The American Journal of Medicines
Added on 2022-09-18
11 Pages2436 Words24 Views
Running head: EDUCATIONAL BOOKLET
Educational Booklet
Name of the Student
Name of the University
Author Note
Educational Booklet
Name of the Student
Name of the University
Author Note
EDUCATIONAL BOOKLET 1
Introduction
Sulfonylureas is an anti-diabetic drug that is used for the treatment of Type 2 Diabetes
Mellitus (T2DM) among the older adults. Despite the presence of the large number of the
anti-diabetic drug in the market, sulfonylureas are regarded as one of the potent drug for the
treatment of T2DM (Kalra et al., 2018). The following educational booklet will highlight the
pathophysiology of T2DM followed by the mode of action of this medication in order to
overcome hyperglycaemic condition of T2DM in relation to the disease pathophysiology. The
educational booklet will also provide necessary details about the medication side-effects,
interactions, contradictions and implications.
Pathophysiology of the disorder: Type 2 Diabetes Mellitus (T2DM)
Normal Pathophysiology of T2DM
Impaired secretion of insulin and development of resistance towards insulin contribute
to development of the complex pathological condition of T2DM. Impaired insulin secretion
leads to decrease in the glucose responsiveness. Impaired glucose tolerance (IGT) is mainly
induced through decrease in the level of glucose-responsive during the early phase of the
insulin secretion and decrease in the additional insulin secretion that is produced after meals
(Postprandial hyperglycemia) (Zaccardi et al., 2016). Impaired insulin secretion is
progressive condition and this leads to the development of glucose toxicity and lipo-toxicity.
Insulin resistance is defined as a condition under which the insulin fails to exert the sufficient
action that is proportional to the amount of glucose present in the blood. Insulin resistance
and high glucose concentration hamper several organs like liver, kidneys and muscles. The
development of insulin resistance is multifactorial as it has both genetic and environmental
influence. The dysfunction of the beta-cells of the Islet of Langerhans present in the pancreas
leads to inappropriate secretion of insulin in response to glucose and thus developing
Introduction
Sulfonylureas is an anti-diabetic drug that is used for the treatment of Type 2 Diabetes
Mellitus (T2DM) among the older adults. Despite the presence of the large number of the
anti-diabetic drug in the market, sulfonylureas are regarded as one of the potent drug for the
treatment of T2DM (Kalra et al., 2018). The following educational booklet will highlight the
pathophysiology of T2DM followed by the mode of action of this medication in order to
overcome hyperglycaemic condition of T2DM in relation to the disease pathophysiology. The
educational booklet will also provide necessary details about the medication side-effects,
interactions, contradictions and implications.
Pathophysiology of the disorder: Type 2 Diabetes Mellitus (T2DM)
Normal Pathophysiology of T2DM
Impaired secretion of insulin and development of resistance towards insulin contribute
to development of the complex pathological condition of T2DM. Impaired insulin secretion
leads to decrease in the glucose responsiveness. Impaired glucose tolerance (IGT) is mainly
induced through decrease in the level of glucose-responsive during the early phase of the
insulin secretion and decrease in the additional insulin secretion that is produced after meals
(Postprandial hyperglycemia) (Zaccardi et al., 2016). Impaired insulin secretion is
progressive condition and this leads to the development of glucose toxicity and lipo-toxicity.
Insulin resistance is defined as a condition under which the insulin fails to exert the sufficient
action that is proportional to the amount of glucose present in the blood. Insulin resistance
and high glucose concentration hamper several organs like liver, kidneys and muscles. The
development of insulin resistance is multifactorial as it has both genetic and environmental
influence. The dysfunction of the beta-cells of the Islet of Langerhans present in the pancreas
leads to inappropriate secretion of insulin in response to glucose and thus developing
EDUCATIONAL BOOKLET 2
hyperglycaemic condition. Presence of obesity along with visceral adiposity for a prolong
period of time increase the level of internal inflammation and this in turn creates de-
sensitization by hampering the sensitivity of the glucose-re-uptake receptors and thereby
developing insulin resistance even under the high concentration of glucose in the blood and
insulin in the plasma. Other factors that promote insulin resistance and subsequent generation
of insulin resistance include presence of ectopic fat storage syndrome, presence of high
adipose tissues in the endocrine organs and high concentration of the non-esterified fatty
acids (Zaccardi et al., 2016).
Dysfunction of pancreatic beta cell
Chronic insulin resistance is regarded as the main pathophysiology of T2DM (Shehata
et al., 2017). Chronic insulin resistance develops when the pancreatic beta cells are unable to
produce insulin to compensate the glucose content in the blood (Shehata et al., 2017). The
worsening of the T2DM condition occurs due to dysfunction of the pancreatic beta cells to
produce insulin followed by the development of insulin resistance in the body under the
action of the Pancreatic Derived Factor (PANDER). Thus insulin resistance, the hepatic cell
fails to re-uptake glucose from the blood leading to the development of T2DM (Shehata et
al., 2017).
PANDER is a 235 amino-acid protein. It is secreted from the pancreatic beta and
alpha cells (MarElia et al., 2018). This protein is involved in regulating the secretary process
of insulin and glucose homeostasis (MarElia et al., 2018). Under hypergycemic action, the
PANDER protein involves negative action on the Islet cells and thus reducing the insulin
secretion and increasing the hyperglycaemic condition further. The concentration of
PANDER is elevated as highlighted in the serum of the diabetic patients and thus it is
concluded that beta-cell dysfunction play an important role in the glycemic control of the
diabetic patient. In obese adolescents, the dysfunction of beta cells plays an importance role
hyperglycaemic condition. Presence of obesity along with visceral adiposity for a prolong
period of time increase the level of internal inflammation and this in turn creates de-
sensitization by hampering the sensitivity of the glucose-re-uptake receptors and thereby
developing insulin resistance even under the high concentration of glucose in the blood and
insulin in the plasma. Other factors that promote insulin resistance and subsequent generation
of insulin resistance include presence of ectopic fat storage syndrome, presence of high
adipose tissues in the endocrine organs and high concentration of the non-esterified fatty
acids (Zaccardi et al., 2016).
Dysfunction of pancreatic beta cell
Chronic insulin resistance is regarded as the main pathophysiology of T2DM (Shehata
et al., 2017). Chronic insulin resistance develops when the pancreatic beta cells are unable to
produce insulin to compensate the glucose content in the blood (Shehata et al., 2017). The
worsening of the T2DM condition occurs due to dysfunction of the pancreatic beta cells to
produce insulin followed by the development of insulin resistance in the body under the
action of the Pancreatic Derived Factor (PANDER). Thus insulin resistance, the hepatic cell
fails to re-uptake glucose from the blood leading to the development of T2DM (Shehata et
al., 2017).
PANDER is a 235 amino-acid protein. It is secreted from the pancreatic beta and
alpha cells (MarElia et al., 2018). This protein is involved in regulating the secretary process
of insulin and glucose homeostasis (MarElia et al., 2018). Under hypergycemic action, the
PANDER protein involves negative action on the Islet cells and thus reducing the insulin
secretion and increasing the hyperglycaemic condition further. The concentration of
PANDER is elevated as highlighted in the serum of the diabetic patients and thus it is
concluded that beta-cell dysfunction play an important role in the glycemic control of the
diabetic patient. In obese adolescents, the dysfunction of beta cells plays an importance role
EDUCATIONAL BOOKLET 3
in predicting the disease progression during the later stages of life (MarElia et al., 2018).
Ageing is also associated with the development of the beta-cell dysfunction and thus the
chances of developing Type 2 Diabetes mellitus are higher among the older adults (MarElia
et al., 2018).
Drug therapies
Sulfonylureas were discovered during 1942. Carbutamide is regarded as first
sulfonylurea that was used for the treatment of T2DM. However due to its adverse effects
over the bone marrow, it was withdrawn from the market. Sulfonylureas are classified into
two generation drugs. Glibenclamide, gluclazide, glimepiride and glipizide are the second
generation drugs. The first generation drug, tolbutamide and chlorpropamide are no longer
used. The second generation drugs are all equally potent towards reducing the concentration
of blood glucose however, there are differences in the rate of absorption, dosing and
metabolism.
in predicting the disease progression during the later stages of life (MarElia et al., 2018).
Ageing is also associated with the development of the beta-cell dysfunction and thus the
chances of developing Type 2 Diabetes mellitus are higher among the older adults (MarElia
et al., 2018).
Drug therapies
Sulfonylureas were discovered during 1942. Carbutamide is regarded as first
sulfonylurea that was used for the treatment of T2DM. However due to its adverse effects
over the bone marrow, it was withdrawn from the market. Sulfonylureas are classified into
two generation drugs. Glibenclamide, gluclazide, glimepiride and glipizide are the second
generation drugs. The first generation drug, tolbutamide and chlorpropamide are no longer
used. The second generation drugs are all equally potent towards reducing the concentration
of blood glucose however, there are differences in the rate of absorption, dosing and
metabolism.
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