Image Source: Diabetes mellitus Checker
Definition:-Diabetes is a chronic disease, which occurs when the pancreas is (located the stomach in the upper left abdomen) does not produce enough insulin, or when the body cannot effectively use insulin produces.
This leads to an increased concentration of glucose in the blood.
Diabetes demographics and statistics:-
»347 million people worldwide have diabetes
»In 2012 an expected 1.5 million deaths were directly caused by diabetes.
»More than 80% of deaths occur in low –and middle – income countries.
»Diabetes increases the risk of heart diseases and stroke.
»50% of people with diabetes die of cardiovascular disease (primarily heat disease and stroke)
»WHO project that diabetes will be 7th primary cause of death in 2030.
Signs and symptoms:-
∗crave extra liquids
∗numbness and tingling of feet
∗unexplained weight loss
∗frequent vaginal infections
∗Poor wound healing.
»Hypoglycemia and ketoacidosis
»Infections (especially fungal infections of skin and mucous membranes, urinary infections, mycobacterial infections, anaerobic infections of deep tissues)
»Atherosclerosis, manifesting in cerebrovascular and coronary artery disease
»Diabetic eye disease( Retinopathy, cataract)
»it is Diabetic kidney disease
»infections and Foot ulceration.
»High blood pressure
»Elevated serum cholesterol
Classification of DM:-
»Insulin dependent diabetes mellitus (IDDM),type-1,juvenile or childhood – onset
»Non-insulin dependent diabetes mellitus NIDDM, type-2 or adult-onset.
»Malnutrition related diabetes (MRD)
»Gestational diabetes mellitus.
Differences between type 1 and type 2 diabetes:-
Insulin dependent diabetes mellitus (IDDM), type-1, juvenile or childhood – onset:-
Type 1:-Type 1 diabetes mellitus is typically characterized by an absolute insulin deficiency attributed to an autoimmune destruction of the
β- cells of the islets of Langerhans. Affected persons will have autoantibodies to glutamic acid decarboxylase, pancreatic islet β-cells, and/
or insulin.T1DM can be diagnosed at any stage, but is most likely to be diagnosed prior to the age of 30 years.
Non-insulin dependent diabetes mellitus NIDDM, type-2 or adult-onset:-
Type 2:- Type 2 diabetes mellitus is the most common form of DM and is typically identified in persons over the age of 30 years; conversely, it has become a more prominent diagnosis in adolescents of assured ethnic origins (eg :- African American, Hispanic).
Those diagnosed with T2DM are characteristically overheavy or obese, have a positive family history of diabetes, and/or exhibit signs of insulin confrontation autoantibodies found in T1DM are absent in T2DM.
Gestational diabetes mellitus:-
Gestational diabetes mellitus (GDM) is a disorder in which women main exhibit levels of elevated plasma glucose during pregnancy.
Women before diagnosed with diabetes prior to pregnancy are excluded from this classification. After pregnancy, the diagnostic classification of May Gestational diabetes mellitus is changed based on postpartum testing.
PATHOPHYSIOLOGY OF THE DIABETIC STATE:-
»Normal glucose regulation involves many factors including insulin, counter regulatory hormones, in cretin hormones, and amylin. Changes to any of these factors may result in an imbalance in glucose levels.
»Promotes the cellular uptake of plasma glucose
»Excites conversion of glucose into energy storage molecules (e.g., glycogen, fat) in the liver, muscles, and adipose cells.
»Facilitates cellular uptake of amino acids and their incorporation into proteins.
»Prevents production of glucose from liver, muscle glycogen, or amino acids.
Counter regulatory hormones:-
Counter regulatory hormones in diabetes are hormones that work against insulin. Thus, where Insulin lowers blood glucose; counter regulatory hormones increase blood glucose. The counter regulatory Hormones include:
»Catecholamines (Epinephrine and Norepinephrine)
Incretion hormones:-Consumed glucose encourages a more quick release of insulin from the pancreas than when glucose is given by intravenous injection.
This occurs because the incretin hormones, gastric inhibitory peptide and glucagon-like peptide-1 are secreted by the intestines in response to glucose ingestion, before the glucose is absorbed.
Postprandial excretion of GLP-1 is diminished in DM, whereas GIP secretion is normal or increased. Actions of GLP-1 include:
»Increases glucose-dependent insulin secretion
»Inhibits inappropriate glucagon secretion
»Increases β-cell growth/replication
»Slows gastric emptying Suppresses appetite.
is a hormone that is consecrated with insulin from the pancreatic β-cells. Hence, in individuals with T1DM, little to no amylin is produced, whereas in T2DM, amylin is produced, but in an insufficient quantity.
Amylin reduces postprandial blood glucose levels by the following actions:
»Prolongs gastric emptying time
»Decreases postprandial glucagon secretion
Development of diabetes:-
T1DM:-Genetic predisposition, environmental factors, and autoimmunity have been proposed as Causes that lead to progressive β-cell dysfunction and eventually, overt diabetes mellitus.
T1DM is the result of immune-mediated destruction of the β-cells and is characterized by the abrupt onset of clinical signs and symptoms.
Environmental triggers such as viral (e.g., rubella, Coxsackie B), chemical, or dietary (e.g. cow’s milk) have been suspected in the development of T1DM.
An autoimmune component, possibly triggered by an environmental factor, is involved in the development of T1DM.
Anti-insulin or anti β-cell antibodies are present in the blood of most individuals at the time of diagnosis of T1DM.
Antibodies to glutamic acid decarboxylase (GAD) are found in the blood of approximately 70% of individuals diagnosed with T1DM.
Thus, the presence of these antibodies may serve as an immunologic predictor of the future development of the disease.
T2DM. Genetic factors, a β-cell defect, and peripheral site defects have been implicated.
»Genetics:- There is greater than a 90% concordance rate in identical twins if one has T2DM, suggesting that the development of T2DM is predominately dependent on genetics.
The risk of off spring development of T2DM is at least 15%.
»A primary β–cell dysfunction has been postulated in the development of T2DM because at diagnosis, typically only about 50% of β-cells are functioning.
The number of functioning nβ-cells continues to decline with duration of the disease.
»A peripheral site defect may also contribute to the expression of T2DM. Faults in marker receptor compulsory or a reduced number of insulin receptors can prime to hyperglycemia.
Secondary diabetes may increase from other conditions (e.g., Cushing syndrome, acromegaly, cystic fibrosis, down syndrome, pancreatic disorders) or treatments (e.g. Antipsychotics ,Glucocorticoids).
NIDDM shows strong family aggregation:-
»Twin studies and familial studies have provided firm evidence that role of genetic factors is relatively high
»Till now, no specific genetic marker has been identified, though some have been proposed
»With current status of knowledge, it seems that diabetes is a “polygenic” disease and not possibly due to defect in a single gene
»History of diabetes among parents, grandparents and first degree relatives predisposes a person to high risk of developing diabetes.
Age, sex and race:-
-Increasing age increases risk
-Most cases are detected during middle age
Sex: -There is no clear difference between sexes as regards risk of diabetes
Race: Some races are known to be at high risk as Polynesians, Eskimos, Pima, Indians, etc.
-Possibility is also strong that South Asian populations including Indians may be at high risk.
If you have any questions and complaints and more information for consult your “Family Doctor” or “Personal “Doctor”.
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