a. Aetiology:Predisposing Factors

Factors Presence Mechanism/JustificationGenetic (-) 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 FactorsFactors Presence Mechanism/JustificationOver weight/Obesity (-) 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.

Environment(intrapartal stage) (-) 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.

Virus Infection (-) Mumps, coxsackeivirusPresence of Toxin 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

Decrease serum potassium level

(-) Low potassium level impairs release of insulin

Development of glucose intolerance during drug therapy

(-) Some drugs like thiazide diuretics, thyroid hormones, sex hormones, corticosteroids and lithium has side effects of glucose intolerance

Gestational Diabetes Mellitus (GDM)

(-) Mother who has GDM has higher chance of having Type2 DM in the near future

Pathophysiology Diabetes Mellitus

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/JustificationPolyuria (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 hunger)

(+) Results from depletion of cellular reserves 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 infections

(-) Hyperglycemia and glycosuria favors 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.