User:Alteripse/diabetes workshop

proposed structure and relationships of diabetes articles- incomplete


 * diabetes (disambig and pointers to d.i. and principal diab articles)
 * diabetes mellitus overview incl section on complications that divides acute & chronic, macro/micro etc and points to individ articles
 * diabetes mellitus type 1 (redirects fr variant nonpreferred versions type 1 diabetes mellitus type I diabetes type 1 diabetes type I diabetes mellitus insulin-dependent diabetes mellitus(this one deserves brief explan of hx & overlapping nature) IDDM insulin-dependent diabetes juvenile diabetes juvenile diabetes mellitus)
 * diabetes mellitus type 2 (redirects fr variant nonpreferred versions type 2 diabetes mellitus type 2 diabetes type II diabetes type II diabetes mellitus non-insulin-dependent diabetes mellitus NIDDM non-insulin-dependent diabetes adult-onset diabetes mellitus maturity-onset diabetes mellitus
 * gestational diabetes mellitus
 * maturity-onset diabetes of the young (rd fr MODY)
 * Other misc types of diab
 * mitochondrial diabetes
 * steroid diabetes
 * cystic fibrosis-related diabetes etc)
 * Long-term complications of diabetes (rd fr diabetic complications long-term diabetic complications Long term complications of diabetes chronic complications of diabetes mellitus chronic complications of diabetes) This is main article laying out pathophys, types, divisions into macro and micro but only brief mention and pointers to each individual condition
 * macrovascular complications of diabetes mellitus rd to long-term compl (also rd fr macrovascular complications of diabetes macroangiopathic complications of diabetes diabetic macroangiopathy)
 * heart disease in diabetes
 * stroke in diabetes
 * peripheral vascular disease in diabetes
 * diabetic foot disease w rd fr diabetic foot ulcer


 * microvascular complications of diabetes mellitus rd to long-term compl (also rd fr microvascular complications of diabetes microangiopathic complications of diabetes mellitus diabetic microangiopathy)
 * diabetic nephropathy
 * diabetic retinopathy
 * diabetic neuropathy


 * acute complications of diabetes mellitus rd to section of overview article that points to specific conditions (also rd acute complications of diabetes)
 * diabetic ketoacidosis (rd fr DKA) ###needs major rewrite / fact check ww
 * hyperosmolar coma (rd fr hyperosmolar nonketotic coma, HHNC, hyperosmolar, non-ketotic coma)
 * diabetic hypoglycemia (rd fr insulin reaction


 * other diabetes related articles
 * insulin sensitivity, insulin resistance
 * glycemic control Diabetes Control and Complications Trial (rd fr DCCT)
 * hemoglobin A1c (rd fr glycosylated hemoglobin) glycosylation
 * glucose meter


 * oral hypoglycemic agent rd diabetes medication
 * sulfonylurea
 * thiazolidinedione
 * metformin
 * insulin, insulin (medication)

Diabetic ketoacidosis (DKA) is an acute metabolic complication of diabetes mellitus, especially type 1 diabetes, in which dehydration is accompanied by ketosis and metabolic acidosis. Moderate or severe degrees of DKA are likely to lead to death without medical treatment. Treatment consists of hospitalization for intravenous administration of insulin, water and electrolytes, and usually results in full recovery.

Pathophysiology
Ketoacidosis is the advanced metabolic decompensation characteristic of insulin-dependent diabetes mellitus. The clinical manifestations include vomiting, dehydration, extreme hyperglycemia, ketosis, and metabolic acidosis. The primary underlying problem in DKA is insufficient insulin action, due to variable combinations of insulin deficiency and reduced insulin sensitivity (Table 1). Insulin deficiency may be absolute (e.g., failure of the islet cells, missed insulin doses) or relative (e.g., failure to take extra insulin during illness). As illness progresses, stress-induced counterregulatory hormones (glucagon, cortisol, and catecholamines) antagonize insulin action, and stimulate lipolysis, ketogenesis, and hepatic glucose production. Insulin sensitivity is further reduced by hyperosmolality and acidosis. Lower insulin and higher glucagon action in the liver lead to gluconeogenesis and ketogenesis. Deficient insulin action in peripheral tissues allows catabolism of fat and muscle. Fat and muscle catabolism leads to ketosis and acidosis, causing anorexia, vomiting, and hyperventilation. Hyperglycemia induces osmotic diuresis, producing dehydration and electrolyte depletion if oral intake is disrupted by vomiting. Vomiting and hyperventilation aggravate dehydration. Without treatment, severe dehydration results in shock, worsening acidosis, and eventually death.

A typical patient with moderately severe DKA would loose 10-15% of body water (sometimes up to 20%) and significant amounts of electrolytes (Table 2). Water is lost about equally from intracellular and extracellular space.

Usual causes
Four circumstances lead to most hospitalizations for DKA. Delayed diagnosis of new-onset type 1 diabetes   About 25% of new IDDM patients have reached a state of acidosis requiring iv fluids by the time diabetes is recognised. Most had been taken for medical attention within the previous week and had been diagnosed with a minor infection. Most parents had noticed weight loss, bedwetting, drinking, or other symptoms of longer duration than the acute illness but had not volunteered them to the physician. Physicians should: (1) be aware of the commonness of IDDM, which develops in about 1 in 400 children; (2) routinely question to distinguish truly acute illnesses from progressive processes present for more than a week (e.g., "When was he last completely well?", "Any changes in drinking, urination, eating, bowels, or weight?"); (3) check urine dipstrips for abdominal complaints of all types. Illness mismanagement in established diabetes   The most common error is insulin reduction despite ketonuria. Patients with IDDM should be provided with Sick Day Rules (written instructions for handling illness by checking urine for ketones and using extra insulin to reverse ketosis) and a telephone contact. In surveys of DKA admissions in adults, respiratory and urinary infections were most often blamed; gastroenteritis leads the list in children. Recurrent admission of a few diabetic patients  A small percentage of people with type 1 diabetes suffer repeated hospitalizations for DKA, sometimes several times a year over many years. Most are 10 to 25 years of age. Common features of recurrent diabetic ketoacidosis include inadeq¬uate diabetes education, lack of supervision and family disorganization in younger patients, and eating disorders, personality disorders or substance abuse in older patients. Family or individual counseling rarely stops the admissions, which are most effectively reduced by assistance of another person in the daily diabetes care and illness management, or by addressing the motivations for insulin omission or hospitalization.

Diagnosis and differential diagnosis of DKA
Table 3 lists the symptoms and signs of DKA as it progresses. The presenting complaint to an emergency department is usually "vomiting." If a patient known to have IDDM has been vomiting, and is visibly dehydrated, a diagnosis of DKA can be confirmed in minutes by demonstrating hyperglycemia with a fingerstick glucose and ketosis with a urine dipstrip. You may safely start isotonic fluids while awaiting lab results. If the patient is not known to have diabetes, a history of polydipsia/polyuria with hyperglycemia, ketonuria, and acidosis confirms a diagnosis of iddm with dka. Although easy to confirm when suspected, dka is often missed by not being considered. Common suspected diagnoses when dka is missed are gastroenteritis ("flu"), and pneumonia. Once DKA is suspected, few conditions need to be excluded. The most common mimic of DKA, especially in young children, is severe gastroenteritis with hypertonic dehydration, when a glucose as high as 400 mg/dl may be accompanied by ketosis and acidosis. This stress hyperglycemia may be tentatively distinguished from DKA by absence of a history of polyuria and polydipsia, and by elevation of the serum Na. When fluids are given, without insulin, the glucose will rapidly fall and remain normal if the child simply has gastroenteritis. Other illnesses and drugs may occasionally produce stress hyperglycemia. Other acute conditions which can partly resemble DKA are nonketotic hyperosmolar coma, Reye’s syndrome, pancreatitis, pyelonephritis, acute renal failure, stroke, asthma, adrenal crisis, hyperventilation, acute surgical abdomen, lactic acidosis, alcoholic ketoacidosis, several congenital metabolic acidosis, starvation ketosis of pregnancy, and various overdoses and poisonings (e.g., salicylate, alcohol, Lomotil, carbon monoxide, toluene).

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