Pathophysiology Diabetes Mellitus

a. Aetiology:
Predisposing Factors
Factors Presence Mechanism/Justification
Genetic (-) Initial decrease in beta cell mass related
to genetic factors responsible for beta cell
differentiation or presence of diabetogenic
gene.
Age >40 (+) Pancreas, similar to several other
components of the body, does not
function well due to old age.
Gender (+) Most frequent in women than in men,
ages 20-40
Race (-) In the report of CDC, the populations most
affected are native Americans,
particularly in the desert Southwest,
Hispanic-Americans, and Asian-
Americans

Precipitating Factors
Factors
Over weight/Obesity
Environment(intrapartal stage)
Virus Infection
Presence of Toxin
Decrease serum potassium
level
Development of glucose
intolerance during drug
therapy
Gestational Diabetes Mellitus
(GDM)
Presence Mechanism/Justification
(-) Obese people have increased resistance
to the action of insulin and impaired
suppression of glucose by liver, resulting
both hyperglycemia and hyperinsulinemia.
85% of all people with diabetes are
obese.
(-) Initial decrease in beta cell mass related
to presence of Maternal Diabetes Mellitus
during pregnancy or in uterine factors
such as intrauterine growth restriction.
High potential that the children of diabetic
mothers will also become diabetic in the
future.
(-) Mumps, coxsackeivirus
unknown Nitrosamines that are found in smoked
and cured meats, are related to
streptozoin that is used to induce DM in
experimental animals, rat poison named
Vacor that induces DM when ingested by
Human
(-) Low potassium level impairs release of
insulin
(-) Some drugs like thiazide diuretics, thyroid
hormones, sex hormones, corticosteroids
and lithium has side effects of glucose
intolerance
(-) Mother who has GDM has higher chance
of having Type2 DM in the near future
Stress (+) Form of stress with neuroendocrine
response increases gluconeogenesis and
glycogenolysis.
Alcohol (+) Alcohol contains 7cal/g. Alcohol intake
increases the risk of sulfonylurea or
insulin induced hypoglycaemia because of
the ability of alcohol to suppress
gluconeogenesis

b. Symptomatology

Symptoms Presence Mechanism/Justification

Polyuria (excessive urination) (+) Glucose exceeds the amount that can be
reabsorbed by renal tubules this results
glycosuria.
Polydipsia (excessive thirst) (+) Excess glucose in the blood pulls water
out of the cell causing intracellular
dehydration, including those in thirst
center.
Polyphagia (excessive (+) Results from depletion of cellular reserves
hunger) of carbohydrates, fats and proteins.
Blurred Vision (+) Lens and retina are exposed to
hyperosmolar fluids
Weakness and fatigue (+) Lowered plasma volume; Degenerative
changes occur in striated muscle in
persons who have long-standing, poorly
controlled diabetes milletus. Diabetic
amyotrophy, a syndrome of muscle
weakness, pain and atrophy occurs
mostly in elderly.
Paresthesias (+) Temporary dysfunction of peripheral
sensory nerves
Pruritus, vaginitis, chronic skin (-) Hyperglycemia and glycosuria favors
infections growth of yeast organisms.
Weight loss (+) Initial loss due to depletion of water,
glycogen, and triglyceride store; chronic
loss secondary to decrease muscle mass
as amino acid are diverted to form
glucose and ketone bodies.
Often Asymptomatic The body is able to adopt to a slow rise of
blood glucose level to a greater extent
than it can to a rapid rise.

Narrative:
 Type two Diabetes Mellitus is a heterogeneous condition that describes the presence of
excess serum glucose level in association with relative insulin deficiency. Type 2 Diabetes is
associated with high, normal, low insulin levels. However there is a presence of insulin
resistance thus the insulin cannot function effectively and hyperglycemia will occur. Most people
with this type of diabetes are older and obese, but type 2 Diabetes is becoming a more common
occurrence in obese adolescent. The metabolic abnormalities that contribute in hyperglycemia
in people with type 2 diabetes are impaired beta cell function and insulin production, peripheral
insulin resistance, and increase hepatic glucose production.
Insulin is a anabolic hormone. Without insulin three major metabolic problems occur:
decrease glucose uptake and utilization, increase fat and lipid mobilization and increased
protein and amino acid utilization.
Beta cells chronically exposed to high blood levels of glucose become progressively less
efficient when responding to further glucose elevation. Insulin resistance initially produces an
increase beta cell secretion of insulin as body attempt to maintain normoglycemic state. In time,
however the insulin response declines because of increasing beta cell dysfunction. This results
to postprandial hyperglycemia. Eventually fasting blood glucose level also rise until frank type 2
Diabetes occurs.
Cells that require insulin as carrier of glucose can take only 25% of glucose they require for
fuel, but nerve tissues, erythrocytes, and cells of intestine, liver, kidney tubules do not require
insulin for glucose transport. However, adipose tissue, along with skeletal and cardiac muscle
requires insulin for glucose transport.
During severe stress such as hospitalization, the body of a type 2 diabetes patient will turn
fat reserves into glucose for energy production when glucose is not available. Fat and lipid
metabolism cause breakdown products called ketones to form. Ketones accumulate in the blood
and excreted through kidneys and lungs. Ketones interfere with the body’s acid base balance by
producing Hydrogen ions. The pH can decrease, and metabolic acidosis can result. In addition
when ketone is excreted in urine, sodium is also eliminated, causing sodium depletion and
further acidosis. The excretion of ketone also increases osmotic pressure, leading to increase
fluid loss.
In this type of Diabetes Mellitus the onset of clinical manifestation may develop gradually
that clients may notice a few or no clinical manifestations for a number of year. Some of the
manifestations are frequency in urination, increase thirst or fluid intake, and as the disease
progresses, weight loss despite hunger and increased food intake.
 In the insulin deficit is severe or prolonged, the process continues to develop, resulting in
additional consequences, ultimately, diabetic ketoacidosis. This occurs more frequently in
persons with type 1 diabetes.
Lack of glucose in cells results in catabolism of fats and proteins leading to excessive
amount of fatty acids and their metabolites, known as ketones or ketoacids, in the blood.
Ketones consist of acetone and two organic acids-beta-hydroxybutyric acid and acetoacectic
acid. Because the liver and other cells are limited in the amount of lipids, fatty acids, or ketones
they can process completely within a given time, excessive amounts of ketones in the blood
cause ketoacidosis. The ketoacids bind with bicarbonate buffer in the blood, leading to
decreased serum bicarbonate and eventually to a decrease in the pH of the body fluids. Some
ketoacids are excreted in the urine. Some diabetic patients test their urine for ketones.
However, as dehydration develops, the glomerular filtration rate in the kidney is decreased, and
excretion of acids becomes more limited, resulting in decompensated metabolic acidosis, which
has life threatening potential.
As diabetes develops, weight gain or increased abdominal girth is common. As blood
glucose rises in the early stage, fluid loss is significant. Polyuria is indicated by urinary
frequency, which is often noticed by the patient at night with the excretion of large volumes of
urine. Thirst and dry mouth occur in response to fluid loss. Fatigue and lethargy develop. Weight
loss may follow. Appetite is increased. Typically, the 3 p’s, polyuria, polydipsia, and polyphagia,
herald the onset of diabetes. If the insulin deficit continues the patient progresses to the stage of
diabetic ketoacidosis. Fasting blood glucose level, the glucose tolerance test, and the
glycosylated hemoglobin test are used to screen people with clinical and subclinical diabetes.
There is less emphasis now on the “prediabetic stage” because tissue and organ damage
appear to commence at an early stage. At present, a fasting blood sugar equal to or greater
than 126 mg/dL, taken on more than one occasion, confirms a diagnosis of diabetes. The test
for glycosylated hemoglobin is used to monitor long-term control of blood glucose levels. The
test should be repeated every three months. The acceptable level for HbA has been lowered to
7.0%, and is likely to be lowered again to 6.0% (normal), in order to reduce the serious long-
term effects of hyperglycemia. Patients with diabetes can monitor themselves carefully at home
by taking a sample of capillary blood from a finger and checking it with a portable monitoring
machine (glucometer). When performined regularly, this self-monitoring test helps reduce the
fluctuations in blood glucose levels and therefore the risk of complications. Urine tests for
ketones are helpful for those who are predisposed to ketoacidosis. Arterial blood gas analysis is
required if ketoacidosis develops. Serum electrolytes may checked as well. Maintenance of
normal blood glucose levels is important to minimize the complications of diabetes mellitus, both
acute and chronic. Glucose intake must be balanced with utilization. Treatment measures
depend on the severity of the insulin deficit and may change overtime. There are essentially
three levels of control, the diet and exercise, oral medication to increase insulin secretion or
reduce insulin resistance and insulin replacement. Therapy is based on maintaining optimum
body weight as well as control of blood glucose levels. This is important for person with both
types of diabetes. Recommended diets include more complex carbohydrates and adequate
protein, as well as maintaining low cholesterol and low lipid levels. Increased fiber with meals
appears to reduce surges in blood sugar associated with food intake. The total amount of food
intake, as well as the distribution of the constituents, is important. Food intake must match
available insulin and metabolic needs, including activity level. Various methods of meal planning
are available from the diabetic associations and local diabetic clinics to ensure that the patient
ingests a good balance of the various nutrients and to provide information on the exchange of
food components without disruption of goals. Nutritionists can be consulted on an individual
basis in many diabetic clinics. A regular moderate exercise program is very beneficial to the
diabetic. Exercise can increase the uptake of glucose b muscles substantially without an
increase in insulin utilization. It also assists in weight control, reduces stress and improves
cardiovascular fitness. There is a risk that hypoglycemia may develop with exercise particularly
strenuous or prolonged exercise. The increased use of glucose by skeletal muscle, plus the
increased absorption of insulin from the injection site, may lower blood glucose levels
precipitously. Increasing carbohydrate intake by eating a snack to compensate for exercise can
decrease this risk. Antidiabetic agents or oral hypoglycemic drugs such as glyburide and
repaglinide are useful in the treatment of type 2 effective. These drugs stimulate the beta cells
of the pancreas to increase insulin release. Drugs such as metformin act to reduce insulin
resistance and reduce hepatic glucose production. The newer drugs increase tissue sensitivity
to insulin, but they do have some side effects. Frequently, a combination of diet, exercise and
oral hypoglycemic drugs is effective in treating mild forms of diabetes. Insulin can be used for
replacement therapy. It must be injected subcutaneously because it is a protein that is
destroyed in the digestive tract if taken orally. Continuous infusion via a small pump are favored
by some diabetics and may provide better control. The primary form of insulin used now is a
biosynthetic form of insulin, identical to human insulin, synthesized by bacteria using
recombinant DNA techniques. Insulin is standardized in units for subcutaneous administration
and is produced in three forms: rapid-onset, short-acting insulin; intermediate acting insulin; and
slow onset, long-acting insulin. Newer insulins in the market have a very rapid onset, 15
minutes, or last for 24 hours, in an attempt to provide better control of serum levels. Any
transition from one type of insulin to another must be carefully monitored by a physician. Blood
glucose levels should be checked at more frequent intervals during any changes. The type of
insulin used and its effective period can be important factors in predicting periods of potential
hypoglycemia in individual patients, and food intake can be timed to coincide with peak insulin
levels, thus avoiding hypoglycemia. Each patient has an individualized schedule of insulin
administration. Injection site must be rotated to minimize skin damage. Insulin types may be
mixed for administration, and several injections may be required in one day. Insulin dosage may
also require adjustment under special circumstances such as infection with high fever or
vomiting, or at the time of surgery.
Continuous control of blood glucose level minimizes the risk of potential complications
for the patient. Improved self-monitoring devices are helpful. Small, computerized recording and
data bank devices have improved the compliance of young adults. Many factors can lead to
fluctuation in serum glucose levels and subsequent changes in cell metabolism throughout the
body. These changes may result from variations in diet or physical activity, the presence of
infections, or alcohol use. Complications may be acute or chronic. Long-term complications
such as vascular disease result from degenerative changes in the tissues. Stable blood glucose
levels reduce the risk of complications. Hypoglycemia is precipitated by an excess of insulin,
which causes a deficit of glucose in the blood. It usually occurs in patients with type 1 diabetes,
often quite suddenly, following strenuous exercise, an error in dosage, vomiting, or skipping a
meal after taking insulin. Many individuals are able to recognize their own response. The lack of
glucose quickly affects the nervous system because neurons cannot use fats or protein as an
energy source. The manifestations of hypoglycemia are related directly to the low blood glucose
levels, not to the high insulin levels. One group of signs is related to impaired neurologic
function resulting from the lack of glucose. These sign include poor concentration, slurred
speech, lack of coordination, and staggering gait. Persons with hypoglycemia are some times
assumed to be intoxicated with alcohol. The second group of signs is related to the
hypoglycemic state stimulating the sympathetic nervous system, resulting in increased pulse;
pale, moist skin; anxiety; and tremors. If hypoglycemia remains untreated, loss of
consciousness, seizures, and death will follow. Treatment consists of immediate administration
of concentrated carbohydrate, such as sweetened fruit juice or candy. If the person is
unconscious, glucose or glucagons may be given parenterally. Hypoglycemia can be life
threatening or can cause brain damage if it is not treated promptly. It is wise to verify that
patients who have come for other treatments have eaten and taken the appropriate medications
before the appointment to minimize the risk of a hypoglycemic episode during the appointment.
Appointments should be scheduled so that meals are not unduly delayed or missed.
As indicated earlier, diabetic ketoacidosis results from insufficient insulin, which leads to
high blood glucose levels and mobilization of lipids. It is more common in type 1 patients.
Ketoacidosis usually develops over a few days and may be initiated by an infection or stress,
which increases the demand for insulin in the body. It may also result from an error in dosage or
overindulgence in food or alcohol. The signs and symptoms of diabetic ketoacidosis are related
to dehydration, metabolic acidosis, and electrolyte imbalances. Signs of dehydration include
thirst; dry, rough oral mucosa; and warm, dry skin. The pulse is rapid but weak and thready, and
the blood pressure is low as the vascular volume decreases. Oliguria indicates that
compensation mechanisms to conserve fluid in the body are taking place. Ketoacidosis leads to
rapid, deep respirations and an acetone breath. Lethargy and decreased responsiveness
indicate depression of the central nervous system owing to acidosis and decreased blood flow.
Metabolic acidosis develops as ketoacids bind with bicarbonate ions in the buffer, leading to
decreased serum pH. As dehydration progresses, renal compensation is reduced, acidosis
becomes decompensated, and serum pH falls, resulting in loss of consciousness. Electrolyte
imbalances include imbalances of sodium, potassium, and chloride. Signs include primarily
abdominal cramps, nausea, and vomiting, as well as lethargy and weakness. Actual serum
values of electrolytes may be misleading because the proportion of water lost can affect the
serum level even though the electrolytes were lost in the urine. Serum sodium is often low, but
the potassium concentration may be elevated because of acidosis. If the condition remains
untreated, central nervous system depression develops owing to the acidosis and dehydration,
leading to coma. Treatment of diabetic ketoacidosis involves administration of insulin as well as
replacement of fluid and electrolytes. Serum potassium levels may decrease when insulin is
administered because insulin promotes transport of potassium into cells. Bicarbonate
administration is essential to reverse the acidosis, as well as specific treatment to resolve the
causative factor of the diabetic ketoacidosis episode. Hyper osmolar hyperglycemic nonketotic
coma develops more frequently in the patients with type 2 diabetes. Often the patient is an older
person with an infection or one who has overindulged in carbohydrates, thereby using more
insulin than anticipated. In these cases, hyperglycemia and dehydration develop because of the
relative insulin deficit, but sufficient insulin is available to prevent keto acidosis. Therefore, the
condition may be difficult to diagnose initially. Severe cellular dehydration results in neurological
deficits, muscle weakness, difficulities with speech, and abnormal reflexes. Degenerative
changes occur in many tissues with both types of diabetes, particularly when blood glucose
levels are poorly controlled. The insulin deficit and glucose excess cause a number of
alterations in metabolic pathways involving carbohydrates, lipids and proteins.
Changes occur in both the small and large arteries because of degeneration related to
the metabolic abnormalities associated with diabetes.
Microangiopathy, in which the capillary basement membrane becomes thick and hard,
causes obstruction or rupture of capillaries and small arteries and results in tissue necrosis and
loss of function. Retinopathy is a leading cause of blindness. Retinal changes can be observed
through the pupil of the eye. Diabetic nephropathy, or vascular degeneration in the kidney
gromeruli, enventually leads to chronic renal failure. It is responsible for 40% of the patients in
end-stage renal failure.

Macroangiopathy, like atherosclerosis, affects the arteries, thus leading to a high

incidence of heart attacks, strokes and peripheral vascular disease in diabetics. Obstruction of
the arteries in the legs frequently results in ulcers on the feet and legs frequently that are slow to
heal. Ulcers are aggravated when peripheral neuropathy is present, reducing pain sensation.
Peripheral vascular disease also causes intermittent claudication, which imapairsmobility.
Decreased blood flow predisposes to frequent infection and gangrenous ulcers. In some cases,
vascular problems necessitate amputation if gangrene develops. New surgical techniques allow
for less invasive, less traumatic surgery to remove vascular obstructions, using angioscopic
bypass surgery. This very helpful to diabetics who tend to have delayed healing.
Peripheral neuropathy is a common problem for diabetics. This leads to impaired
sensation, numbness, tingling, weakness and muscle wasting. It results from ischemia and
altered metabolic processes. Degenerative changes occur in both unmyelinated and myelinated
nerve fibers. The risks of tissue trauma and infection are greatly increased when vascular
impairment and sensory impairment coexist.
Infections are common and tend to be more severe in diabetics, probably because of the
vascular impairment, which decreases tissue resistance, the delay in healing because of insulin
deficit, and the increased glucose levels in body fluids that support infection. Wound healing is
slow, predisposing to infection in case of trauma or surgery. Diabetics are also susceptible to
tuberculosis, which is increasing in incidence.
Infections in the feet and legs tend to persist because of vascular impairment, and
healing is slow, contributing to a high incidence of gangrene and resultant amputation.
 Fungal infections such as Candida occur frequently and persist on the skin in the body
folds, in the oral cavity and vagina. The urinary tract is a common site of infection, particularly if
bladder function is compromised, and predisposes the patient to cystitis and pyelonephritis.
Periodontal disease are much more common in diabetics.
Due to DM and CRF which leads to accumulation of toxic substances in the body ,
functions of other organs are affected. Cirrhosis represents the end stage of chronic liver
disease in which the functional liver tissue has been replaced by fibrous tissue. It is
characterized by diffused fibrosis and conversion of normal liver architecture into structurally
abnormal nodules. The fibrous tissue replaces normally functioning liver tissue and forms
constrictive bands that disrupt flow in the vascular channels and biliary duct systems of the liver.
The disruption of vascular channels predisposes to portal hypertension and its complications;
obstruction of biliary channels and exposure to the destructive effects of bile stasis and loss of
liver cells. Although cirrhosis is usually associated with alcoholism, it can develop in the course
of other disorders, including viral hepatitis, toxic reactions to drugs and chemicals, biliary
obstruction and liver failure. Cirrhosis also accompanies metabolic disorders that cause the
deposition of minerals in the liver. The manifestations of liver cirrhosis are variable, rangng from
asymptomatic hepatomegaly to hepatic failure. Often, there are no symptoms of cirrhosis until
the disease is far advanced. The common signs and symptoms of cirrhosis are weight loss
(sometimes masked by ascites), weakness and anorexia. Jaundice usually not a clear sign, is
mild at first but increase in severity during the later stages of the disease. There may be
abdominal pain because of liver enlargement or stretching of Glisson’s capsule.This pain is at
the epigastric area or in the upper right quadrant and is described as dull, aching, and causing a
sensation of fullness. The late manifestations of cirrhosis are related to portal hypertension and
liver failure. Splenomegaly, ascites, and portosystemic shunts (esophageal varices, aorectal
varices, and caput medsae) result from portal hypertension. Other late complication include
bleeding due to decreased clotting factors, thrombocytopenia due to splenomegaly,
gynecomastia, and a feminizing pattern of pubic hair distribution in men because of testicular
atrophy, spider angioma, palmar erythema, and encephalopathy with asterixis and neurologic
signs.
Further impairment in the function of the liver can affect its nearby organs. Cholelithiasis
or gallstones is caused by precipitation of substances contained in the bile, mainlu cholesterol
and bilirubin. The bile of which gallstones are formed usually is supersaturated with cholesterol
and bilirubinate. Approxmately 80% of gallstones are composed primarily of cholesterol; other
20% are black or brown pigment stones consisting of calcium salts with bilirubin. Three factors
contribute to the formation of gallstones: abnormalities to the composition of bile, stasis of bile
and inflammation of the gallbladder. All these factors cause liver to excrete more cholesterol into
the bile. Gallbladder sludge(thickened gallbladder mucoprotein with tiny trapped cholesterol
crystals) is thought to be precursor of gallstones. Malabsorption disorders stemming from ileal
disease or intestinal bypasss surgery, for example, interfere with the absorption of bile salts
which are needed to maintain the solubility of cholesterol. Inflammation of the gallbladder
alters absorption characteristics of the mucosal layer allowing excessive absorption of water
and bile salts. Pigment stones containing bilirubin are seen in persons with hemolytic disease
and hepatic cirrhosis.
Many persons with gallstones have no symptom. Gallstones cause symptoms when they
obstruct bile flow. Small stones pass into common duct, producing symptoms of indigestion and
biliary colic. Larger stones are more likely to obstruct flow and cause jaundice. The pain of
biliary colic is abrupt in onset and increases steadily in intensity until it reaches the climax in 30
to 60 minutes. The upper right quadrant, or epigastric area, is the usual location of pain.
Cholecystitis (inflammation of the gallbladder) is associated with cholelithiasis.
Choledocholithiasis refers to the stones in the common duct and cholangitis to the inflammation
of the common duct.
 c. Narrative

Type two Diabetes Mellitus is a heterogeneous condition that describes the presence of
excess serum glucose level in association with relative insulin deficiency. Type 2 Diabetes is
associated with high, normal, low insulin levels. However there is a presence of insulin
resistance thus the insulin cannot function effectively and hyperglycemia will occur. Most people
with this type of diabetes are older and obese, but type 2 Diabetes is becoming a more common
occurrence in obese adolescent. The metabolic abnormalities that contribute in hyperglycemia
in people with type 2 diabetes are impaired beta cell function and insulin production, peripheral
insulin resistance, and increase hepatic glucose production.
Insulin is a anabolic hormone. Without insulin three major metabolic problems occur:
decrease glucose uptake and utilization, increase fat and lipid mobilization and increased
protein and amino acid utilization.
Beta cells chronically exposed to high blood levels of glucose become progressively less
efficient when responding to further glucose elevation. Insulin resistance initially produces an
increase beta cell secretion of insulin as body attempt to maintain normoglycemic state. In time,
however the insulin response declines because of increasing beta cell dysfunction. This results
to postprandial hyperglycemia. Eventually fasting blood glucose level also rise until frank type 2
Diabetes occurs.
 Cells that require insulin as carrier of glucose can take only 25% of glucose they require for
fuel, but nerve tissues, erythrocytes, and cells of intestine, liver, kidney tubules do not require
insulin for glucose transport. However, adipose tissue, along with skeletal and cardiac muscle
requires insulin for glucose transport.
During severe stress such as hospitalization, the body of a type 2 diabetes patient will turn
fat reserves into glucose for energy production when glucose is not available. Fat and lipid
metabolism cause breakdown products called ketones to form. Ketones accumulate in the blood
and excreted through kidneys and lungs. Ketones interfere with the body’s acid base balance by
producing Hydrogen ions. The pH can decrease, and metabolic acidosis can result. In addition
when ketone is excreted in urine, sodium is also eliminated, causing sodium depletion and
further acidosis. The excretion of ketone also increases osmotic pressure, leading to increase
fluid loss.
In this type of Diabetes Mellitus the onset of clinical manifestation may develop gradually
that clients may notice a few or no clinical manifestations for a number of year. Some of the
manifestations are frequency in urination, increase thirst or fluid intake, and as the disease
progresses, weight loss despite hunger and increased food intake.
Clients with diabetes mellitus are living longer, with an increased risk for development of
chronic complications. Chronic complication are the major cause of morbidity and mortality in
client with diabetes mellitus. Diabetes mellitus-related complications are classified into two
types: macrovascular, including coronary artery diseases, cerebrovascular disease,
hypertension, peripheral vascular disease and infection; and microvascular, including
retinopathy, nephropathy, and neuropathy.
The very-low density lipoprotein and low density lipoprotein level are increased and high
density lipoproteins are decreased, and the most characteristic of lipid abnormality in diabetes
mellitus is an increase triglyceride level. Therefore the influence of diabetes in these disease are
not additive, it is multiplicative. Macrovascular disease tends to occur year before the onset of
clinical diabetes mellitus.
Clients with DM are two to four times more likely to have coronary artery disease than those
who do not have DM. In many clients with DM, often presents atypical or silent CAD, that often
presents as indgestion, or unexplained heart failure, dyspnea or excretions, or epigastric pain.
CAD is common in clients younger than 40 years old, of diabetes mellitus is of long duration.
DM patients with history of myocardial infarction have higher chance of having second infarct
than the patient who does not have DM. The incidence of cerebrovascular disease is two to
three times greater in diabetic client, and is more severe. Atherothromboembolic infarction
manifested by transient ischemic attracts and cerebrovascular accidents are the most commont
incidence of CVD that are the complication of DM.
Hypertension has increased of 40% occurrence in diabetic population. Hypertension is a
major risk factor for stroke and nephropathy.
Diabetis mellitus augments the process of atherosclerosclerosis by variety of mechanism
thus causing peripheral vascular disease. Hyperglycemia and insulin resistance contribute to
endothelial dysfunction by decreasing available nitric oxide bioavailability and altering the
function of various cell mediators.
Clients with diabetes are susceptible to different type of infection. Three factors may
contribute to the development of infection are impaired polymorphonuclear-leukocyte function,
diabetic nephropathies and vascular insufficiencies. Damaged area heals slowly because the
damaged vascular system cannot carry sufficient amount of oxygen, white blood cells, nutrients
and antibodies to the injured site. Infection increases the need for insulin and enhances the
possibility of ketoacidosis. Urinary tract infection is the most common infection especially in
women. Factors that impairs the polymorphonuclear-leukocyte is the presence of glycosuria and
the development of neurogenic bladder, which results in incomplete emptying and or urinary
stasis.
About 80% of clients with DM have some form of retinopathy, the exact cause of retinopathy
is not understood but it is probably a multifactorial and associated with protein glycosylation,
ischemia, and hemodynamics mechanism that increases the permeability and decreases the
elasticity of capillaries.
About 20% of diagnosed DM type 2 patients have nephropathy 5 to 10 years after
diagnosis. A consequence of microangiopathy, nephropathy involves damage to and eventual
obliteration of the capillaries that supply the glomeruli of the kidney. This damage leads to
complex pathologic changes and manifestations such as intercapillary glomerolonecrosis,
nephrosis, gross albuminuria and hypertension. Unsuccessful treatment of nephropathy will lead
to stage 5 chronic kidney disease. Like retinopathy, diabetic nephropathy is irreversible.
Neuropathy, the most common chronic complication of diabetes mellitus. Nearly 60% of
diabetic patients experience it. Because nerve fibers do not have their own blood supply, they
depend on diffusion of nutriens, and oxygen across membrane. When axon and dendrites do
not receive nourishment their transmission of impulses becomes slow. Both temporary and
permanent neurologic problem may develop. The neuropathy might be mild that causing minor
inconveniences or severe that quality of life is affected. Clients might present mononeuropathy
or polyneuropathy and may have motor or sensory impairment, depending on which nerve that
are involved. Mononeuropathy usually involves single or group nerves. It produces sharp,
stabbing pain and is usually caused by an infarction of blood supply. Polyneuropathy also
known as diffuse neuropathy, which involves both sensory and autonomic nerves. Sensory
neuropathy is most common type. It is commonly assed as bilateral, symmetrical and is
affecting the lower extremity. Client may describe tingling, numbness, burning, and mild to
severe sensory loss, a major factor in injuries to the legs.
Autonomic neuropathy affects the nerves that regulate vital functions, including the heart muscle
and smooth muscles. Autonomic neuropathy involves damage to the nerves that run through a
part of the peripheral nervous system. The peripheral nervous system includes the nerves used
for communication to and from the brain and spinal cord (central nervous system) and all other
parts of the body, including the internal organs, muscles, skin, and blood vessels. Damage to
the autonomic nerves affects the function of areas connected to the problem nerve. Some of the
autonomic neuropathy are: autonomic neuropathy of the pupil which interferes with pupils ability
to adapt to dark because pupils dilation is inadequate; autonomic neuropathy of the
cardiovascular system is evidence by abnormal response to exercise, fixed heart maybe noted;
autonomic neuropathy of gastrointestinal, client may have dysphagia, abdominal pain, nausea,
vomiting, diarrhea malabsorption, post prandial hypoglycemia, constipation, or fecal
incontinence and gastroparesis. Bladder hypotonisity of neurogenic bladder is common
manifestation of autonomic neuropathy of genitourinary organs. In male client it can contribute
to erectile dysfunction and retrograde ejaculation. Women may experience painful coitus.
All of these complications can be prevented by good control of blood sugar level,
exercise and diet modification.