part 1 contd
PATHOGENESIS
The pathogenesis of each type of Diabetes mellitus is different and discussed separately.
TYPE 1: This type of DM is characterized by an absolute lack of insulin, which is why patient always wants insulin. It is previously called as IDDM. The absolute lack of insulin is due to the beta cell destruction. There are three main mechanisms responsible for beta cell destruction that is genetic susceptibility, autoimmunity, and environment insult. These factors of genetic predisposition and environmental insult causes unnecessary immune response against normal functioning beta cells. This immune response triggers the auto immunity, which causes beta cell destruction. When complete destruction of beta cells occurs, no insulin secretion occurs in the bloodstream that causes type 1 Diabetes mellitus.
TYPE 2: Type 2 Diabetes mellitus is characterized by decrease in beta cell secretion of insulin or a decrease response of the tissues to respond to insulin, i.e. insulin resistance. The main factor involved in the pathogenesis of type 2 Diabetes mellitus is environmental factor. Obesity is one of the most important cause although genetic predisposition is also important which causes deranged insulin secretion and cause hyperglycemia. This hyperglycemia causes ß cell exhaustion and decrease in insulin secretion. Other metabolic disturbances cause reduced responsiveness of tissues to insulin action called as insulin resistance. It is a major factor in the development of type 2 Diabetes mellitus.
Gestational Diabetes mellitus (GDM): GDM is a prodromal form of type 2 DM being unmarked by pregnancy. Pregnancy is associated with insulin resistance that necessitates an increase in insulin production to maintain euglycemia (a normal insulin concentration of glucose in blood). Placental hormones that rise late in pregnancy induce the insulin resistance in GDM. Gestational Diabetes mellitus itself is typically found late in the second or early third trimester. Some studies suggest that there is an exaggeration of the pregnancy induced insulin resistance in GDM, but it appears that the major determinant of whether a woman develops DM is likely insulin reserve. This reserve is blunted in women with GDM. In severe GDM an element of glucose toxicity supervenes which may further blunt the insulin sensitivity. The elevated free acids that are also found in GDM may be a further cause of insulin resistance as may be a manifestation of the disease process itself. Thus, GDM is similar to type 2 DM with insulin resistance and impaired insulin secretion, and persistence of these abnormalities postpartum contributes to the increased risk of type 2 DM in the long term.
DIAGNOSIS
New revised criteria for the diagnosis of DM from the expert panel of WHO and National Diabetes Data Group emphasize the FPG as the most reliable and convenient test for diagnosing Diabetes mellitus in asymptomatic individual.
Glucose tolerance is classified in to three categories based on the FPG
• FPG < 110 mg/dl is considered as normal
• FPG = 110 mg/dl but < 126 mg/dl is defined as IFG (Impaired Fasting Glucose)
• FPG = 126 confirm the diagnosis of DM
IFG is a new diagnostic category analogous to IGT, which is defined as the plasma glucose level between 140mg/dl and 200mg/dl, 2 hour after a 75gm oral glucose load.
A random plasma glucose concentration = 200 accompanied by classic symptoms of Diabetes mellitus, for example polydipsia (increased thirst), polyuria (increased micturation), polyphagia (increased appetite), weight loss is sufficient for the diagnosis of DM.
The two-hour plasma glucose commonly referred to post parendial is still a valid mechanism for diagnosing DM but is not recommended as a part of routine screening.
CLINICAL FEATURES
contd in part 3
by Dr. Abhishek Pandey
PATHOGENESIS
The pathogenesis of each type of Diabetes mellitus is different and discussed separately.
TYPE 1: This type of DM is characterized by an absolute lack of insulin, which is why patient always wants insulin. It is previously called as IDDM. The absolute lack of insulin is due to the beta cell destruction. There are three main mechanisms responsible for beta cell destruction that is genetic susceptibility, autoimmunity, and environment insult. These factors of genetic predisposition and environmental insult causes unnecessary immune response against normal functioning beta cells. This immune response triggers the auto immunity, which causes beta cell destruction. When complete destruction of beta cells occurs, no insulin secretion occurs in the bloodstream that causes type 1 Diabetes mellitus.
TYPE 2: Type 2 Diabetes mellitus is characterized by decrease in beta cell secretion of insulin or a decrease response of the tissues to respond to insulin, i.e. insulin resistance. The main factor involved in the pathogenesis of type 2 Diabetes mellitus is environmental factor. Obesity is one of the most important cause although genetic predisposition is also important which causes deranged insulin secretion and cause hyperglycemia. This hyperglycemia causes ß cell exhaustion and decrease in insulin secretion. Other metabolic disturbances cause reduced responsiveness of tissues to insulin action called as insulin resistance. It is a major factor in the development of type 2 Diabetes mellitus.
Gestational Diabetes mellitus (GDM): GDM is a prodromal form of type 2 DM being unmarked by pregnancy. Pregnancy is associated with insulin resistance that necessitates an increase in insulin production to maintain euglycemia (a normal insulin concentration of glucose in blood). Placental hormones that rise late in pregnancy induce the insulin resistance in GDM. Gestational Diabetes mellitus itself is typically found late in the second or early third trimester. Some studies suggest that there is an exaggeration of the pregnancy induced insulin resistance in GDM, but it appears that the major determinant of whether a woman develops DM is likely insulin reserve. This reserve is blunted in women with GDM. In severe GDM an element of glucose toxicity supervenes which may further blunt the insulin sensitivity. The elevated free acids that are also found in GDM may be a further cause of insulin resistance as may be a manifestation of the disease process itself. Thus, GDM is similar to type 2 DM with insulin resistance and impaired insulin secretion, and persistence of these abnormalities postpartum contributes to the increased risk of type 2 DM in the long term.
DIAGNOSIS
New revised criteria for the diagnosis of DM from the expert panel of WHO and National Diabetes Data Group emphasize the FPG as the most reliable and convenient test for diagnosing Diabetes mellitus in asymptomatic individual.
Glucose tolerance is classified in to three categories based on the FPG
• FPG < 110 mg/dl is considered as normal
• FPG = 110 mg/dl but < 126 mg/dl is defined as IFG (Impaired Fasting Glucose)
• FPG = 126 confirm the diagnosis of DM
IFG is a new diagnostic category analogous to IGT, which is defined as the plasma glucose level between 140mg/dl and 200mg/dl, 2 hour after a 75gm oral glucose load.
A random plasma glucose concentration = 200 accompanied by classic symptoms of Diabetes mellitus, for example polydipsia (increased thirst), polyuria (increased micturation), polyphagia (increased appetite), weight loss is sufficient for the diagnosis of DM.
The two-hour plasma glucose commonly referred to post parendial is still a valid mechanism for diagnosing DM but is not recommended as a part of routine screening.
CLINICAL FEATURES
| Type 1 DM | Type 2 DM |
| Increased thirst Increased micturation Weight loss in spite of Increased/normal appetite Fatigueness Nausea Vomiting | Increased thirst Increased micturation Increased appetite Blurred vision Slow healing infections Fatigueness Impotency in men |
contd in part 3
by Dr. Abhishek Pandey
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