CHAPTER I INTRODUCTION 1.

1 Background Diabetes mellitus is a chronic disease that is genetic sistemetik and clinically heterogeneous acquired and that can interfere with the metabolism of carbohydrates, proteins and fats due defesiasi or ineffectiveness of insulin function, which can affect many body systems, which can cause long-term complications and decreased quality of life of patients. In 2000 in Indonesia is estimated there are at least million people disbetes

mellitus and !"#. million worldwide sufferers. $ada estimated 20!0 estimated that diabetes mellitus in Indonesia to be at least # million and 2%&.% million in the 'orld. (rom the literature it was mentioned that treatment failure and diabetes mellitus nurses caused by various factors. (actor is the main cause of indiscipline or ignorance )knowlegge deficit* patients about the disease, treatment and care programs. +o overcome this problem various attempts have been made include counseling and education. +he importance of counseling and education on diabetes mulitus is to increase knowledge about the disease and basically more geared to the planning aspects dining, sporting, drug use insulin, self-monitoring of blood glucose levels , urine and increased motivation for regular medical treatment aimed at relieving symptoms, creating and maintaining a sense of healthy, prevent acute and chronic complications, reduce the complications that have been there, treat disease broadcaster, improve quality of life and reduce mortality. -part from that desired behavior change pad sipenderita diabetes mellitus to be obedient in implementing disease management programs affected by the sharing factor.
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.upporting factors are e/ternal factors that are important in influencing the behavior of people to be obedient after getting counseling for patients with diabetes mellitus. 0esides, there are also factors would include education level, economic status , income, family support, community support, and the distance of travel time to reach the health services. (acing this phenomenon concluded that although patients with diabetes mellitus have to know the procedures of handling the disease, tetapai there are other factors that mermpengaruhi that problem as mentioned above ter1adi.berdasarkan the problem can get clear about the factors that affect people with diabetes mellitus who had get counseling on how to handle the disease. 1.2 Purposes +his paper have a several purpose first in future we hope student can e/plain about anatomy and physiology diabetic mellitus, +wice .tudent can e/plain about sign and medical tests detect diabetic mellitus . +hird student can e/plain about etiology of diabetic mellitus, -nd the last but not least .tudent know how to deal with diabetic mellitus nursing. 1.3 Benef !s +he benefits of this paper are students will know how to make a good makalah and students will e/plore more about their vocabulary and their tenses skill writing scientific paper in 2nglish also students can develop their knowledge about many disease like diabetic mellitus. and also student can writing scientific writing like 2nglish in

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2.1 D a"e!es #e$$ !us Diabetes mellitus is a disease in which glucose )simple sugar* in the blood is high because the body can not release or use insulin adequately ).oegondo, 200#*. Diabetes 8ellitus )D8* is a metabolic disease that mostly hereditary, demham sign - a sign of hyperglycemia and glucosuria, or not accompanied by clinical symptoms of acute or chronic, as a result of the lack of effective insulin in the body, located in the primary disorder of carbohydrate metabolism that is usually accompanied also fat and protein metabolism disorders. )-skandar, 2000*. 2.2 Ana!o%& P'&s o$og&

+he pancreas is a flattened organ that lies behind and slightly below the stomach in the abdomen. +his organ has two functions9 the function of the endocrine and e/ocrine function ).loane, 200%*. 5art of e/ocrine pancreatic acinar cells serve as pancreatic, pancreas produce fluid that is secreted through the pancreatic duct into the small intestine ).loane, 200%*. +he pancreas consists of two main tissue, .loane )200%*, namely9 a. :afplion secretion of digestive 1uices into the duodenum. b. islets of ;angerhans that secrete sekretnya out. 4owever, secrete insulin and glucagon directly into the blood. +he islets of ;angerhans of the pancreas become endocrinological systems scattered through out the pancreas with a weight of only !-%< of the total weight of the pancreas. ;angerhans islets shaped opioids with each of the different islets. +he smallest of the islets of ;angerhans is #0=, %00= while the biggest, most is that the amount of !00-22#=. :umber of all the islets of ;angerhans in the pancreas is estimated between !-2 million ).loane, 200%*. 2ndocrine cells can be found in the islets of ;angerhans, which are collections of small cells scattered throughout the organ. +here are .loane )200%*9 a. -lpha cells, an amount of about 20- 0<, producing hyperglycemic factor glucagon, a hormone that has antiinsulin like activity. b. 0eta cells secrete insulin which lowers blood sugar levels. >niversity of :orth .umatra c. .omastatin delta cells secrete hormones barrier that inhibits the secretion of growth hormones glucagon and insulin.
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types of hormone-producing cells were identified in these islets,

d. ( cells secrete pancreatic polypeptide, similar to the function of the digestive hormone is not clear. Insulin is a hormone that is made up of a series of amino acids, produced by the beta cells of the pancreas gland. >nder normal circumstances, when there is stimulation of the beta cells, insulin is synthesi?ed and then secreted into the blood in accordance with the needs of the body for the purposes of regulation of blood glucose )8anaf, 200@*. Insulin synthesis begins in the form of prepoinsulin )precursor of the hormone insulin* on beta cell endoplasmic reticulum. 'ith the help of peptidase en?ymes, prepoinsulin had split to form proinsulin, which is then collected in the bubbles )secretory vesicles* in these cells. 4ere, with the help of peptidase en?ymes, insulin and proinsulin decomposed into 3-peptide )3-peptide* that they are ready to simultaneously secreted through the cell membrane )Auyton, 200"*. 5hysiological mechanisms above, is necessary for the continuity of the process of glucose metabolism, insulin function in relation to glucose in the body utilasi process. Increased blood glucose levels, is a ma1or component that gives the stimulation of insulin-producing beta cells, although some types of amino acids and drugs, can also have the same effect. 8echanisms of insulin synthesis and secretion after stimulation of the beta cells is quite complicated, and not yet fully understood clearly )8anaf, 200@*. +here are several stages in insulin secretion after glucose molecules provide stimulus to the beta cells. (irst, the process to be able to pass through the cell membrane that requires other compounds. Alucose transporter )A;>+* is an amino acid compound found in a variety of cells involved in glucose metabolism process. (unction as a BvehicleB glucose transporters in from the outside into the body tissues. Alucose transforter 2 )A;>+ 2* . 5resent in beta cells, for e/ample, is needed in the process of entry of glucose from the blood, through the membrane, into the cell. +his process is an important step, so that further into the cell, the glucose molecule can
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undergo glycolysis and phosphorylation process that will liberate -+5 molecules. -+5 molecules are liberated, needed to activate the process of closing C channels contained in cell membranes. Inhibition of C ions e/penditure in the cells causes cell membrane depolari?ation, which was followed later by the opening of 3a channels. +his condition allows the entry of 3a D ions thereby increasing the levels of intracellular 3a D , the atmosphere needed for the process of insulin secretion via a mechanism is quite comple/ and not yet completely une/plained )8anaf, 200@*. 2.3 C$ass f ca! on of D a"e!es #e$$ !us -lthough clinically there are two kinds of diabetes, but actually there who think diabetes is only a spectrum of insulin deficiency. Individuals who lack insulin completely or almost total say as 1uvenile onset diabetes or insulin-dependent or ketosis prone, because without insulin can occur within a few days of death caused by ketoacidosis. -t the other e/treme there are individuals who are stable or maturity onset or noninsulin dependent. +hese people only show relative insulin deficiency, and although many of them may require supplementation of insulin )insulin requiring*, there will be no deaths due to ketoacidosis despite e/ogenous insulin was stopped. 2ven among them there may be an increase in the absolute amount of insulin when compared to normal people. 0ut this is usually due to obesity and , or physical activity )Austaviani, 200@*. D8 classification according to the 'orld 4ealth $rgani?ation )200&* are9 I. +ype ! Diabetes9 Insulin Dependent Diabetes 8ellitus )IDD8* II. +ype 2 diabetes9 insulin-dependent diabetes mellitus not )noninsulin Dependent Diabetes 8ellitus* E:IDD8F. Decreased insulin production or reduction in insulin action or both III. -nother type of diabetes according to )5owers, 200#*9 -. Aenetic defect of G-cell function characteri?ed by mutations in9

!. +ranscription factor hepatocyte nuclei )4:(* H )8$DI !* 2. Alucokinase )8$DI 2* %. 4:(-!H )8$DI %* . Insulin promoter factor )I5(* ! )8$DI * #. 4:(-!G )8$DI #* @. :euroD! )8$DI @* ". mitochondrial D:J. Insulin or proinsulin conversion 0. Defective insulin on insulin action !. +ype - insulin resistance 2. ;eprekaunism %. 6abson-8endenhall syndrome . lipodystrophy syndrome 3. Diseases of the e/ocrine pancreas-pancreatitis, pankreatektomi, neoplasia, cystic fibrosis, hemochromatosis, pankreatopati fibrokalkulous. D. 2ndokrinopati-acromegaly,3ushingKs syndrome,glukagonoma, feokromasitoma, hyperthyroidism, stomatostatinoma, aldosteronoma. 2. Induction of drug or chemical-pentamidine, nicotinic acid, glucocorticoids, thyroid hormone, G-blockers. (. -3ongenital rubella infection, citomegalivirus, koksakie. A. >nusual forms of immune-mediated diabetes Bstiff-manB syndrome.

I7. Aestational diabetes mellitus )diabetes during pregnancy* )-D-, 200%*. 2.( E! o$og& of D a"e!es #e$$ !us :on Insulin Dependent Diabetes 8ellitus ):IDD8* or :ot Dependent Diabetes 8ellitus Insulin )D8++I* due to the relative failure of the cell and insulin resisitensi. Insulin resistance is a decrease in the ability of insulin to stimulate glucose uptake by peripheral tissues and to inhibit the production of glucose by the liver. 3ells are not able to fully compensate for the insulin resistance, relative insulin resistance occurs means. +his inability can be seen from the reduced stimulation of insulin secretion in glucose, but the glucose stimulation of insulin secretion stimulants with other materials. 8ean pancreatic cells undergo desensiti?ation to glucose )3apita .electa 8edicine, 200!*. 2.) Pa!'op'&s o$og& of D a"e!es #e$$ !us *Brunner and +uddar!', 2--2. !. Diabetes +ype !

+here is an inability to produce insulin because the cells of the pancreas have been destroyed by an autoimmune process. Alucose derived from food can not be stored in the liver although it remains in the blood and cause hyperglycemia posprandial )after meals*.

If the concentration of glucose in the blood is high, the kidneys can not reabsorb all of the glucose that is filtered out as a result of glucose e/creted in the urine )glucosuria*. +his will be accompanied by the e/cretion of fluid and electrolyte overload, a condition called osmotic diuresis. 5atients e/perienced an increase in urination )polyuria* and thirst )polydipsia*. 2. Diabetes +ype II

+here are two main problems related to insulin, namely9 insulin resistance and impaired insulin secretion. :ormally, insulin would be bound to specific receptors on the cell surface. -s a result of the binding of insulin to the receptor, there is a series of reactions in the metabolism of glucose in the cells. Insulin resistance in diabetes >niversity of :orth .umatra +ype II accompanied by a decrease in intracellular reactions, thus becoming ineffective insulin to stimulate glucose uptake by the tissues. +o overcome insulin resistance and prevent the formation of glucose in the blood should be a rise in insulin that is secreted. In patients with impaired glucose tolerance, a condition caused by e/cessive secretion of insulin and glucose levels will be maintained at a normal level or slightly increased. 4owever, if the cells are not able to keep pace with the increased demand for insulin increases glucose levels and type II diabetes happens.

Despite the impaired insulin secretion, which is a hallmark of type II diabetes, but there is an adequate amount of insulin to prevent the breakdown of fat and ketone body production. +herefore, diabetic ketoacidosis does not occur in type II diabetes. 4owever, type II diabetes that is not controlled can lead to other problems called acute hyperglycemic syndrome hiperosmoler nonketotik. Alucose intolerance due to a slow and progressive, then the onset of type II diabetes can go undetected, symptoms are often mild and may include fatigue, irritability, polyuria, pilidipsia, sores on the skin that does not heal, infections and blurred vision. %. Aestational Diabetes Defined as glucose intolerance beginning or first once obtained during pregnancy )8ichael (. Areenean and 3aren A. .olomon, 200#*. $ccurred in women who did not have diabetes before pregnancy. 4yperglycemia occurs during pregnancy due to hormone-placental hormone secretion. -fter giving birth, blood glucose levels in women with gestational diabetes will go back to normal. 2./ Ep de% o$og& of D a"e!es #e$$ !us +he prevalence rate of diabetes mellitus is high. -llegedly there are appro/imately !@ million cases of diabetes in the >nited .tates each year and @00,000 thousand new cases are diagnosed. Diabetes is the third leading cause of death in the >nited .tates and is the leading cause of blindness in adults due to diabetic retino. -t the same age, people with diabetes for at least 2 L times more likely to have a heart attack than those who do not have a heart attack. +hirty-five percent of diabetics eventually die from vascular disease. 4eart attack, kidney failure, stroke, and gangrene are the most important complications. In addition to intrauterine fetal death in mothers with poorly controlled diabetes mellitus also increased ).chteingart, 200#*.

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2.0 R sk 1ac!ors for D a"e!es #e$$ !us 6isk factors for diabetes mellitus from e8edicine 4ealth9 !. $besity )overweight* +here is a significant correlation between obesity and blood glucose levels, the degree of obesity with 08IM 2% may lead to increased blood glucose levels to 200 mg<. 2. hypertension Increased blood pressure in hypertension is closely linked to improper storage of salt and water, or increased pressure in the body of the peripheral vascular circulation. %. (amily 4istory of Diabetes 8ellitus - person who is suffering from Diabetes 8ellitus is suspected to have diabetes genes. .uspected that diabetes is a recessive gene talents. $nly people who are homo?ygous with the recessive gene that suffering Diabetes 8ellitus. . Dislipedimia Is a condition characteri?ed by increased levels of blood fats )triglyceridesM 2#0 mg , dl*. +here is a relationship between the increase in plasma insulin with low 4D; )N%# mg , dl* are often obtained in patients with diabetes. #. age 0ased on research, the most affected age Diabetes 8ellitus isM # years. @. history of childbirth 6ecurrent miscarriage, birth defects or birth weightM 000 grams.

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2.2 C$ n ca$ +&%p!o%s of D a"e!es #e$$ !us -ccording :ewsroom )200&* a person can be said to suffer from diabetes mellitus suffer if two of the three symptoms, namely9 a. +6I-. complaint9 8any drinks, lot of urine and weight loss. b. 0lood glucose levels at fasting more than !20 mg , dl. c. 0lood glucose levels two hours after eating more than 200 mg , dl. 3omplaints are common in patients with Diabetes 8ellitus are9 5olyuria, polydipsia, polyphagia, enurun 'eight, 'eakness, tingling, itching, decreased visual acuity, ulcer , wound, 'hitish )'aspad1i, !&&@*. 2.3 D a"e! c #e$$ !us d agnos s In preparation of the new classification system, the american diabetes association also presents diagnostic criteria and recommendations new screening for diabetes mellitu. :ew criteria for the diagnosis of diabetes mellitus is as follows9 !. .ymptoms of diabetes )ie polyuria, polydipsia, weight loss, pengelihatn blurred* plus the concentration glukosaplasma while )any time, without considering the last meal* O 200 mg , dl. 2. (asting plasma glucose )(5A* )no caloric intake dive at least J hours* O !2@mg,dl %. Alucose 2 hours after a glucose load )2h5A* O 200 mg , dl, to use it only dose burden of oral "#g glucose anhydrous dissolved in water. Diagnosis occur if one of these three criteria are met followed by confirmation by other criteria on the ne/t day. .ome group also known to e/ist with glucose levels do not meet the criteria for diabetes but is too high to be considered normal
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Aroup between is characteri?ed by9 !. (5A O !!0 and N!2@ mg , dl )(5A normal is N!!0 mg , dl* 2. 2h5A O ! 0 and N200 mg , dl )2h5A normal is N! 0 mg , dl* 3riteria earlier than 'orld 4ealth $rgan?ation ntuk diagnosis of diabetes mellitus is a (5A O ! 0 mg , dl and 2h5A O 200 mg , dl. Criteriayang new better at identifying (5A upon which complications mikrovascular diabetes began to appear and comparability between the thresholds abnormal (5A and 2h5A. 3hange threshold (5A of ! 0 to !2@ mg , dl, fueled by clinical findings and epidemiologicalP benchmark is likely to cause confusion in patients who previously have e/amination results between !2@ and ! 0 mg , dl. (5A easy and accurate so that a screening test is most commonly used for diabetes mellitus. :ow is also recommended that those asymptomatic following undergo screening tests9 !. -ll people aged # years or moreP when normal repeat every % years. 2. 5eople who are younger who have risk factors for the following9 !. $besity 2. Immediate family have diabetes %. 2thnic groups at high risk . 4ypertension #. 4D; cholesterol Q %# mg , dl and or triglycerides O 2#0 mg , dl @. Alucose measurements before showing the results intermediates. +able 2.!. -nd blood glucose levels during fasting as a standard filter and the diagnosis of D8 Aolongan klinik
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:on D8

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Alucose blood 5lasma vena rate in the time )mg,dl* Darah kapiler 5lasma vena

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Alukosa rate (asting )mg,dl* 0lood

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.ources9 3onsensus 8anagement of +ype-2 diabetes mellitus in Indonesia, 5erkeni 2002 2.3.1 Tes d agnos! c for D a"e! #e$$ !us .ymptoms of type ! diabetes often appear suddenly and are often the reason for checking blood sugar levels. 0ecause symptoms of other types of diabetes and prediabetes come on more gradually or may not be evident, the -merican Diabetes -ssociation )-D-* has recommended screening guidelines. +he -D- recommends that the following people be screened for diabetes9 -nyone with a body mass inde/ higher than 2#, regardless of age, who has additional risk factors, such as high blood pressure, a sedentary lifestyle, a history of polycystic ovary syndrome, having delivered a baby who weighed more than & pounds, a history of diabetes in pregnancy, high cholesterol levels, a history of heart disease, or having a close relative with diabetes. -nyone older than age # is advised to receive an initial blood sugar screening, and then, if the results are normal, to be screened every three years thereafter.

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+ests for prediabetes +he primary test to screen for prediabetes is9
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+he glycated hemoglobin )-!3* test. +his blood test indicates your average blood sugar level for the past two to three months. It works by measuring the percentage of blood sugar attached to hemoglobin, the o/ygen-carrying protein in red blood cells. +he higher your blood sugar levels, the more hemoglobin youKll have with sugar attached. -n -!3 level between #." and @. percent suggests you have prediabetes. :ormal levels are below #." percent. If the -!3 test isnKt available, or if you have certain conditions that can make the -!3 test inaccurate R such as if youKre pregnant or have an uncommon form of hemoglobin )known as a hemoglobin variant* R your doctor may use the following tests to diagnose diabetes9 (asting blood sugar test. - blood sample will be taken after an overnight fast. blood sugar level from !00 to !2# mg,d; )#.@ to @.& mmol,;* is considered prediabetes, sometimes referred to as impaired fasting glucose. :ormal is below !00 mg,d;. $ral glucose tolerance test. - blood sample will be taken after you fast for at least eight hours or overnight. +hen youKll drink a sugary solution, and your blood sugar level will be measured again after two hours. - blood sugar level less than ! 0 mg,d; )".J mmol,;* is normal. - blood sugar level from ! 0 to !&& mg,d; )".J to !! mmol,;* is considered prediabetes. +his is sometimes referred to as impaired glucose tolerance. 2. +ests for type ! and type 2 diabetes Alycated hemoglobin )-!3* test. +his blood test indicates your average blood sugar level for the past two to three months. It measures the percentage of blood sugar attached to hemoglobin, the o/ygen-carrying protein in red blood cells. +he higher your blood sugar levels, the more hemoglobin youKll have with sugar attached. -n -!3 level of @.# percent or higher on two separate tests indicates that you have diabetes.

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If the -!3 test results arenKt consistent, the test isnKt available, or if you have certain conditions that can make the -!3 test inaccurate R such as if youKre pregnant or have an uncommon form of hemoglobin )known as a hemoglobin variant* R your doctor may use the following tests to diagnose diabetes9 6andom blood sugar test. - blood sample will be taken at a random time. 6egardless of when you last ate, a random blood sugar level of 200 milligrams per deciliter )mg,d;* R !!.! millimoles per liter )mmol,;* R or higher suggests diabetes. (asting blood sugar test. - blood sample will be taken after an overnight fast. fasting blood sugar level between !00 and !2# mg,d; )#.@ and @.& mmol,;* is considered prediabetes. If itKs !2@ mg,d; )" mmol,;* or higher on two separate tests, youKll be diagnosed with diabetes. If type ! diabetes is suspected, your urine will be tested to look for the presence of ketones, a byproduct produced when muscle and fat tissue are used for energy when the body doesnKt have enough insulin to use the available glucose. $ccasionally a 3 peptide level R a test used to measure the ability of the pancreas to secrete insulin R may be ordered. ;evels of 3 peptide are usually low in people with type ! diabetes, but may be normal or high in people with type 2 diabetes. %. Aestational diabetes mellitus In the >..., gestational diabetes mellitus )AD8* occurs in about < of all pregnancies. Detection of AD8 mengharuska we ad1ust meals, provide therapy, perform surveillance of the fetus, and set up special procedures for labor. :ormal glucose tolerance to fluctuate during pregnancy, so the criteria for AD8 were made to identify women who berisikomengalami diabetes during pregnancy. ma1ority of women with AD8 will show recovery to normal glucose levels after childbirth, but bnayak who remain at risk of diabetes mellitus in the future.

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.creening tests for AD8 consists of measurements of plasma glucose ! hour after a #0g oral glucose administration )usually given as a solution of the type-kola suatau specially formulated for this purpose*. +his e/amination should be performed in advance of pregnancy week 2 to week 2J. If the !-hour plasma glucose greater than or equal to ! 0 mg , dl, should be performed oral glucose tolerance test % hours straight )A++* at a dose of !00 g of glucose. plasma glucose less than !0# mg , dl in the fasting state, less than !&0 mg , dl at ! hour, less than !@# mg , dl at 2 hours and less drai ! # mg , dl at % oKclock. Diagnosis of AD8 is based on the fulfillment of two of four between plasma glucose levels above. If the patient is unable to support the weight of glucose and then vomiting, A++ invalid and stopped samplingP re-A++ on subsequent days. 2ven though the combination of screening tests and e/aminations konfimatorik !00g #0g is never recommended for pregnant women smeua, now considered that the tests are not necessary for women younger than 2# years with normal body weight, no history of diabetes in the family, and not from of ethnic diabtes have high numbers. -ll perumpuan pregnancy outside of these criteria must undergo e/amination. Alucose tolerance test -lthough not part of the standard of the new recommendations for screening and diagnosing diabetes e/cept AD8, glucose tolerance test )A++* may be used by some physicians to evaluate cases of hyperglycemia or hypoglycemia even that is not clear. $ral A++ is influenced by many physiological variables and the sub1ect of many interpretations of different diagnostic. Intravenous tolerance test, which is even more difficult for interpretation, seldom indicated for diagnosis purposes. 5atients who underwent A++ should be in a state of normal nutritional statusP should not take salicylates, diuretics, anticonvulsants, steroids or oral contraceptives and do not smoke, eat and drink anything other than water dive !2 hours before the e/amination.

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.ome researchers use a standard dose of glucose )varies #0g, "#g, !00g* while others menyesuaikandosi glucose with body si?e, using the benchmark of !."# g , kg body weight or body surface area #0g,m2. 5rotocols for taking samples variesP researchers are generally evaluated during fasting and at ! and 2 hoursP ma1ority also took specimen at the third hour, while some are also taking on the half hour and !.# hours. Interpretation -ccount after two hours of administration of glucose load, blood glucose levels should fall to fasting. 5ersistent increase in 2 hours is abnormal. 8odest increase in 2 hours and % hours of normal levels suggests a clear interruption of glucose metabolism without diabetes. 7ery sharp increase followed by a decrease to subnormal levels may occur in hyperthyroidism and alcoholic liver disease. 'ith age velocity decreased glucose levels 2 hours reduced levels in people who do not have diabetes and those with a negative family history increased an average of @ mg , dl for each decade after age %0 years >rine decision simultaneously is essential but is often done. 'hen glucose is given along with large amounts of fluid in the urine taking !.# to 2 hours is not difficult, and the results might show how much glucose is released by the patient at a certain level of hyperglycemia. In the event of glucosuria without hiperglekemia patients should be evaluated to determine whether there is impaired renal tubular function. 2.1- Co%p$ ca! ons of D a"e! c #e$$ !us -ccording to )8ans1oer et al, !&&&* some of the complications of Diabetes 8ellitus is

2.1-.1 Acu!e co%p$ ca! ons a. hypoglycemia

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4ypoglycemia literally means blood glucose levels below the normal price. -lthough fasting plasma glucose levels in normal people rarely e/ceeded && mg< )#.# mmol , ;*, but levels of N!J0 mg< )@ mmol , ;* is considered normal. 5lasma glucose levels appro/imately !0< higher than whole blood glucose levels )whole blood* because erythrocytes containing glucose levels are relatively lower. Alucose levels are higher than the venous artery, while the capillary blood glucose levels between arteries and veins )'ahono .oemad1i, 200@*. b. hyperglycemia 4yperglycemia may occur due to increased intake of glucose and increased liver glucose production. +his e/cess glucose will not run normally metaboli?ed through glycolysis. 0ut, partly through the aldose reductase en?yme intermediate is converted into sorbitol, which in turn will accumulate in cells , tissues and cause damage and the change in function )-rifin*. 4yperglycemia consists of9 !. Diabetic Ceto -cidosis )DC-* Diabetic Cetoacidosis )DC-* is a state-clutter metabolic decompensation characteri?ed by the triad of hyperglycemia, acidosis and ketosis, mainly caused by absolute or relative insulin deficiency ).oewondo, 200@*. 2. :on-ketotic hyperglycemic hyperosmolar coma )C44:C* C44:C syndrome characteri?ed by hyperglycemia, hyperosmolar without the presence of ketosis. +he main clinical symptom is severe dehydration, severe hyperglycemia and are often accompanied by disturbances neurolis with or without the presence of ketosis ).oewondo, 200@*.

2.1-.2 C'ron c co%p$ ca! ons

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a. macrovascular disease 6egarding the large blood vessels, coronary heart disease )cerebrovascular, capillary blood vessel disease* )-vicenna, 200&*. -lertness to the possibility of coronary artery disease should be improved, especially for those who have a high risk of atherosclerotic disorders such as those who have a family history of coronary artery disease or a strong family history of D8 )'aspad1i, 200@*. b. 8icrovascular disease, the small blood vessels, retinopathy, nephropathy 6enal abnormalities that occur in people with diabetes begins with microalbuminuria, and then developed into clinical proteinuria, continues to decline in glomerular filtration rate and the function ended with renal failure yangmemerlukan management with substitution treatment )'aspad1i, 200@*. 7arious disorders caused by diabetes can occur in the retina, ranging from diabetic retinopathy retinal hemorrhages nonproliferatif up, then also retinal detachments and further can cause blindness. 2arly diagnosis of retinopathy can be detected through a routine e/amination of the retina )'aspad1i, 200@* c. .ensory nerve neuropathy )affects the e/tremities*, an effect on the autonomic nervous gastrointestinal, cardiovascular ).uddarth and 0runner, 2002*. d. >lcer , gangrene )-vicenna, 200&*. 2.11 Pre4en! on of D a"e! c #e$$ !us 3omplication when it occurs, attempt to heal the situation is very difficult for the normal direction, the damage will generally be settled. +herefore, early prevention efforts for these complications is necessary and e/pected to be very useful to avoid many of the disadvantages )Sunita, 200@*.

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-ccording to the '4$ in !&& , diabetes prevention efforts there are % types or stages9 2.11.1 Pr %ar& pre4en! on -ll activities are aimed at preventing the onset of hyperglycemia in individuals at risk for diabetes or so in the general population. 2.11.2 +econdar& pre4en! on (ind people with diabetes as early as possible, for e/ample by screening tests, especially in high risk populations, thus patients who previously undiagnosed D8 can netted, so that efforts can be made to prevent complications or complications if there is still reversible. +herefore, in !&& the '4$ declared that the new detection by screening patients included in secondary prevention efforts to make it more known early complications can be prevented due to reversible. (or developing countries, including IndonesiaKs efforts include e/pensive. 2.11.3 Ter! ar& pre4en! on -ll efforts to prevent complications or disability from complications of it. +o prevent disability course should begin with early detection of diabetes complications to later complications can be managed with good course management in addition to controlling blood glucose levels. +hese efforts include9 a. 5revent complications of diabetes. b. 5revent the progress )progression* does not lead to complications for organ failure. c. 5revent disability caused by the failure of the body organ or tissue.

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2.12 #anage%en! of D a"e! c #e$$ !us Diabetes management starts with setting eating and physical activity for some time )2weeks*. 'hen blood glucose levels have not reached the target, pharmacological intervention with oral hypoglycemic medication )$4$* or insulin in1ections. In certain circumstances $4$ can soon be given as indicated. In case of severe metabolic decompensation, such as ketoacidosis, severe stress, weight decreased rapidly, insulin can be given immediately. In both these circumstances need to be aware of the possibility of hypoglycemia. 8onitoring of blood glucose levels can be done independently, after receiving special training )Iuli, 20!0*. +here are main pillars of diabetes management that is used for a long time, in

the management of diabetic patients are as follows9 !. 3ounseling Implementation of the diabetes educator should provide an integrated service in an installation such as the central form imformasi who works 2 hours a day and will serve patients or anyone who asks about the ins and outs of diabetes especially about diet and its management including complications ).uyono, 200@*. 3ounseling Diabetes 8ellitus can be done for primary prevention, secondary and tertiary )4iwani 8kes (C >.>*. -ccording to Iuli )20!0* +he e/tension includes an understanding of9 a. D8 disease. b. .ignificance and need for control and monitoring of diabetes mellitus. c. D8 complications. d. 5harmacological and non-pharmacological interventions. e. 4ypoglycemia.

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f. .pecial problems faced. g. (oot care in diabetes. h. 4ow to support system development and teaching skills. i. 4ow to use the health care facility. 2. 5lanning 8eal +he recommended standard is food with a balanced composition in terms of carbohydrates, protein, and fat, according to nutritional adequacy both as follows9 @0"0< carbohydrate, 20-2#< fat, !0-!#< protein. +he number of calories ad1usted to growth, nutritional status, age, acute stress and physical activity to achieve and maintain ideal body weight. (ood composition to "0-"#< still give good results. 6ecommended amount of cholesterol N%00 mg , day, the fat comes from cultivated sources of unsaturated fatty acids 8>(- )8ono >nsaturated (atty -cids*, and limiting 5>(- )5oly >nsaturated (atty -cid* and saturated fatty acids. +he amount of fiber T 2# g , day, preferably soluble fiber )Iuli, 20!0*. (or the determination of nutritional status, used 0ody 8ass Inde/ )08I* U body mass inde/ )08I*. 08I U 08I U weight )kg* , +0 )m* D. 3lassification of nutritional status based on 08I )2m Iunir, .uharko .oebardi, 200@*9 a. >nderweight b. :ormal 00 c. 00 over d. 'ith the risk of e. I $bese f. $bese II N!J.# !J.# - 22.& 2%.0 O 2% to 2 .& 2# to 2&.& O %0

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2.12.1 Nu!r ! ona$ Needs +u"s!ance D a"e! c #e$$ !us !. 5rotein $nly a few scientific data to make strong recommendations about the protein intake of people with diabetes. -D- currently recommends consuming !0< to 20< of energy from total protein. -ccording to consensus management of diabetes in Indonesia needs protein for people with diabetes is !0-!#< of energy )D6 4iswani 8kes*. 2. (ats 6ecommendations of fat )2m Iunir, .uharko .oebardi, 200@*9 a. ;imit the consumption of foods that contain saturated fat, the amount of a ma/imum of !0< of the total calories per day. b. If the ;D; cholesterol level O !00 mg , dl, the intake of saturated fatty acids lowered to a ma/imum of "< of total calories per day. c. 8a/imum cholesterol intake %00 mg , day, if the ;D; cholesterol level O !00 mg , dl, the ma/imum that can be consumed cholesterol 200 mg per day. d. ;imit your intake of trans fatty acids. e. 3onsumption of fish 2-% times a week to meet the needs of unsaturated fatty acids chain length. f. Intake of unsaturated fatty acid chain length of up to !0< of calorie intake per day. %. 3arbohydrate 3arbohydrates are given to diabetics should not be more than ##-@#< of total daily energy needs, or should not be more than "0< when combined with the provision of unsaturated fatty acids single chain )8>(- U monounsaturated fatty
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acids*. $n each gram of carbohydrates are an energy content equal to )2m Iunir, .uharko .oebardi, 200@*. . 7itamins and 8inerals

kilocalories

7itamins and minerals found in vegetables and fruits, weeks to help smooth functioning of the body. 'hen we eat a varied diet every day then no longer need additional vitamins. Diabetes need to achieve and maintain normal blood pressure. +herefore, the need to limit sodium consumption. -void foods high in salt and 8.A. +he recommended daily salt meal appro/imately @-" grams )! teaspoon*. #. (iber (iber intake recommendations for people with diabetes the same as for people who are not diabetic. It is recommended to consume 20-%# grams of dietary fiber from different food sources. -dvocacy in Indonesia is appro/imately 2# grams per day with emphasis on soluble fiber )D6 4iswani 8kes*. @. .odium +he recommended intake for people with diabetes is the same as the general population is not more than %000 mg )D6 4iswani 8kes*. 2.12.2 Ca$or e con!en! of D a"e! c #e$$ !us 3alories in the diet of people every day is determined by the circumstances of her illness. If the patient is also classified as obese people, then in addition to restriction of carbohydrate and fat, as well as to limit the calories in the diet. In 3ipto 8angunkusumo used eight raw diet with various levels of calories )Sune, 200@*, namely9 Diet I Diet II Diet III !000 calories !%00 calories !#00 calories
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Diet I7 Diet 7 Diet 7I Diet 7II Diet 7III

!"00 calories !&00 calories 2!00 calories 2%00 calories 2#00 calories

Diet I to III given to diabetics who are classified as obese. Diet I7 to 7 is given to patients with normal weight, Diet 7I to 7III are given to people with thin, diabetes with complications, people with diabetes or who are pregnant. 2.13 P'ar%aco$og ca$ T'erap'& of D a"e!es #e$$ !us 1or%a! on of Insu$ n Increased insulin levels when blood glucose increases. 3ertain amino acids, ketones, and fatty acids also increase the secretion of insulin, as well as increased levels of growth hormone, -3+4, glucagon, gastrin, and sekretin. 4igh insulin levels in the blood, somatosin, epinephrine, and norepinephrine inhibit insulin secretion. 0eta cells normally produce cutting proinsulin to insulin and 3 peptide. equimolar amounts of both issued into circulation. 8etabolically inactive peptide c )and cleared from the circulation more rapidly than insulin*, but keberadaannyan serves as an inde/ of beta cell activity outside measurement of serum insulin, which is influenced by e/ogenous hormones. :ormal fasting serum insulin levels were Jsamapi !# > , 8l )0.%-0.@ ng , ml*. concentration of glucose and insulin in normal circumstances changing in parallel. $n serum glucose levels were very low, insulin may decrease to levels below the sensitivity of the e/amination. .erum insulin measured by radioimmunoassay, but also digunaknan antibodies react with inactive precursor form, proinsulin. It becomes significant only when suspected abnormalities of insulin activity, or in certain pancreatic tumor that emit more than the active hormone prohormone.
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!.

insulin

Insulin is a hormone that is produced from pancreatic V cells in response to glucose. Insulin is a polypeptide consisting of #! amino acids arranged in 2 chain, chain consists of 2! amino acids and the 0 chain consists of %0 amino acids. Insulin has a very important role in the control of metabolism and e/tensive, the effect of insulin is to help transport glucose from the blood into the cells. 7arious insulin preparations9 !. .hort-acting insulin +his preparation consists of a single insulin regular, starting new work after half an hour )subcutaneous in1ection*, eg -ctrapid, 7elosulin, 4umulin 6egular. 2. ;ong-acting insulin )long-acting* +he insulin dosage works by making the dissolution in tissue fluids and inhibit resorpsinya from the in1ection site into the blood. +he method used is to mi/ insulin with ?inc or protein or alter its physical form, e/ample9 4uman 8onotard. %. 8edium-acting insulin )medium-acting* +his insulin preparation period effect can be varied by mi/ing some form of insulin with different length of employment, for e/ample9 8i/tard %0 48 )+1ay and 6ahard1a, 2002*. - total of 20-2#< of patients with type 2 diabetes will require insulin later to control blood glucose levels. (or patients who are not able to control their blood glucose levels with a combination of metformin and a sulfonylurea, the ne/t step is possible given insulin )'aspad1i, 20!0*. 2. $ral -ntidiabetic Drugs $ral antidiabetic medications intended to help treat patients with type 2 diabetes mellitus. $ral antidiabetic pharmacotherapy can be done using a single drug
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or a combination of two drugs )Directorate Aeneral of 5harmaceutical and 8edical Devices, 200#*. a. 3lass of sulfonylureas +his class of drugs works dikelen1ar stimulate pancreatic insulin secretion, and therefore the only effective if ;angerhans cells of pancreatic V-cells can still produce Decreased levels of blood glucose that occurs after administration of sulfonylurea compounds due to the stimulation of insulin secretion by the pancreas gland. +his class of drugs is a new option for adult diabetes with normal body weight and less, and have never e/perienced before ketoacidosis )Directorate Aeneral of 5harmaceutical and 8edical Devices, 200#*. +he first-generation sulfonylureas +olbutamide well absorbed but rapidly metaboli?ed in the liver. 6elatively short tenure, the elimination half-life -# hours )Cat?ung, 2002*. +olbutamide in blood plasma protein bound. +his drug in the liver and converted into karboksitolbutamid e/creted through the kidneys )4andoko and .uharto, !&&#*. -sektoheksamid quickly in the body undergo biotransformation, plasma half-life of 0.#-2 hours. 0ut these drugs in the body is converted into !hidroksilheksamid which turned out to be stronger than the effects of hypoglycemia asetoheksamid own. 0esides the !-hidroksilheksamid also showed a longer half-life, appro/imately -# hours )4andoko and .uharto, !&&#*. 3hlorpropamide quickly absorbed by the intestine, "0-J0< is metaboli?ed in the liver and its metabolites are rapidly e/creted through the kidneys. 0ound to albumin in the blood, a half-life of appro/imately %@ hours so that the effect is still visible a few days after treatment was stopped )4andoko and .uharto, !&&#*.

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+ola?amid absorbed more slowly in the colon than other sulfonylureas and their effect on blood glucose is not immediately apparent within a few hours after administration. +he half-life of about " hours )Cat?ung, 2002*. .econd-generation sulfonylureas Alyburide )glibenclamide* hipoglikemisnya efficacy that is appro/imately !00 times more potent than tolbutamide. $ften potent where other drugs are not effective anymore, the risk of hypoglycemia is also larger and frequent. Different work patterns with other sulfonylureas, namely the single-dose morning stimulates insulin secretion at any glucose infusion )during meals* )+1ay and 6ahard1a, 2002*. +his drug is metaboli?ed in the liver, only 2!< diekresi metabolites in urine and the remainder is e/creted via the bile and kidney )4andoko and .uharto, !&&#*. Alipi?ide has a half-life of 2- hours, &0< Alipi?ide is metaboli?ed in the liver to the active product and !0< is e/creted unchanged by the kidney )Cat?ung, 2002*. Alimepiride can achieve a reduction in blood glucose with the lowest dose of the sulfonylurea compounds. ;arge single dose of ! mg proved effective and the recommended ma/imum daily dose is J mg. Alimepiride possessed a half-life of # hours and completely metaboli?ed by the liver into inactive products )Cat?ung, 2002*. b. 3lass 0iguanides +his class is available is metformin, metformin lowers blood glucose through their effects on insulin action at the cellular level and lower liver glucose production. 8etformin also suppress appetite until weight does not increase, so itKs worth given to patients who are overweight )Directorate Aeneral of 5harmaceutical and 8edical Devices, 200#*. c. 3lass +ia?olidindion

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+his new class of drugs has broad pharmacological activity and a decrease in glucose and insulin levels by increasing sensitivity to insulin of muscle, fat and liver tissue, as the effect is the absorption of glucose into fat and muscle tissue increased. +ia?olidindion e/pected to be more appropriate to work on targets aberration that insulin resistance without causing hypoglycemia and also does not cause pancreatic V cell e/haustion. 2/ample9 5ioglita?one, +roglita?on. d. -lfa glucosidase Inhibitor class +his drug works by competitively inhibiting the en?yme alpha-glucosidase in the digestive tract so that it can reduce hyperglycemia postprandrial. +his drug works in the intestinal lumen and does not cause the >niversity of :orth .umatra hypoglycemia and also had no effect on insulin levels. 2/ample9 -carbose )+1ay and 6ahard1a, 2002* 2.1( Nurs ng Care P$an Pa! en! 5 !' D a"e!es #e$$ !us Data the patient is an obese, @2-years-old married woman with an J-years history of type 2 diabetes mellitus controllled by oral hypoglycemic agents. .he has been refferd to a short-term ambulatory diabetes education program for intruction on insulin administratation to achieve better blood glucose control. +he patient states that she has an inconsisitent sleep-activity schedule and does not e/ercise regulary. .he has accurate knowledge of dietary modifications and has succesfully lost weightP however, within a few month she gains the weight back. .he performs regular foot checks, wears well-fitted shoes, and has no skin breakdown, but complains of loss of sensation in both feet. -lthough she performed self-glucose monitoring in the past, she does not currently have a working blood glucose monitoring at home. 4er fasting blood glucose is 220mg,dl. 5hysical assessment reveals !W peripheral pulsesP e/termities warm and dry, with color consistent with the rest of her bodyP patellar and achilles tendon refle/es %W )on scale of ! to *P decreased perception to touch in
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lower e/tremitiesP and decreased vibration and pinprick sensation to great toes billatery. .he wieght 200 pounds and is # foot, inches tall. 4er blood pressure is !% ,J mm hgP heart rate, &2 beats,minP and respiration, 2 breaths,min. her urine is negative for microalbuminoria. 4er vision is 20, 0 on the snellen chart. Nurs ng D agnos! c R sk for def c en! f$u d 4o$u%e re$a!ed !o '&perg$&ce% a $utcomes !. patient will maintain serum glucose level within normal parameters. 2. patient will remain free of fluid imbalance. Re$a!ed NOC Ou!co%es !. blood glucose level 2. fluid balance %. hydration Re$a!ed NIC In!er4en! ons !. (luid management 2. (luid monitoring %. 4ypoglycemia mangement :ursing Interventions,6ationales !. 8onitoring blood glucose levels. Increased blood glucose levels increase the osmolarity of the serum, which results in fluid being pulled from yhe tissue into the vascular space and elimination by the kidneys via osmotic diuresis

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2. -sses and monitoring for fluid volume deficiency. Diabetic patients are at increased risk for hypovolemia caused by osmotic diuresis secondary to hyperglyemia. +he earlier fluid volume deficiencies are identified, the quicker fluid balance can be restored. %. 2ncourage the intake of 2 to % ; of fluid per day. +o replace fluid losses and prevent hypervolemia and cellular dehydration. . +each patient the relationship between high blood glucose levels and fluid loss. +o help the patient understand the need for blood glucose control and to increase the likehood og complience with therapeutic regimen. #. +each patient signs and symptoms of fluid volume depletion and the need to report such menifestations quickly. +o facillitate early recognition and treatment. Nurs ng D agnos! c I%"a$ance nu!r ! on6 %ore !'an "od& re7u re%en!s $utcomes !. 5atient will achieve weight loss to within 20 pounds of ideal weight. 2. 5atient will select correct dietay choices within prescribed diet.

Re$a!ed NOC Ou!co%es !. :utritional status 2. :utritional status 9 food and fluid intake %. :utritional status 9 nutrient intake Re$a!ed NIC In!er4en! ons
32

!. 2ating disorders management 2. :utrition management %. 'eight management . 'eight reduction assistance :ursing Interventions,6ationales !. $btain a thorough diet history. +o asses the patientXs current dietary intake so that dietary alterations to maintain blood glucose control can be planned. 2. 2ncourage patient to become involved in setting goals for dietary changes, documenting food intake, and planning meals. 3hanges are more likely to be made when the patient is involved in planning those changes. 5atients know their own likes and dislikes, financial resources, and abillity to make dietary changes. 5articipation allows the patient greater control over situasion. %. .et realistic weight control goals. .etting goals that are unrealistic and unachievable produces frustation and hopelessnes, which may discourage the patient from trying to control her weight. . 4elp the patient identify an acceptable weight loss schedule permanent weight loss generally gradual and based on sound dietary principles. (ad diets should be avoided. +he patientXs agreement with thw weight loss plan increases the probability of complience. #. +each or reinforce earlier teaching about the selected system of dietary management. Cnowladge increases the likehood of complience. @. +each the patient how to handle sick days and unplanned social events. +o prepare the patient to deal appropriately with unusual dietary events or inability to intake food.

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". +each the patient the need for maintaining food intake distribution throughout the day. +o maintain consistency of blood glucose levels after the administration of insulin. Nurs ng D agnos! c R sk for nfec! on re$a!ed !o a$!ered ! ssue perfus on secondar& !o c'ron c '&perg$&ce% a $utcomes !. 5atient will remain free from infection. 2. 5atient will accurately verbali?e the relationship between poor blood glucose control and risk for infection. %. 5atient will accurately list signs and symptoms of infection. Re$a!ed NOC Ou!co%es !. Immune status 2. Cnowledge 9 infection control %. +issue integrity9 skin and mucous membaranes Re$a!ed NIC In!er4en! ons !. .kin surveillance 2. .urveillance %. +eaching 9 disease process :ursing Interventions,6ationales !. +each the patient the relationship between infection and metabolic control. If the patient understands that good metabolic control decreases the risk for
34

infection, she is more likely to comply with prescribed treatments. 8etabolic control reduces the e/tent of neoropathy that occurs from choronic hyperglycemia 2. 8onitor for signs of locali?ed infections )heat, redness, warmth, pain* and systemic infections )elevated white blood cell count, fever, lethargy*. 2arly detection of infection results in treatment being implemented more quickly. %. +each the patient the signs of locali?edand systemic infection. +he patient is usually the first to identify early infections. . +each patient to inspect feet dialy for signs of infection. Diabetic neuropathy )sensory loss* increases the patientXs risk for foot infections. +he need for foot care cannot be overemphasi?ed. Nurs ng D agnos! c Def c en! kno5$edge *se$f8ad% n s!ra! on of nsu$ n, care of e7u p%en!, 'o%e %on !or ng of "$ood g$ucose. re$a!ed !o $ack of pre4 ous e9posure !o nfor%a! on or sk $$. $utcomes !. 5atient will accurately verbali?e disease processP need for blood glucose controlP and signs of infection, hyperglycemia, and hypoglycemia. 2. 5atient will accurately demonstrate self-administration of insulin.

Re$a!ed NOC Ou!co%es !. Cnowledge 9 medication 2. Cnowledge 9 treatment regimen Re$a!ed NIC In!er4en! ons
35

!. +eaching 9 prescribed medication 2. +eaching 9 psycomotor skill %. :ursing Interventions,6ationales !. .upport and encourage patient as necessary to self-in1ect insulin. -t first patients may be afraid to self-in1ect. -dults who perform self-in1ections have minimal discomfort and come to reali?e they are capable of performing this skill. 2. Demonstrate and have patient return demonstrate home bloos glucose monitoring )4A08*, correcting technique as neede. +he patient needs to be taught the skill before performing it. 2valuation of patient skill is necesssary to ensure accuracy. %. +each the patient about the effect of activity,dietary intake, and insulin on blood glucose. Instruct patient on timing of blood glucose monitoring. +o help the patient understand that all aspects of care interaled. 4A08 provides immediete feedback about previous behaviors and reinforces the value of therapetic measures. . +each the signs and symptoms and treatment measures for hyperglycemia and hypoglycemia. +his knowledge decrease the fear of reactions and allows for quick intervention if hyperglycemia or hypoglycemia does occur. #. +each about the care of insulin and supplies. +o ensure that insulin remains stable and equipment is sterile. @. 6efer to dietitian for further teaching regarding any deitary modifications that need to be made now that the patient is receiving insulin. +he dietitian enforces previous teaching, assesses for new dietary needs, and teaches new information.
36

Nurs ng D agnos! c Ineffec! 4e 'ea$!' %a n!enance re$a!ed !o neffec! 4e cop ng sk $$s. $utcomes !. 5atient will independently maintain blood glucose control via diet, monitoring, and self-administration of insulin. 2. 5atient will state at least one change that will help her improve her blood glucose control. Re$a!ed NOC Ou!co%es !. 4ealth promoting behavior 2. Cnowedge 9 health resources %. Cnowledge 9 treatment regimen . 5articipation in health care decisions Re$a!ed NIC In!er4en! ons !. 3oping enhancement 2. 4ealth system guidence %. .elf-modifications assistance . +eaching 9 disease process :ursing Interventions,6ationales !. 3ounsel patient regarding effects of lack of e/ercise and diet on blood glucose levels. 3hange in behavior is more likely to occur if the patient understand the relationships between lifestyle , activity, diet, and glucose cotrol.

37

2. 2/plore willingness and abillity to change behaviors 9 sleep-activity, diet, and e/ercise. Aoals are more likely to be achieved if the patient agrees that the changes will be benefical. %. 2ngage patient in mutual problem solving as opposed to prescribing, increasing patients sesnse of control can help with self-esteem and enhance attitudes toward change . 2/plore sources for long-term support in learning more effective ways of coping )i.e., weight los, e/ercise, diabetes management*. 3hanging lifestyle, eating behaviors, and coping skills is diffcultP support over long periods is usually required. E4a$ua! on 2valuation is based on comparing the patient,s outcomes with desired outcomes.

CO:ER

3onclusion - Diabetes 8ellitus is a collection of symptoms that occur in a person who is caused by an increase in blood glucose levels due to insulin deficiency both in absolute and relative ).ubekti, et al .., !&&&*. 2tiological classification of diabetes mellitus -ccording to the -D- 200% terdriri on +ype ! Diabetes 8ellitus, Diabetes 8ellitus +ype 2 Diabetes 8ellitus and $ther +ypes.
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2pidemiologically D8 is often not detected. - variety of genetic, environmental and lifestyle play a role in the course of diabetes. +here is a tendency these diseases arise in the family. 0esides, it was also found differences in prevalence and complications among races, nations and cultures. +ype 2 diabetes will increase to #-!0 times as much as a change in the behavior of the traditional rural-to urban. 3hanging risk factors are increasing age epidemiologically, the number and duration of obesity, body fat distribution, lack of physical activity and hyperinsulinemia. -ll these factors interact with genetic factors associated with type 2 diabetes mellitus ).oegondo, !&&&*. 'ithout effective intervention, the incidence of type 2 diabetes increases caused by many things such as increased life e/pectancy, reduced deaths due to infection and increased risk factors are caused by wrong lifestyle such as obesity, lack of e/ercise , activity and unhealthy eating patterns and not regular ).lamet .uyono In Diabetes and ;ipid 3enter, 200"*. Aenesis D8 begins with insulin deficiency as a ma1or cause. $n the other hand the onset of diabetes can be derived from the relative lack of insulin caused by insulin resistance )insuline recistance*. +his situation is characteri?ed by ketidakrentanan , organ inability to use insulin, so insulin can not function optimally in regulating glucose metabolism. -s a result, increased blood glucose levels )hyperglycemia* )8: 0ustan, 200"*. 0oth the D8 type ! or type 2 diabetes mellitus clear blood glucose levels rise and when it passes the threshold level of the kidney, the glucose it will come out through the urine. 5erhaps this is why this disease is also called diabetes ).uyono, !&&&*. D8 diagnosis should be based on e/amination of blood glucose levels, can not be established only on the basis of glucosuria alone. In determining the diagnosis of diabetes should be considered the origin of the material is taken and the way blood e/amination used. +o diagnose diabetes, the recommended inspection is an
39

e/amination of glucose by en?ymatic method with capillary blood material )5erkeni, !&&J*. If the blood glucose is not well controlled, a few years later, almost always complications will arise. 3omplications from diabetes can be divided into two ma1or groups9 a*. -cute complications and b*. 3hronic complications. -ccording .idartawan while .oegondo, principles of drug delivery , treatment of diabetic patients consisted of 2, namely9 a. +reatment with insulin and, b. +reatment with antidiabetic medication. .uggestion .uggestions from our group is that we all maintain health and healthy living patterns. -void foods, activities that may trigger the occurrence of a disease. If there are symptoms of a disease such as Deabetes 8ellitus immediately come to the hospital to be addressed and to avoid any further complications. -s well as doing a diet low in protein and carbohydrates because it can increase the levels of sugar in the blood. RE1ERENCE+ -merican Diabetes -ssociation, e/pert committee on the diagnosisand classification of diabetes mellitus9 6eport of the e/pert committeeon the Diagnosis and classification of diabetes mellitus -merican Diabetes -ssosiation9 economic costs of diabetes in the us in 2002, diabetes care -hern S- et al9 insulin pump theraphy in pediatric9 a therapeutic alternativeto safely lower 4b- levels across all age groups, pediatric diabetes

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http9,,books.google.co.id,booksY idUZ+[":uDt?223\pgU5-#!&\dqUpemeriksaanWdiagnosticWdiabetesWmelitus\h lUid\saUZ\eiU!+Ci>ey;2seIr[egwoDw0-\redir]escUy^vUonepage\qUpemerik saan<20diagnostic<20diabetes<20melitus\fUfalse in access may 2" 20!%

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