diabetes mellitus kad
DESCRIPTION
all about diabetes mellitus and it's complicationsTRANSCRIPT
Ronald Chrisbianto Gani405090223
Faculty of Medicine 2009Tarumanagara University
ENDOCRINE SYSTEM BLOCK
CASE 1
DIABETES MELLITUS
DEFINISI
• Sindrom kronik gangguan metabolisme karbohidrat, protein, dan lemak akibat ketidak cukupan sekresi insulin atau resistensi insulin pada jaringan yang dituju
Dorland Medical Dictionary 29th Ed
EPIDEMIOLOGY
Harrison’s Principal of Medicine 18th Ed
TOP 10 COUNTRIES
• China• India• USA• Indonesia• Brazil
• Russia• Japan• Pakistan• Bangladesh• Nigeria
International Diabetes Federation 2011
Nelson’s Textbook of Pediatrics 19th Ed
CLASSIFICATION & ETIOLOGY• Type I Diabetes (beta cell destruction, usually
leading to absolute insulin deficiency)– Immune-mediated– Idiopathic
• Type 2 diabetes (may range from predominantly insulin resistance with relative insulin deficiency to a predominantly insulin secretory defect with insulin resistance)
• Gestational diabetes mellitus (GDM)
Harrison’s Principal of Medicine 18th Ed
Harrison’s Principal of Medicine 18th Ed
CLASSIFICATION
Harrison’s Principal of Medicine 18th Ed
CLASSIFICATION
Sherwood’s Human Physiology 7th Ed
CLASSIFICATION
Robbin’s Basic Pathology 8th Ed
DIAGNOSIS
Harrison’s Principal of Medicine 18th Ed
Diagnostic Criteria for Impaired Glucose Tolerance (IGT) and Diabetes Mellitus (DM)
IGT• Fasting Glucose 110-125
mg/dL (6,1-7,6mmol/L)• 2-hr plasma glucose during
OGTT <200mg/dL but <140mg/dL
DM• Symptoms of DM plus
random plasma glucose >= 200mg/dL or
• Fasting Plasma Glucose >= 126mg/dL or
• 2-hr plasma glucose during OGTT >= 200mg/dL
Nelson’s Textbook of Pediatrics 19th Ed
INSULIN SECRETION
Harrison’s Principal of Medicine 18th Ed
INSULIN ACTION
Harrison’s Principal of Medicine 18th Ed
TYPE I DIABETES
PATHOGENESIS OF TYPE I DIABETES
Nelson’s Textbook of Pediatrics 19th Ed
PATHOGENESIS OF TYPE I DIABETES
Harrison’s Principal of Medicine 18th Ed
PATHOPHYSIOLOGY
OF TYPE I DIABETES
Nelson’s Textbook of Pediatrics 19th Ed
Sherwood’s Human Physiology 7th Ed
CLINICAL MANIFESTATION
Classic Sign• Polyuria• Polydipsia• Polyphagia
Other• Nocturnal Enuresis• Monolial Vaginitis• Weight loss• Diminished subcutaneous
fat stores• Complications
Nelson’s Textbook of Pediatrics 19th Ed
TREATMENT
GOAL :Eliminate symptoms related to hyperglycemia (<200mg/dL)Reduce or eliminate complicationsAllow the patient to achieve as normal a lifestyle as possible
Harrison’s Principal of Medicine 18th Ed
NUTRITIONAL RECCOMENDATION
Harrison’s Principal of Medicine 18th Ed
EXERCISE
• Benefits :– Cardiovascular risk
reduction– BP reduction– Maintaining muscle mass– Body fat reduction– Weight loss– Lowering plasma glucose– Increasing insulin sensitivity
• Reccomended :– 150mins/week– Aerobic physical activity
• Caution– DM type I, pre-exercise
plasma glucose• Low ketone body
formation ketoacidosis• High hypoglycemia
Harrison’s Principal of Medicine 18th Ed
EXERCISE
• To avoid exercise related hypo-hyperglycemia– Monitor blood glucose before, during, after exercise– Delay if BG >250mg/dL or ketone is present– If BG <100mg/dL, ingest carbohydrate first– Decrease insulin dose before exercise and inject
insulin into non-exercising area– Learn individual glucose responses to different type
of exercise and increase food intake up to 24hr after exercise, depending on intensity and duration of exercise
Harrison’s Principal of Medicine 18th Ed
BLOOD GLUCOSE MONITORING
• Self-Monitoring Blood Glucose (SMBG)– Used to modify doses of insulin– Must be performed several times per day
• Current Continuous Glucose Monitoring System (CGMS)
• Ketones monitoring, especially when blood glucose is >300mg/dL, blood β-hydroxybutirate is preferred
• Long-term Glycemic Control– HbA1c / glycated hemoglobin : reflects alteration of
glycemic control over previous 2-3months
Harrison’s Principal of Medicine 18th Ed
BLOOD GLUCOSE MONITORING
• Mean Plasma Glucose based on HbA1c
• Reccomended to be performed at least twice a year
HbA1c Mean Plasma Glucose
6% 135mg/dL
7% 170mg/dL
8% 205mg/dL
(1% increase of HbA1c ~ 35mg/dL blood glucose increase)
Harrison’s Principal of Medicine 18th Ed
INSULIN
Harrison’s Principal of Medicine 18th Ed
CONTINUOUS SUBCUTANEOUS INSULIN INFUSION (CSII)
• Advantages– Multiple basal infusion rates can be programmed to
accomodate nocturnal vs daytime basal insulin requirement– Basal infusion rates can be altered during periods of exercise– Different waveforms of insulin infusion with meal related
bolus allow better matching of insulin depending meal composition
– Programmed algorithm consider prior insulin administration and blood glucose values in calculating insulin dose
• Disadvantages : require very frequent interaction with helath proffesional and alteration of device can be fatal
Harrison’s Principal of Medicine 18th Ed
INSULIN REGIMENT
Harrison’s Principal of Medicine 18th Ed
OTHER AGENTS THAT IMPROVE GLUCOSE CONTROL
• Pramlintide – Analogue of amylin (peptide cosecreted with insulin)– Injected before meal– Slows gastric emptying– Supress glucagon– Does not alter insulin level– Side effect : nausea and vomiting
(dose-dependent) – Influence absorbtion of other medication
Harrison’s Principal of Medicine 18th Ed
PREVENTION
• Many prevention has been performed and success in animals, but no satisfactory results in human
TYPE II DIABETES
RISK FACTOR
Individual with high risk is recommended to do a screening test
PATHOGENESIS
OFTYPE II
DIABETESMELLITUS
MECHANISM OFINSULIN
RESISTANCE
PATHOPHYSIOLOGY
• Metabolic Abnormalities– Abnormal Muscle and
Fat Metabolism– Impaired insulin
secretion– Increased Hepatic
Glucose and Lipid Production
TREATMENT
TREATMENT
ONGOING CARE
ANTIDIABETIC AGENT
ANTIDIABETIC AGENT
INSULIN SECRETAGOGUE
ANTIHIPERGLYCEMIC ORAL• Insulin Sensitizing
– Biguanid• Contoh : metformin• Meningkatkan pemakaian
glukosa oleh sel dan menstimulasi produksi GLP-1menekan fungsi sel alfa
• DOC pd awal pengelolaan diabetes
• Bisa diberikan monoterapi atau kombinasi dg SU / insulin
• ES: asidosis laktat• KI : gangguan ginjal, hati,
infeksi beratm, gangguan jantung, anemia (gangguan vit B12)
– Glitazone• Agonist PPAR• Merangsang ekspresi bbrp
protein u/ memperbaiki sensitivitas insulin
• Rosiglitazone : meningkatkan LDL dan HDL
• Pioglitazon : menurunkan TG meningkatkan HDL
• Monoterapi, atau kombinasi dg metformin dan sekretagok
• ES: BB ↑, ISPA, sakit kepala, anemia dilusional
• KI : dihentikan jk kenaikan ALT / AST 3x BANN, hati2 pd NYHA kelas 3 dan 4
ANTIHYPERGLICEMIC ORAL
• Sekretagok Insulin– Sulfonilurea
• Merangsang sel B pankreas melepas insuli
• SU gen I : acetohexamide, tolbutamide
• SU gen II : glibenclamide• SU gen III : glimepiride• Kombinasi dg insulin• ES: Hipoglikemik, BB ↑,
gangguan pencernaan, fotosensitivitas, gangguan enzim hati, flushing
• KI : DM tipe I, hamil, menyusui
– Glinid• Mirip SU, masa kerja pendek• Obat prandial (2-3x/day)
• Penghambat Alfa Glukosidase
• Menghambat kerja enzim alfa glukosidase penurunan penyerapan glukosa, menurunkan hiperglikemia postprandial
• Mek kerja : memperlambat pemecahan dan penyerapan karbohidrat kompleks
• ES: metrorismus, flatulence, diare
• KI : IBS, sirosis, gangguan ginjal
ANTIHYPERGLYCEMIC ORAL
• Incretin– Penghambat DPP-IV• Memperpanjang masa kerja GLP-1 (menekan kerja sel
alfa dan menghambat pengsongan lambung)• Sitagliptin dan vildaglitin• ES: nasofaringitis, resiko infeksi sal kemih, sakit kepala
KETOASIDOSIS DIABETIC AND HYPERGLYCEMIC HYPEROSMOLAR STATE
DKA & HHS
CLINICAL MANIFESTATION
MANAGEMENT
DIABETIC RETINOPATHY
DIABETIC RETINOPATHY
• Leading causes for blindness in US
• Risk for blind diabetic : non diabetic = 25 : 1
• Classified into : – Proliferative– Non-Proliferative
• Treatment : prophilactic photocoagulation, proliferative : panretinal laser
DIABETIC NEPHROPATHY
SCREENING DIAGNOSIS
INTERVENTION
• Normalization of hyperglycemia• Strict blood pressure control• Administration of ACE inhibitor or ARB, if not
possible, CCB, B-Blocker, or diuretic• Dyslipidemia should be treated• Nephrologist consult if GFR <60mL/min
DAFTAR PUSTAKA
• Fauci AS, Braunwald E, Kasper DL, Longo DL, Jameson JL, et al, editors. Harrison’s Principle of Internal Medicine. 18th ed. USA : McGraw Hill Medical, 2011
• Sudoyo AW, Setiyohadi B, Alwi I, Simadibrata M, Setiadi S, et al, editors. Buku Ajar Ilmu Penyakit Dalam 5th ed. Jakarta : Pusat Penerbitan Ilmu Penyakit Dalam FKUI, 2006
• Kumar V, Abbas AK, Fausto N. Robbins and Cotran Pathologic Basis of Disease 7th ed. Philadelphia : Elsevier Saunders 2005
• Kliegman, Behrman, Jenson, Stanton ; 2007 ; NELSON TEXTBOOK OF PEDIATRICS 18th Edition Volume II ; Philadelphia : Sunders Elsevier