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Diabetes mellitus

is a syndrome of disordered metabolism, usually due to a combination of hereditary and environmental causes, resulting in abnormally high blood sugar levels (hyperglycemia).

often referred to simply as diabetes ( Greek: to pass through <urine>).

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Normal Glucose Metabolism

the sugars and starches within the foods we eat are broken down into glucose, and are absorbed into the blood stream. This absorption causes a rise in the blood glucose level.

As the blood containing elevated glucose levels circulates, it comes into contact with the pancreas, and certain other specific parts of the pancreas, which are contained in a sub structure called the islets of Langerhans.

These other specialized parts are the alpha, beta, and delta cells, which produce particular homones, which drastically affect blood sugar levels.

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When an inreased blood sugar level is sensed by the beta cells, they secrete insulin directly into the bloodstream. Insulin is a powerful hormone which allows cell membranes to change, (become more permeable to glucose), so that they allow the glucose molecule to be pulled into the cell interior, where it can be broken down into energy.

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In another example, when you've just gotten done with a bunch of work, and your blood sugar level begins to fall, the other type of cell, the alpha cell, senses a low blood sugar condition, and it releases another hormone, called glucagone. Glucagone goes out into the blood stream in the same fashion as the insulin did, however, the glucagone tells the liver cells to release some of their stored sugars back into the blood stream, thus raising the blood sugar levels back into an operating range.

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Insulin is also the principal control signal for conversion of glucose to glycogen for internal storage in liver and muscle cells. Lowered glucose levels result both in the reduced release of insulin from the beta cells and in the reverse conversion of glycogen to glucose when glucose levels fall. This is mainly controlled by the hormone glucagon which acts in an opposite manner to insulin. Glucagon and insulin are part of a feedback system that keeps blood glucose levels at a stable level. Glucose thus recovered by the liver re-enters the bloodstream; muscle cells lack the necessary export mechanism.

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When energy is required, glycogen stores in the liver are converted into glucose via glycogenolysis, elevating blood glucose levels and providing the needed cellular energy source.The liver also produces glucose from fat (fatty acids) and proteins (amino acids) through the process of gluconeogenesis. Glycogenolysis and gluconeogenesis both serve to increase blood glucose levels. Thus, glycemia is controlled by a complex interaction between the gastrointestinal tract, the pancreas, and the liver.

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Multiple hormones may affect glycemia. Insulin is the only hormone that lowers blood glucose levels. The counter-regulatory hormones such as glucagon, catecholamines, growth hormone, thyroid hormone, and glucocorticoids all act to increase blood glucose levels, in addition to their other effects .

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Abnormal Glucose MetablolismThe destruction of beta cells by a virus or an auto-immune response from our own bodies, are two reasons which have so far been found for beta cell destruction in clinical studies.

When this sort of destruction occurs, it impairs the body's ability to manufacture insulin. In the case of someone with type 1, insulin-dependent diabetes, the beta cell destruction may be complete and may never be repaired by the body. In the case of type 2 diabetes, some beta cells remain, however they may not be able to keep up with the body's demand for insulin unless a low carbohydrate or complex carbohydrate diet is followed.

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Other conditionsSteroid diabetes(also "steroid-induced diabetes") is a medical term

referring to prolonged hyperglycemia due to glucocorticoid therapy for another medical condition. It is usually, but not always, a transient condition.

The most common glucocorticoids which cause steroid diabetes are prednisolone and dexamethasone given systemically in "pharmacologic doses" for days or weeks. Typical medical conditions in which steroid diabetes arises during high-dose glucocorticoid treatment include severe asthma, organ transplantation, cystic fibrosis, inflammatory bowel disease, and induction chemotherapy for leukemia or other cancers.

Topical steroids can also cause hyperglycemia if used in large quantities and high doses over prolonged time periods, but this usually resolves with discontinuation of the medication.

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Types of Diabetes

• Type 1 diabetes. results from autoimmune destruction of insulin-producing beta cells of the pancreas.

• Type 2 diabetes: The bodyproduces insulin, but the cells have developed a resistance to it, often because the pt is overweight or obese. Watching fat intake is a necessary part of losing weight and keeping diabetes under control.

• Gestational diabetes. It usually develops during the third trimester and significantly increases perinatal morbidity and mortality. the pathophysiology of gestational diabetes is associated with increased insulin resistance.

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Impaired Glucose Tolerance and Impaired Fasting Glucose

The conditions known as impaired glucose tolerance (IGT) and impaired fasting glucose (IFG) represent metabolic states lying between diabetes and normoglycemia. People with IFG have increased fasting blood glucose levels but usually have

normal levels following food consumption. they are risk factors for future diabetes. Pathophysiology of

IFG and IGT is related primarily to increased insulin resistance whereas endogenous insulin secretion is normal in most patients. Approximately 30 to 40% of individuals with IGT or IFG will develop type 2 diabetes within 10 years after onset.

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Diabetes and Fat Intake

people with diabetes need to limit their fat intake to decrease their risk of developing heart disease.That is diabetes slowly damages the arteries in the body unless blood sugar is very tightly controlled.

The increased risk of cardiovascular disease exists no matter which of the three types of diabetes the pt has.

Obesity contributes greatly to insulin resistance, even in the absence of diabetes. In fact, weight loss is a cornerstone of therapy for obese type 2 diabetic patients. Insulin resistance generally decreases with weight loss.

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There is some evidence that fat cells are more resistant to insulin than muscle cells. If a person has more fat cells than muscle cells, then the insulin becomes less effective overall, and glucose remains circulating in the blood instead of being taken in to the cells to be used as energy.

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Why Do Type 1 Diabetes Patients Slim Down Even Eating Much

Due to the fact that Type 1 Diabetes patients lack insulin in body, patients’ body cannot make the best of glucose. This stimulates protein and fat in body to acceleratory decomposition, which contributes to supplying energy and heat for body. By this, large quantity of carbohydrate, protein and fat will be consumed. Besides, Type 1 Diabetes patients are always in a state of water loss; even they have had more water. when the sugar levels are high, they will want to pass urine quite a few times. This will naturally result in dehydration. The loss of sugar in the urine means a loss of calories which provide energy and therefore many people with high sugars lose weight.

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Polyuria,polydipsia,polyphagia

When the glucose concentration in the blood is raised beyond the renal threshold, reabsorption of glucose in the proximal renal tubuli is incomplete, and part of the glucose remains in the urine ( glycosuria). This increases the osmotic pressure of the urine and inhibits the reabsorption of water by the kidney, resulting in increased urine production ( polyuria) and increased fluid loss. Lost blood volume will be replaced osmotically from water held in body cells, causing dehydration and

increased thirst(polydipsia).

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reason for polyphagia is the intracellular starvation. As in diabetes either there is absence or the resistance to insulin action so glucose cannot move into the cells and thus cells are starved of glucose.

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Permanent Teeth Erupt Early in Diabetic Children

The reasons for the speedier tooth eruption may have to do with gum inflammation, which tended to be greater in children with diabetes. Gum inflammation may diminish the mass of the bones supporting the teeth, shortening the distance that developing teeth need to progress to break through the gums. This could potentially increase their risk of dental problems liket they could raise the odds of misaligned or crowded teeth, which, lead to cosmetic effects, and can make it harder to clean the teeth and keep the gums healthy.

Clinical differentiation betweenhypoglycemia and hyperglycemia

hypoglycemia• hunger and weakness followed

bysweating.• Rapid pulse• Shakiness, dizziness,

weakness• Decreased coordination• Difficulty concentrating• Blurred vision• Headache• Trouble performing routine

tasks• Note: Symptoms can vary

from person to person and episode to episode.

hyperglycemia

• Warm, dry skin that does not sweat

• Dry, parched mout• Extreme thirst• Frequent urination • General weakness• Loss of appetite• Fruity breath• Nausea and vomiting• Abdominal pain• Deep, rapid breathing• High fever

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Diabetic ketoacidosis

People with type 1 diabetes are highly susceptible to diabetic ketoacidosis. Because the pancreas produces no insulin, glucose cannot enter cells and remains in the bloodstream. To meet cellular energy needs, fat is broken down through lipolysis, releasing glycerol and free fatty acids. Glycerol is converted to glucose for cellular use. Fatty acids are converted to ketones, resulting in increased ketone levels in body fluids and decreased hydrogen ion concentration (pH). Ketones are excreted in the urine, accompanied by large amounts of water. The accumulation of ketones in body fluids, decreased pH, electrolyte loss and dehydration from excessive urination, and alterations in the bicarbonate buffer system result in diabetic ketoacidosis (DKA). Untreated DKA can result in

coma or death.

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Many patients with type 1 diabetes are initially diagnosed with the disease following a hospital admission for DKA. In a known diabetic patient,

periods of stress or infection may precipitate DKA. More often, however, DKA results from poor daily glycemic control. Patients who remain severely hyperglycemic for several days or longer due to inadequate insulin administration or excessive glucose intake are prone to developing DKA.

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ORAL COMPLICATIONS OF DIABETES

• Gingivitis and periodontal disease.

• Salivary gland dysfunction and xerostomia.• Candidiasis.• Burning mouth syndrome.• Lichen planus.• Acute oral infections• delayed wond healing• Early tooth loss in IDDM.

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Gingivitis and periodontal disease

Is related to the altered response to infection, microvascular changes and, possibly, increased glucose concentrations in the saliva (salivary hyperglycemia) and gingival crevicular fluid. Increased salivary glucose results in additional bacterial substrate and plaque formation.29 Increased gingival crevicular fluid glucose may diminish the ability of periodontal fibroblasts to contribute to periodontal healing.

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Salivary gland dysfunction and xerostomia.

Is due to polyuria, or an underlying metabolic or endocrine problem. When the normal environment of the oral cavity is altered because of a decrease in salivary flow or alteration in salivary composition, a healthy mouth can become susceptible to dental caries and tooth deterioration. Dry, atrophic and cracking oral mucosa is the eventual complication from insufficient salivary production. Accompanying mucositis, ulcers and desquamation, as well as an inflamed, depapillated tongue, are also common problems. Difficulty in lubricating, masticating, tasting and swallowing are among the most devastating complications from salivary dysfunction and may contribute to impaired nutritional intake.

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Candidiasis

Salivary dysfunction, compromised immune function and salivary hyperglycemia that provides a potential substrate for fungal growth are the major contributing factors for oral candidiasis in patients with diabetes. Oral lesions associated with candidiasis include median rhomboid glossitis atrophic glossitis, denture stomatitis, (thrush) and angular cheilitis.

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Mechanism of increased risk ofinfection

• Macrophage metabolism alteration occurs, with inhibition of phagocytosis.

• Immunological defect and deficient leucocytes functions.Functions of immune cells, including neutrophil, monocytes and

macrophages are altered.• Decrease production of antibodies.• Peripheral neuropathy and poorperipheral circulation.• All steps of PMN functioning which include PMN chemotaxis,spontaneous activation of PMN cells, increased free radical

production; after stimulation are altered, which may increase the risk of vascularcomplications and infectious episodes.• Neutrophil adherence, chemotaxis and phagocytosis are alsoimpaired thus inhibiting bacteria killing.

Infection is a possible consequence of wounds that remain open for an extended period to time. Another complication of poorly controlled diabetes is a decreased immune response. So diabetes makes infections both more likely to occur and harder for the body to fight off.

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DELAYED HEALING OF WOUNDS

• Microangiopathy and utilization

of protein for energy may retardthe repair of tissues.• There is altered cellular activities and failure of

PMNs to migrate toward the area ofwound healing.

• Collagen synthesis isdecreased. Decreased crosslinking and glycosylation of collagenrenders collagen produced inDM more soluble and possiblywith a decrease remodelingtime.

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Burning mouth syndrome

in uncontrolled or marginally controlled diabetes, these etiologic factors can include salivary dysfunction, candidiasis and neurological abnormalities such as depression. Neuropathy

may lead to oral symptoms of paresthesias and tingling, numbness, burning or pain caused by pathological changes involving the nerves in the oral region.

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