PATOFISIOLOGI DAN DIAGNOSA OBESITAS Bambang Suprapto
OBESITASDEFINISIKLASIFIKASISIAPA OBESE?KOMPLIKASIPENURUNAN BERAT BADANPATOFISIOLOGIDIAGNOSA
DEFISINSI OBESITASBMI >25 (ASIA)BMI>30 (EROPA + AMERIKA)KELEBIHAN LEMAK:- WANITA: N = 20 -27% BB- PRIA : N = 12 15% BB
BODY MASS INDEX BMI = BB (kg) : TB (m)2BB = Berat badanTB = Tinggi badan
LEMAK TUBUH(Deurenberg et al, 1991)% lemak = 1,2 (BMI) + 0,23(umur) 10,8 (gender) 5,4
% lemak= persen lemak tubuhBMI = kg/m2Umur = tahunGender: laki-laki = 1 wanita = 0
KLASIFIKASI OBESITAS (2)WHO (2000) WPRO (2000) < 18,5 UNDERWEIGHT < 18,5 18,5 24,9 NORMAL 18,5 22,9 25,0 29,9 Pre-obese/overweight 23,0 24,9 30,0 34,9 OBESE I 25,0 29,9 35,0 39,9 OBESE II > 30,0>40,0 OBESE IIISumber: Anuurad, et al (2003)
KLASIFIKASI OBESITAS (3)SEX-SPECIFIC CUT-OFF-POINTS FOR WAIST CIRCUMFERENCE: Level 1 Level 2(alerting zone) (action level)Men > 94 cm > 102 cmWanita > 80 cm > 88 cm(Sumber; Kopelman et al, 2005)
KLASIFIKASI OBESITAS (4)
Underweight 23,0 At risk 23,0 24,9 Increased ModerateObese class I 25,0 29,9 Moderate SevereObese Class II > 30,0 Severe Very severeBMI (Kg/m2) Risk of comorbidities Waist circumference < 90 cm (men) > 90 cm < 80 cm (women) > 80 cm
(Sumber: WHO, IASO, IOTF, 2000)
SIAPA KEGEMUKAN?FAKTOR DEMOGRAFIK (umur, gender, etnisitas)FAKTOR SOSIAL BUDAYA (tingkat pendidikan, penghasilan, status perkawinan)FAKTOR BIOLOGIS (paritas)FAKTOR PERILAKU (asupan makanan, merokok, konsumsi alkohol, kegiatan jasmani)
KOMPLIKASI OBESITASDIABETES MELLITUS TIPE 2PENYAKIT JANTUNG KORONERKANKEROSTEOARTRITISBATU EMPEDUSLEEP APNOEAGANGGUAN REPRODUKSIGANGUAN KEHAMILANGANGGUAN PSIKOLOGISSOCIAL PENALTIES
MANFAAT PENURUNAN BERAT BADAN (5-10%BB)MORTALITAS UMUM: TURUN 20%KEMATIAN AKIBAT DM: TURUN 30%KEMATIAN AKIBAT KANKER: TURUN 40%TEKANAN DARAH: TURUN 10 mm HgLIPID: CHOLESTEROL TURUN 15%DIABETES: PENGENDALIAN KADAR GULA DARAH LEBIH BAIK
PATOFISIOLOGI OBESITAS (1) ENERGY - ENERGY = ENERGY IN OUT STOREDENERGY STORED = FAT STORAGE
ENERGY STORESENERGY INTAKE ENERGY OUTPUTFecal energy(2)
PATOFISIOLOGI OBESITAS (2)MOLECULARBEHAVIORALPRADER WILLI SYNDROMEPEGULATSUMO
ADIPOSE TISSUELeptinLep-RAnabolic pathway Catabolic pathwayNeuronsNeurons POMCHypothalamusAGRP MC4R
Food intakeMSH------------- +-+-PC1
Components of energy expenditureBMRTEF-------------------------Spontaneous activityEXERCISERestingMetabolic RateNon restingMetabolicrate_________________Beyond
Voluntary
control
THERMOGENESISISOMETRIC THERMOGENESISDYNAMIC THERMOGENESISPSYCHOLOGICAL THERMOGENESISCOLD-INDUCED THERMOGENESISDIET-INDUCED THERMOGENESISDRUG-INDUCED THERMOGENESIS
CONTROL OF FOOD INTAKEHUNGER-SATIETY CONTROL CENTRES IN THE BRAIN:-NPY/AgRP NEURONS = OREXIGENIC- POMC/CART NEURONS= ANOREXIGENIC- LATERAL HYPOTHALAMUS = OREXIGENIC
HUNGER-SATIETY SIGNALS FROM THE PERIPHERYSIGNALS FROM THE GASTROINTESTINAL TRACTAMINOSTATIC SIGNALSGLUCOSTATIC AND GLYCOGENOSTATIC SIGNALSLIPOSTATIC AND ADIPOSITY SIGNALSLEPTIN AND INSULINHEPATIC NUTRIENT METABOLISM SIGNALS
INTEGRATED MODELS OF FOOD INTAKE CONTROLSHORT-TERM (HOUR TO HOUR) BLOOD GLUCOSE HOMEOTSTASISMEDIUM-TERM (DAY-TO-DAY) MAINTENANCE OF ADEQUATE HEPATIC STORES OF GLYCOGENLONG-TERM (WEEKS, MONTHS OR YEARS) MAINTENANCE OF THE BODYS FAT AND PROTEIN COMPARTMENTS
Blood metabolites Higher centres Gut Glucose Cognition CCK Fatty acids Sensorial Ghrelin Amino acids Learning GIP.GLP-1,PYYEPISODIC SIGNALSHYPOTHALAMUSSNSEnergyexpenditureADIPOSE TISSUEEnergy intakeTONIC SIGNAL Leptin Insulin
Major effectsMinor effectsAdditive over timeOutcomeLow SESGenderEnvironmentEconomicsNutritionActivityInactivitySmokingPrevalence ofoverweight orobesity+Schematic representation of the determinants ofOverweight and obesity
DIAGNOSA OBESITASBMI > 25; BMI>30TRICEPS SKINFOLD:LAKI-LAKI > 16 MM WANITA > 28 MMWAIST CIRCUMFERENCELAKI-LAKI: > 102 CMWANITA : > 88 CM
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