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CARBOHYDRATE METABOLISM CARBOHYDRATE BLOOD GLUCOSA GLYCOGEN FFA TRIGLYSERIDA LIVER TISSUE AMINO ACID PYRUVATE - LACTATE ENERGY ATP + H 2 O + CO 2.

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Presentasi berjudul: "CARBOHYDRATE METABOLISM CARBOHYDRATE BLOOD GLUCOSA GLYCOGEN FFA TRIGLYSERIDA LIVER TISSUE AMINO ACID PYRUVATE - LACTATE ENERGY ATP + H 2 O + CO 2."— Transcript presentasi:

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2 CARBOHYDRATE METABOLISM CARBOHYDRATE BLOOD GLUCOSA GLYCOGEN FFA TRIGLYSERIDA LIVER TISSUE AMINO ACID PYRUVATE - LACTATE ENERGY ATP + H 2 O + CO 2

3 NORMAL BLOOD SUGAR CONTROLE BY HORMONAL REGULATION BLOOD SUGAR (CONC.) 1. INSULIN 2. GLUCAGON 3. THYROXINE 4. GROWTH HORMONE 5. A.C.T.H 6. CORTICOSTEROID 7. EPINEPHRINE

4 NORMAL BLOOD SUGAR CONTROLE BY INTERMEDIARY REGULATION 1. GLYCOGENESIS 2. GLYCOGENOLYSIS 3. GLUCONEOGENESIS 4. GLUCOLYSIS

5 BLOOD SUGAR CONCENTRATION NORMAL DM 1. FASTING mg/dl > 126 mg./dl 2. POST PRAN 200 mg/dl DIAL 3. NON FASTING mg/dl > 200 mg/dl

6 CARBOHYDRATE METABOLISM DISORDERS - HYPERGLYCEMIC SYNDROME - HYPOGLYCEMIC SYNDROME - INBORN ERROR - HORMONAL DISORDERS

7 DISTURBANCE OF CARBOHYDRATE METABOLISM - INSULIN DEFICIENCY, INSULIN RESISTENCY - HORMONAL DISORDERS CAUSES : DIABETES MELLITUS

8 IS CHARACTERIZED BY CHANGES IN THE METABOLISM OF EACH OF THE MAJOR BODY FUELS (CARBOHYDRATE - FAT AND PROTEIN) AND IS ASSOSIATED BY DISTURBANCES OF A VARIETY OF HORMONES.

9 1. IDDM INSULIN DEPENDENT DM TYPE I DM 2. NIDDM NONINSULIN DEPENDENT DM TYPE II DM 3. GESTATIONAL DM 4. MALNUTRITION RELATED DM A. FCPD (FIBROCALCULOUS PANCREATIC DM) B. PDPD (PROTEIN DEFICIENT PANCREATIC DM) 5. DM OTHER CAUSES CLASSIFICATION OF DIABETES MELLITUS

10 PATHOPHYSIOLOGY D.M D.M INSULIN DEFICIENT HYPERGLYCEMIA GLUCOSURIA ACUTE CHONIC D.M + STRESSMICROANGIOPATHY D. KETO-ACIDOSIS D. COMA MACROANGIOPATHY

11 COMPLICATIONS OF DM - MACROANGIOPATHY - MICROANGIOPATHY - DIABETIC RETINOPATHY - DIABETIC NEPHROPATHY - DIABETIC NEUROPATHY - INFECTION, ABSCESS, GANGRENE - HYPERLIPIDEMIA -DIABETES KETOACIDOSIS - COMA KETON BODIES ACETO ACETIC ACID B.HIDROXY BUTYRIC ACID ACETON

12 1. URINE GLUCOSE (screening) 2. BLOOD GLUCOSE (diagnostic) 3. ORAL GLUCOSE TOLERANCE TEST (confirmatory test) 4. IV- GLUCOSE TOLERANCE TEST (confirmatory test) 5. HbA1C TEST (follow-up) 6. FRUCTOSAMIN TEST (follow-up) 7. C-PEPTIDE CONC (confirmatory test) 8. URINARY KETON (complication) 9. BLOOD KETON (complication) 10. MICROALBUMIN IN URINE (complication) LABORATORY EXAMINATIONS

13 DIAGNOSIS BS mg/dlBS FASTINGPOSTPR NORMAL < 110 < 150 GLUCOSE < 126 < 200 INTOLERANCE DIABETES > 126 >200 MELLITUS

14 ORAL GLUCOSE TOLERANCE TEST (OGTT) Hours BS mg/dl NORMALDM SEVERE MILD

15 BLOOD GLUCOSE PRE-ANALYTIC STEPS  Specimen of choice : venous blood; in certain condition/instruments : capillary blood  Sample of choice : serum or plasma, others : whole blood (venous or capillary blood)  Fasting : 8-10 hours  Meal after fasting : food in usual amount

16 PRE-ANALYTIC STEPS (contd….)  Specimens handling :  Glycolysis ± 7 mg/dl/h in WB w/o inhibitors  At 4ºC ± 2 mg/dl/h will lost  Bacterial contamination will decrease glucose level  Delay time in serum containing blood clot : < 90 minutes

17 PRE-ANALYTIC STEPS (contd….) OGTT Diet : must consists of > 159g of carbohydrate per day, over a period of 3 days Discontinue any drugs that can affect glucose plas-ma level 3 days before the test Fasting : 12 hours

18 PRE-ANALYTIC STEPS (contd….) OGTT A parallel urine sample must be taken for fasting glucose and ketone. A positive test strip results is a contraindication for OGTT

19 PRE-ANALYTIC STEPS (contd….) OGTT D-glucose : 75 g (adult) 1.75 g/kgBW (children) max up to 75 g 50 g for pregnant women Patients should remain seated during the test Blood samples are collected in 0; 60; 120 minutes

20 ANALYTICAL STEPS METHODS : chemical & enzymatic  Chemical methods are no longer used, because of lack of specificity, except ortho-toluidine method  ENZYMATIC method :  Glucose oxidase (less specific than hexokinase)  Hexokinase (generally accepted reference method)

21 GLUCOSE OXIDASE-PAP : glucose H 2 O ß-D-glucose + O 2 gluconolactone oxidase O 2 gluconic acid + H 2 O 2 peroxidase H 2 O 2 + phenylamine-phenazone color changes + H 2 O Measured by photometer in specific wavelength

22 HEXOKINASE : hexokinase Glucose + ATP glucose 6-phosphate + ADP Mg ++ G6PD Glucose 6-phosphate + NADP 6- phosphoglucono- lactone + NADPH + H + More expensive, but better in specificity and precision

23 INTERPRETATION : Normoglycemia Hyperglycemia Hypoglycemia “Amended” insulin-to-glucose ratio : Insulin µU/ml Glucose – 30 (mg/dl) Normal : 50 – 100 µU/mg X 100

24 INTERFERING FACTORS :  Falsely high : dextrose iv-infusion, steroids, stress, infection, caffeine, nicotine, ß-blockers, adrenal gland infection, total parenteral nutrition (TPN), diuretics, estrogen, phenytoin  Falsely low : insulin, alcohol, anabolic steroids, OAD

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26 Principle : Glucose reduces Cu 2+ to become Cu + and precipitated as Cu2O( red brick color substance)

27 3 ml benedict sol + 3 drops urine 100 °C

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29 Result ; Blue : negative Green : (+) Yellowish green : (++) Yellow : (+++) Red brick : (++++)

30 Glycohemoglobin Glycated Hemoglobin Hb A 1 C atau A 1 c

31 Glukosa plasma bila kadarnya lebih dari normal, akan bereaksi dengan Hb di dalam eritrosit, menjadi glycated hemoglobin secara ireversibel sepanjang masa hidup eristrosit (120 hari).

32 Glycated hemoglobin yang terbentuk proporsional terhadap rerata kadar glukosa plasma selama 6-12 minggu dengan kadar ± 5% kadar total Hb A Normal kadar Hb A1c : 3% kadar Hb A kadar Hb A1a < 1% kadar Hb A1b < 2%  Bila terjadi hiperglikemia, yang meningkat adalah HbA1C

33 Glycated hemoglobin memberikan prediksi risiko progresif dari komplikasi diabetik. Pemeriksaan A1c digunakan untuk kontrol DM tentang kepatuhan pengobatan 2-3 bulan yang lalu. Tidak direkomendasi untuk diagnosis DM

34 Hasil: HbA1c HbA1-total Kontrol DM baik 2,5-6,0% < 7,5% Kontrol DM kurang baik 6,1-8,0% 7,6- 9,0% Kontrol DM buruk > 8% > 9%

35 Metode pemeriksaan : Ion exchange column chromatography; HPLC. Untuk cut off A1c diambil sesuai dengan kadar Hb A1 total yaitu = 5 % dari Hb dewasa (HbA) Bila < 1,1 x batas atas normal; komplikasi renal dan retinal jarang dijumpai. Bila > 1,7 x batas atas normal; pada > 70% kasus sudah terjadi komplikasi renal dan retinal.

36 HbF lebih dari normal CRF tanpa/dengan hemodialisa Splenomegali Serum trigliserida tinggi Alkoholisme Keracunan Pb atau opiat. Fe defisiensi anemia

37 1. Masa hidup eritrosit menurun misalnya pada penyakit : Hemoglobinopati (HbS, HbC, HbD) Anemia hemolitik Perdarahan akut atau kronis

38 2. Sesudah transfusi 3. Kehamilan 4. Penggunaan dosis tinggi Vit C atau E A 1 c normal, tidak menghilangkan kemungkinan IGT

39 A 1 c dapat meningkat bila kadar glukosa meningkat setelah terapi dihentikan dan tetap tinggi 2 – 4 minggu setelah terapi dilanjutkan.

40 Bila kadar glukosa puasa<110 mg/dl; A 1 c normal pada > 96% kasus Bila kadar glukosa puasa 110–125 mg/dl; A 1 c normal pada > 80% kasus Bila kadar glukosa puasa > 126 mg/dl; A 1 c normal pada > 60% kasus

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