ASKEP KLIEN DGN DIABETES MELLITUS

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1 ASKEP KLIEN DGN DIABETES MELLITUS
Ns. Yani Sofiani, M. Kep., Sp KMB

2 ANATOMI KELENJAR PANKREAS EKSOKRIN * PROTEASE * AMILASE ENZIM:
* LIPASE ENDOKRIN * GLUKAGON (SELα) * INSULIN (SELβ)

3 DEfinition A group of conditions characterised by chronically raised plasma glucose concentrations. This glucose abnormality is due to an absolute or relative lack of insulin and has many causes, though commonest are type 2 and type 1 diabetes

4 Plasma glucose controlled :
Plasma glucose are controlled within a narrow range by the beta cells in the pancreatic islets of Langerhans. Rise of plasma glucose will stimulate the secretion of insulin which will increase glucose uptake in the liver and storage as glycogen and also in muscle.

5 etiological classification
Type 1(beta cell destruction, usually leading to absolute insulin deficiency) Autoimmune Idiopathic Type 2 (may range from predominantly insulin resistance with relative insulin deficiency to a predominantly secretory defect with or without insulin resistance)

6 WHO diagnostic criteria
Plasma glucos concentration mmol/L mg/dl Diabetes mellitus Fasting Or 2-hour post glucose load Or both > 7.0 > 11.1 126 > 200 Impaired glucose tolerance And 2-hour post glucose load < 7.0 7.8 and < 7.0 <126 > 140 and < 200 Impaired fasting glycemia 2 hour 6.1 and < 7.0 < 7.8 110 and < 126 < 140

7 Diabetes Mellitus Type 2
Endogenous insulin is sufficient to prevent ketoacidosis but inadequate to prevent hyperglycemia Strong genetic influence Prevalence : Chinese & Japanese 30%, North American, European, African %, Pima Indian, Pacific Islanders Nauru & Samoa nearly 100% Aging, sedentary life style, abdominal visceral obesity enhance of insulin resistance

8 Diabetes Mellitus Type 2
Essentials of diagnosis Typically > 40 years of age Obesity Polyuria and polydipsia Candial vaginitis sometimes an initial manifestations Often few or no symptoms Often associated with hypetension, dyslipidemia, atherosclerosis

9 Diabetes Mellitus Type 2
Syptoms & signs Polyuria and thirst Weakness or fatigue Recurrent blurred vision Vulvovaginitis and pruritus Peripheral neuropathy Often asymptomatic

10 Diabetes Mellitus Type 2
Laboratory tests Fasting plasma glucose 2 hour after glucose load Glucosuria Ketonuia HbA1cLipid profile

11 Diabetes Mellitus Type 2
Treatment Diet Excercise Oral agents single or combination Insulin Tim-oriented educational approach Treat other risk factors

12 OAD (oral antidiabetic Drug)
Biguanide : ­ Metformin Insulin secretagogue a. Sulfonilurea : ­ glibenclamide ­ gliclazide ­ glipizide ­ glimepiride b. Meglitinide: repaglinide & nateglinide AGI (-glukosidase inhibitor): acarbose Insulin sensitizer: thiazolidinedione (TZD)

13 Diabetes Mellitus Type 2
Complications ( acut >< cronik ) acut : hipo/hiperglikemia cronik : mikro/makrovaskuler  retinopati, nefropati, neuropati, stroke, CHF dll Hospitalization : Altered mental status, ketoacidosis, volume disorders, electrolyte disorders, unstable comorid conditions

14 Perkembangan Diabetes Tipe 2
Resistensi Insulin Fungsi Sel-Beta SU ? Resistensi Insulin & Hiperinsulinemia dg Toleransi Glucosa Normal Insulin resistance and impaired beta-cell function are primary defects that occur early in the course of development of type 2 diabetes. Insulin resistance leads to an obligatory hyperinsulinemia in order to maintain normal glucose tolerance. In most cases of type 2 diabetes, beta-cell dysfunction develops subsequent to the development of insulin resistance and it is not until such beta-cell dysfunction develops that any abnormality in glucose tolerance is seen. The condition which results is termed impaired glucose tolerance. In some cases individuals may develop beta-cell dysfunction in the absence of early insulin resistance. However, exposure of tissues to hyperglycemia in the face of beta-cell dysfunction adds resistance to the effects of insulin whether or not insulin resistance was present to begin with. Ultimately, type 2 diabetes is the result of worsening beta-cell function, either in the most common situation of chronic pre-existing insulin resistance or, in the less common scenario of decreased beta-cell function without pre-existing insulin resistance. It is interesting to note that animal studies have demonstrated that the beta-cell dysfunction that occurs most commonly following pre-existing insulin resistance may actually be a function of the pre-existing insulin resistance itself. Resistensi Insulin & Kadar Insulin Menurun dg Toleransi Glucosa Terganggu (IGT) Diabetes Tipe 2 Adapted from Diabetes 1996;45:1661

15 Insulin Resistance: Associated Conditions
Type 2 diabetes Impaired glucose tolerance Atherosclerosis Dyslipidemia Hypertension Insulin Resistance Decreased fibrinolytic activity Obesity (central) In addition to type 2 diabetes, insulin resistance is a pathogenic factor in the development of a broad spectrum of clinical conditions. These include hypertension, atherosclerosis, dyslipidemia, decreased fibrinolytic activity, impaired glucose tolerance, acanthosis nigricans, hyperuricemia, polycystic ovary disease, and obesity. Polycystic ovary disease Hyperuricemia KLINIS

16 Diabetes Type 1 Differences
Absence of significant insulin secretion, less than 10%, and none after 5 years Largely immunological process Require insulin treatment within short period Weight loss Ketonemia or ketonuria or both The need of insulin does not change Type 2 into type 1, a misunderstanding

17 Diabetes Type 1 Treatment
Insulin : rapid, short, intermediate-acting, premixed, long-acting

18 Pengkajian Keperawatan
Data Subyektif Important Health Information ¤ Riwayat kesehatan yang lalu: mumps, rubella,coxsakievirus atau infeksi virus lain; trauma yang terakhir dialami, infeksi atau stres; kehamilan; pankreatitis kroni; cushing syndrome, akromegaly; adanya riwayat DM tipe I atau tipe II pada keluarga.

19 Obat-obatan: kepatuhan penggunaan insulin
Obat-obatan: kepatuhan penggunaan insulin atau OHO (oral agents, seperti: Sulfonylureas, Meglitinides, Biguanides, dll); penggunaan kortikosteroid, diuretik, phenytoin (Dilantin) ¤ Pembedahan atau pengobatan lain: pembedahan yang terakhir dilakukan

20 ¤ Persepsi kesehatan – health. management: adanya riwayat keluarga;
¤ Persepsi kesehatan – health management: adanya riwayat keluarga; malaise; pemeriksaan mata dan gigi yang terakhir ¤ Nutritional – metabolic: obesitas; kehilangan BB (tipe I); penambahan BB (tipe II): haus, lapar; nausea dan muntah; penyembuhan yang lama terutama luka di kaki, kepatuhan terhadap program diet, terutama pada klien yang sebelumnya telah didiagnosa diabetes.

21 ¤ Eliminasi: konstipasi atau diare;. frekuensi
¤ Eliminasi: konstipasi atau diare; frekuensi urinasi, nokturia, inkotinensia urin; infeksi kulit ¤ Aktifitas – exercise: kelemahan otot, fatigue ¤ Kognitif – persepsi: nyeri abdomen, sakit kepala; penglihatan kabus; numbness (mati rasa) atau tingling (rasa geli) pada ekstremitas; pruritus

22 ¤ Seksual-reproduksi: impotensi,. seringnya
¤ Seksual-reproduksi: impotensi, seringnya infeksi vaginal; penurunan libido ¤ Koping – toleransi stress: depresi, iritabilitas, apatis ¤ Nilai – keyakinan: komitmen terhadap perubahan gaya hidup meliputi diet, pengobatan dan pola aktifitas

23 Data Obyektif ¤ Mata: lembut, sunken eyeballs ; perdarahan badan kaca (vitreous) pada mata, katarak ¤ Integumen: kering, hangat, kulit yang tidak elastis; pigmented lesions (pada kaki); ulser (terutama pada kaki), kehilangan rambut pada kaki

24 ¤Pernafasan: cepat dan dalam (kusmaul)
¤Kardiovaskular: hipotensi; kelemahan, nadi cepat ¤Gastrointestinal: mulut kering, muntah, fruity breath ¤Neurologi: gangguan refleks, kelemahan, bingung, stupor, koma

25 ¤Muskuloskeletal: muscle wasting (penurunan massa otot)
¤ lab

26 Diagnosa keperawatan Resiko/gangguan keseimbangan volume cairan dan / atau elektrolit : kurang dari kebutuhan tubuh b.d. diuresis osmotik Gangguan nutrisi kurang dari kebutuhan tubuh b.d. defisiensi insulin Resiko infeksi Resiko penyebaran infeksi dll