Pathophysiology of Diabetes MellitusStudies conducted on the pathophysiology of diabetes mellitus suggested that abnormal metabolism of insulin hormone is the primary cause for the development of this complex syndrome. Even though the etiologies and triggering factors of the three types of diabetes mellitus are different, they cause nearly the same symptoms and complications.

What is Diabetes Mellitus

Diabetes mellitus (DM) or simply diabetes, is a chronic health condition in which the body either fails to produce sufficient amounts of insulin or it responds abnormally to insulin. Commonly referred to as a syndrome, diabetes is classified into three types, namely, Type 1 diabetes, Type 2 diabetes, and Gestational diabetes. The ultimate outcome for all three types of diabetes is high blood glucose level. The pathophysiology of diabetes mellitus is very complex, as this ailment is characterized by different etiologies while sharing similar signs, symptoms, and complications.

Diabetes Mellitus: Pathophysiology

The pathophysiology of all types of diabetes is related to the hormone insulin, which is secreted by the beta cells of the pancreas. In a healthy person, insulin is produced in response to the increased level of glucose in the bloodstream, and its major role is to control glucose concentration in the blood. What insulin does is, allowing the body cells and tissues to use glucose as a main energy source. Also, this hormone is responsible for conversion of glucose to glycogen for storage in the muscles and liver cells. This way, sugar level is maintained at a near stable amount.

In a diabetic person, there is an abnormal metabolism of insulin hormone. The actual reason for this malfunction differs according to the type of diabetes. Whatever the cause is, the body cells and tissues

do not make use of glucose from the blood, resulting in elevated blood glucose (a typical symptom of diabetes called hyperglycemia). This condition is also exacerbated by the conversion of stored glycogen to glucose, i.e., increased hepatic glucose production. Over a period of time, high glucose level in the bloodstream can lead to severe complications, such as eye disorders, cardiovascular diseases, kidney damage, and nerve problems.

In Type 1 diabetes, the pancreas cannot synthesize enough amounts of insulin as required by the body. The pathophysiology of Type 1 diabetes mellitus suggests that it is an autoimmune disease, wherein the body's own immune system generates secretion of substances that attack the beta cells of the pancreas. Consequently, the pancreas secretes little or no insulin. Type 1 diabetes is more common among children and young adults (around 20 years). Since it is common among young individuals and insulin hormone is used for treatment, Type 1 diabetes is also referred to as Juvenile Diabetes or Insulin Dependent Diabetes Mellitus (IDDM).

In case of Type 2 diabetes mellitus, the insulin hormone secreted by the beta cells is normal or slightly lower than the ideal amount. However, the body cells are not responding to insulin as they do in a healthy person. Since the body cells and tissues are resistant to insulin, they do not absorb glucose, instead it remains in the bloodstream. Thus, the Type 2 diabetes is also characterized by elevated blood sugar. It is commonly manifested by middle-aged adults (above 40 years). As insulin is not necessary for treatment of Type 2 diabetes, it is known as Non-insulin Dependent Diabetes Mellitus (NIIDM) or Adult Onset Diabetes.

The third type of diabetes is called Gestational diabetes. As the term clearly suggests, it is exhibited by pregnant women. Over here, high level of blood glucose is caused by hormonal fluctuations during pregnancy. Usually, the sugar concentration returns to normal after the baby is born. However, there are also instances, in which it remains high even after childbirth. This is an indication for increased risks of developing diabetes in the near future.

As already mentioned, the symptoms and effects of all the three forms of diabetes are similar. The noticeable symptoms include increased thirst (polydipsia), increased urination (polyuria), and increased appetite (polyphagia). Other diabetes signs and symptoms include excessive fatigue, presence of sugar in the urine (glycosuria), body irritation, unexplained weight loss, and dehydration. Elevated blood sugar and glycosuria are interrelated; when sugar amount in the blood is abnormally high, the reabsorption by proximal convoluted tubule is reduced, thereby retaining some glucose in the urine.

Diabetes Mellitus: Diagnosis and Treatment

Regarding the definition of diabetes mellitus, it is often described as a fasting blood glucose level of 126 milligrams per deciliter (mg/dL) or more. As per statistics, Type 2 diabetes is the most commonly occurring type, in comparison to the other two forms of diabetes mellitus. Early and correct detection of the diabetes is necessary to prevent severe health effects. After diagnosis, the physician prescribes appropriate medication for treatment of diabetes, which may include insulin injections or oral insulin

medicines, depending upon the type of diabetes mellitus.

In addition to the therapeutic intervention, healthy lifestyle modifications, especially in terms of diet and exercises are recommended for effective management of diabetes symptoms and long-term effects. Since it is a global health issue, studies regarding the diabetes mellitus pathophysiology are currently in progress in order to minimize its associated health effects, and also, to treat it effectively.

By Ningthoujam SandhyaraniLast Updated: 11/16/2011

http://www.buzzle.com/articles/pathophysiology-of-diabetes-mellitus.html

Gestational Diabetes- Carla Janzen, MD, Jeffrey S. Greenspoon, MD

Essentials of Diagnosis

Any degree of glucose intolerance with onset or first recognition during pregnancy. In the majority of cases of GDM, glucose regulation will return to normal after delivery.

Definition

The above definition applies regardless of whether insulin or only diet modification is used for treatment or whether the condition continues after pregnancy. It is possible that unrecognized glucose intolerance may have antedated or begun concomitantly with pregnancy.

Gestational diabetes may be screened for by drawing a 1-hour glucose level following a 50-gram glucose load, but is definitively diagnosed only by an abnormal 3-hour GTT following a 100-gram glucose load. Such persons are not within the norm (95%) for pregnancy.

Significance

The growth and maturation of the fetus are closely associated with the delivery of maternal nutrients, particularly glucose. This is most crucial in the third trimester and is directly related to the duration and degree of maternal glucose elevation. Thus the negative impact is as highly diverse as the variety of carbohydrate intolerance that women bring to pregnancy. In those with severe abnormalities, there is an increased rate of miscarriage, congenital malformations, prematurity, pyelonephritis, preeclampsia, in utero meconium, fetal distress, cesarean section deliveries, and stillbirth.

Incidence & Etiology

Inability to maintain glucose levels required by the body for proper functioning is a growing health problem in the United States; thus it is not surprising that more women are found during pregnancy to be unable to attain the low glucose levels required for proper fetal growth. The incidence of gestational diabetes varies from 12% in racially heterogeneous urban regions to 1% in rural areas with a predominantly white population.

Pathophysiology

Gestational diabetes is pathophysiologically similar to type 2 diabetes. Approximately 90% of the persons identified have a deficiency of insulin receptors (prior to pregnancy) or a marked increase in weight in the abdominal region. The other 10% have deficient insulin production and will proceed to develop mature-onset insulin-dependent diabetes.

Similarly to women with type 2 diabetes, the women most likely to develop gestational diabetes are those who are overweight, with a body habitus often described as "apple shaped." HPL blocks insulin receptors and increases in direct linear relation to the length of pregnancy. Insulin release is enhanced in an attempt to maintain glucose homeostasis. The patient experiences increased hunger due to the excess insulin release as a result of elevated glucose levels. This insulin release further decreases insulin receptors due to elevated hormonal levels. Thus the vicious cycle of excess appetite with weight gain occurs. Few other symptoms mark this condition.

Diagnosis

Glucosuria is a common finding in pregnancy due to increased glomerular filtration and is therefore unreliable as a means of diagnosis. Glucose screening should be done in every pregnant patient at or no later than 28 weeks' gestation, since risk factors are insufficient to identify all women with gestational diabetes. Ultrasound findings of fetal weight ≥ 70% for gestational age, polyhydramnios (AFI ≥ 20), midline congenital anomalies, or an abdominal circumference measurement that exceeds the femur growth by 2 weeks merit an immediate 3-hour GTT. Other

Diabetes Mellitus & Pregnancy

Introduction Metabolism in Normal & Diabetic Pregnancy Diagnostic Criteria for Diabetes Mellitus Prior to Pregnancy Diagnostic Criteria for Gestational Diabetes Mellitus Pregestational Diabetes L Type 1 Diabetes (Insulin-Dependent) L Type 2 Diabetes (Non-Insulin Dependent) Gestational Diabetes Antepartum Care Neonatal Complications Intrapartum & Postpartum Management

L Prognosis References

clinical findings indicating possible diabetes are edema developing early in pregnancy and excessive weight gain.

Initial screening is accomplished by ingestion of 50 grams of glucose (usually chilled glucola) at any time of the day and without regard to prior meal ingestion. The sensitivity and specificity are based on the cutoff value used to indicate a positive result (Table 18-4); however, screening is not as reproducible from day to day as would be desired. If screening is positive, the patient is advised to follow a carbohydrate loading diet for 3 days and then have a full 3-hour glucose tolerance test. A simple carbohydrate loading diet is all the pasta and starches she can eat at each meal and one candy bar per day. For the GTT, the patient fasts, then receives 100 grams of glucose after a fasting glucose level is obtained. A blood sample is then taken every hour for 3 hours. The patient is advised to sit quietly during the test to minimize the impact of exercise on glucose levels.

The glucose values initially used to detect gestational diabetes were determined by O'Sullivan and Mahan in a retrospective study designed to detect risk of developing type 2 diabetes in the future. The values were set using whole blood and required two values reaching or exceeding the value to be positive. Subsequent information has led to alteration in O'Sullivan's criteria. For example, there is growing evidence that one value is sufficient to make an impact on the health of the fetus, and is now the criterion used by most clinicians to initiate treatment. Whole blood glucose values are lower than plasma levels due to glucose uptake by hemoglobin. The present values used by the American College of Obstetricians and Gynecologists are based on a theoretical increase in hemoglobin and plasma with pregnancy. Recently, a study using all three methods of glucose determination on the same samples have disproved the theoretical values and are listed in Table 18-5.

Treatment

The key to therapy in most patients is diet and exercise (because of the paucity of insulin receptors). This makes therapy more difficult than with the insulin-deficient patient, in whom exogenous insulin may be easily administered. Therapy in the type 2 diabetic is based on the patient's motivation and ability to change lifestyle. Exercise of the non-weight-bearing type (noted previously) is encouraged as even short exercise periods have a major benefit.

Every care provider must stress the importance of diet. Soluble fiber is invaluable to provide satiety and improve insulin receptor numbers and sensitivity. Carbohydrate restriction has been shown to improve glycemic control in diet-controlled GDM. Fats must be reduced because of their negative impact on insulin receptors. Calories should be prescribed at 20-25/kcal per kilogram of present body weight (generally 1800-2400 kcal). Massively obese patients have a reduction in their metabolism rate; therefore, it is better to start low and increase the calories as needed. Food records are kept for 1 week, and the content and calories are reviewed by the dietitian with helpful suggestions on improving favorite dishes to be included in the diet. The patient is instructed to particularly note all food taken in when a 1-hour postprandial glucose value is 130 mg/dL or greater. The memory reflectance glucose meters are invaluable in assisting the patient to learn the proper diet and the impact of her actions on glucose levels. Insulin is added as needed for glucose control only after clear dietary errors are noted and attempts at

correction are done. Approaches to initiating insulin therapy vary, but should remain as simple as possible.

A minimum of 2 visits to the dietitian encourages education and interaction over dietary questions. The customization of diet to ethnic foods is often invaluable in obtaining dietary compliance. The encouragement of other family members to participate in dietary counseling assists their support for the patient and is key to making familial dietary changes. The patient often benefits from direct contact with the dietitian when glucose levels are erratic, when her weight fails to meet expected guidelines, when she is having difficulty with calorie counting, or when she increases daily calories more than 300 kcal over guidelines.

The patient checks her glucose 4 times daily (eg, fasting, and 1-hour postprandial breakfast, lunch, dinner). The desired values are a fasting level of 70-90 mg/dL and a 1-hour level of 130 mg/dL. The average glucose levels should be 90 mg/dL.

http://www.health.am/pregnancy/gestational-diabetes/

Human placental lactogen Human placental lactogen (HPL), also called human chorionic somatomammotropin, is a polypeptide placental hormone. Its structure and function is similar to that of human growth hormone. It modifies the metabolic state of the mother during pregnancy to facilitate the energy supply of the fetus. HPL has anti-insulin properties. HPL is a hormone secreted by the syncytiotrophoblast during pregnancy. Like human growth hormone, HPL is encoded by genes on chromosome 17q22-24. It was identified in 1963.[2]

http://en.wikipedia.org/wiki/Human_placental_lactogen

glycogenolysis /gly·co·ge·nol·y·sis/ (-jĕ-nol´ĭ-sis) the splitting up of glycogen in the liver, yielding glucose.glycogenolyt´icDorland's Medical Dictionary for Health Consumers. © 2007 by Saunders, an imprint of Elsevier, Inc. All rights reserved.

gluconeogenesis [gloo″ko-ne″o-jen´ĕ-sis] the synthesis of glucose from noncarbohydrate sources, such as amino acids and glycerol. It occurs primarily in the liver and kidneys whenever the supply of carbohydrates is insufficient to meet the body's energy needs. Gluconeogenesis is stimulated by cortisol and other GLUCOCORTICOIDS and by the thyroid hormone thyroxine. Formerly called glyconeogenesis.Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition. © 2003 by Saunders, an imprint of Elsevier, Inc. All rights reserved.

glycogenesis /gly·co·gen·e·sis/ (gli″ko-jen´ĕ-sis) the conversion of glucose to glycogen for storage in the liver.glycogenet´icDorland's Medical Dictionary for Health Consumers. © 2007 by Saunders, an imprint of Elsevier, Inc. All rights reserved.

glycolysis [glīkol′isis]

Etymology: Gk, glykys + lysis, loosening

a series of enzymatically catalyzed reactions by which glucose and other sugars are broken down to yield lactic acid (anaerobic glycolysis) or pyruvic acid (aerobic glycolysis). The breakdown releases energy in the form of adenosine triphosphate. Also called Embden-Meyerhof pathway. See also aldolase, citric acid cycle, lactic acid.

Mosby's Medical Dictionary, 8th edition. © 2009, Elsevier.

lip·o·gen·e·sis (l p -j n -s s)

n.

1. Production of fat, either fatty degeneration or fatty infiltration. Also called adipogenesis.

2. The normal deposition of fat or the conversion of carbohydrate or protein to fat.

lip o·gen ic (-j n k), li·pog e·nous (l -p j -n s) adj.

The American Heritage® Medical Dictionary Copyright © 2007, 2004 by Houghton Mifflin Company. Published by Houghton Mifflin Company. All rights reserved.

gly·co·gen (gl k -j n)

n.

A polysaccharide that is the main form of carbohydrate storage in animals and occurs mainly in liver and muscle tissue; it is readily converted to glucose. Also called animal starch.

gly co·gen ic (-j n k) adj.

The American Heritage® Medical Dictionary Copyright © 2007, 2004 by Houghton Mifflin Company. Published by Houghton Mifflin Company. All rights reserved.

glucagon [glo ̅o̅′kəgon]

Etymology: Gk, glykys, sweet, agaein, to lead

a polypeptide hormone, produced by alpha cells in the islets of Langerhans, that stimulates the conversion of glycogen to glucose in the liver. Secretion of glucagon is stimulated by hypoglycemia and by growth hormone from the anterior pituitary. A preparation of purified crystallized glucagon is used in the treatment of certain hypoglycemic states. Also called hyperglycemic-glycogenolytic factor (HGF).

glucagon (recombinant),

a form of recombinant DNA origin, having the same actions and uses as that of animal origin.

Mosby's Medical Dictionary, 8th edition. © 2009, Elsevier.

>sometimes used to treat insulin shock.

>a polypeptide hormone secreted by the alpha cells of the ISLETS OF LANGERHANS in response to HYPOGLYCEMIA or to stimulation by GROWTH HORMONE . It increases blood glucose concentration by stimulating GLYCOGENOLYSIS in the liver and can be administered parenterally to relieve severe HYPOGLYCEMIA from any cause, especially HYPERINSULINISM . Because it slows motility of the gastrointestinal tract, it is also used as an aid in gastrointestinal radiography.

glucagon stimulation test a provocative test of growth hormone (GH) function in which the fasting serum level of GH is measured after administration of glucagon.

Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition. © 2003 by Saunders, an imprint of Elsevier, Inc. All rights reserved.

>raises the blood sugar by increasing hepatic glycogenolysis.

Mosby's Dental Dictionary, 2nd edition. © 2008 Elsevier, Inc. All rights reserved.

glucagon diabetesglucagon elevates blood glucose levels and may contribute to the severity of diabetes if there is already an insulin deficit but it is not necessary to, nor sufficient for, the development of diabetes.glucagon stimulation testa provocative test of growth hormone (GH) function in which the fasting serum level of GH is measured before and after administration of glucagon.glucagon tolerance testevaluates the insulin response to elevation of blood glucose induced by administration of glucagon. Used in diagnosing hyperinsulinism.Saunders Comprehensive Veterinary Dictionary, 3 ed. © 2007 Elsevier, Inc. All rights reserved

Somatostatin

From Wikipedia, the free encyclopedia

Jump to: navigation, search

Somatostatin

Available structures

PDBOrtholog search: PDBe, RCSB

[show]List of PDB id codes

Identifiers

Symbols SST; SMST

External

IDs

OMIM: 182450 MGI: 98326 HomoloGene: 819

GeneCards: SST Gene

[show]Gene Ontology

RNA expression pattern

More reference expression data

Orthologs

Species Human Mouse

Entrez 6750 20604

Ensembl ENSG00000157005 ENSMUSG00000004366

UniProt P61278 P60041

RefSeq

(mRNA)NM_001048.3 NM_009215.1

RefSeq

(protein)NP_001039.1 NP_033241.1

Location

(UCSC)

Chr 3:

187.39 – 187.39 Mb

Chr 16:

23.89 – 23.89 Mb

PubMed

search[1] [2]

This box:

view

talk

edit

Somatostatin (also known as growth hormone-inhibiting hormone (GHIH) or somatotropin release-inhibiting factor (SRIF)) or somatotropin release-inhibiting hormone[citation needed] is a peptide hormone that regulates the endocrine system and affects neurotransmission and cell proliferation via interaction with G-protein-coupled somatostatin receptors and inhibition of the release of numerous secondary hormones.

Sphincter of Oddi Dysfunction

Sphincter of Oddi dysfunction refers to abnormal function of the sphincter muscle at the end of the bile and pancreatic ducts, the tubes that drain the liver and pancreas into the small intestine through a small nipple-like opening called the papilla. The sphincter is a circular band of muscle tissue which controls the release of bile and pancreatic juices though an opening in the papilla into the intestine. Abnormal relaxation of the sphincter prevents normal flow of bile or pancreatic juices into the intestine. This may cause episodic upper abdominal pain and even pancreatitis (see separate discussion under pancreatic disorders). The diagnosis is considered in

patients with typical pain and abnormally elevated liver enzymes in the absence of gallstones or other causes of bile duct obstruction. The diagnosis should also be considered in patients with repeated and unexplained episodes of pancreatitis. The diagnosis can be confirmed by Endoscopic Retrograde Cholangiopancreatography (ERCP). After the patient is deeply sedated, the physician passes a flexible tube (endoscope) through the mouth, esophagus and stomach and into the beginning of the small intestine called the duodenum. At this location the bile duct drains into the intestine through a small nipple-like opening called the papilla. A plastic tube called a catheter is then passed through the scope, into the papilla and up into the bile duct. The pressure within the sphincter can be assessed. An elevated sphincter pressure is suggestive of sphincter dysfunction. Treatment consists of cutting the sphincter muscle (sphincterotomy) during ERCP using a thin wire attached to a catheter. ERCP and sphincterotomy are associated with a significant risk of a complication called pancreatitis when performed on patients with Sphincter of Oddi dysfunction or in patients suspected to have the condition.

http://www.rgal.com/our-services/conditions/gall-bladder-conditions/sphincter-of-oddi-dysfunction

Diabetes overviewReviewed by Professor   Ian W   Campbell , consultant physician, adult diabetes

93

What is diabetes?

Diabetes affects 2.3 million people in the UK.

Diabetes is a condition where the blood sugar level is higher than normal.

There are two main types of diabetes.

Type 1 diabetes or insulin-dependent diabetes. It is usually seen in young people. Type 2 diabetes - usually non insulin-dependent diabetes. It tends to affect adults over 40 and

overweight people.

There are also other types of diabetes.

Pregnancy diabetes . This is known as gestational diabetes. It's associated with pregnancy and symptoms usually disappear after the birth. If you get gestational diabetes, you have an increased risk of developing one of the main types of diabetes later in life.

Secondary diabetes. This is when diabetes is caused as the result of another condition, eg inflammation of the pancreas, or by the use of certain medication such as diuretics or steroids (the most common cause).

How common is diabetes?

There are currently 2.3 milion people with diabetes in the UK. However, it's estimated that more than half a million people have the condition but are unaware of it.

The last 30 years has seen a threefold increase in the number of cases of childhood diabetes. This is especially worrying in respect of the rising numbers of children and teenagers with type 2 diabetes, usually only seen in older people, and which reflects obesity levels in young people.

Obesity levels have also risen and this has led to Type 2 diabetes, which is linked to diet, being seen for the first time in young people in Europe and America.

But obesity doesn't explain the increase in the numbers of Type 1 diabetes in children, who make up the majority of new cases.

What causes diabetes?

Term watch

Glucose is sugar. Blood sugar level is the same as blood glucose level.

Insulin is a hormone produced by the pancreas gland in the abdomen. It controls the use of glucose within the body.

The blood sugar level will rise if:

the pancreas produces little or no insulin (Type 1 diabetes) the pancreas produces insulin, but it's inadequate for the body’s needs and its effectiveness is

reduced (Type 2 diabetes).

It's thought Type 2 diabetes is related to factors associated with a Western lifestyle, since it's most common in people who are overweight and who don't get enough exercise.

Gestational diabetes is brought about by the many hormone changes and demands placed upon the body during pregnancy.

Secondary diabetes is much like Type 2 diabetes. It's quite variable, depending on the underlying cause. It can be caused by damage to the pancreas (eg by alcohol), and drugs such as steroids and diuretics can impair insulin secretion from the pancreas.

Common symptoms of diabetes

Glucose is one of the body’s main fuels. If there isn't enough, blood sugar levels rise and glucose is secreted into urine. This causes:

Good advice

If you experience any of these symptoms on a regular basis, see your GP and get tested for diabetes.

increased thirst frequent urination tiredness weight loss, although appetite often increases (especially in Type 1 diabetes) itchiness, especially around the genitals recurrent infections on the skin, eg boils.

People with Type 1 diabetes usually develop these symptoms within days or weeks.

In Type 2 diabetes, these symptoms often don't show for years. Many are diagnosed by chance through routine medical check-ups.

Heredity plays a part in diabetes, but only 10 per cent of people with Type 1 have a family history of diabetes. For Type 2, this rises to 30 per cent.

How is a diagnosis made?

Type 2 traits

People with Type 2 diabetes often have:

a family history of diabetes obesity increased blood pressure premature vascular problems such as heart attacks and stroke raised level of triglyceride (a type of fat) in the blood impotence (erectile dysfunction) .

Glucose levels are measured in blood samples. This is done using the following tests:

random glucose test: glucose levels are taken at a random time on two occasions. Any figure above 11.1mmol/l is a diagnosis of diabetes

fasting glucose test: the glucose level is measured after an overnight fast and on two different days. Above 7.0mmol/l is a diagnosis of diabetes.

You may only need to give one blood sample if you have other symptoms of diabetes.

Glucose tolerance test

If the diagnosis is still unclear from these tests, a glucose tolerance test can be carried out.

A glucose drink is given containing a standard amount of glucose (75g). Blood samples are taken before the drink is given and two hours later. The test is done after an overnight fast.

A two-hour blood glucose level above 11.1mmol/l is a diagnosis of diabetes. A level below 7.8mmol/l is normal.

What if I have IGT?

If you have IGT, you should take similar steps to people with diabetes:

lose weight if you are overweight exercise more stop smoking .

You should also be kept under review and checked at least annually for the development of diabetes.

If the level falls between these values, it suggests a decreased tolerance for glucose.

This is known as impaired glucose tolerance (IGT).

Impaired glucose tolerance is more than just a pre-diabetic state.

People who have IGT are at increased risk of developing some of the conditions associated with diabetes, such as heart disease.

Pregnant women with IGT have an increased risk of miscarriage and stillbirth.

How is diabetes treated?

Diabetes is treated in two ways:

Diet and diabetes

A special diet used to be recommended for diabetes.

It's now thought a normal, well-balanced diet is best.

But calorie intake is still important.

People with diabetes who are overweight need to think of weight loss as part of their treatment.

a combination of healthy diet and exercise medication with tablets and/or insulin.

Insulin injections increase the amount of insulin in your body and bring down the blood sugar level. Insulin injections are used in Type 1 diabetes and in some cases of Type 2.

These can be given once a day as a long-acting insulin, or as shorter-acting injections given more frequently through the day, and can be used in combination with tablet treatment if necessary.

There are different types of oral medication for treating Type 2 diabetes:

some increase the amount of insulin secreted by the pancreas some increase the action of insulin in the body some delay the absorption of glucose from the digestive system some suppress a hormone called glucagon, which is secreted by the pancreas and stops insulin

from working.

Treatment for diabetes depends on the individual.

It starts the first time you give yourself an insulin injection or take a diabetes tablet, and continues through eating a well-balanced diet and starting an exercise programme.

To help you get the most out of treatment, consult your GP or hospital healthcare team, which should include a diabetes nurse specialist.

Blood sugar levels

Monitoring blood sugar levels is an important aspect of treatment, especially in Type 1 diabetes where levels can change markedly.

This can be done easily at home with a small blood glucose meter.

Depending on the reading, you may need to adjust your diet, the amount you exercise or your insulin intake.

Managing diabetes

In the long term, diabetes is monitored through routine check-ups by your doctor and/or annual check-ups at the hospital on an outpatient basis.

Their purpose is to determine if treatment is satisfactory and to look out for any evidence of longer-term complications such as eye or kidney disease.

Tests for these complications are usually done at the annual check-up, while routine check-ups may be carried out every three to six months.

Routine check-ups

Blood sample to check the level of HbA1c (a measure of long-term glucose) in the blood. Evaluation of home glucose readings. Discussion of diet. Blood pressure . Weight check. Other tests and examinations as determined by your doctor.

Annual check-ups

Blood sample to check the amount of HbA1c in the blood. Blood sample to determine the amount of fats in the blood. Blood sample to check kidney function and various salts in the blood (mainly sodium and

potassium). Blood pressure. Urine sample to determine the presence of protein (albuminuria). The appearance of protein

can indicate that the small blood vessels (capillaries) in the kidneys are beginning to be affected by the diabetes.

Foot examination, including a check of various pulse points on the foot to assess circulation, and a check for vibration sensation to determine if there's any neuropathy (nerve damage) to the foot.

Weight check. Measuring the waistline. Discussion of exercise habits. Discussion of smoking habits.

Long-term prospects

Both types of diabetes have the risk of complications.

Acute complications

Low glucose level, caused by treatment with insulin or oral hypoglycaemic drugs that increase insulin secretion from the pancreas.

Diabetic acidosis , a life-threatening condition caused by the lack of insulin.

Late-stage diabetic complications

Retinopathy (eye disease) that can cause blindness. Diabetic kidney disease that can lead to kidney failure. Diabetic neuropathy (nerve disease) that can cause foot ulcers and foot infections.

Atherosclerosis (hardening of the arteries), particularly in smokers and those with high blood pressure and abnormal fat levels in the blood.

Late-stage complications do not usually develop for 10 to 15 years with Type 1 diabetes.

In Type 2 diabetes, however, symptoms can appear close to the time of actual diagnosis because the disease may go undetected for longer.

Many studies now show that good glucose control can significantly reduce or even stop complications. This means keeping the blood sugar level as close to normal as possible.

Recent studies have also confirmed the need for people with diabetes to reduce their risk of atherosclerosis (fatty deposits in your arteries).

This is because if you have Type 2 diabetes, you have a four to five times greater risk of developing serious problems with your circulation that can lead to a heart attack or a stroke.

The main factors that increase your risk are:

smoking high blood pressure raised levels of fats such as cholesterol in the blood.

By taking measures to address these issues, you will reduce your chance of developing complications such as heart disease.

Based on a text by Dr   Jan Erik   Henriksen , Dr   Ole Hother   Nielsen  and Professor   Henning   Beck- Nielsen

Last updated 29.09.2008

http://www.netdoctor.co.uk/diseases/facts/diabetes.htm

What diseases cause secondary diabetes0 comments 2011-10-10 8:57:35 4 views

Diabetes is a common metabolic endocrine disease, the vast majority of primary, genetic tendency, a few other diseases may be due to secondary. Disease and diabetes can lead to many reasons, according to etiology can be divided into the following categories:

(1) pancreatic disease. Such as pancreatitis, pancreatic cancer, pancreatic sections addition, pancreatic injury, deposition of iron (hemochromatosis), congenital defects caused by the pancreas trunk of insulin secretion.

(2) endocrine diseases. As the secretion of hormones antagonistic to insulin caused by excessive secondary diabetes, Cushing's syndrome, acromegaly, pheochromocytoma, tumor glucagon,

somatostatin tumors. In addition, some endocrine and metabolic syndrome, such as primary aldosteronism, hypoparathyroidism, hyperthyroidism, carcinoid syndrome, PRL tumors, may also be secondary to diabetes.

(3) hepatic disease. Glucose metabolism in the liver plays an important role in hepatitis, cirrhosis of the liver can also be secondary to diabetes.

(4) drug-induced. A variety of drugs, chemicals can affect glucose metabolism. Such as thiazide diuretics (hydrochlorothiazide urea thiophene), glucocorticoids (dexamethasone, prednisone, methylprednisolone, etc.), oral contraceptives, tricyclic antidepressants (Miami for the forest to Jiabing imipramine), phenytoin, analgesic antipyretic drugs (aspirin, indomethacin) receptor blockers (propranolol, metoprolol), etc., can cause impaired glucose tolerance.

(5), insulin receptor abnormalities. Congenital abnormalities such as fat, nutrition, women with acanthosis nigricans masculine.

(6) genetic syndrome associated with diabetes. Type 1 glycogen calm, acute intermittent porphyria disease, progeria syndrome.

http://www.toprank365.com/Diabetes/243.html

Causes of Secondary Diabetes Mellitus

Jul 26, 2010 | By Ngozi Oguejiofo

Ngozi Oguejiofo has been writing on a freelance basis since 2009 and most of her writings are focused on health. She is currently a registered nurse. She is interested in teaching, and writes articles focused on student nurses for various online publications.

Photo Credit Diabetic Tools image by painless from Fotolia.com

Diabetes is a condition in which blood glucose levels are high. It's caused by inadequate production of insulin, a hormone that transports blood sugar from the bloodstream to the cells. It can also result from insulin resistance, the body's inability to use insulin effectively. All forms of diabetes are associated with high levels of glucose in the blood. Diabetes is typically classified into Type 1 and Type 2 diabetes. However, diabetes that develops as a result of factors such as disease or hormonal problems is called secondary diabetes.

Diseases of The Pancreas

Insulin is produced by the islets of Langerhans, found in the pancreas. "The Diabetes Answer Book: Practical Answers to More Than 300 Top Questions" by David K. McCulloch says secondary diabetes can happen if the pancreas is destroyed by disease or some other condition. This is because it may not be able to produce enough insulin. Pancreatic problems such as pancreatitis, an inflammation of the pancreas; cystic fibrosis, a genetic disorder that clogs up the pancreas; hemochromatosis, a condition in which there is too much iron in the blood; and surgical removal of the pancreas can lead to secondary diabetes.

Hormonal Disease

Certain hormonal imbalances affect blood glucose levels in the body. Pheochromocytoma is a tumor of the adrenal glands. It makes the adrenal glands release large amounts of a class of hormones called catecholamines. "Textbook of Type 2 Diabetes" by Barry J. Goldstein and Dirk Müller-Wieland suggests that enhanced glucose output, inhibition of insulin secretion and insulin resistance are all effects of catecholamines that can lead to secondary diabetes. Cushing's disease exposes the body to high levels of cortisol, an adrenal hormone. Excessive amounts of cortisol causes insulin resistance and leads to high blood glucose levels.

Acromegaly is a hormonal disorder in which the pituitary gland secretes too much growth hormone. High amounts of growth hormone in the body can eventually lead to insulin resistance and too much glucose in the blood. Other hormonal diseases such as hyperthyroidism can also cause secondary diabetes.

Genetic Diseases

Secondary diabetes can occur in the presence of certain rare genetic disorders. The stiff-person syndrome is a neurological disorder that's characterized by muscle spasms. It's associated with the development of diabetes.

Wolfram's syndrome is a recessive genetic disease that can cause secondary diabetes. Characteristics of this disorder are encapsulated in the acronym DIDMOAD, which stands for diabetes insipidus, diabetes mellitus, optic atrophy and deafness.

Rabson-Mendenhall syndrome is a genetic disease in which there is a mutation in the insulin receptor genes. In this disorder, there is severe insulin resistance, high blood insulin levels and high blood sugar levels.

References

"The Diabetes Answer Book: Practical Answers to More Than 300 Top Questions"; David K. McCulloch; 2008

"Textbook of type 2 diabetes"; Barry J. Goldstein, Dirk Müller-Wieland; 2003 "Nursing Practice: Hospital and Home : The Adult"; Margaret F. Alexander, Josephine N. Fawcett,

Phyllis J. Runciman; 2006 The University of Kansas Hospital: Rabson-Mendenhall Syndrome PubMed: Stiff-person syndrome

Article reviewed by Anton Alden Last updated on: Jul 26, 2010

http://www.livestrong.com/article/185566-causes-of-secondary-diabetes-mellitus/