CARBOHYDRATE METABOLISM AND THE LABORATORY TESTS

Presentasi berjudul: "CARBOHYDRATE METABOLISM AND THE LABORATORY TESTS"— Transcript presentasi:

1 CARBOHYDRATE METABOLISM AND THE LABORATORY TESTS

2 GLYCOGEN FFA TRIGLYSERIDA
CARBOHYDRATE METABOLISM CARBOHYDRATE BLOOD GLUCOSA GLYCOGEN FFA TRIGLYSERIDA LIVER TISSUE AMINO ACID PYRUVATE - LACTATE ENERGY ATP + H2O + CO2

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 < 150 mg/dl > 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 DIABETES MELLITUS 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 CLASSIFICATION OF DIABETES MELLITUS
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

10 D.M + STRESS MICROANGIOPATHY D. KETO-ACIDOSIS D. COMA MACROANGIOPATHY
PATHOPHYSIOLOGY D.M D.M INSULIN DEFICIENT HYPERGLYCEMIA GLUCOSURIA ACUTE CHONIC D.M + STRESS MICROANGIOPATHY 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 LABORATORY EXAMINATIONS
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)

13 DIAGNOSIS BS mg/dl BS FASTING POSTPR NORMAL < < 150 GLUCOSE < < 200 INTOLERANCE DIABETES > >200 MELLITUS

14 ORAL GLUCOSE TOLERANCE TEST
(OGTT) BS mg/dl NORMAL DM 300 300 SEVERE 200 200 MILD 100 100 1 2 3 Hours 1 2 3 Hours

15 LABORATORY TESTS 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 BLOOD GLUCOSE 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 OGTT BLOOD GLUCOSE PRE-ANALYTIC STEPS (contd….)
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 BLOOD GLUCOSE 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 BLOOD GLUCOSE 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 BLOOD GLUCOSE 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 Measured by photometer in specific wavelength
BLOOD GLUCOSE GLUCOSE OXIDASE-PAP : glucose H2O ß-D-glucose + O gluconolactone oxidase O2 gluconic acid + H2O2 peroxidase H2O2 + phenylamine-phenazone color changes + H2O Measured by photometer in specific wavelength

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

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

24 POST-ANALYTICAL STEPS
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

25 Benedict’s tes

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

28

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

30 Glycohemoglobin Glycated Hemoglobin Hb A1C atau A1c

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 Kontrol DM baik 2,5-6,0% < 7,5%
Hasil: HbA1c HbA1-total Kontrol DM baik ,5-6,0% < 7,5% Kontrol DM kurang baik 6,1-8,0% ,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 Peningkatan kadar A1c menunjukkan pasti DM bila tak ada faktor-faktor lain yang menyebabkan A1c meningkat : HbF lebih dari normal CRF tanpa/dengan hemodialisa Splenomegali Serum trigliserida tinggi Alkoholisme Keracunan Pb atau opiat. Fe defisiensi anemia

37 A1c menurun pada : Hemoglobinopati (HbS, HbC, HbD) Anemia hemolitik
1. Masa hidup eritrosit menurun misalnya pada penyakit : Hemoglobinopati (HbS, HbC, HbD) Anemia hemolitik Perdarahan akut atau kronis

38 A1c menurun pada : 2. Sesudah transfusi 3. Kehamilan
4. Penggunaan dosis tinggi Vit C atau E A1c normal, tidak menghilangkan kemungkinan IGT

39 INTERPRETASI A1c dapat meningkat bila kadar glukosa meningkat setelah terapi dihentikan dan tetap tinggi 2 – 4 minggu setelah terapi dilanjutkan.

40 INTERPRETASI Bila kadar glukosa puasa<110 mg/dl;
A1c normal pada > 96% kasus Bila kadar glukosa puasa 110–125 mg/dl; A1c normal pada > 80% kasus Bila kadar glukosa puasa > 126 mg/dl; A1c normal pada > 60% kasus

41 thankyou