Presentasi sedang didownload. Silahkan tunggu

Presentasi sedang didownload. Silahkan tunggu

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

Presentasi serupa


Presentasi berjudul: "ASKEP KLIEN DGN DIABETES MELLITUS Ns. Yani Sofiani, M. Kep., Sp KMB."— Transcript presentasi:

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

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

3 DE FINITION 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 P LASMA 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 Diabetes mellitus Fasting Or 2-hour post glucose load Or both > 7.0 > 11.1  126  > 200 Impaired glucose tolerance Fasting And 2-hour post glucose load < 7.0  7.8 and < 7.0 <126 > 140 and < 200 Impaired fasting glycemia Fasting 2 hour  6.1 and < 7.0  < 7.8  110 and < 126  < 140 Plasma glucos concentration mmol/L mg/dl

7 D IABETES M ELLITUS T YPE 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 D IABETES M ELLITUS T YPE 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 D IABETES M ELLITUS T YPE 2 Syptoms & signs Polyuria and thirst Weakness or fatigue Recurrent blurred vision Vulvovaginitis and pruritus Peripheral neuropathy Often asymptomatic

10 D IABETES M ELLITUS T YPE 2 Laboratory tests Fasting plasma glucose 2 hour after glucose load Glucosuria Ketonuia HbA1cLipid profile

11 D IABETES M ELLITUS T YPE 2 Treatment Diet Excercise Oral agents single or combination Insulin Tim-oriented educational approach Treat other risk factors

12 1. Biguanide: ­ Metformin 2. Insulin secretagogue a. Sulfonilurea: ­ glibenclamide ­ gliclazide ­ glipizide ­ glimepiride b. Meglitinide: repaglinide & nateglinide 3. AGI (  -glukosidase inhibitor): acarbose 4. Insulin sensitizer: thiazolidinedione (TZD) OAD (oral antidiabetic Drug)

13 D IABETES M ELLITUS T YPE 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 P ERKEMBANGAN D IABETES T IPE 2 Resistensi Insulin Resistensi Insulin & Hiperinsulinemia dg Toleransi Glucosa Normal Resistensi Insulin & Kadar Insulin Menurun dg Toleransi Glucosa Terganggu (IGT) Diabetes Tipe 2 Fungsi Sel-Beta Adapted from Diabetes 1996;45:1661 ? SU

15 I NSULIN R ESISTANCE : A SSOCIATED C ONDITIONS Atherosclerosis Type 2 diabetes Impaired glucose tolerance Polycystic ovary disease Obesity (central) Dyslipidemia Hypertension Hyperuricemia Decreased fibrinolytic activity Insulin Resistance KLINIS

16 D IABETES T YPE 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 D IABETES T YPE 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 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; 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 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 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 D IAGNOSA 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


Download ppt "ASKEP KLIEN DGN DIABETES MELLITUS Ns. Yani Sofiani, M. Kep., Sp KMB."

Presentasi serupa


Iklan oleh Google