Page 902 - Cardiac Nursing

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878 PA R T V / Health Promotion and Disease Prevention
Another group of newly discovered intestinal hormones, the in- triggers the autoimmune attack against the pancreas, but several
cretins, are also released in response to nutrient ingestion. The in- agents are suspected. 15 Viral triggers such as enteroviruses, cox-
cretins include glucose-dependent insulin-releasing peptide (GIP) sackie virus B, congenital rubella, cytomegalovirus, and mumps
and glucagon-like peptide-1 (GLP-1). GIP is secreted by the K are suspected culprits. However, these agents are only theorized
cells of the upper intestine and GLP-1 is released from the L cells to initiate the autoimmunity of type 1 diabetes, and research on
of the intestine. 13 Both are secreted in response to postmeal glu- causation is ongoing. From a prevention perspective, it appears
cose elevations and stimulate -cell insulin secretion. In addition that children who are breastfed are less likely to develop type 1
to increasing glucose-dependent insulin secretion, incretin hor- diabetes. 13
mones inhibit glucagon secretion, slow gastric emptying, and in- When 90% of the pancreas is destroyed, there is no longer
crease feelings of satiety. Incretins help to keep postmeal blood enough insulin available to maintain euglycemia and the symp-
glucose levels within normal ranges. Both GIP and GLP-1 are toms of hyperglycemia are expressed. The rate of destruction of
rapidly degraded by the enzyme dipeptidyl-peptidase-inhibitor- the -cell mass with type 1 diabetes is rapid in youth and more
IV. (New therapies that imitate the incretins and inhibit their gradual in the older age group. 13 Although the destruction of the
breakdown will be discussed in the section “Medication for Type -cells is progressive, the onset of type 1 diabetes is usually
2 Diabetes.”) People with type 1 diabetes make normal amounts abrupt. With only 10% of the pancreas working, there is no
of the incretins, while those with type 2 secrete less of this power- longer adequate insulin to maintain euglycemia. Without suffi-
ful glucose-lowering hormone. 13 cient insulin to utilize glucose for energy, the body starts break-
Four to 16 hours after eating, the body enters the phase II or ing down fat stores for fuel. The pace of this fat breakdown and
the postabsorptive state. This phase most often occurs during resulting ketone bodies overwhelms the liver and, in a short
sleep and marks the end of anabolism or energy storage and be- time, it can no longer clear ketones at a fast enough pace. High
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gins the phase of catabolism or energy production. During this levels of circulating ketones result in ketosis and acidosis⎯also
phase, since the body is not exposed to food, it must revert to called diabetes ketoacidosis. At this point, the body cells are
stored energy for fuel. Glucagon levels rise and insulin levels de- starved for glucose and the person usually feels ill enough to seek
crease to a steady state, often termed basal insulin release. The medical help. Depending on the duration and severity of keto-
main function of insulin during this phase is not to promote en- sis, the person with a new case of type 1 diabetes appears mal-
ergy storage, but to prevent hyperglycemia. The high levels of cir- nourished due to inability to store fuel, dehydrated due to
culating glucagon increase the breakdown of glycogen stores in osmotic diuresis, and may have abdominal pain and nausea from
the liver (glycogenolysis) to ensure an adequate supply of glucose the ketone bodies. In an effort to blow off excess acids, the per-
to the brain and other glucose-dependent tissues. In addition, fat son may have rapid respirations and a their breath may smell
cells (adipocytes) break down triglycerides and release free fatty fruity. Treatment includes fluids, insulin, electrolyte replace-
acids (FFAs) to be used as energy by the liver and skeletal muscles. ment, and patient and family education. Clinical presentation is
The brain will only use glucose for fuel due to its inability to use usually enough to make a diagnosis of type 1 diabetes. If unsure,
FFAs as fuel. Many individuals with type 2 diabetes experience a diagnosis can be confirmed by antibody blood tests. Some tests
morning fasting hyperglycemia due to the dominance of glycogen used to confirm autoimmune -cell destruction include anti-
and the relative lack of insulin during this phase. 13 bodies to glutamic acid decarboxylase, islet cell autoantibodies,
In addition to glucagon, there are other catabolic hormones and insulin autoantibodies. 15 Patients with type 1 diabetes will
that increase the breakdown of stored fuel supplies and increase require insulin replacement for the rest of their lives. There is
circulating glucose. They increase insulin resistance and glycogen ongoing investigation to evaluate if type 1 diabetes can be pre-
breakdown, causing a net increase in blood glucose levels. The hor- vented or delayed in individuals at high risk of developing type
mones released from the kidney, corticosteroids and epinephrine, 1 diabetes. To date however, large, randomized clinical trials
are activated during flight-or-fight response or hypoglycemia. have failed to demonstrate treatment effect. 16,17 These studies
Other hormones including growth hormone and cortisol increase have improved the understanding of the immunopathogenesis
insulin resistance in early morning, causing many people with type and will hopefully lead to future strategies and treatments to
1 diabetes to experience the “dawn” phenomena, or an elevation in prevent type 1 diabetes.
morning glucose. 14
Glucose homeostasis is reliant on a complex interrelationship Type 2 Diabetes Mellitus
of hormones that activate anabolic and catabolic processes. When
this precise balance is disrupted through the loss or dysfunction of Unlike type 1 diabetes, type 2 diabetes (formerly referred to as
insulin and other hormones, the end result is hyperglycemia. adult onset or non-insulin-dependent diabetes) is not an autoim-
mune condition. Of all people with diabetes, 90% to 95% have
Type 1 Diabetes Mellitus type 2. Most people with type 2 diabetes are overweight and de-
velop hyperglycemia as a result of insulin resistance and insulin
Previously labeled “juvenile diabetes” or “insulin-dependent dia- deficiency. Besides being overweight, some of the risk factors for
betes,” type 1 diabetes affects approximately 10% of all people developing type 2 diabetes include physical inactivity, first-degree
6
with diabetes. The unique feature of type 1 is its’ progressive au- relative with diabetes, women who delivered a baby bigger than
toimmunity resulting in complete destruction of the pancreatic 9 lb (4.2 kg), or who had gestational diabetes. Other risk factors
-cells. Although it can occur at any age, most new cases are include hypertension, impaired glucose tolerance, elevated triglyc-
expressed during childhood and puberty, when insulin-resistant erides, and other conditions associated with insulin resistance. 11
pubertal hormones are at their peak. To express type 1 diabetes, In addition to these risk factors, the social milieu into which a
a genetic propensity and an environmental trigger are neces- person is born can also increase or decrease the likelihood of the
sary. 13 Research has not identified any one causative agent that expression of type 2 diabetes. Social research reveals that people of