APPENDIX B PATHOPHYSIOLOGY OF DM TYPE 2

Alpha glucosidase inhibitor: a category of oral agents are used to treat type 2 diabetes that delay the absorption of carbohydrate, resulting in lower postprandial blood glucose level. Continuous subcutaneous insulin infusion: a small device that delivers insulin on a 24-hour basis as basal insulin; it is also programmed by the patient to deliver a bolus dose before eating a meal in attempt to mimic normal pancreatic function.

Diabetes mellitus: a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion,insulin action or both.

Diabetic ketoacidosis (DKA): a diabetic derangement in type 1 diabetes that results from a deficiency of insulin. Highly acidic ketone bodies are formed, resulting in acidosis; usually requires hospitalization for treatment and is usually caused by nonadherence to the insulin regimen, concurrent illness, or infection.

Fasting plasma glucose (FPG): blood glucose determination obtained in the laboratory after fasting for more than 8 hours. Although plasma levels are specified in diagnostic criteria, blood glucose levels, which are slightly higher than plasma levels, are more commonly used.

 Glycosylated hemoglobin (hemoglobin A1c): a-long term measure of glucose control that is the result of glucose attaching to hemoglobin for the life of the red blood cell (120 days). The goal of diabetes therapy is a normal to near-normal level of glycosylated hemoglobin(referred to as HgbA1c or A1C), the same as in nondiabetic population.

Hyperglycemia: elevated blood glucose level-fasting level greater than 110mg/dL (6.1mmo/L); 2-hour postprandial greater than 140mg/dL(7.8mmo/L) Hyperglycemic hyperosmolar nonketotic syndrome(HHNS): a metabolic disorder of type 2 diabetes resulting from a relative insulin difeciency initiated by an intercurrent illness that raises the demand for insulin; associated with polyuria and severe dehydration.

Hypoglycemia: low blood glucose level (less than 60 mg/dL [less than 2.7mmo/L])

Insulin: a hormone secreted by the beta cells of the islets of langerhans of the pancreas that is necessary for th e metabolism of carbohydrates, proteins, and fats; a deficiency of insulin results in d iabetes mellitus.

 Impaired fasting glucose(IFG), impaired glucose tolerance(IGT): a metabolic stage intermediate between normal glucose homeostasis and diabetes; not clinical intities in their own right but risk factors for future diabetes and cardiovascular disease Islet cell transplant: an investigational procedure in which purified islet cells from cadaver donors are injected into the portal vein of the liver, with the goal of having these cells secrete insulin and cure type1 diabetes.

Ketone: a highly acidic substance formed when the liver breaks down free fatty acids in the absence of insulin. The result is diabetic ketoacidosis. Nephropathy: a long-term complication of diabetes in which the kidney cells are damaged; characterized by albuminoria in early stages progressing to end-stage renal disease.

Neuropathy: a long- term complication of diabetes resulting from damaged to nerve cell. Retinopathy: a long-term complication of diabetes in which the microvascular system of the eye is damaged.

 Self-monitoring of blood glucose (SMBG)2: a method of capillary blood glucose testing in which the patient pricks his/her finger and applies a drop of blood to a test strip that is ready by a meter.

Sulfunyurea: a classifaction of oral antidaibetic medication for treating type 2 diabetes; enhances insulin secretion and insulin action. Thiazolidinedione: a class of oral antidiabetic medications that reduce insulin resistance in target tissues, enhancing insulin action without directly stimulating insulin secretion.

RISKS FACTORS Family history of diabetes (ie. Parents or sibling with diabetes) Race/ethinicity (eg. African Americans,Hispanic American , Native Americans, Asian American) Age > 45 y.o. Previously identified impaired fasting glucose or impaired glucose tolerance Hypertension (>140/90mm Hg) HDL cholesterol level <35 mg/dl (0.90mmol/L)and / or tri-glyceride level>250 mg/dl (2.8mmol/L) History of gestational diabetes or delivery over 9 lbs

ANATOMY AND PHYSIOLOGY system

of the endocrine

hypothalamus The hypothalamus is located in the brain, near the optic chiasm. It secretes hormones that stimulate or suppress the release of hormones in the pituitary gland, in addition to controlling water balance, sleep, temperature, appetite, and blood pressure. pineal body The pineal body is located below the corpus callosum, a part of the brain. It produces the hormone melatonin. pituitary The pituitary gland is located at the base of the brain. No larger than a pea, the gland controls many functions of the other endocrine glands. thyroid and parathyroids The thyroid gland and parathyroid glands are located in front of the neck, below the larynx (voice box). The thyroid plays an important role in the body's

metabolism. Both the thyroid and parathyroid glands also play a role in the regulation of the body's calcium balance.

thymus The thymus is located in the upper part of the chest and produces T-lymphocytes (white blood cells that fight infections and destroy abnormal cells). What are hormones? Hormones are chemical substances created by the body that control numerous body functions. They actually act as "messengers" to coordinate functions of various body parts. Most hormones are proteins consisting of amino acid chains. Some hormones are steroids, fatty cholesterol-produced substances. Functions controlled by hormones include activities of entire organs; growth and development; reproduction; sexual characteristics; usage and storage of energy; and levels of fluid, salt, and sugar in the blood.

adrenal gland The pair of adrenal glands are located on top of both kidneys. Adrenal glands work hand-in-hand with the hypothalamus and pituitary gland. kidney The pair of kidneys are located near the middle of the back, just below the rib cage. The kidneys process the blood to sift out waste products and extra water. This waste and extra water becomes urine, which is stored in the bladder. pancreas The pancreas is located across the back of the abdomen, behind the stomach. The pancreas plays a role in digestion, as well as hormone production. ovary A female's ovaries are located on both sides of the

uterus, below the opening of the fallopian tubes (tubes that extend from the uterus to the ovaries). In addition to containing the egg cells necessary for reproduction, the ovaries also produce estrogen and progesterone.

testis A male's testes are located in a pouch that hangs suspended outside his body. The testes produce testosterone and sperm.

Figure 2. Pathophysiology

Disease Process Type 2 diabetes is characterized by the 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 in plasma leads to decreased glucose transport into muscle cells, elevated hepatic glucose production, and increased breakdown of fat. For type 2 diabetes mellitus to occur, both defects must exist. For example, 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.

Beta cell dysfunction is a major factor across the spectrum of pre-diabetes to diabetes. A study of obese adolescents by Bacha et al confirms what is increasingly being stressed in adults as well: Beta cell function happens early in the pathological process and does not necessarily follow stage of insulin resistance. Singular focus on insulin resistance as the "be all and end all" is gradually shifting, and hopefully better treatment options that focus on the beta cell pathology will emerge to treat the disorder early. In the progression from normal glucose tolerance to abnormal glucose tolerance, postprandial blood glucose levels increase first; eventually, fasting

hyperglycemia develops as suppression of hepatic gluconeogenesis fails.

During the induction of insulin resistance, such as is seen after high-calorie diet, steroid administration, or physical inactivity, increased glucagon levels and increased glucose-dependent insulinotropic polypeptide (GIP) levels accompany glucose intolerance; however, postprandial glucagonlike peptide-1 (GLP-1) response is unaltered. This has physiologic implications; for example, if the GLP-1 level is unaltered, GLP-1 may be a target of therapy in the states mentioned above.

The high mobility group A1 (HMGA1) protein is a key regulator of the insulin receptor gene (INSR). Functional variants of the HMGA1 gene are associated with an increased risk of diabetes. These variants were shown to lead to reduction in protein content of both HMGA1 and INSR. Although the pathophysiology of the disease differs between the types of diabetes, most of the complications, including microvascular, macrovascular, and neuropathic, are similar regardless of the type of diabetes.

Hyperglycemia appears to be the determinant of microvascular and metabolic complications. Macrovascular disease, however, is much less related

to glycemia. Insulin resistance with concomitant lipid abnormalities (ie, elevated levels of small dense lowdensity lipoprotein cholesterol [LDL-C] particles, low levels of high-density lipoprotein cholesterol [HDL-C], elevated levels of triglyceride-rich remnant lipoproteins) and thrombotic abnormalities (ie, elevated type-1 plasminogen activator inhibitor [PAI1], elevated fibrinogen), as well as conventional atherosclerotic risk factors (eg, family history, smoking, hypertension, elevated LDL-C, low HDL-C), determine cardiovascular risk. Unlike liver and smooth muscle, insulin resistance is not associated with increased myocardial lipid accumulation. Increased cardiovascular risk appears to begin prior to the development of frank hyperglycemia, presumably because of the effects of insulin resistance. Stern in 1996 and Haffner and D'Agostino in 1999 developed the "ticking clock" hypothesis of complications, asserting that the clock starts ticking for microvascular risk at the onset of hyperglycemia, while the clock starts ticking for macrovascular risk at some antecedent point, presumably with the onset of insulin resistance.

Gestational diabetes mellitus (GDM) is defined as any degree of glucose intolerance with onset or first recognition during pregnancy. Gestational diabetes mellitus is a complication of approximately 4% of all pregnancies in the United States.

 Untreated gestational diabetes mellitus can lead to fetal macrosomia, hypoglycemia, hypocalcemia, and hyperbilirubinemia. In addition, mothers with gestational diabetes mellitus have increased rates of cesarean delivery and chronic hypertension. See appendix B Clinical manifestation the three Ps ;POLYURIA, POLYDIPSIA, POLYPHAGIA Polyuria Polyphagia Fatigue & weakness sudden vision changes tingling or numbness in hands or feet dry skin, skin lesions, or wounds that are slow to heal recurrent infections.

The onset of type 1 diabetes may also be associated with sudden weight or nausea , vomiting or abdominal pains ,if DKA has developed. DIAGNOSTIC PROCEDURES
LABORATORY ASSESSMENT BLOOD TESTS

The nurse, the client or a family member monitors the ongoing status of the disease by performing capillary blood glucose testing using a blood glucose meter. FASTING BLOOD GLUCOSE TEST Fasting blood glucose test are most accurate when the blood is obtained by venipuncture. The client should fast for at least 8hours (water is permitted). Draw the blood before insulin or oral antidiabetic agents have been taken. Diabetes is diagnosed when two separate test

results exceed 126 mg/dL. (7 mmol/L) (ADA,2003a). ORAL GLUCOSE TOLERANCE TEST The oral glucose tolerance test (OGTT) is the most sensitive test for diagnosing diabetes, although it is not routinely used except in gestational diabetes. The test is inconvenient to clients, costly, and time consuming compared with the fasting blood glucose measure. Carbohydrate restriction or bedrest before the test alters glucose tolerance. The client drinks a beverage containing a glucose load of 75 g, and blood samples are collected at 30-minute intervals for 2 hours. A diagnosis of diabetes is made if the blood glucose is greater than 200mg/dL (11.1 mmol/L) at 120mins. GLYCOSYLATED HEMOGLOBIN ASSAYS > Blood glucose permanently attaches to hemoglobin. The higher the blood glucose level is over time, the more glycosyted hemoglobin becomes. Thus glycosylated hemoglobin (HbA1c) is a good indicator of the average blood glucose level B. pharmacology The goal of medical treatment is to return the patient to as near a euglycemic state as possible and correct any related metabolic disorders.

Oral Hypoglycemic Sulfonylureas (SUFs) Orinase (Tolbutamide) Tolinase (Tolazamide) Diabinese (Chlorpropamide)

Action These medications act on the pancreatic tissue to produce insulin.

Biguanides Glucophage (Metformin)

Alpha-glucosidase inhibitors Precose (Acarbose) Glyset (Miglitol)

These medications act by lowering the cells resistance to insulin and they decrease excess sugar production from the liver by making the body more sensitive to natural insulin. These medications delay the absorption of glucose from the intestine by slowing the bodys digestion of carbohydrates.

Thiazolidinediones These medications assist the Rezulin body by sensitizing body (Troglitazone) tissues to insulin. Avandia (Rosiglitazone DIET These will help to improve glycemic (blood sugar) control and prevent or minimize complications of diabetes. Diet: A healthy diet is key to controlling blood sugar levels and preventing diabetes complications.

He or she can be recommend a dietitian or a weight modification program to help the patient reach a goal.

Eat a consistent, well-balanced diet that is high in fiber, low in saturated fat, and low in concentrated sweets. It will also help to keep blood sugar at a relatively even level and avoid excessively low or high blood sugar levels, which can be dangerous and even lifethreatening. SAMPLE MENU

Exchanges (2-starch, 3-meat, 1-vegetable, 1-fat, 1-fruit Freeitems (optional)) SAMPLE LUNCH #1 2 slices bread , 2 oz sliced turkey and 1 oz low fat cheese, lettuce,tomato,onion, 1tsp mayonnaise, 1 medium apple, Unswetened iced tea, mustard, pickled, hot pepper SAMPLE LUNCH #2 Hamburger bun, 3 oz lean beef patty, green salad, 1tbsp salad dressing, 1/4cup watermelons, diet soda, 1tbsp catsup,pickle,onions SAMPLE LUNCH #3 1 cup cooked pasta 3 oz boiled shrimp, cup plum tomatoes, 1tsp olive oil, 1 cup fresh strawberries, ice water with lemon, garlic and basil SPECIAL CONSIDERATIONS FOR TYPE 2 DIABETES. A moderate caloric restriction (250 to 500 calories less than average daily intake) and an increase in physical activity improves diabetic control and weight control. Decrease of more than 10% of body weight can result in significant improvement in glycosylated hemologbin(hemoglobin A1c).

EXERCISE THERAPY Regular exercise is an essential part of a diabetic treatment plan. Reduce the risk for atherosclerosis. 1. Exercise in the client with uncontrolled diabetes results in further hyperglycemia and the formation of ketone bodies. Diabetic clients may have prolonged elevated blood glucose levels after vigorous exercise. 2. Exercise in the person with the diabetes can cause hypoglycemia because of increased muscle glucose uptake and inhibited glucose release from the liver. Benefits of exercise.

Improves control by increasing insulin sensitivity, enhancing cell uptake of glucose, and promoting weight loss. Regular exercise decreases risk factors for cardiovascular disease. Exercise decreases blood pressure and improves cardiovascular function. Regular vigorous physical activity prevents or delays type 2 diabetes by reducing body weight, insulin resistance, and glucose intolerance.

Risk related to exercise prolonged hypoglycemia or hyperglycemia can occur, particularly after sustained high-intensive exercise.

 Several complications of diabetes can be made worse by exercise: 1. Proliferative retinopathy is advised to avoid the Valsalva maneuver(breathe-holding while bearing down ) and 2. Activities that increase blood pressure. Heavy lifting , rapid head motion, or jarring activities can cause eye hemorrhage or retinal detachment. 3. Exercise may increase proteinuria in clients with diabetic nephropathy. 4. The for foot and joint injury rises for clients with peripheral neuropathy. Client education: exercise promotion. 1. Instruct the client to wear shoes with good traction and cushioning and to examine The feet daily and after exercise. 2. Discourage exercise in the extreme heat or cold or during periods of poor blood glucose control. 3. Advise the client to stay hydration specially during and after exercise in a warm environment. 4. Exercise can increase absorption of insulin from the injection site. 5. The risk for hypoglycemia increases when insulin is injected into an area that is exercised. NURSING MANAGEMENT ASSESSMENT Obtain a history of current problems, family history, and general health history. Has the patient experienced polyuria, polydipsia, polyphagia, and any other symptoms? Number of years since diagnosis of diabetes Family members diagnosed with diabetes, their subsequent treatment, and complications

o o

o o

Perform a review of systems and physical examination to assess for signs and symptoms of diabetes, general health of patient, and presence of complications. General: recent weight loss or gain, increased fatigue, tiredness, anxiety Skin: skin lesions, infections, dehydration, evidence of poor wound healing Eyes: changes in visionfloaters, halos, blurred vision, dry or burning eyes, cataracts, glaucoma Mouth: gingivitis, periodontal disease Cardiovascular: orthostatic hypotension, cold extremities, weak pedal pulses, leg claudication GI: diarrhea, constipation, early satiety, bloating, increased flatulence, hunger or thirst Genitourinary (GU): increased urination, nocturia, impotence, vaginal discharge Neurologic: numbness and tingling of the extremities, decreased pain and temperature perception, changes in gait and balance Nursing Diagnosis:

Alteration in Nutrition (hypo/hyperglycemia) Alteration in Cardiac Output (atherosclerosis) Knowledge Deficit (treatment regimen) Ineffective Coping Individual (denial, lifetime alteration) Ineffective Coping Family (care giver strain) Potential for Fluid Volume Excess (cardiovascular/renal complications) Potential for Fluid Volume Deficit (polyuria) Potential for Social Isolation (BBQs, cocktail parties, work potlucks)

PLANNING The patient must have a good understanding of both hypo and hyperglycemia and be able to verbalize treatment for both.

The patient should be provided support information such as groups and organizations that can assist with the necessary life style changes associated with a diagnosis of Diabetes Type II. Dietician referral may be necessary. The patient needs to be aware that periodic lab testing will be required (usually life long). Originally every 3 months and when stable usually every 6 months. INTERVENTION

Monitoring blood glucose Administering antidiabetics/insulin Full body assessment, special attention made to circulatory and skin Prevention of ulcer formation Monitoring VS Monitoring for hyper/hypoglycemia Offering snacks at bedtime if permitted.

E- Patients is able to avoid further complication in relevance to disease