DIABETES MELLITUS TA SON TEDAVI YAKLASIMLARI

DIABETES MELLITUS TA SON TEDAVI YAKLASIMLARI PowerPoint PPT Presentation


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DIABETES MELLITUS TA SON TEDAVI YAKLASIMLARI

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1. DIABETES MELLITUS’TA SON TEDAVI YAKLASIMLARI Doç.Dr.Fulya AKIN PAÜTF Endokrinoloji ve Metabolizma Hastaliklari

2. Diyabet Tedavisinde Dönüm Noktalari Uzun-etkili insulin analoglari • It has been more than 80 years since the discovery of insülin, and as this timeline shows, there has been continuing progress. In fact, much of our current understanding of diabet, its devastating consequences, and its effective management has been attained during the latter part of this timeline. As this presentation will discuss, despite the progress of science, there are still many challenges to be overcome Researchers at the University of Toronto discovered insülin in 19211 The first sulphonylureas appeared during the early 1940s1 Hans Christian Hagedorn’s delayed-action preparation, “neutral protamine Hagedorn,” appeared in 1946; we know it as NPH1 The Lente series appeared in 19521 Metformin became available (outside the United States) in 19601 Portable insülin infusion pumps were introduced during the late 1970s1 The Diabet Control and Complications Trial was published in 19931 Rapid-acting insülin analogues became available in 19962 The United Kingdom Prospective Diabet Study was published in 19981 Lantus? (insülin glargine; the first long-acting insülin analogue) received US Food and Drug Administration approval in 20003• It has been more than 80 years since the discovery of insülin, and as this timeline shows, there has been continuing progress. In fact, much of our current understanding of diabet, its devastating consequences, and its effective management has been attained during the latter part of this timeline. As this presentation will discuss, despite the progress of science, there are still many challenges to be overcome Researchers at the University of Toronto discovered insülin in 19211 The first sulphonylureas appeared during the early 1940s1 Hans Christian Hagedorn’s delayed-action preparation, “neutral protamine Hagedorn,” appeared in 1946; we know it as NPH1 The Lente series appeared in 19521 Metformin became available (outside the United States) in 19601 Portable insülin infusion pumps were introduced during the late 1970s1 The Diabet Control and Complications Trial was published in 19931 Rapid-acting insülin analogues became available in 19962 The United Kingdom Prospective Diabet Study was published in 19981 Lantus? (insülin glargine; the first long-acting insülin analogue) received US Food and Drug Administration approval in 20003

3. Diabetes Mellitus’ta Glisemik Kontrol Hedefleri

4. Tip 2 Diabet nasil tedavi edilmelidir?

5. Tip 2 diyabet tedavisinde kalici ve sürekli glisemi kontrolü ile komplikasyonlara bagli morbidite ve mortaliteyi azaltmak hedeflenmelidir.1 1Reusch JE, Gadsby R: Thiazolidinedione Therapy: The benefits of agressive and early use in type 2 diabetes.Diabetes Technol Ther. 5. 4(2003): 685-93.

6. Yasam tarzi degisiklikleri Ilk basamak tedavidir1 Belfast Diet Study: 223 yeni tani Tip 2 DM, ~80% taniyi takiben 6 yil sadece diyet tedavisi verilmis.2 Ilk birkaç ay, kan sekeri ve agirlikta azalma gözlenmis.2 Diyet tedavisini sürdüren hastalarin ?-hücre fonksiyonunda azalma ile birlikte progresif kan sekeri yükseklikleri oldugu görülmüstür.3

7. Glisemik kontrol diyet veya konvansiyonel monoterapilerle saglanamaz.* Traditional monotherapy generally fails Treatment with diet alone, insulin or sulphonylurea is known to improve glycaemia in patients with Type 2 diabetes, but which treatment most frequently attained HbA1c below 7% was unknown. The UKPDS study aimed to assess how often each therapy can achieve the glycaemic control target levels set by the American Diabetes Association. Newly diagnosed Type 2 diabetes patients were followed up every 3 months for 3, 6 and 9 years after enrollment. After 3 months on a low-fat, high-carbohydrate, high-fibre diet, patients were randomised to therapy with diet alone, insulin or sulphonylurea. The proportion of patients who maintained target glycaemic levels declined markedly over 9 years of follow-up. After 9 years of monotherapy with diet, insulin, or sulphonylurea, 8%, 42% and 24%, respectively, achieved FPG levels of less than 7.8 mmol/L (140 mg/dL) and 9%, 28% and 24% achieved HbA1c levels below 7%. Link to next slide: Is combination therapy the answer? Reference Turner RC et al. JAMA 1999; 281: 2005–2012.Traditional monotherapy generally fails Treatment with diet alone, insulin or sulphonylurea is known to improve glycaemia in patients with Type 2 diabetes, but which treatment most frequently attained HbA1c below 7% was unknown. The UKPDS study aimed to assess how often each therapy can achieve the glycaemic control target levels set by the American Diabetes Association. Newly diagnosed Type 2 diabetes patients were followed up every 3 months for 3, 6 and 9 years after enrollment. After 3 months on a low-fat, high-carbohydrate, high-fibre diet, patients were randomised to therapy with diet alone, insulin or sulphonylurea. The proportion of patients who maintained target glycaemic levels declined markedly over 9 years of follow-up. After 9 years of monotherapy with diet, insulin, or sulphonylurea, 8%, 42% and 24%, respectively, achieved FPG levels of less than 7.8 mmol/L (140 mg/dL) and 9%, 28% and 24% achieved HbA1c levels below 7%. Link to next slide: Is combination therapy the answer? Reference Turner RC et al. JAMA 1999; 281: 2005–2012.

8. OAD monoterapisi zaman içinde A1C hedefini sürdürmede yetersiz kalir

9. Çalismalar hastalarin çogunun A1C hedeflerine ulasamadiklarini göstermistir.1,2 Tip 2 diyabet ilerledikçe3 etkin kontrol saglamak için sonunda insülin gerekinceye kadar diger OAD’ler eklenir Çoklu ilaç tedavisi gerekliligi4 Tanidan ~ 3 yil sonra hastalarin ~ %50’sinde Tanidan ~ 9 yil sonra hastalarin ~ %75’inde

10. Tip 2 diyabet tedavisinde güncel yaklasim Diyabet komplikasyonlarini belirgin sekilde azaltabilir1,2 Son yillarda tip 2 diyabetli hastalarin tedavisine yaklasim biçimi büyük ölçüde degismistir3,4 Glisemik kontrol hedeflerinin asagi çekilmesi ve geleneksel basamakli tedavinin yerine insülin ve kombinasyon tedavilerine daha erken baslanmasi benimsenmistir3,4

11. Tip 2 Diyabette Tedavi Yaklasimi This slide illustrates the current treatment algorithm for type 2 diabetes patients. Initially, there is a pre-diabetes period, where normal glucose tolerance shifts into a state of impaired glucose tolerance (IGT). This initial phase probably starts at the age of 20 to 30 years, but is usual undiagnosed because few, if any, clinical symptoms present. As IGT worsens, symptoms become apparent, and type 2 diabetes is diagnosed. Following modification of lifestyle with diet and exercise, monotherapy with an oral antidiabetic agent is the first pharmaco-therapeutic intervention. As the disease progresses, most patients need a combination of agents to control their glycemia. Treatment with insulin, alongside combination therapy might eventually be needed and, if pancreatic failure occurs, intravenous insulin may be administered. Key studies, such as the United Kingdom Prospective Diabetes Study (UKPDS), show that aggressive pharmacotherapy significantly reduces the risk and incidence of microvascular complications, and might reduce the risk of macrovascular complications. Consequently, a global trend is developing to treat diabetes earlier and more aggressively to manage glycemia, delay disease progression, and minimize the development of complications that increase morbidity and mortality in patients with type 2 diabetes.This slide illustrates the current treatment algorithm for type 2 diabetes patients. Initially, there is a pre-diabetes period, where normal glucose tolerance shifts into a state of impaired glucose tolerance (IGT). This initial phase probably starts at the age of 20 to 30 years, but is usual undiagnosed because few, if any, clinical symptoms present. As IGT worsens, symptoms become apparent, and type 2 diabetes is diagnosed. Following modification of lifestyle with diet and exercise, monotherapy with an oral antidiabetic agent is the first pharmaco-therapeutic intervention. As the disease progresses, most patients need a combination of agents to control their glycemia. Treatment with insulin, alongside combination therapy might eventually be needed and, if pancreatic failure occurs, intravenous insulin may be administered. Key studies, such as the United Kingdom Prospective Diabetes Study (UKPDS), show that aggressive pharmacotherapy significantly reduces the risk and incidence of microvascular complications, and might reduce the risk of macrovascular complications. Consequently, a global trend is developing to treat diabetes earlier and more aggressively to manage glycemia, delay disease progression, and minimize the development of complications that increase morbidity and mortality in patients with type 2 diabetes.

12. Tip 2 diyabet tedavisinde güncel yaklasim Hedef A1C degeri Genel olarak: <%7 Bireysel olarak: Hipoglisemi yasanmamasi kosulu ile <%6 Yasam beklentisi düsük ve hipoglisemi riski varsa hedefler gözden geçirilmeli A1C ölçümü Hedef degere ulasilana dek: 3 ayda bir Hedefe ulasildiktan sonra: En az 6 ayda bir

13. Tip 2 diyabet tedavisinde güncel yaklasim KG hedefi Önce açlik ve ögün öncesi KG hedeflenmeli Hedefi 70-130 mg/dl (kapiler) Açlik ve ögün öncesi KG hedefleri sürdürülemiyorsa veya A1C =%7 ise postprandiyal KG Hedef: <180 mg/dl Ögünlerden 90-120 dk sonra

14. Tip 2 diyabet tedavisinde güncel yaklasim Tedavi seçiminde glukoz düsürücü etkinin yaninda güvenlik, tolerabilite ve maliyet önemli Siklikla diyabete eslik eden hipertansiyon ve hiperlipidemi vb. güncel kilavuzlara uygun tedavi edilmeli

15. Tip 2 diyabet tedavisinde güncel yaklasim Taniyi takiben yasam tarzi düzenlemeleri ve metformin Beslenme Fiziksel aktivite Kilo kaybi (en az 4 kg veya agirligin %5’i) Evde kan sekeri takibi Metformin 2 X 500 mg baslanmali ve 1-2 ay içinde etkili dozlara çikilmali: 2 X 850 mg (maksimum 3.000 mg/gün)

16. Tip 2 diyabet tedavisinde güncel yaklasim Glisemik hedeflere ulasilamazsa veya hedefler sürdürülemiyorsa kisa sürede yeni ilaç ve yeni tedavi rejimi A1C =%7 ise ikinci bir ilaç eklenmeli (bazal insülin en etkili seçenek) A1C >%8.5 ise ve diyabet semptomlari varsa insülin (tercihen bazal insülin) baslanmali

17. Tip 2 diyabet tedavisinde güncel yaklasim Glisemik hedeflere ulasilamadiginda zaman kaybetmeden insülin tedavisine baslanmali veya insülin tedavisi yogunlastirilmali A1C <%8 ? Üçüncü bir ilaç (Tedavi maliyeti!) Hizli/kisa etkili insülin ile ? Salgilatici ilaçlar kesilmeli (sulfonilüre veya glinidler) Insülin tedavisi + insülin duyarlilastirici bir ilaç (tercihen metformin) Insülin + glitazon sivi retansiyonu riskini artirabilir!

20. OAD’ lerin Metabolik Etkileri

22. RECORD: yorumlar Metformin ve sülfonilüre alan hastalarla kiyaslandiginda, rosiglitazon olan hastalarda genel kardiyovasküler (KV) hospitalizasyon ve KV ölüm oranlarinda bir artis gözlenmedi1 Genel KV sonuçlar, KKY parametresinin eklendigi durumda bile, metformin ve sülfonilüreye kiyasla rosiglitazon için benzerdi1 Metformin , UKPDS çalismasinda MI ve herhangi bir nedene bagli ölümü azaltmada bir fayda ortaya koymustu2 Sekonder birlesik sonlanim noktasi olan KV ölüm, MI veya inme, rosiglitazon veya aktif kontrol grubundaki hastalarda benzer bulundu1 Metformin veya sülfonilüreye eklenen rosiglitazon, 5 yilda hastalarda HbA1c ‘de sürekli bir azalma sergiledi1 Metformin ve sülfonilüre alan hastalarla kiyaslandiginda, rosiglitazon olan hastalarda genel kardiyovasküler (KV) hospitalizasyon ve KV ölüm oranlarinda bir artis gözlenmedi.1 Genel KV sonuçlar, KKY parametresinin eklendigi durumda bile, metformin ve sülfonilüreye kiyasla rosiglitazon için benzerdi. UKPDS çalismasinda, asiri kilolu hastalarda olusan metformin grubunda, miyokard infarktüsünde (%39, P = 0.01) ve herhangi bir nedene bagli ölümde (%36, P = 0.01) önemli risk azalmalari, orijinal çalismada intensif tedavi grubunda gözlendi. Bu risk azalmalari çalisma sonrasi dönemde de korundu.2 Sekonder birlesik sonlanim noktasi olan kardiyovasküler ölüm, miyokard infarktüsü veya inme, rosiglitazon veya aktif kontrol grubundaki hastalarda benzer bulundu.1 Metformin veya sülfonilüreye eklenen rosiglitazon, 5 yilda hastalarda HbA1c ‘de sürekli bir azalma sergiledi.1 Tiazolidindionlarla önceden bilinen, konjestif kalp yetmezligi ve kemik kirigi riskindeki artis bu çalismada teyit edildi.1 Home PD, et al. Lancet 2009;373:2125–2135. Holman RR, et al. N Engl J Med 2008;359:1577–1589. Metformin ve sülfonilüre alan hastalarla kiyaslandiginda, rosiglitazon olan hastalarda genel kardiyovasküler (KV) hospitalizasyon ve KV ölüm oranlarinda bir artis gözlenmedi.1 Genel KV sonuçlar, KKY parametresinin eklendigi durumda bile, metformin ve sülfonilüreye kiyasla rosiglitazon için benzerdi. UKPDS çalismasinda, asiri kilolu hastalarda olusan metformin grubunda, miyokard infarktüsünde (%39, P = 0.01) ve herhangi bir nedene bagli ölümde (%36, P = 0.01) önemli risk azalmalari, orijinal çalismada intensif tedavi grubunda gözlendi. Bu risk azalmalari çalisma sonrasi dönemde de korundu.2 Sekonder birlesik sonlanim noktasi olan kardiyovasküler ölüm, miyokard infarktüsü veya inme, rosiglitazon veya aktif kontrol grubundaki hastalarda benzer bulundu.1 Metformin veya sülfonilüreye eklenen rosiglitazon, 5 yilda hastalarda HbA1c ‘de sürekli bir azalma sergiledi.1 Tiazolidindionlarla önceden bilinen, konjestif kalp yetmezligi ve kemik kirigi riskindeki artis bu çalismada teyit edildi.1 Home PD, et al. Lancet 2009;373:2125–2135. Holman RR, et al. N Engl J Med 2008;359:1577–1589.

23. Tiazolidindionlarla önceden bilinen bir sinif etkisi olan, konjestif kalp yetmezligi ve kemik kirigi riskindeki artis bu çalismada teyit edildi1

24. Yeni oral tedaviler adacik disfonksiyonunu hedef almaktadirlar The primary metabolic defects of T2DM are pancreatic islet dysfunction (?-cell and ?-cell dysfunction) and impaired insulin action (insulin resistance); another contributing factor is uncompensated glucose influx. Many of these specific problems are addressed by one or another existing class of oral antihyperglycemic drugs, each of which has distinctive mechanisms.1 ?-Glucosidase inhibitors moderate glucose influx by delaying intestinal carbohydrate absorption, thereby mitigating postprandial glucose excursions.1 The utility of these agents depends in part on proper dietary compliance and is more effective in populations whose diet does not consist of highly processed foods. The widespread use of these agents in Japan and Spain is an excellent example of their utility in populations where a rice and fish diet is prevalent. Thiazolidinediones (TZDs) work primarily by enhancing both basal and insulin-mediated suppression of hepatic glucose production and to some extent by augmenting insulin-stimulated muscle glucose utilization.2 Metformin (of the biguanide drug class) lowers glucose levels, chiefly by reducing heptic glucose production.1 Sulfonylureas lower the glucose threshold for triggering ?-cell insulin release.1 Glinides resemble sulfonylureas in enhancing acute ?-cell function. Their short metabolic half-lives enable them to produce brief, episodic stimulation of insulin secretion.1 Of the glinides, nateglinide is rapidly reversible, whereas repaglinide is not. No currently available therapy addresses ?-cell function (glucagon) and chronic ?-cell function. References 1. Inzucchi SE. Oral antihyperglycemic therapy of type 2 diabetes: scientific review. JAMA. 2002;287-360–372. 2. DeFronzo RA. Impaired glucose tolerance: do pharmacological therapies correct the underlying metabolic disturbance? Br J Diabetes Vasc Dis. 2003;3(suppl 1):S24–S40. The primary metabolic defects of T2DM are pancreatic islet dysfunction (?-cell and ?-cell dysfunction) and impaired insulin action (insulin resistance); another contributing factor is uncompensated glucose influx. Many of these specific problems are addressed by one or another existing class of oral antihyperglycemic drugs, each of which has distinctive mechanisms.1 ?-Glucosidase inhibitors moderate glucose influx by delaying intestinal carbohydrate absorption, thereby mitigating postprandial glucose excursions.1 The utility of these agents depends in part on proper dietary compliance and is more effective in populations whose diet does not consist of highly processed foods. The widespread use of these agents in Japan and Spain is an excellent example of their utility in populations where a rice and fish diet is prevalent. Thiazolidinediones (TZDs) work primarily by enhancing both basal and insulin-mediated suppression of hepatic glucose production and to some extent by augmenting insulin-stimulated muscle glucose utilization.2 Metformin (of the biguanide drug class) lowers glucose levels, chiefly by reducing heptic glucose production.1 Sulfonylureas lower the glucose threshold for triggering ?-cell insulin release.1 Glinides resemble sulfonylureas in enhancing acute ?-cell function. Their short metabolic half-lives enable them to produce brief, episodic stimulation of insulin secretion.1 Of the glinides, nateglinide is rapidly reversible, whereas repaglinide is not. No currently available therapy addresses ?-cell function (glucagon) and chronic ?-cell function. References 1. Inzucchi SE. Oral antihyperglycemic therapy of type 2 diabetes: scientific review. JAMA. 2002;287-360–372. 2. DeFronzo RA. Impaired glucose tolerance: do pharmacological therapies correct the underlying metabolic disturbance? Br J Diabetes Vasc Dis. 2003;3(suppl 1):S24–S40.

25. Tip 2 diabet ve obezitede yeni tedaviler Inkretinler: 1.GLP-1 mimetikler, 2.DPP inhibitörleri Inhale/oral insulinler Rimonabant Dual PPAR agonistleri

26. Inkretinler (GLP-1 ve GIP) glukoz homeostazini adacik hücre fonksiyonlari üzerinden etkilerler Incretins (GLP-1 and GIP) Regulate Glucose Homeostasis Through Effects on Islet Cell Function The presence of nutrients in the gastrointestinal tract rapidly stimulates the release of incretins: GLP-1 from L cells located primarily in the distal gut (ileum and colon) and GIP from K cells in the proximal gut (duodenum).1,2 Collectively, GLP-1 and GIP exert several beneficial actions, including stimulating the insulin response in pancreatic beta cells (GLP-1 and GIP) and inhibiting glucagon secretion from pancreatic alpha cells when glucose levels are elevated.2-4 Increased insulin levels improve glucose uptake by peripheral tissues, while the combination of increased insulin and decreased glucagon reduce hepatic glucose output.5,6Incretins (GLP-1 and GIP) Regulate Glucose Homeostasis Through Effects on Islet Cell Function The presence of nutrients in the gastrointestinal tract rapidly stimulates the release of incretins: GLP-1 from L cells located primarily in the distal gut (ileum and colon) and GIP from K cells in the proximal gut (duodenum).1,2 Collectively, GLP-1 and GIP exert several beneficial actions, including stimulating the insulin response in pancreatic beta cells (GLP-1 and GIP) and inhibiting glucagon secretion from pancreatic alpha cells when glucose levels are elevated.2-4 Increased insulin levels improve glucose uptake by peripheral tissues, while the combination of increased insulin and decreased glucagon reduce hepatic glucose output.5,6

27. Inkretinlerin Karsilastirilmasi

28. Mevcut Stratejiler DPP-4 aktivitesini inhibe etmek (DPP-4 inhibitörleri; inkretin artiricilar)

29. Artiricilar (DPP-4 inhibitörleri) Oral aktiftir, günde bir kez alinirlar. Orta derecede (fizyolojik dozda) inkretin hormon konsantrasyonlarini artirirlar. Her iki inkretin hormon (GIP and GLP-1) üzerine etkileri vardir. Kilo üzerine etkileri nötrdür ve GI yan etkileri yoktur.

30. Mimetikler (GLP-1 reseptör aktivatörleri) Injektabl formdadirlar; farkli doz skalalari (2 x günde ? 1 x haftada) vardir. Yüksek (farmakolojik dozda) of GLP-1-reseptör aktivatör plazma konsantrasyonlarini artirirlar. BütünGLP-1 reseptörleri üzerine güçlü etkileri vardir. (a- ve ß-hücreleri, istah, yiyecek alimi, vücut agirligi) Kilo kaybina sebep olurlar. GI yan etkileri vardir. Bazan antikor olusumuna sebep olabilirler.

31. Tip 2 diyabette glisemik kontrolün saglanmasi

32. Insülin Tedavisi Rejimleri Konvansiyonel insülin tedavisi Günde 1-2 enjeksiyon Intensif insülin tedavisi Multipl enjeksiyon (bazal-bolüs insülin tedavisi) Sürekli subkutan insülin enjeksiyonu (pompa tedavisi)

33. Bazal Insülin Destegi (Endojen insülin rezervi olmasi gerekir) Tek doz NPH/Glargin/Detemir* + SU/MGT Tek veya iki doz NPH /Glargin/Detemir + MF/TZD Tek doz NPH /Glargin/Detemir + SU/MGT + MF

34. Klasik Insülinlerin Etki Profili

35. Insülin Tedavisi Endikasyonlari Tip 1 Diyabet LADA GDM (diyetle kontrol saglanamazsa) Tip 2 Diyabette OAD’ler ile iyi metabolik kontrol saglanamamasi Asiri kilo kaybi Agir hiperglisemik semptomlar Akut miyokard infarktüsü Akut atesli, sistemik hastaliklar Hiperozmolar veya ketotik koma (HONK, DKA) Major cerrahi operasyon Gebelik ve laktasyon Böbrek veya karaciger yetersizligi OAD’lere allerji veya agir yan etkiler Agir insülin rezistansi (?)

36. Insan Insülinlerinin Kisitlamalari Regüler insülin (ögünlerle iliskili) Emilimi yavas oldugu için yemeklerden yarim saat önce enjekte edilmeli Erken post-prandiyal hiperglisemi riski Geç post-prandiyal hipoglisemi riski NPH insülin (bazal) Erken hiperglisemi kontrol edilemez Geç dönemde hipoglisemi riski artar Hazir karisim insan insülinleri Regüler ve NPH insülinin kisitlamalarini içerir

37. Günde Iki Kez Uygulanan NPH Tedavisinin Sinirli Yönleri The regimen of twice-daily NPH and regular insulin attempts to mimick physiologic insulin secretion. However, this regimen results in many gaps in insulin coverage, during which the patient is at risk for hyperglycaemia, leading to poor long-term control1,2 As a result, NPH and regular insulin profiles do not come close to matching the normal endogenous secretory pattern1,2 “Dawn phenomenon” refers to the early morning fall in tissue insulin sensitivity counteracted by increased insulin secretion in individuals without diabetes but manifested as rising glycaemia in some patients with diabetes3The regimen of twice-daily NPH and regular insulin attempts to mimick physiologic insulin secretion. However, this regimen results in many gaps in insulin coverage, during which the patient is at risk for hyperglycaemia, leading to poor long-term control1,2 As a result, NPH and regular insulin profiles do not come close to matching the normal endogenous secretory pattern1,2 “Dawn phenomenon” refers to the early morning fall in tissue insulin sensitivity counteracted by increased insulin secretion in individuals without diabetes but manifested as rising glycaemia in some patients with diabetes3

38. Normal Insülin Sekresyonu: Bazal-Bolus Insülin Kavrami In individuals with normal weight who do not have diabetes, 2 patterns of insulin output are seen: basal insulin, which is secreted at a fairly constant rate between meals and at night to maintain euglycaemia, and during early morning hours; and bolus insulin, which is meal-related1 The therapeutic challenge for patients with diabetes is to provide enough basal insulin to control between-meal hyperglycaemia—which is due to hepatic glucose production—and enough bolus insulin to minimise hyperglycaemia immediately after meals. The provision of adequate levels of basal and bolus insulin may reduce risk for hypoglycaemia in individuals with erratic schedules or in those who have greater insulin requirements1 In individuals with normal weight who do not have diabetes, 2 patterns of insulin output are seen: basal insulin, which is secreted at a fairly constant rate between meals and at night to maintain euglycaemia, and during early morning hours; and bolus insulin, which is meal-related1 The therapeutic challenge for patients with diabetes is to provide enough basal insulin to control between-meal hyperglycaemia—which is due to hepatic glucose production—and enough bolus insulin to minimise hyperglycaemia immediately after meals. The provision of adequate levels of basal and bolus insulin may reduce risk for hypoglycaemia in individuals with erratic schedules or in those who have greater insulin requirements1

39. Bazal/Bolus Insülin Tedavisi Anlayisi

40. Insülin Analoglari A. Hizli ve kisa etkili Lispro: Humalog Aspart: NovoRapid Glulisin: Apidra B. Uzun etkili ve piksiz Glargin: Lantus Detemir: Levemir

41. Etki Süresine göre Insülin Analoglari

43. Insülin Doz Hesabi Bazal %50 (%40-60) Bolüs %50 (%40-60)

44. Bazal Insülin Dozu Hedef AKS 100-120 mg/dl Tip 2 diyabette tek doz 10 iu basla Veya 0.1-0.2 iu/kg/gün tek doz basla Tek doz NPH’tan Glargine ayni dozda geç, 2 doz NPH’dan geçiste %20-30 azalt NPH’dan Detemir’e %10-15 artir

46. ÖZET Tip 2 diyabet hastalarinda uzun dönemde glisemik kontrol hedeflerine ulasilamamaktadir. Erken, yogun glisemi kontrolü gereklidir.Insulin direnci ve ?-hücre disfonksiyonunu hedef alan tedavi, hastaligin önlenmesi ve klinik sonuçlarda iyilesmeyi saglayacaktir. CORE SLIDECORE SLIDE

47. TEMD-2009

49. Global Trend Daha erken ve daha agressif tedavi

50. VAKA 1

51. Ü.Ö. 27.04.06 56 y , erkek 5 yildir tip 2 DM tanisi olan hasta 1.5 yildir novomix sabah 16ü aksam 8ü kullaniyor AKS; 120-150 TKS; 150 civari max KS; 300 hiperglisemik koma veya hipoglisemik atak tariflemiyor

52. 1 yil önce DRP: - MAÜ: 128 mg /gün ( 25/ 4/ 06) EMG yapilmamis

53. Özgeçmis: ? DM tip 2:+ ? HT: 5 Yildir accuzide 1x1 aliyor ; TA takibi yok ? Dislipidemi: var ancak medikal tedavi almiyor ? Lumbal herni op:+ ? sigara:+ Soygeçmis: Anne DM:+

54. Sistemlerin gözden geçirilmesi ( + bulgular) ? Nokturi ? Klaudia kasyo intermittant+ FM: BOY: 1.63 KILO: 65 BMI: 23 TA: 140/ 90 BB: Tiroid non –palpable, lap:- SS: Bilat ac sesleri aliniyor ral:- ronkus:- KVS: ritmik s1+ s2+ ek ses: - üfürüm:- Batin: HSM:- defans:- rebound:- Extr: sol dorsalis pedis ve tibialis post alinmiyor

55. laboratuar

56. 27.4.2006 AKS:159 TKS:308 HbA1C: 7.6

57. Bilat alt ext arterial doppler: bilat alt ekst arterlerinde intimal refleksiyonda artis, monofazik paternede akim

58. Tedavi: 1800 kcallik diyabetik 200 mg / gün kol içeren diyabetik diyet 8Ü Ax3, 12 ü lantus ASA 1x1 ACCUZIDE 1X1 FLUVASTATIN 1X1 Trental 1x1 Sigara stop

59. takip 22.06.06 fluvastatin ile ciddi kas agrilarindan dolayi atorvastatin 40 mg a geçildi. TA diastolik 50 civari AKS: 125 Tkol: 109 TKS: 180 TG: 102 HbA1c: 6.8 HDL: 40 LDL: 49 DEGISIKLIK; atorvastatin 20 mg 1x1 acuitel 1X1

60. 27.09.06 KILO:70 AKS: 132 TKS: 160 HbA1c: 6.2 metformin 2x1 gr eklendi

61. 28.06.07 AKS: 127 TKS: 280 HbA1c: 6 27.09.07 5 kg 1 ayda verdi AKS: 120 TKS: 143 HbA1c: 5.5

62. VAKA 2

63. V.S. 05.10.06 54 y , erkek 3 yildir tip 2 DM tanisi olan hasta Diamicron MR 1X1, glukofen 2X1 kullaniyor AKS; 140-190 TKS; 180 civari max KS; 360 hiperglisemik koma tarifliyor o dönemde hastaya intensif insülin tedavisi önerildi ancak hasta tedaviyi kabul etmedi,hipoglisemik atak tariflemiyor Diyet ve egzersiz uyumu kötü

64. 1 yil önce DRP: - MAÜ: 14.7 mg /gün ( 23/ 2/ 06) ancak daha önce iki kez + tespit edildigi için ACE inh aliyor EMG yapilmamis

65. Özgeçmis: ? DM tip 2:+ ? HT:- ? Dislipidemi: +, lipidor 1x1 ? ? sigara:+ Soygeçmis: özellik yok

66. Sistemlerin gözden geçirilmesi ( + bulgular) ? Nokturi ? poliuri FM: BOY: 1.65 KILO: 67 BMI: 24.5 TA: 130/ 90 BB: Tiroid non –palpable, lap:- SS: Bilat ac sesleri aliniyor ral:- ronkus:- KVS: ritmik s1+ s2+ ek ses: - üfürüm:- Batin: HSM:- defans:- rebound:- Extr: nabizlar bilat +, PTÖ: -

67. laboratuar

68. 5.10.2006 AKS:229 TKS:262 HbA1c:8.3

69. Tedavi: 1800 kcallik diyabetik 200 mg / gün kol içeren diyabetik diyet 12 ü lantus GLIKLAZIDE MR 1X2 METFORMIN 2X1 ASA 1x1 GOPTEN 1X1 ATORVASTATIN 1X1 Sigara stop

70. takip 16.02.07 AKS: 120 TKS: 92 HbA1c: 6.3 LDL: 69 TEDAVI AYNEN DEVAM

71. 03 .07 hasta MI geçirdi ve intensif insülin tedavisine geçildi. diyet uyumu ile de birlikte KS hipoglisemik seyredince oad+ lantus ( 10ü) ile devam edildi Tedaviye karvedilol eklendi

72. 17.05.07 AKS: 143 TKS: 162 HbA1c: 6.3 20.09.07 AKS: 117 TKS: 112 HbA1c: 5.3

73. VAKA 3

74. A.G. 5.4.07 46 Y , erkek 7 yildir tip 2 DM mevcut daha öncesinde diamicron MR 1X1 kullanan hasta 3 aydir ilacini kesmis , evde AKS nin 160-230 mg /dl civarinda oldugunu ifade ediyor. Max KS : 414 mg/dl imis. Daha önce komplikasyon arastirisi yapilmamis

75. Özgeçmis: ? DM tip 2:+ ? HT: - ? Dislipidemi: var ancak medikal tedavi almiyor ? ses tellerinden op:+ ( etyo?) ? sigara:+ Soygeçmis: özellik yok

76. Sistemlerin gözden geçirilmesi ( + bulgular) ? Nokturi ? Poliüri FM: BOY: 1.71 KILO: 65 BMI: 22.5 TA: 160/ 90 BB: Tiroid non –palpable, lap:- SS: Bilat ac sesleri aliniyor ral:- ronkus:- KVS: ritmik s1+ s2+ ek ses: - üfürüm:- Batin: HSM:- defans:- rebound:-

77. laboratuar

78. 5.4.2007 AKS:266 TKS:333 HbA1c:11

79. Tedavi: 1800 kcallik diyabetik diyet 8Ü Ax3, 10 ü lantus ASA 1x1 Metformin 2X1 GR Sigara stop

80. takip 04.07.07 AKS: 146 TKS: 63 HbA1c: 5.6 DEGISIKLIK; analog insülinler kesilip lantus 16ü ve metformin 2x1 gr ile devam

81. 18 .09.07 AKS: 135 Hba1C: 5.5 Metformin 2x1 , lantus 14ü gr ile devam 14.11.07 KS hioglisemik seyretmeye basladigi için lantus dozu azaltiliyor, takipte kesilip oad kombinasyonu düsünülebilir

82. Tip2 DM vaka çalismalari IDF Diyabet egitim modülleri

83. Vaka 1 58 y,erkek 10 yildir Tip 2DM. KS’ine daha önce hiç bakilmamis ve ilaç kullanimi yok. Random KS:576mg/dl Ketonüri yok HbA1c:8.5 BMI:32 Agirlik:113.6

84. Hasta doktorun acil hastaneye gitmesi teklifini reddediyor,ama diyabet klinigine gelebilecegini belirtiyor. Daha önce hiç DM egitimi almamis. Kendini iyi hissettigini söylüyor.Esi ise çok ajite oldugunu ifade ediyor. Son 6 haftadir yurtdisindan ziyaretçileri oldugunu ve aksam yemeklerini disarida yedigini belirtiyor.

85. Hastanin durumu nedir?Hangi ek bilgileri bilmek istersiniz?

86. Sizce bu kisinin tedaviye ihtiyaci var mi? Hangi tip tedavi verirsiniz?

87. Bu kisiye nasil bir diyet tavsiye edersiniz?

88. Vaka 2 53 y bayan,evli, 2 çocugu var. Agirlik:91.5 kg, Boy:165cm TA:140/95-160/110 mm Hg Bazen kahvaltilarini kaçirabiliyor. 30dk hergün yürüyor.Yürüyüsünü artirma fikrini kabul etmiyor.

89. KS Profili 1.gün AKS:260mg/dl ögle KS: 230 mg/dl Aksam yemegi öncesi KS:245mg/dl 2.Gün AKS:232mg/dl ögle KS:240mg/dl Aksam yemegi öncesi KS:225mg/dl 3.Gün AKS:226mg/dl ögle KS:230mg/dl Aksam yemegi öncesi KS:234 mg/dl

90. Tedavi: Metformin 1000mg 2*1+Gliburid 10 mg 2*1 HbA1c:9.5

91. Tedavisi yeterli seviyede mi?

92. DM tedavisinde ne gibi degisiklikler yapmak istersiniz? Niçin?

93. Hastayi bazi degisiklikler yapmaya nasil ikna edersiniz?

94. Hedef kan glikoz seviyesi ne olmali? Hangi siklikta takibe alirsiniz ve ne zaman degisiklik yapmayi planlarsiniz?

95. Vaka 3 50 y erkek hasta, isçi. 10 yildir diyabetik. Agirlik:81.8 kg, Boy:178 cm. TA:155/94 mmHg. Son HbA1c:8.5

96. Tedavi: Metformin 1000mg 2*1, Gliburid 10 mg 2*1 ve gece yatarken 30Ü NPH insülin aliyor. KS profili 1.Gün AKS:180, ögle KS:287 aksam KS:40 2. Gün AKS:153, ögle KS:257, aksam KS:270 3.Gün AKS:162, ögle KS:268, aksam KS:290

97. Ögünlerini düzenli yapiyor. Isinde çok aktif.

98. Tedavisi yeterli mi? Ne gibi degisiklikler yapmayi planlarsiniz ? Neden?

99. Hastayi bazi degisiklikler yapmaya nasil ikna edersiniz?

100. Hedef kan glikoz seviyesi ne olmali? Hangi siklikta takibe alirsiniz ve ne zaman degisiklik yapmayi planlarsiniz?

101. TESEKKÜRLER

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