Post on 24-Feb-2016
description
CARBOHYDRATE METABOLISM
CARBOHYDRATE
BLOODGLUCOSA
GLYCOGEN FFA TRIGLYSERIDA
LIVER TISSUE AMINO ACID PYRUVATE - LACTATE
ENERGY ATP + H2O + CO2
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
NORMAL BLOOD SUGAR CONTROLE
BY INTERMEDIARY REGULATION
1. GLYCOGENESIS
2. GLYCOGENOLYSIS
3. GLUCONEOGENESIS
4. GLUCOLYSIS
BLOOD SUGAR CONCENTRATION
NORMAL DM
1. FASTING 70-110mg/dl > 126 mg./dl
2. POST PRAN < 150 mg/dl > 200 mg/dl DIAL
3. NON FASTING 100-150 mg/dl > 200 mg/dl
CARBOHYDRATE METABOLISM
DISORDERS
- HYPERGLYCEMIC SYNDROME
- HYPOGLYCEMIC SYNDROME
- INBORN ERROR
- HORMONAL DISORDERS
DISTURBANCE OF CARBOHYDRATE
METABOLISM
- INSULIN DEFICIENCY, INSULIN RESISTENCY
- HORMONAL DISORDERS
CAUSES :
DIABETES MELLITUS
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.
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
PATHOPHYSIOLOGY D.M
D.M INSULIN DEFICIENT
HYPERGLYCEMIA
GLUCOSURIA
ACUTE CHONIC
D.M + STRESS MICROANGIOPATHY
D. KETO-ACIDOSIS
D. COMA MACROANGIOPATHY
COMPLICATIONS OF DM- MACROANGIOPATHY- MICROANGIOPATHY
- DIABETIC RETINOPATHY- DIABETIC NEPHROPATHY- DIABETIC NEUROPATHY- INFECTION, ABSCESS, GANGRENE- HYPERLIPIDEMIA-DIABETES KETOACIDOSIS - COMA
KETON BODIESACETO ACETIC ACIDB.HIDROXY BUTYRIC ACIDACETON
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
DIAGNOSIS
BS mg/dl BSFASTING POSTPR
NORMAL < 110 < 150
GLUCOSE < 126 < 200INTOLERANCE
DIABETES > 126 >200MELLITUS
ORAL GLUCOSE TOLERANCE TEST
(OGTT)
100
200
300
100
200
300
1 2 30 1 2 30Hours Hours
BS mg/dlNORMAL DM
SEVERE
MILD
BLOOD GLUCOSEPRE-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
LABORATORY TESTS
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
BLOOD GLUCOSE
PRE-ANALYTIC STEPS (contd….)
OGTTDiet : must consists of > 159g of carbohydrate
per day, over a period of 3 daysDiscontinue any drugs that can affect glucose
plas-ma level 3 days before the testFasting : 12 hours
BLOOD GLUCOSE
PRE-ANALYTIC STEPS (contd….) OGTTA parallel urine sample must be taken for fasting
glucose and ketone. A positive test strip results is a contraindication for OGTT
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 womenPatients should remain seated during the testBlood samples are collected in 0; 60; 120 minutes
BLOOD GLUCOSE
ANALYTICAL STEPSMETHODS : 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)
BLOOD GLUCOSE
GLUCOSE OXIDASE-PAP : glucose
H2O
ß-D-glucose + O2 gluconolactone
oxidase O2
gluconic acid + H2O2 peroxidaseH2O2 + phenylamine-phenazone
color changes + H2O
BLOOD GLUCOSE
Measured by photometer in specific wavelength
HEXOKINASE : hexokinaseGlucose + ATP glucose 6-phosphate +
ADP Mg++
G6PDGlucose 6-phosphate + NADP 6-
phosphoglucono-
lactone + NADPH + H+
More expensive, but better in specificity and precision
BLOOD GLUCOSE
INTERPRETATION :NormoglycemiaHyperglycemiaHypoglycemia
“Amended” insulin-to-glucose ratio : Insulin µU/ml Glucose – 30 (mg/dl)Normal : 50 – 100 µU/mg
POST-ANALYTICAL STEPS
X 100
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
POST-ANALYTICAL STEPS
BENEDICT’S TES
Principle :
Glucose reduces Cu 2+ to become Cu +
and precipitated as Cu2O( red brick color substance)
3 ml benedict sol + 3 drops urine
100 °C
Result ;
Blue : negativeGreen : (+)Yellowish green : (++)Yellow : (+++)Red brick : (++++)
GlycohemoglobinGlycated Hemoglobin
Hb A1C atau A1c
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).
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
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
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%
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.
HbF lebih dari normalCRF tanpa/dengan hemodialisaSplenomegaliSerum trigliserida tinggi AlkoholismeKeracunan Pb atau opiat.Fe defisiensi anemia
Peningkatan kadar A1c menunjukkan pasti DM bila tak ada faktor-faktor lain yang menyebabkan A1c meningkat :
1. Masa hidup eritrosit menurun misalnya pada penyakit : Hemoglobinopati (HbS, HbC, HbD)Anemia hemolitikPerdarahan akut atau kronis
A1c menurun pada :
2. Sesudah transfusi3. Kehamilan4. Penggunaan dosis tinggi Vit C atau E
A1c normal, tidak menghilangkan kemungkinan IGT
A1c menurun pada :
A1c dapat meningkat bila kadar glukosa meningkat setelah terapi dihentikan dan tetap tinggi 2 – 4 minggu setelah terapi dilanjutkan.
INTERPRETASI
Bila kadar glukosa puasa<110 mg/dl; A1c normal pada > 96% kasusBila kadar glukosa puasa 110–125 mg/dl;
A1c normal pada > 80% kasusBila kadar glukosa puasa > 126 mg/dl; A1c normal pada > 60% kasus
INTERPRETASI
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