: Lippincott Williams & Williams, 2000;298-309. ISBN 0-683-30417-8. # Heart Protection Study Collaborative Group. MRC/BHF Heart Protection Study of cholesterol-lowering with simvastatin in 5963 people with diabetes: a randomised placebo-controlled trial. Lancet 2003;361(9374):2005-16. PMID 12814710. # Patlak M. New Weapons to Combat an Ancient Disease: Treating Diabetes. [http://www.fasebj.org/cgi/content/full/16/14/1853e FASEB J 2002;16:1853E]. PMID 12468446. # Banting FG, Best CH, Collip JB, Campbell WR, Fletcher AA. Pancreatic extracts in the treatment of diabetes mellitus. Canad Med Assoc J 1922;12:141-146. # Himsworth HP. Diabetes mellitus: its differentiation into insulin-sensitive and insulin-insensitive types. Lancet 1936;i:127-130. # Colhoun HM, Betteridge DJ, Durrington PN, Hitman GA, Neil HA, Livingstone SJ, Thomason MJ, Mackness MI, Charlton-Menys V, Fuller JH on behalf of the CARDS Investigators. Primary prevention of cardiovascular disease with atorvastatin in type 2 diabetes in the Collaborative Atorvastatin Diabetes Study (CARDS): multicenter randomized placebo-controlled trial. Lancet 2004; 364: 685-96. PMID 15325833 #MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomised placebo-controlled trial. Lancet, 2002; 360: 7-22. PMID 12114036 #.Kaiserman I, Kaiserman N, Nakar S, Vinker S. Dry eye in diabetic patients. Am J Ophthalmol. 2005 Mar;139(3):498-503. PMID 15767060 #Li HY, Pang GX, Xu ZZ. [Tear film function of patients with type 2 diabetes]. Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2004 Dec;26(6):682-6. PMID 15663232 #Sendecka M, Baryluk A, Polz-Dacewicz M. [Prevalence and risk factors of dry eye syndrome]. Przegl Epidemiol. 2004;58(1):227-33. PMID 15218664 #Stuebe AM, Rich-Edwards JW, Willett WC, Manson JE, Michels KB. Duration of lactation and incidence of type 2 diabetes. JAMA 2005;294:2601-10. PMID 16304074. #American Diabetes Association. "Total Prevalence of Diabetes and Pre-diabetes." www.diabetes.org/diabetes-statistics/prevalence.jsp

External links

- [http://www.diabetes.org American Diabetes Association]
- [http://www.diabetes.ca Canadian Diabetes Association]
- [http://www.nlm.nih.gov/medlineplus/diabetes.html MedlinePlus Diabetes from the U.S. National Library of Medicine]
- [http://www.childrenwithdiabetes.com Children with Diabetes]
- [http://www.jdrf.org Juvenile Diabetes Research Foundation]
- [http://www.womens-health-club.com/diseases/diabetes-mellitus.htm More Information on Diabetes Mellitus]
- [http://www.who.int/diabetes/en/ WHO — The Diabetes Programme]
- [http://www.cdc.gov/diabetes Center for Disease Control Diabetes Section]
- [http://www.idsoc.org The Immunology of Diabetes Society]
- [http://www.uchsc.edu/misc/diabetes/books.html Informative Book on Basic and Clinical information on Type 1 Diabetes from Barbara Center for Childhood Diabetes]
- [http://diabetes.niddk.nih.gov/dm/pubs/riskfortype2/ Diabetes Type 2 Risks]
- [http://www.joinleenow.org/ The Iacocca Foundation supporting diabetes]
- [http://www.newonsetdiabetes.org Clinical trials for newly diagnosed type 1 diabetes patients] Category:Diabetes Category:Nutrition Category:Medical_conditions_related_to_obesity ko:당뇨병 ms:Kencing manis ja:糖尿病 simple:Diabetes mellitus

Hyperglycemia

Hyperglycemia or High Blood Sugar is a condition in which an excessive amount of glucose circulates in the blood plasma. The term is from Greek: hyper-, prefix meaning "too much"; -glyc-, root meaning "sweet"; -emia, suffix meaning "of the blood".

Causes

Diabetes

Hyperglycemia is one of the classic symptoms of diabetes mellitus, the others being frequent and excessive thirst accompanied by frequent and excessive urination. But caution: A hyperglycemic condition without other classic symptoms is not dispositive of a diagnosis of diabetes mellitus, but hyperglycemia is also an independent medical condition with other causes. By comparison to hyperglycemia as an independent non-diabetic condition, Diabetes mellitus, in its organic form, is an apparently auto-immune disease of unknown cause and unknown cure, in which the islets of Langerhans (a subordinate organ within the pancreas) fail to produce sufficient quantities of the hormone insulin or produce no insulin at all. Non-organic diabetes mellitus can be caused by accidental damage to the islets of Langerhans, or to the pancreas itself (the islets being subordinate, they cannot function without the pancreas); or by other diseases affecting the pancreas, such as pancreatic cancer and other causes of pancreatic failure (which, thus, causes the islets to fail); or by surgical removal of the pancreas (thus, of the islets), usually for one of the reasons noted above.

Non-diabetic hyperglycemia

The most common cause of chronic non-diabetic hyperglycemia is obesity, the cure for which is proper diet and exercise to reduce the body's excess white fat reserves. The presence of excessive white fat reserves interferes with the body's ability to properly absorb and use insulin that is otherwise produced in sufficient quantity. Chronic non-diabetic hyperglycemia can produce some of the same complications as diabetic hyperglycemia; however, some of the complications of diabetes mellitus (especially juvenile-onset diabetes mellitus) can occur even if blood sugar levels are kept under control, because the disease operates beyond just the condition of hyperglycemia. Certain eating disorders can produce acute non-diabetic hyperglycemia, as in the binge phase of bulimia nervosa, when the subject consumes an incredible number of calories at once, frequently from foods that are high in both simple and complex carbohydrates - the body simply having a fierce craving for the energy that carbohydrates provide.

History

Diabetes is Greek for "passing through" (i.e., frequent and excessive thirst and urination; and Mellitus is Latin for "honey-sweet." Historically, diabetes was a collective name for a number of diseases, each of which affected a different endocrine gland but all of which had in common the classic symptoms of frequent and excessive thirst accompanied by frequent and excessive urination. Except for diabetes mellitus and diabetes insipidus, the other diabetic diseases have been renamed.

Measurement

Glucose levels are measured in either: 1. Milligrams per deciliter (mg/dL), in the United States and other countries (Myanmar, Liberia) that do not yet use the International or "Metric" System of measurement; or, 2. Millimoles per liter (mmol/L) in the rest of the "metrified world." Comparatively:
- 72 mg/dL = 4 mmol/L
- 90 mg/dL = 5 mmol/L
- 108 mg/dL = 6 mmol/L
- 126 mg/dL = 7 mmol/L Glucose levels vary before and after meals, and at various times of day; and what is "normal" varies among medical professionals, and can vary between patients. (As in other facets of life, the "average patient" does not exist as a real person.) In general, the "home" normal range for most people is about 80 to 120 mg/dL or 4 to 7 mmol/L. A subject with a "home" range above 126 mg/dL or 7 mmol/L is generally held to have hyperglycemia, whereas a "home" range below 70 mg/dL or 4 mmol/L is considered hypoglycemic. In fasting adults, blood plasma glucose should not exceed 126 mg/dL or 7 mmol/L. Sustained higher levels of blood sugar cause damage to the blood vessels and to the organs they supply, leading to the complications of diabetes.

Common Symptoms of Diabetic Hyperglycemia

If you have diabetes mellitus, the presence of these symptoms can indicate that blood sugar levels are too high:
- Polyphagia (frequent hunger, especially pronounced hunger)
- Polydipsia (frequent thirst, especially excessive thirst)
- Polyuria (frequent urination, especially excessive urination) But caution: Frequent hunger without the other two symptoms (which invariably occur together, absent renal complications, bladder infections, etc.), can also indicate that blood sugar levels are too low. This commonly occurs when people who have type 2 diabetes mellitus take too much oral hypoglycemic medication for the amount of food they eat. The resulting drop in blood sugar level to below the normal range prompts a hunger response. This hunger is not usually as pronounced as in type 1 diabetes mellitus (especially the juvenile onset form). People with chronic non-diabetic hyperglycemia who take oral hypoglycemic mediation can have the same problem (again, not as pronounced a hunger. In particular, if the hyperglycemia is caused by obesity, prescription of oral hypoglycemic medication can be ill advised. This is because the medication typically interferes with the subject's weight reduction plan by artificially lowering the blood sugar levels, so that a strong hunger response occurs when the subject attempts to naturally lower the blood sugar levels through a programme of proper diet and exercise. A vicious cycle can result, in which the more the subject exercises to lose weight, the greater the hunger caused by the medication, so that subject eats more to compensate for the oral hypoglycemic and, thus, cannot lose weight. The average blood sugar levels thus do not change, which can lead to an increase in the dosage of the oral hypglycemic medication, which only perpetuates the problem. Other symptoms of diabetic hyperglycemia may include:
- Blurred vision
- Fatigue
- Weight loss
- Poor wound healing (cuts, scrapes, etc.)
- Dry mouth
- Dry or itchy skin
- Impotence (male)
- Recurrent infections such as vaginal yeast infections, groin rash, or external ear infections (swimmers ear) These symptoms do not normally occur with acute non-diabetic hyperglycemia (it just doesn't last long enough), but some of them can occur in chronic non-diabetic hyperglycemia. The notable exception is weight loss, which almost never happens in chronic non-diabetic hyperglycemia - especially if the hyperglycemia is caused by obesity. Instead, the subject either maintains a stable obese weight, or gains weight. This is one of the ways non-diabetic hyperglycemia can be distinguished from diabetic hyperglycemia.

Blood sugar

In medicine, blood sugar is a term used to refer to levels of glucose in the blood. Blood sugar concentration, or serum glucose level, is tightly regulated in the human body. Glucose, transported via the bloodstream, is the primary source of energy for the body's cells. Normally, blood glucose levels stay within narrow limits throughout the day: 4 to 8 mmol/l (70 to 150 mg/dl). Levels rise after meals and are usually lowest in the morning, before the first meal of the day. Diabetes mellitus is the most prominent disease related to failure of blood sugar regulation. Though it is called "blood sugar", other sugars besides glucose are found in the blood, like fructose and galactose. However, only glucose levels are regulated via insulin and leptin.

Direct health effects of blood sugar problems

If blood sugar levels drop too low, a potentially fatal condition called hypoglycemia develops. Symptoms may include lethargy, impaired mental functioning, irritability, and loss of consciousness. If levels remain too high, appetite is suppressed over the short term. Long-term hyperglycemia causes many of the long-term health problems associated with diabetes, including eye, kidney, and nerve damage.

Mechanisms of blood sugar regulation

Blood sugar levels are regulated by negative feedback in order to keep the body in homeostasis. The levels of glucose in the blood are monitored by the pancreas. When the concentration of glucose falls, as it is consumed to meet the body's energy demands, the pancreas releases glucagon, a hormone which targets cells in the liver. These cells then convert glycogen into glucose (this process is called glycogenolysis). The glucose is released into the bloodstream, increasing blood sugar levels. When levels of blood sugar rise, whether as a result of glycogen conversion, or from digestion of a meal, a different hormone is released from islet cells found in the pancreas. This hormone, insulin, causes the liver to convert more glucose into glycogen (this process is called glyogenosis), decreasing blood sugar levels. Diabetes mellitus type 1 is caused by insufficient or non-existent production of insulin, while type 2 is due to inadequate response to released insulin ( "insulin resistance"). Both types of diabetes result in too much glucose remaining in the blood.

Low blood sugar

Some people report drowsiness or impaired cognitive function several hours after meals, which they believe is related to a drop in blood sugar, or "low blood sugar". For more information, see: idiopathic postprandial syndrome hypoglycemia

Dehydration

Dehydration is the removal of water (hydor in ancient Greek) from an object. Medically, dehydration is a serious and potentially life-threatening condition in which the body contains an insufficient volume of water for normal functioning. The term "volume depletion" is similar to dehydration, but it refers to the loss of salts as well as water. Also see Hypovolemia.

Medical causes of dehydration

In humans, dehydration can be caused by a wide range of diseases and states that impair water homeostasis in the body. These include:
- External or stress-related causes
- Blood loss or hypotension due to physical trauma
- Diarrhea
- Hyperthermia
- Shock
- Prolonged physical activity without consuming adequate water, especially in a hot environment
- Survival situations, especially desert survival conditions
- Vomiting
- Infectious diseases
- Cholera
- Gastroenteritis
- Shigellosis
- Yellow fever
- Malnutrition
- Electrolyte imbalance
- Hypernatremia (also caused by dehydration)
- Hyponatremia, especially from restricted salt diets
- excessive consumption of alcohol
- Fasting
- Patient refusal of nutrition and hydration
- Other causes of obligate water loss
- Severe hyperglycemia, especially in Diabetes mellitus
- Glycosuria

Symptoms and prognosis

Symptoms may include headaches similar to what is experienced as a hangover, a sudden episode of visual snow, decreased blood pressure (hypotension), and dizziness or fainting when standing up due to orthostatic hypotension. Untreated dehydration generally results in delirium, unconsciousness, and death. Dehydration symptoms generally become noticeable after 2% of one's normal water volume has been lost. Initially, one experiences thirst and discomfort, possibly along with loss of appetite and dry skin. Athletes may suffer a loss of performance of up to 50%, and experience flushing, low endurance, rapid heart rates, elevated body temperatures, and rapid onset of fatigue. The symptoms become increasingly severe with greater water loss. One's heart and respiration rates will increase to compensate for decreased plasma volume and blood pressure, while body temperature may rise due to decreased sweating. Around 5% to 6% water loss, one may become groggy or sleepy, experience headaches or nausea, and may feel tingling in one's limbs (paresthesia). With 10% to 15% fluid loss, muscles may become spastic, skin may shrivel and wrinkle, vision may dim, urination will be greatly reduced and may become painful, and delirium may begin. Losses of greater than 15% are usually fatal. [http://faculty.washington.edu/kepeter/118/notes/water_balance.htm]

Treatment

Correction of a dehydrated state is accomplished by the replenishment of necessary water and electrolytes (rehydration). Even in the case of serious lack of fresh water (e.g. at sea or in a desert), drinking seawater or urine does not help, nor does the consumption of alcohol. When dehydrated, unnecessary sweating should be avoided, as it wastes water. If there is only dry food, it is better not to eat, as water is necessary for digestion. The best treatment for minor dehydration is consumption of an electrolyte-balanced fluid like a sports drink. For severe cases of dehydration where fainting, unconsciousness, or any other severely inhibiting symptom is present (the patient is incapable of standing or thinking clearly), emergency attention is required. Fluids will be given through an IV, and within a few hours, the patient will return to normal unless a complication occurred.

Avoiding dehydration

A person's body loses, during an average day in a temperate climate such as the United Kingdom, approximately 2.5 litres of water. This can be through the lungs as water vapor, through the skin as sweat, or through the kidneys as urine. Some (a less significant amount, in the absence of diarrhea) is also lost through the bowels. During vigorous exercise or in a hot environment, it is easy to lose several times this amount. Heavy exercise in high temperatures could cause the loss of over 2.5 litres of fluid per hour, which exceeds the body's absorptive capacity.

Ethical concerns

Judge Lynch of the Massachusetts Supreme Judicial Court argued that death by dehydration symptoms was "cruel and violent" in his opinion on the 1986 Brophy case:
- The mouth would dry out and become caked or coated with thick material.
- The lips would become parched and cracked.
- The tongue would swell, and might crack.
- The eyes would recede back into their orbits and the cheeks would become hollow.
- The lining of the nose might crack and cause the nose to bleed.
- The skin would hang loose on the body and become dry and scaly.
- The urine would become highly concentrated, leading to burning of the bladder.
- The lining of the stomach would dry out and the sufferer would experience dry heaves and vomiting.
- The body temperature would become very high.
- The brain cells would dry out, causing convulsions.
- The respiratory tract would dry out, and the thick secretions that would result could plug the lungs and cause death.
- At some point within five days to three weeks, the major organs, including the lungs, heart, and brain, would give out and the patient would die. Be advised the death due to dehydration can occur in 3 days (or less in hot weather) and no one normally lives more than about 5-6 days

External links

- [http://www.uga.edu/nchfp/how/dry/dehydrator.html National Center for Home Food Preservation - Food Dehydrators]
- [http://www.acs.ucalgary.ca/~smzess/survival/water.htm Tips from the SAS Survival Guide by John Wiseman]
- [http://www.surviveoutdoors.com/reference/dehydration.asp Dehydration Information]
- [http://www.safetycenter.navy.mil/media/approach/issues/mar02/cool.htm Report of a navy officer including some tips]
- [http://www.water.org.uk/home/resources-and-links/water-for-health/ask-about/adults Water requirements in adults]
- [http://www.nlm.nih.gov/medlineplus/ency/article/000982.htm#visualContent Definition of Dehydraton by the US National Institutes of Health]

References

- Ira R. Byock, M.D., [http://www.dyingwell.com/prnh.htm Patient Refusal of Nutrition and Hydration: Walking the Ever-Finer Line]. American Journal Hospice & Palliative Care, pp. 8-13. (March/April 1995) Category:Electrolyte disturbance Category:Nutrition

Cardiovascular disease

Cardiovascular disease refers to the class of diseases that involve the heart and/or blood vessels (arteries and veins). While the term technically refers to any disease that affects the cardiovascular system, it is usually used to refer to those related to atherosclerosis (arterial disease). These conditions have similar causes, mechanisms, and treatments. Over 50 million Americans have cardiovascular problems, and most other Western countries face high and increasing rates of cardiovascular disease. It is the number 1 cause of death and disability in the United States and most European countries. By the time that heart problems are detected, the underlying cause (atherosclerosis) is usually quite advanced, having progressed for decades. There is therefore increased emphasis on preventing atherosclerosis by modifying risk factors, such as healthy eating, exercise and avoidance of smoking.

Forms

Cardiovascular disease usually occurs as a result of arterial damage. The symptoms and treatments depend on which set (or sets) of arteries are affected. In coronary heart disease, atherosclerotic plaques (inflamed fatty deposits in the blood vessel wall) obstruct the coronary arteries (blood vessels supplying the heart). Narrowing of arteries is called arterial stenosis. When the blockages become severe enough, the blood flow to the heart is restricted (cardiac ischemia), especially during increased demand (i.e. during exertion or emotion). This results in angina pectoris. The acute stage of coronary heart disease occurs when one of the plaques ruptures, forming a thrombus (blood clot) that acute occludes the whole artery. The portion of the heart muscle supplied by that artery dies; this is known as a myocardial infarction (or a heart attack in lay parlance). This may result in the death of the patient if the affected area is large enough. If the patient survives, congestive heart failure may result. Similarly, inflammation and blood clots may obstruct the cerebral arteries (those supplying the brain). As the disease progresses, an artery may be transiently blocked, causing cerebral ischemia. This results in a transient ischemic attack (TIA), called a mini-stroke in lay parlance. If the obstruction is severe, a cerebrovascular accident, or stroke may result, due to the death of brain tissue supplied by the artery. In peripheral artery disease, obstruction occurs in the arteries of the arms or legs. This results initially in pain, during temporary obstruction, and finally in tissue death and gangrene if not treated. There are many specific illnesses that may occur in association with these and other cardiovascular disease. In addition to the ones mentioned above, these include hypertension (high blood pressure), arterial aneurysms (arterial enlargement and weakening), cardiomegaly (abnormal enlargement of the heart), tachycardia/bradycardia/arrhythmia (fast/slow/irregular heart rates), cardiac arrest (heart stoppage), cardiomyopathy (heart muscle weakness), heart valve regurgitation (leakage), and heart valve stenosis (narrowing).

Risk factors

There are many risk factors which predispose to various forms of cardiovascular disease. These include the following:
- Age
- Diabetes mellitus
- Hypercholesterolemia (elevated cholesterol levels) and less than excellent lipoprotein particle profile (cholesterol subtypes)
- Tobacco smoking
- Higher fibrinogen and PAI-1 blood concentrations
- Elevated homocysteine, or even upper half of normal
- High blood pressure
- Obesity, especially central or male-type obesity; apart from being linked to diabetes, this form of obesity independently increases cardiovascular risk, presumedly by inducing an inflammatory and procoagulant state
- Genetic factors/Family history of cardiovascular disease
- Physical inactivity
- Male sex
- Although men have a higher rate of cardiovascular disease than women, it is also the number one health problem for women in industrialized countries. After menopause, the risk for women approaches that of men. Hormone replacement therapy alleviates a number of post-menopausal problems, but appears to increase the risk of cardiovascular disease.

Prevention

Attempts to prevent cardiovascular disease take the form of modifying risk factors. Some, such as gender, age, and family history, cannot be modified. Smoking cessation (or abstinence) is one of the most effective and easily modifiable changes. Also important is a low-fat, low-calorie diet, which helps one to maintain a healthy body mass index (BMI) and preventing obesity. Regular cardiovascular exercise (aerobic exercise) complements the healthful eating habits. Sometimes, the combination of diet and exercise will improve lipoprotein (cholesterol) levels; if not, a physician may prescribe "cholesterol-lowering" drugs, such as the statins. These medications have additional protective benefits aside from their lipoprotein profile improvement. Aspirin may also be prescribed, as it has been shown to decrease the clot formation that may lead to myocardial infarctions and strokes; it is routinely prescribed for patients with one or more cardiovascular risk factors. Eating oily fish at least twice a week may help reduce the risk of sudden death and arrhythmias. Studies of individual heart cells showed that the fatty acids blocked excessive sodium and calcium currents in the heart, which could otherwise cause dangerous, unpredictable changes in its rhythm (Leaf et al 2003).

Treatment

Treatment of cardiovascular disease depends on the specific form of the disease in each patient, but effective treatment always includes preventetive lifestyle changes discussed above. Medications, such as blood pressure reducing medications, aspirin and other treatments may be involved. In some circumstances, surgery or angioplasty may be warranted to reopen, repair, or replace damaged blood vessels.

Research

The causes, prevention, and treatment of all forms of cardiovascular disease are active fields of biomedical research, with hundreds of scientific studies being published on a weekly basis. A fairly recent emphasis is on the link between low-grade inflammation that hallmarks atherosclerosis and its possible interventions. C-reactive protein (CRP) is an inflammatory marker that may be present in increased levels in the blood in patients at risk for cardiovascular disease. Its exact role in predicting disease is the subject of debate. Some areas currently being researched include possible links between infection with Chlamydia pneumoniae and coronary artery disease. The Chlamydia link has become less plausible with the absence of improvement after antibiotic use (Andraws et al 2005).

Reference

- Andraws R, Berger JS, Brown DL. Effects of antibiotic therapy on outcomes of patients with coronary artery disease. JAMA 2005;293:2641-7. PMID 15928286.
- Leaf A, Kang JX, Xiao YF, Billman GE. Clinical prevention of sudden cardiac death by n-3 polyunsaturated fatty acids and mechanism of prevention of arrhythmias by n-3 fish oils. Circulation 2003;107:2646-52. PMID 12782616. Category:Medical conditions related to obesity

Renal dialysis

In medicine, renal dialysis is a method for removing waste such as urea from the blood when the kidneys are incapable of this (i.e. in renal failure).

Initiation of Dialysis

In acute renal failure, (renal) dialysis is generally initiated when the renal function has deteriorated to an extent that it is threatening the body's physiology. Volume overload (i.e. hypervolemia) that is unresponsive to strong diuretics, such as furosemide, and severe hyperkalemia are two common indications for dialysis. In chronic renal failure the problem is usually longstanding, and the decision is based on the level of kidney function (GFR or creatinine clearance), possibility of a renal transplant and complications of the malfunctioning kidney (e.g. hyperkalemia, uremia). Chronic renal failure that does not have an acute (i.e. reversible) component and requires dialysis is called end-stage renal disease (ESRD). There is no general agreement among nephrologists on when to start dialysis. In Canada some nephrologists advocate that patients with CRF should start dialysis when the GFR is below 15 mL/min and below 20 mL/min for patients with diabetes mellitus. Canadian guidelines suggest considering dialysis when the GFR is less than 12 mL/min. In the United States, dialysis is initated at a GFR of 15 mL/min in diabetics and 10mL/min in non-diabetics, in conjuction with uremic sypmtoms. Most guidelines agree that dialysis should be started before the GFR drops below 6 mL/min. The rationale for starting dialysis early is that it prevents illness associated with severe uremia and may minimize long-term complications associated with kidney failure. Studies have shown that starting dialysis with a lower GFR is associated with a poor nutritional status which is associated with a higher mortality in the first two years of treatment. Acute renal failure can present on top of (i.e. in addition to) chronic renal failure. This is called acute-on-chronic renal failure (AoCRF) and may require dialysis temporarily (until the acute component of the renal failure resolves).

Types of dialysis

uremia There are two main types of dialysis, hemodialysis and peritoneal dialysis, and several subtypes.
- In hemodialysis, also known as artificial kidney, the patient's blood is passed through a tube to a semipermeable membrane (dialyser) that filters out waste products. The cleansed blood is then returned back to the body. The procedure is monitored by a machine, which also provides the dialysis fluid, mixing it from a concentrate and water. Depending on where the treatment is done, dialysis is either:
- Hospital Hemodialysis
- Satellite Hemodialysis (a specialized unit outside a hospital, but managed by professional staff)
- Home Hemodialysis
- In peritoneal dialysis, a special solution is run through a tube into the peritoneal cavity, the abdominal body cavity around the intestine. The fluid is left there for a while to absorb waste products, and then removed through the tube. Subtypes of peritoneal dialysis are:
- Continous Ambulatory Peritoneal Dialysis (CAPD)
- Continous Cyclic Peritoneal Dialysis (CCPD)
- Intermittent Peritoneal Dialysis (IPD)
- Nocturnal Intermittent Peritoneal Dialysis (NIPD)

Measures of dialysis treatment adequacy

Several measures of dialysis adequacy exist. The most widespread is Kt/V, but its utility has been questioned. The hemodialysis product (HDP) has been proposed as an alternative. Urea reduction ratio (URR) is another measure of dialysis adequacy. It has also been suggested that a 'holistic attitude', which takes overall patient wellbeing should be taken into account rather than mere numbers. The measurement of treatment adequacy is an unresolved issue. None of the commonly used dialysis treatment adequacy measures accurately models the mass transfer phenomena that underlie the physics of dialysis.

Hemodialysis

physics The principle of hemodialysis (UK: haemodialysis) is somewhat different. It works by having the blood flow along one side of a semipermeable membrane, with the dialysis solution flowing along the other side, usually in the opposite (countercurrent) direction. Due to the difference in osmolarity between the two solutions, solutes diffuse across the membrane along their concentration gradient. A difference in pressure drives water across the membrane, which also pulls along some solutes (solvent drag). The dialysis solution is used at about the body temperature, and consists of a sterilized solution of mineral ions. Urea and other uremic toxins diffuse into the dialysis solution, which does not have any urea. However, concentrations of most mineral ions (eg sodium) are similar to those of normal plasma to prevent loss. Concentrations of certain other ions, such as potassium and phosphate are lower than in the normal plasma because they accumulate in renal failure. Dialysis is conducted in a dedicated facility, either a special room in a hospital or a clinic that specializes in hemodialysis. Nurses and technicians working in the facility have special training specific to dialysis. Dialysis can also be done in the patient's home. Although this is currently rare in the USA, home hemodialysis has numerous advantages over in-center dialysis such as greater control over the therapy for the patient and better symptom control due to longer and/or more frequent dialysis sessions. A prescription for dialysis by the renal physician (nephrologist) will specify various parameters for setting up dialysis machines, times and durations of dialysis sessions. In the North America and UK, 3-4 hour sessions, 3 times a week are typical, although there are patients who dialyse 2 or 4 or 5 per week. There are also a small number of patients who undergo nocturnal dialysis for 8 hours per night 6 nights per week. Step-by-step description of hemodialysis: #Before or around the time the patient arrives for his/her scheduled session, a dialysis machine will be prepared. There are many models of dialysis machines, but typically in modern machines there will be a computer, CRT, a pump, and facility for disposable tubing and filters. The filters (the actual artificial kidneys) are cylindrical, clear plastic outside with the filter materiel visible inside (looks like thick paper). They are perhaps 15-18 inches long, and 2-3 inches thick. They have tubing connectors at both ends. The technician or nurse will set up plumbing on the machine in a moderately complex pattern that has been worked out to move blood through the filter, allow for saline drip (or not), allow for various other medications/chemicals to be administered. How the plumbing is set up may vary between models of machine and they types of filters. For some filters, it is necessary to clear sterilizing fluid from the filter before connecting the patient. This is done by altering the plumbing to push saline through the filter, and carefully checked with a type of litmus test. # The pump does not directly contact the blood or fluid in the plumbing — it works by applying pressure to the tubing, then moving that pressure point around. Think of a disk with a protrusion in it. Put this into a close fitting 270 degree enclosure. Put plastic tubing between the enclosure and the disk, entering and exiting in the 90 open degrees. Now imagine the disk turning. It will put pressure on the tubing, and the pressure point will roll around through the 270 degrees, forcing the fluid to move. It is characteristic of dialysis machines that most of the blood out of the patients body at any given time is visible. This facilitates troubleshooting, particularly detection of clotting. #The patient arrives and is carefully weighed. Standing and sitting blood pressures are taken. Temperature is taken. #Access is set up. For patients with a fistula (a surgical modification to an arm or leg vein to make it more robust, and therefore usable for high capacity blood movement required by dialysis) this means inserting two large gauge needles into the fistula. This is painful for the patient but there are various methods of numbing the entry sites before the needles are inserted — the two most common are lignocaine (lidocaine), a local anaesthetic injected under the skin, and there is also a cream called EMLA which is applied to the skin 45 minutes before the needles are inserted. Fistulas are widely considered the desirable way to get access for hemodialysis, but they take time to set up and mature (anywhere between 5 weeks to 15 weeks). For other patients, access may be via a catheter installed to connect to large veins in the chest. Other arrangements can be made as well. #When access has been set up, the patient is then connected to the preconfigured plumbing, creating a complete loop through the pump and filter. The pump and a timer are started. Hemodialysis is underway. #Periodically (every half hour, nominally) blood pressure is taken. As a practical matter, fluid is also removed during dialysis. Most dialysis patients are on moderate to severe fluid restrictive diets (in addition to other dietary restrictions), since kidney failure usually includes an inability to properly regulate fluid levels in the body. A session of hemodialysis may typically remove 2-5 kilograms (5-10 pounds) of fluid from the patient. The amount of fluid to be removed is set by the dialysis nurse according to the patient's "estimated dry weight." This is a weight that the care staff believes represents what the patient should weigh without fluid built up because of kidney failure. Removing this much fluid can cause or exacerbate low blood pressure. Monitoring is intended to detect this before it becomes too severe. Low blood pressure can cause cramping, nausea, shakes, dizziness, lightheadedness, and unconsciousness. #At the end of the prescribed time, the patient is disconnected from the plumbing (which is removed and discarded, except perhaps for the filter, which may be sterilized and reused with the same patient at a later date). Needle wounds (in case of fistula) are bandaged with gauze, held for up to 1 hour with direct pressure to stop bleeding, and then taped in place. The process is similar to getting blood drawn, only it is lengthier, and more fluid or blood is lost. #Temperature, standing and sitting blood pressure, and weight are all measured again. Temperature changes may indicate infection. BP discussed above. Weighing is to confirm the removal of the desired amount of fluid. #Care staff verifies that the patient is in condition suitable for leaving. The patient must be able to stand (if previously able), maintain a reasonable blood pressure, and be coherent (if normally coherent). Different rules apply for in-patient treatment. Following haemodialysis, patients may experience a syndrome called "washout". The patient feels weak, tremulous, extreme fatigue. Patients report they "are too tired, too weak to converse, hold a book or even a newspaper." It may also vary in intensity ranging from whole body aching, stiffness in joints and other flu-like symptoms including headaches, nausea and loss of appetite. The syndrome may begin toward the end of treatment or minutes following the treatment. It may last 30 minutes or 12-14 hours in a dissipating form. Patients though exhausted have difficulty falling to sleep. Eating a light meal, rest and quiet help the patient cope with washout until it has 'worn away.'

Hemodialysis Access

There are three primary modes of access to the blood in Hemodialysis: catheter, AV fistula, or graft. There are also less common methods such as the "LifeSite" access. The selection of an access is influenced by factors such as the patient's stability and the condition of his or her vasculature. Only a single access may be used in a given hemodialysis session, but patients frequently have multiple accesses, whether it is because one is still maturing, or perhaps one or more are in poor condition.

Catheter

Catheter access, often called a CVC (Central Venous Catheter), is usually the first access a dialysis patient receives because it is quick and easy to place. Also, it is ready for use immediately, as opposed to other forms of access. It consists of a pair of lines encased in a single long tube, with the tip placed inside the vena cava or atrium of the heart and one exiting the body, usually in the neck area. The two ends of the catheter (one for drawing blood and one for returning it) attach directly to the dialysis lines when performing hemodialysis, and are covered by disposable plastic caps between sessions. Blood circulating in the machine from catheter patients is visibly darker than that from fistula or graft patients, because the access is drawing deoxygenated blood. Aside from quickness, catheters have other advantages. No needle is necessary during treatment with catheter access. Also, for some patients catheters are the only option, if the vasculature is in no condition to create a fistula or graft. Catheters have a number of disadvantages, however. Their maximum blood flow rate is usually lower than that of fistulas and grafts, meaning that the dialysis treatment will be less effective. They have a tendency to clot, rendering them unusable. Furthermore, they are highly prone to infection. Since they open directly to the heart, any bacterial colonization can be very serious and lead to sepsis.

AV Fistula

AV (ateriovenous) fistulas are recognized as the preferred access method. To create a fistula, a vascular surgeon joins an artery and a vein together through anastomosis. Since this bypasses the capillaries, blood flows at a very high rate through the fistula. One can feel this by placing one's finger over a mature fistula. This is called feeling for "thrill". Fistulas are usually created in the non-dominant arm. A common approach is to join the brachial artery and the cephalic vein. A fistula will take a number of weeks to mature, on average perhaps 3 months. During treatment, two needles are inserted into the fistula in opposite directions, one to draw blood and one to return it. The advantages of AV fistula use are lower infection rates, higher blood flow rates (which translates to more effective dialysis), and a lower incidence of clotting. The disadvantage of fistula access is primarily the maturation time and the surgical procedure. Also, it requires the blood vessels to be in good shape.

AV Graft

AV (arteriovenous) grafts are much like fistulas in most respects, except that an artificial vessel is used to join the artery and vein, often made of Gore-Tex. Grafts are used when the patient's native vasculature does not permit a fistula. They mature faster than fistulas, in about one month.

Hemodialysis Equipment

Hemodialysis Machine

The hemodialysis machine performs the function of pumping the patient's blood and the dialysate through the dialyzer. The newest dialysis machines on the market are highly computerized and continuously monitor an array of safety-critical parameters, including blood and dialysate flow rates, blood pressure, heart rate, conductivity, pH, etc. If any reading is out of normal range, an audible alarm will sound to alert the patient-care technician who is monitoring the patient. Two of the largest manufacturers of dialysis machines are Fresenius and Gambro.

Water System

An extensive water purification system is absolutely critical for hemodialysis. Since dialysis patients are exposed to vast quantities of water, which is mixed with the acid bath to form the dialysate, even trace mineral contaminants or bacterial endotoxins can filter into the patient's blood. Because the damaged kidneys are not able to peform their intended function of removing impurities, ions that are introduced into the blood stream via water can build up to hazardous levels, causing numerous symptoms including death. For this reason, water used in hemodialysis is typically purified using reverse osmosis. It is also checked for the absence of chlorine ions and chloramines, and its conductivity is continuously monitored, to detect the level of ions in the water.

Dialyzer

The dialyzer, or artificial kidney, is the piece of equipment that actually filters the blood. One of the most popular types is the hollow fiber dialyzer, in which the blood is run through a bundle of very thin capillary-like tubes, and the dialysate is pumped in a chamber bathing the fibers. The process mimics the physiology of the glomerulus and the rest of the nephron. Pressure gradients are used to remove fluid from the blood. The membrane itself is often synthetic, made of a blend of polymers such as Polyarylethersulfone, Polyamide and Polyvinylpyrrolidone. Dialyzers come in many different sizes. A larger dialyzer will usually translate to an increased membrane area, and thus an increase in the amount of solutes removed from the patient's blood. Different types of dialyzers have different clearances for different solutes. The nephrologist will prescribe the dialyzer to be used depending on the patient. The dialyzer may either be discarded after each treatment or reused. If it is reused, there is an extensive procedure of sterilization. Dialyzers are not shared between patients in the practice of reuse.

Peritoneal dialysis

There are three types of peritoneal dialysis. Continuous ambulatory peritoneal dialysis (CAPD), the most common type, needs no machine and can be done at home. Continuous cyclic peritoneal dialysis (CCPD) uses a machine and is usually performed at night when the person is sleeping. Intermittent peritoneal dialysis (IPD) uses the same type of machine as CCPD, but is usually done in the hospital because treatment takes longer. Prior to any peritoneal dialysis, a catheter is placed in the patient's abdomen, running from the peritoneum out to the surface, near the navel. This is done as a short surgery. CAPD is typically done in the patient's home and workplace, but can be done almost anywhere; a clean area to work, a way to elevate the bag of dialysis fluid and a method of warming the fluid are all that is needed. The main consideration is the very high potential for infection with an open catheter; peritonitis is a common complication, as are infections of the catheter exit site or "tunnel" (path from the peritoneum to the exit site). Because of this, patients are advised to take a number of precautions against infection. Step-by-step description of peritoneal dialysis (a CAPD exchange): #The supplies and materials needed for an exchange are gathered in one clean location. Notable amongst these is a bag of dialysis fluid (also called dialysis solution), a solution comprised of a known amount of a glucose dissolved in water. The strength of this solution determines the osmotic gradient, and therefore the amount of water that diffuses out of the bloodstream. Common strengths of glucose are 0.5%, 1.5%, 2.5% and 4.25%. 1.5% is approximately fluid-neutral; it neither adds nor removes fluid and is used for patients who are primarily concerned with waste removal rather than fluid regulation. Higher concentrations lead to greater water removal. Electrolytes are also present in the fluid to maintain proper body levels. Patients weigh themselves, and measure temperature and blood pressure daily to determine whether the body is retaining fluid and, thus, what strength of fluid to use. Dialysis fluid typically comes premixed in a disposable bag-and-tube apparatus; no additional equipment is needed. The apparatus consists of two bags, one empty and one with the fluid, connected via flexible tubing to a Y-shaped fitting. The bag is heated to body temperature, to avoid causing cramping. Dry heat is used; common methods include microwaves, heating pads and solar radiation (often using the dashboard of a car, for instance while travelling). #The patient, who performs the entire procedure themselves, dons a disposable surgical mask, scrubs their hands using antibacterial soap, and tucks a clean towel into the waistband of their pants to protect their clothing. The bag of dialysis fluid is removed from the protective packaging, and is hung from an IV stand or other elevated location, such as a coat hook. The tubing attached to the bag of fluid is uncoiled, and the second (empty) bag is placed on the floor. The Y-shaped connector is attached to the catheter tip; a protective cap must be removed from both of these before the connection is made, and the two portions of the connector are not permitted to touch anything, to avoid possible contamination. #Once connected to the system, the patient clamps the tubing connected to the full bag of dialysis fluid and then releases the twist valve located in the tip of their catheter; this permits fluid to flow into or out of the peritoneal cavity. Because the full bag of fluid is clamped off but the empty bag is not, the effluent (used dialysis fluid) from within the peritoneum can drain out of the catheter and into the lower, waste bag. Emptying the abdomen of fluid takes approximately fifteen minutes, and the patient is free to perform tasks such as reading, watching television and browsing the internet. #When the abdomen has drained, the lower, drain, bag is clamped off. The twist valve in the catheter is also closed. The clamp is then removed from the upper tubing, permitting dialysis fluid to drain out. The clamp to the drain bag is briefly opened and some fluid is drained directly from the upper bag into the lower bag. This clears the line of air and other impurities. The drain line is then clamped off and the twist valve on the catheter end is opened. This permits fluid to enter the peritoneum. Filling the abdomen with fresh fluid takes about fifteen minutes, and the patient enjoys the same freedoms as while draining. #Once the entire bag of fluid (an amount varying primarily based on body size, ranging from 1500 to 3000 mL) has been introduced to the abdomen, the patient then cleans their hands again (typically using an antiseptic alcohol-based cleanser) and puts the surgical mask on. The Y-connector is detached from the catheter tip and a protective cap is placed on the end of the catheter. #The effluent is inspected after a dialysis exchange is complete; a cloudy effluent indicates probable peritoneal infection. The effluent is drained into a toilet, and the various dialysis supplies are discarded with normal garbage.

Side-effects and complications

Intermittent dialysis is associated with a steep drop in blood pressure, and dialysis patients are warned not to travel without assistance. The treatment may cause fatigue. All forms of dialysis require access to either the circulatory system or the peritoneum. As this access breaks normal skin barriers, and as people with renal failure generally have a suppressed immune system, infection is a relatively common problem, which may require antibiotics and supportive care. Infection rates are much higher with catheter patients than patients with AV fistulas or grafts, and the use of catheters is therefore discouraged. Similarly, hemorrhage from the access system is a risk; this is especially so in the hours after dialysis, when heparin (which is used in dialysis) may impair blood clotting. First Use Syndrome is a severe anaphylactic reaction to the dialyzer. Its symptoms include sneezing, wheezing, shortness of breath, back pain, chest pain, or sudden death. It can be caused by residual sterilant in the dialyzer or the material of the membrane itself. In recent years, the incidence of First Use Syndrome has fallen off, due to an increased use of gamma irradiation instead of chemical sterilants, and the development of new dialyzer membranes of higher biocompatibility.

Economics of Dialysis in the United States

Dialysis is very expensive, averaging over $63,000 per year for each patient . In the United States, outpatient dialysis is paid for primarily by the government, through the Medicare and Medicaid programs. Medicare alone currently spends over $18.1 billion (2003) on dialysis patients annually, or 6.7% of its total budget . Commercial insurance (private insurance companies) also pays for some patients, typically paying providers more than twice the amount as Medicare. Though in most cases, only those over 65 years of age are eligible for Medicare, patients of any age who have ESRD (End Stage Renal Disease), meaning they require dialysis, are eligible as a special exception. Individuals who do not have the employment history required for Medicare eligibility are usually covered by the Medicaid program, which varies from state to state. A large portion of the cost associated with dialysis is the drug erythropoietin, also known as Epogen or EPO. It is given intravenously during the dialysis procedure, and replaces the hormone normally secreted by the healthy kidney, stimulating the bone marrow to produce red blood cells. Though it is necessary to prevent possibly fatal progressive anemia, it is also extremely costly. A single dose of 10,000 units costs around $100. This would be given 3 times a week, and assuming a patient did not miss a dose, would cost over $15,000 a year. Medicare spent $1.6 billion on EPO alone in 2003, or, by comparison, about the same as the entire budget of the FDA. The vast majority of US outpatient dialysis clinics are owned and operated by one of a small number of large dialysis corporations, or the "chains," as they are known in the industry. As of 2005, there are two main "chains": Fresenius Medical Care and DaVita. The two other largest dialysis corporations, Renal Care Group and Gambro Healthcare US, were acquired by Fresenius and DaVita, respectively, in 2005.

References

# Tattersall J, When to start dialysis, 3rd Congress of Nephrology in Internet, URL: http://www.uninet.edu/cin2003/conf/tattersall/tattersall.html, Accessed on July 21, 2005. # Churchill DN, Blake PG, Jindal KK, Toffelmire EB, Goldstein MB. Clinical practice guidelines for initiation of dialysis. Canadian Society of Nephrology. J Am Soc Nephrol. 1999 Jun;10 Suppl 13:S289-91. PMID 10425611 [http://csnscn.ca/local/files/guidelines/CSN-Guidelines-1999.pdf Full text] available from the [http://www.csnscn.ca Canadian Society of Nephrology] # Ibid. # [http://www.kdigo.org/guidelines/content-startdialysis.htm Guideline Comparison Table] from [http://www.kdigo.org/welcome.htm Kidney Disease - Improving Global Outcomes] # Oreopoulos DG. Beyond Kt/V: redefining adequacy of dialysis in the 21st century. Int Urol Nephrol. 2002;34(3):393-403. Review Article. PMID 12899236 # United States Renal Data System, [http://www.usrds.org/atlas.htm 2005 Annual Data Report Atlas], Chapter Eleven. # Ibid.

External links

- [http://kidney.niddk.nih.gov/kudiseases/pubs/kidneyfailure/index.htm Treatment Methods for Kidney Failure] - National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), NIH website
- [http://www.dialysistips.com/ Dialysis Tips] Resource for dialysis personnel general background with good understanding of the basic problems of dialysis therapy.
- [http://www.globaldialysis.com Global Dialysis] Resource and community for dialysis patients and professionals
- [http://www.uremic-toxins.org EUTox Uremic Toxins Work Group by ESAO] Resource on the topic of uremic toxins for professionals and scientifically interested dialysis patients Category:Nephrology Category:Medical treatments ja:人工透析

Blindness

:This article is about the visual condition. For a novel by the same name, see here. Blindness can be defined physiologically as the condition of lacking visual perception. The definition as it applies to people thus legally classified is, however, more complex. "Blindness" also applies to partial visual impairment: In North America and most of Europe, legal blindness is defined as visual acuity (vision) of 20/200 (6/60) or less in the better eye with best correction possible. This means that a legally blind individual would have to stand 20 feet from an object to see it with the same degree of clarity as a normally sighted person could from 200 feet. In many areas, people with average acuity who nonetheless have a visual field of less than 20 degrees (the norm being 180 degrees) are also classified as being legally blind. Approximately ten percent of those deemed legally blind, by any measure, are fully sightless. The rest have some vision, from light perception alone to relatively good acuity. Those who are not legally blind, but nonetheless have serious visual impairments, possess low vision. By the 10th Revision of the WHO International Statistical Classification of Diseases, Injuries and Causes of Death, low vision is defined as visual acuity of less than 6/18, but equal to or better than 3/60, or corresponding visual field loss to less than 20 degrees, in the better eye with best possible correction. Blindness is defined as visual acuity of less than 3/60, or corresponding visual field loss to less than 10 degrees, in the better eye with best possible correction. Visual impairment includes low vision as well as blindness.

Causes of blindness

Serious visual impairment has a variety of causes:

Diseases

Most visual impairment is caused by disease and malnutrition. According to WHO estimates in 2002, the most common causes of blindness around the world are:
- cataracts (47.8%),
- glaucoma (12.3%),
- age-related macular degeneration (AMD) (8.7%),
- trachoma (3.6%),
- corneal opacity (5.1%), and
- diabetic retinopathy (4.8%), among other causes. People in developing countries are significantly more likely to experience visual impairment as a consequence of treatable or preventable conditions than are their counterparts in the developed world. While vision impairment is most common in people over age 60 across all regions, children in poorer communities are more likely to be affected by blinding diseases than are their more affluent peers. The link between poverty and treatable visual impairment is most obvious when conducting regional comparisons of cause. Most adult visual impairment in North America and Western Europe is related to age-related macular degeneration and diabetic retinopathy. While both of these conditions are subject to treatment, neither can be cured. In developing countries, wherein people have shorter life expectancies, cataracts and water-borne parasites—both of which can be treated effectively—are most often the culprits. Of the estimated 40 million blind people located around the world, 70–80% can have some or all of their sight restored through treatment.

Abnormalities and injuries

Eye injuries, most often occurring in people under 30, are the leading cause of monocular blindness (vision loss in one eye) throughout the United States. Both of these conditions, injuries and cataracts, affect the eye itself. Abnormalities such as optic nerve hypoplasia affect the nerve bundle that sends signals from the eye to the back of the brain, which can lead to decreased visual acuity. People with injuries to the occipital lobe of the brain can, despite having perfectly normal eyes and optic nerves, still be legally or totally blind.

Genetic defects

People with albinism often suffer from visual impairment to the extent that many are legally blind, though few of them actually cannot see.

Adaptive techniques

Visually impaired and blind people have devised a number of techniques that allow them to complete daily activities using their remaining senses. These might include the following:
- Adaptations of banknotes so that the value can be determined by touch. For example:
- In some currencies, such as the euro and pound sterling, the physical size of a note increases with value.
- A lot of banknotes from around the world have a tactile feature to indicate denomination in the upper right corner. This tactile feature is a series of raised dots, but it is not standard Braille [http://www.bankofcanada.ca/en/banknotes/accessibility.html].
- It is also possible to fold notes in different ways to assist recognition.
- Labeling and tagging clothing and other personal items
- Placing different types of food at different positions on a dinner plate
- Marking oven, dishwasher, and dryer dials for ease of use Most people, once they have been visually impaired for long enough, devise their own adaptive strategies in all areas of personal and professional management.

Tools

Designers, both visually impaired and sighted, have developed a number of tools for use by blind people.

Mobility

People with serious visual impairments can travel independently using a white cane, the international symbol of blindness. A long cane is used to extend the user's range of touch sensation, swung in a low sweeping motion across the intended path of travel to detect obstacles. However, some visually impaired persons do not carry these kinds of canes, opting instead for the shorter, lighter identification (ID) cane. Still others require a support cane. Each of these is painted white for maximum visibility, and to denote visual impairment on the part of the user. In addition to making rules about who can and cannot use a cane, some governments mandate the right-of-way be given to users of white canes or guide dogs. A small number of people, about one percent, employ guide dogs. These companions are trained to lead blind individuals around obstacles on the ground and overhead. Though highly intelligent, guide dogs neither interpret street signs nor determine when the team ought to cross a street. Visually impaired people who employ these animals must already be competent travelers.

Reading and magnification

Most blind and visually impaired people read print, either of a regular size or enlarged through the use of magnification devices. A variety of magnifying glasses, some of which are handheld while others rest on desktops, can make reading easier for those with decreased visual acuity. The rest read Braille and Moon type or rely on talking books and readers. They use computers with special hardware such as scanners and refreshable Braille displays as well as software written specifically for the blind, like optical character recognition applications and screen reading software. Some people access these materials through agencies for the blind, such as the National Library Service for the Blind and Physically Handicapped in the United States, the National Library for the Blind or the RNIB in the United Kingdom. Closed-Circuit Televisions, equipment that enlarge and contrast textual items, are a more high-tech alternative to traditional magnification devices. So too are modern web browsers, which can increase the size of text on some web pages through browser controls or through user-controlled style sheets.

Computers

Access technology such as Freedom Scientific's JAWS for Windows screen reading software enable the blind to use mainstream computer applications. Most legally blind people (70% of them across all ages, according to the Lighthouse for the Blind) do not use computers. Only a small fraction of this population, when compared to the sighted community, have Internet access. This bleak outlook is changing, however, as availability of assistive technology increases, accompanied by concerted efforts to insure the accessibility of information technology to all potential users, including the blind. The movement towards greater web accessibility is opening a far wider number of websites to adaptive technology, making the web a more inviting place for visually impaired surfers. Experimental approaches such as the seeing with sound project are beginning to provide access to arbitrary live views from a camera.

Other aids

People may use talking thermometers, enlarged or marked oven dials, talking watches, talking clocks, talking scales, talking calculators, talking compasses and other talking equipment.

Social attitudes towards blindness

Historically, blind and visually impaired people have either been treated as if their lack of sight were an outward manifestation of some internal lack of reason, or as if they possessed extrasensory abilities. Stories such as The Cricket on the Hearth by Charles Dickens provided yet another view of blindness, wherein those affected by it were ignorant of their surroundings and easily deceived. The authors of modern educational materials (see: blindness and education for further reading on that subject), as well as those treating blindness in literature, have worked to paint a truer picture of blind people as three-dimensional individuals with a range of abilities, talents, and even character flaws. Certain individuals are gifted, and others licentious, but nothing definitive can be said of the blind as a class but that they cannot see well.

External links

- [http://www.accesswatch.info Access Watch: Blind users review accessibility of mainstream software]
- [http://www.question-mark.ca ?.Ca: A Comprehensive Directory of Blindness Information]
- [http://www.acb.org American Council of the Blind]
- [http://www.afb.org American Foundation for the Blind]
- [http://www.blindaccessjournal.com Blind Access Journal: Visual impairment in the real world]
- [http://www.v2020.org VISION 2020: The Right to Sight]
- [http://www.iapb.org International Agency for the Prevention of Blindness (IAPB)]
- [http://www.braille.org International Braille Research Center]
- [http://www.growingstrong.org/bvi/resource.html Literature Bibliography and Resources List]
- [http://www.nbp.org National Braille Press]
- [http://www.nfb.org National Federation of the Blind: Civil rights and consumer advocacy]
- [http://www.nlb-online.org/ National Library for the Blind]
- [http://www.loc.gov/nls National Library Service for the Blind and Physically Handicapped]
- [http://www.rfbd.org Recording for the Blind and Dyslexic]
- [http://www.rnib.org.uk/xpedio/groups/public/documents/code/InternetHome.hcsp Royal National Institute for the Blind]
- [http://www.ssc.mhie.ac.uk/ Scottish Sensory Centre]
- [http://www.who.int/mediacentre/factsheets/fs282/en/ WHO Fact Sheet on Visual Impairment]
- ja:失明 simple:Blindness

Erectile dysfunction

Erectile dysfunction, also known as impotence, is the inability to develop or maintain an erection of the