NUR 521 Exam 2 Study Guide Part 3(Diabetes & thyroid Review)
Module 6: Chapters 48 & 49
Diabetes:
??? Define & differentiate between the different types of diabetes:
Diabetes is primarily a disorder of carbohydrate metabolism. Symptoms mainly result from a deficiency
of insulin or from cellular resistance to insulin's actions. The principal sign of diabetes is sustained
hyperglycemia, which results from impaired glucose uptake by cells and from increased glucose
production. When hyperglycemia develops, it can quickly lead to polyuria, polydipsia, ketonuria, and
weight loss. Over time, hyperglycemia can lead to heart disease, renal failure, blindness, neuropathy,
amputations, impotence, and stroke. There is an often-overlooked point about diabetes: in addition to
affecting carbohydrate metabolism, insulin deficiency disrupts metabolism of proteins and lipids. We
refer to regulation of blood glucose levels as glycemic control.
Type 1 diabetes accounts for approximately 5% of all diabetes cases. In the past, type 1 diabetes
was called juvenile-onset diabetes mellitus or insulin-dependent diabetes mellitus (IDDM). However,
these terms have fallen out of favor because type 2 diabetes is becoming more common in children, and
many people with type 2 diabetes use insulin to manage their diabetes. In general, type 1 diabetes
develops during childhood or adolescence, and symptom onset is relatively abrupt. That being said, type
1 diabetes can develop during adulthood.
The primary defect in type 1 diabetes is destruction of pancreatic β cells—the cells responsible for
insulin synthesis and release into the bloodstream. Insulin levels are reduced early in the disease and
usually fall to zero later. β cell destruction is the result of an autoimmune process (i.e., the patient's
immune system inappropriately wages war against its own β cells). The trigger for this immune
response is not entirely known, but genetic, environmental, and infectious factors likely play a role.
Symptoms of type 2 diabetes usually result from a combination of insulin resistance and impaired insulin
secretion. In contrast to patients with type 1 diabetes, those with type 2 diabetes are capable of insulin
synthesis. In fact, early in the disease, insulin levels tend to be normal or slightly elevated, a state known
as hyperinsulinemia. However, although insulin is still produced, its secretion is no longer tightly coupled
to plasma glucose level: release of insulin is delayed, and peak output is subnormal. More important, the
target tissues of insulin (liver, muscle, adipose tissue) exhibit insulin resistance: for a given blood insulin
level, cells in these tissues are less able to take up and metabolize the glucose available to them. Insulin
resistance appears to result from three causes: reduced binding of insulin to its receptors, reduced
receptor numbers, and reduced receptor responsiveness. Over time, hyperglycemia leads to diminished
,pancreatic β cell function, and hence insulin production and secretion eventually decline as the β cells
work harder to overcome insulin resistance within the tissues.
Although the underlying causes of type 2 diabetes are not entirely known, there is a strong familial
association, suggesting that genetics play a role.
The pathogenesis of type 2 diabetes involves insulin resistance, impaired insulin secretion, and
elevated glucose production by the liver. With insulin resistance, circulating insulin concentrations
increase as compensation. Researchers have hypothesized that in type 2 diabetes, the ability of insulin
to inhibit hepatic glucose production and to stimulate its uptake and use by adipose and muscle cells is
diminished. In lean patients with type 2 diabetes, the primary defect appears to occur in the beta cells.
In overweight patients, who represent most patients with type 2 diabetes, the most likely primary defect
is impairment of the target cells.
Gestational diabetes is defined as diabetes that appears in the pregnant patient during pregnancy and
then subsides rapidly after delivery. Gestational diabetes is managed in much the same manner as any
other diabetic pregnancy: blood glucose should be monitored and then controlled with diet and insulin.
In most cases the diabetic state disappears almost immediately after delivery, permitting discontinuation
of insulin. However, if the diabetic state persists beyond parturition, it is no longer considered
gestational and should be rediagnosed and treated accordingly.
In women taking an oral drug for type 2 diabetes, current practice is to discontinue the oral drug and
switch to insulin. Women who discontinue oral medications during pregnancy can resume oral therapy
after delivery.
Successful management of the diabetic pregnancy remains a challenge. Three factors contribute to the
problem. First, the placenta produces hormones that antagonize insulin's actions. Second, production
of cortisol, a hormone that promotes hyperglycemia, increases threefold during pregnancy. Both
factors increase the body's need for insulin. And third, because glucose can pass freely from the
maternal circulation to the fetal circulation, hyperglycemia in the mother will stimulate excessive
secretion of insulin in the fetus. The resultant hyperinsulinism can have multiple adverse effects on the
fetus.
, Successful management of diabetes during pregnancy demands that proper glucose levels be
maintained in both the mother and fetus; failure to do so may be teratogenic or may otherwise harm
the fetus. Achieving glucose control requires diligence on the part of the mother and her prescriber.
Some experts on diabetes in pregnancy advise that blood glucose levels must be monitored six to
seven times a day. Insulin dosage and food intake must be adjusted accordingly.
Diagnostic Criteria:
Diagnosis of diabetes was once made solely by measuring blood levels of glucose. However, hemoglobin
A1c—a test that provides an estimate of glycemic control over the previous 2 to 3 months is now
considered a standard test as well.
What is the screening criteria for prediabetes and diabetes in adults, children, and adolescents???
, Level of Evidence:
Module 6: Chapters 48 & 49
Diabetes:
??? Define & differentiate between the different types of diabetes:
Diabetes is primarily a disorder of carbohydrate metabolism. Symptoms mainly result from a deficiency
of insulin or from cellular resistance to insulin's actions. The principal sign of diabetes is sustained
hyperglycemia, which results from impaired glucose uptake by cells and from increased glucose
production. When hyperglycemia develops, it can quickly lead to polyuria, polydipsia, ketonuria, and
weight loss. Over time, hyperglycemia can lead to heart disease, renal failure, blindness, neuropathy,
amputations, impotence, and stroke. There is an often-overlooked point about diabetes: in addition to
affecting carbohydrate metabolism, insulin deficiency disrupts metabolism of proteins and lipids. We
refer to regulation of blood glucose levels as glycemic control.
Type 1 diabetes accounts for approximately 5% of all diabetes cases. In the past, type 1 diabetes
was called juvenile-onset diabetes mellitus or insulin-dependent diabetes mellitus (IDDM). However,
these terms have fallen out of favor because type 2 diabetes is becoming more common in children, and
many people with type 2 diabetes use insulin to manage their diabetes. In general, type 1 diabetes
develops during childhood or adolescence, and symptom onset is relatively abrupt. That being said, type
1 diabetes can develop during adulthood.
The primary defect in type 1 diabetes is destruction of pancreatic β cells—the cells responsible for
insulin synthesis and release into the bloodstream. Insulin levels are reduced early in the disease and
usually fall to zero later. β cell destruction is the result of an autoimmune process (i.e., the patient's
immune system inappropriately wages war against its own β cells). The trigger for this immune
response is not entirely known, but genetic, environmental, and infectious factors likely play a role.
Symptoms of type 2 diabetes usually result from a combination of insulin resistance and impaired insulin
secretion. In contrast to patients with type 1 diabetes, those with type 2 diabetes are capable of insulin
synthesis. In fact, early in the disease, insulin levels tend to be normal or slightly elevated, a state known
as hyperinsulinemia. However, although insulin is still produced, its secretion is no longer tightly coupled
to plasma glucose level: release of insulin is delayed, and peak output is subnormal. More important, the
target tissues of insulin (liver, muscle, adipose tissue) exhibit insulin resistance: for a given blood insulin
level, cells in these tissues are less able to take up and metabolize the glucose available to them. Insulin
resistance appears to result from three causes: reduced binding of insulin to its receptors, reduced
receptor numbers, and reduced receptor responsiveness. Over time, hyperglycemia leads to diminished
,pancreatic β cell function, and hence insulin production and secretion eventually decline as the β cells
work harder to overcome insulin resistance within the tissues.
Although the underlying causes of type 2 diabetes are not entirely known, there is a strong familial
association, suggesting that genetics play a role.
The pathogenesis of type 2 diabetes involves insulin resistance, impaired insulin secretion, and
elevated glucose production by the liver. With insulin resistance, circulating insulin concentrations
increase as compensation. Researchers have hypothesized that in type 2 diabetes, the ability of insulin
to inhibit hepatic glucose production and to stimulate its uptake and use by adipose and muscle cells is
diminished. In lean patients with type 2 diabetes, the primary defect appears to occur in the beta cells.
In overweight patients, who represent most patients with type 2 diabetes, the most likely primary defect
is impairment of the target cells.
Gestational diabetes is defined as diabetes that appears in the pregnant patient during pregnancy and
then subsides rapidly after delivery. Gestational diabetes is managed in much the same manner as any
other diabetic pregnancy: blood glucose should be monitored and then controlled with diet and insulin.
In most cases the diabetic state disappears almost immediately after delivery, permitting discontinuation
of insulin. However, if the diabetic state persists beyond parturition, it is no longer considered
gestational and should be rediagnosed and treated accordingly.
In women taking an oral drug for type 2 diabetes, current practice is to discontinue the oral drug and
switch to insulin. Women who discontinue oral medications during pregnancy can resume oral therapy
after delivery.
Successful management of the diabetic pregnancy remains a challenge. Three factors contribute to the
problem. First, the placenta produces hormones that antagonize insulin's actions. Second, production
of cortisol, a hormone that promotes hyperglycemia, increases threefold during pregnancy. Both
factors increase the body's need for insulin. And third, because glucose can pass freely from the
maternal circulation to the fetal circulation, hyperglycemia in the mother will stimulate excessive
secretion of insulin in the fetus. The resultant hyperinsulinism can have multiple adverse effects on the
fetus.
, Successful management of diabetes during pregnancy demands that proper glucose levels be
maintained in both the mother and fetus; failure to do so may be teratogenic or may otherwise harm
the fetus. Achieving glucose control requires diligence on the part of the mother and her prescriber.
Some experts on diabetes in pregnancy advise that blood glucose levels must be monitored six to
seven times a day. Insulin dosage and food intake must be adjusted accordingly.
Diagnostic Criteria:
Diagnosis of diabetes was once made solely by measuring blood levels of glucose. However, hemoglobin
A1c—a test that provides an estimate of glycemic control over the previous 2 to 3 months is now
considered a standard test as well.
What is the screening criteria for prediabetes and diabetes in adults, children, and adolescents???
, Level of Evidence:
