Pathophysiology

Type 2 diabetes is characterized by a combination of peripheral insulin resistance and inadequate insulin
secretion by pancreatic beta cells. Insulin resistance, which has been attributed to elevated levels of free
fatty acids and proinflammatory cytokines in plasma, leads to decreased glucose transport into muscle
cells, elevated hepatic glucose production, and increased breakdown of fat.
role for e!cess glucagon cannot be underestimated" indeed, type 2 diabetes is an islet paracrinopathy
in which the reciprocal relationship between the glucagon#secreting alpha cell and the insulin#secreting
beta cell is lost, leading to hyperglucagonemia and hence the consequent hyperglycemia.
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'or type 2 diabetes mellitus to occur, both insulin resistance and inadequate insulin secretion must e!ist.
'or e!ample, all overweight individuals have insulin resistance, but diabetes develops only in those who
cannot increase insulin secretion sufficiently to compensate for their insulin resistance. Their insulin
concentrations may be high, yet inappropriately low for the level of glycemia.
simplified scheme for the pathophysiology of abnormal glucose metabolism in type 2 diabetes mellitus
is depicted in the image below.
(implified scheme for the pathophysiology of type 2 diabetes mellitus.
)ith prolonged diabetes, atrophy of the pancreas may occur. study by Philippe et al used computed
tomography *+T, scan findings, glucagon stimulation test results, and fecal elastase#% measurements to
confirm reduced pancreatic volume in individuals with a median %-#year history of diabetes mellitus
*range, -#2. years,.
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This may also e!plain the associated e!ocrine deficiency seen in prolonged
diabetes.
Beta-cell dysfunction
0eta#cell dysfunction is a ma1or factor across the spectrum of prediabetes to diabetes. study of obese
adolescents by 0acha et al confirms what is increasingly being stressed in adults as well2 0eta#cell
dysfunction develops early in the pathologic process and does not necessarily follow the stage of insulin
resistance.
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(ingular focus on insulin resistance as the 3be all and end all3 is gradually shifting, and
hopefully better treatment options that address the beta#cell pathology will emerge for early therapy.
Insulin resistance
In the progression from normal to abnormal glucose tolerance, postprandial blood glucose levels increase
first. 4ventually, fasting hyperglycemia develops as suppression of hepatic gluconeogenesis fails.
5uring the induction of insulin resistance *such as occurs with a high#calorie diet, steroid administration,
or physical inactivity,, increased glucagon levels and increased glucose#dependent insulinotropic
polypeptide *6IP, levels accompanyglucose intolerance. 7owever, the postprandial glucagonlike peptide#
% *68P#%, response is unaltered.
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Pathology of type 2 diabetes
In type 2 diabetes, the body either produces inadequate amounts of insulin to meet the
demands of the body or insulin resistance has developed. Insulin resistance refers to when
cells of the body such as the muscle, liver and fat cells fail to respond to insulin, even when
levels are high. In fat cells, triglycerides are instead broken down to produce free fatty acids
for energy; muscle cells are deprived of an energy source and liver cells fail to build up
glycogen stores.
This also leads to an overall rise in the level of glucose in the blood. Glycogen stores become
markedly reduced and there is less glucose available for release when it may be
needed. besity and lack of physical activity are thought to be ma!or causes of insulin
resistance.
INTRODUCTION:
5iabetes mellitus is a condition in which the pancreas no longer produces
enough insulin or cells stop responding to the insulin that is produced, so that
glucose in the blood cannot be absorbed into the cells of the body. (ymptoms
include frequent urination, lethargy, e!cessive thirst, and hunger. The
treatment includes changes in diet, oral medications, and in some cases, daily
in1ections of insulin.
The most common form of diabetes is Type II, It is sometimes called age#
onset or adult#onset diabetes, and this form of diabetes occurs most often in
people who are overweight and who do not e!ercise. Type II is considered a
milder form of diabetes because of its slow onset *sometimes developing over
the course of several years, and because it usually can be controlled with diet
and oral medication. The consequences of uncontrolled and untreated Type II
diabetes, however, are the 1ust as serious as those for Type I. This form is
also called noninsulin#dependent diabetes, a term that is somewhat
misleading. 9any people with Type II diabetes can control the condition with
diet and oral medications, however, insulin in1ections are sometimes
necessary if treatment with diet and oral medication is not working.
The causes of diabetes mellitus are unclear, however, there seem to be both
hereditary *genetic factors passed on in families, and environmental factors
involved. :esearch has shown that some people who develop diabetes have
common genetic markers. In Type I diabetes, the immune system, the body;s
defense system against infection, is believed to be triggered by a virus or
another microorganism that destroys cells in the pancreas that produce
insulin. In Type II diabetes, age, obesity, and family history of diabetes play a
role.
In Type II diabetes, the pancreas may produce enough insulin, however, cells
have become resistant to the insulin produced and it may not work as
effectively. (ymptoms of Type II diabetes can begin so gradually that a person
may not know that he or she has it. 4arly signs are lethargy, e!treme thirst,
and frequent urination. <ther symptoms may include sudden weight loss,
slow wound healing, urinary tract infections, gum disease, or blurred vision. It
is not unusual for Type II diabetes to be detected while a patient is seeing a
doctor about another health concern that is actually being caused by the yet
undiagnosed diabetes.
Individuals who are at high risk of developing Type II diabetes mellitus include
people who2
are obese *more than 2=> above their ideal body weight,
have a relative with diabetes mellitus
belong to a high#risk ethnic population *frican#merican, ?ative
merican, 7ispanic, or ?ative 7awaiian,
have been diagnosed with gestational diabetes or have delivered a
baby weighing more than @ lbs */ kg,
have high blood pressure *%/=A@= mm7g or above,
have a high density lipoprotein cholesterol level less than or equal to B-
mgAd8 andAor a triglyceride level greater than or equal to 2-= mgAd8
have had impaired glucose tolerance or impaired fasting glucose on
previous testing
5iabetes mellitus is a common chronic disease requiring lifelong behavioral
and lifestyle changes. It is best managed with a team approach to empower
the client to successfully manage the disease. s part of the team the, the
nurse plans, organizes, and coordinates care among the various health
disciplines involved" provides care and education and promotes the client;s
health and well being. 5iabetes is a ma1or public health worldwide. Its
complications cause many devastating health problems.
ANATOMY AND PHYIO!O"Y:
4very cell in the human body needs energy in order to function. The body;s
primary energy source is glucose, a simple sugar resulting from the digestion
of foods containing carbohydrates *sugars and starches,. 6lucose from the
digested food circulates in the blood as a ready energy source for any cells
that need it. Insulin is a hormone or chemical produced by cells in the
pancreas, an organ located behind the stomach. Insulin bonds to a receptor
site on the outside of cell and acts like a key to open a doorway into the cell
through which glucose can enter. (ome of the glucose can be converted to
concentrated energy sources like glycogen or fatty acids and saved for later
use. )hen there is not enough insulin produced or when the doorway no
longer recognizes the insulin key, glucose stays in the blood rather entering
the cells.

PATHOPHYIO!O"Y:


Other patho: