Download blood glucose

CARBOHYDRATE METABOLISM
CARBOHYDRATE
BLOOD
GLUCOSA
GLYCOGEN
LIVER TISSUE
ENERGY
FFA
TRIGLYSERIDA
AMINO ACID
PYRUVATE - LACTATE
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
DIAL
< 150 mg/dl
> 200 mg/dl
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.
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
PATHOPHYSIOLOGY D.M
D.M
INSULIN DEFICIENT
HYPERGLYCEMIA
GLUCOSURIA
ACUTE
D.M + STRESS
CHONIC
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 BODIES
ACETO ACETIC ACID
B.HIDROXY BUTYRIC ACID
ACETON
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)
DIAGNOSIS
BS mg/dl
FASTING
BS
POSTPR
NORMAL
< 110
< 150
GLUCOSE
INTOLERANCE
< 126
< 200
DIABETES
MELLITUS
> 126
>200
ORAL GLUCOSE TOLERANCE TEST
(OGTT)
BS mg/dl
NORMAL
DM
300
300
SEVERE
200
200
MILD
100
100
0
1
2
3 Hours
0
1
2
3 Hours
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
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
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
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
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
 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)
 GLUCOSE OXIDASE-PAP :
glucose
ß-D-glucose + O2
H2O
gluconolactone
O2
oxidase
gluconic acid + H2O2
peroxidase
H2O2 + phenylamine-phenazone
changes + H2O
Measured by photometer in specific wavelength
color
 HEXOKINASE :
hexokinase
Glucose + ATP
glucose 6-phosphate + ADP
Mg++
G6PD
Glucose 6-phosphate + NADP
phosphoglucono-
6-
lactone + NADPH + H+
More expensive, but better in specificity and precision
 INTERPRETATION :
 Normoglycemia
 Hyperglycemia
 Hypoglycemia
 “Amended” insulin-to-glucose ratio :
Insulin µU/ml
Glucose – 30 (mg/dl)
Normal : 50 – 100 µU/mg
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
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
: negative
Green
: (+)
Yellowish green : (++)
Yellow
: (+++)
Red brick : (++++)
Glycohemoglobin
Glycated 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-
> 8%
> 9%
9,0%
Kontrol DM buruk
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 normal
 CRF tanpa/dengan hemodialisa
 Splenomegali
 Serum trigliserida tinggi
 Alkoholisme
 Keracunan Pb atau opiat.
 Fe defisiensi anemia
1. Masa hidup eritrosit menurun misalnya pada
penyakit :
 Hemoglobinopati (HbS, HbC,
HbD)
 Anemia hemolitik
 Perdarahan akut atau kronis
2. Sesudah transfusi
3. Kehamilan
4. Penggunaan dosis tinggi Vit C atau E
A1c normal, tidak menghilangkan kemungkinan IGT
 A1c dapat meningkat bila kadar glukosa meningkat
setelah terapi dihentikan dan tetap tinggi 2 – 4
minggu setelah terapi dilanjutkan.
 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