Oral glucose Tolerance Test and Factors Influencing Blood Glucose Level.

Done ByAbdulaziz Massoud Alfaydi

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•Blood Glucose Level•Normal:70-110 mg%•Abnormal :

▫A.Hyperglycemia,glycosuria-diebetes▫B.Hypoglycemia

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HOMEOSTASIS NORMAL

•3Mechanisms:.1Metabolic.2Hormonal.3Renal

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Metabolic

•Dietary-Primary source of all body components

•Glycogen-Initial-liver(92%), later-muscle(8%),sufficient for 18 hrs

•Gluconeogenesis:Non-cabohydrates▫Glucogenic amino acids all except ,lys, leu▫TG Glycerol DHAP▫Odd chain FA-Propionic Acid Succinyl CoA▫Lactate Pyruvate Oxaloacetate

PEP▫Shuttle mechanisms-Ala,asp,glycerol

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Hormonal•Insulin- β cell of Langerhans favours

uptake into cell•Glucagon,

epinephrine,glucocorticoids,GH,thyroxin-antagonists to insulin,favours excessive

glycogenolysis and release of more glucose in blood

•Cooperative action of both types of hormones help maintaining the blood

glucose

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Renal

•Rates of Glomerular filtration and Tubular absorption maintain blood

glucose•Kidney threshold for glucose-180 mg%,

more than this spillover in urine –glycosuria

•TMG-375 mg/min,more accurate index than kidney threshold

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ABNORMAL

•HYPERGLYCEMIA•HYPOGLYCEMIA

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HYPERGLYCEMIA :DIABETES:

10 % population worldwide affected, 2 %>50 y

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:Iry (Known causes) I.IDDM- Insulin deficiency

•Autoimmune-Immunity mediated(Antibodies to insulin 50%,antibodies to islet cell cytoplasmic

proteins 80%), idiopathic( damage of β cell of islet of Langerhans or viral infection)

•II.NIDDM-Normal insulin but unavailable(insulin resistance)-Obese(60%),non-obese(40%)

(antibodies),MODY (maturity onset diebetes of young)(Glucokinase ↑,gene mutated-KT↑insulin↓)

•III.Prone-i)Gestation-occurs 15% nondiabetes→diabetes, ↑Child

riskmortality↑,BWt ↑,ii)IFG, iii)IGT

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IIry (Unknown causes) •Pancreatic diseases-pancreatitis,cystic fibrosis•Endocrinopathies-cushing syndrome,thyrotoxicosis,acromegaly•Drug induced-steroids, β blockers

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GLYCOSURIA

GFR-NC,KT & TMG ↓ A. HYPERGLYCEMIC:

•Alimentary-IFG•Emotional-sympathetic and splanic nerve

excitation↑•Endocrinal•Experimental-alloxan

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GLYCOSURIA

•B.RENAL:•Hereditary•Acquired•Threshold –( 180 mg%) ↓•Tubular reabsorption ↓•Experimental-phloridzine

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II.HYPOGLYCEMIA

•Risk-50 mg%,fatal < 30 mg%•Insulin ↑•Thyroid ↓•Liver diseases•Severe exercise•Glycogen storage diseases•Alcohol ingestion

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DIEBETES STATUS•MONITORING•A.Conventional:•Glucose-Blood (GOD-POD)•- Urine• Benedict reagent• G Y O R• 0.5% 1% 1.5% 2>-2%•GTT: 1.Lab-Oral GTT (OGTT)• 2.Clinic-Post-prandial (meal)

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B. Modern investigations

1.Glycated Hb (HbA1c) (Normal 4-8%)-1%↓30% risk (life span 120D)

2.Glycated albumin-fructosamine(life span 20D)3.Lipid profile4.Microalbuminuria- >300 mg%/D excretion5.Ketone bodies (Bl.0-2 mg % →125 mg%,urine 20-60

mg% → 5000 mg% /D )

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Factors affecting GTT

•Concerned with the blood glucose regulation

•1.Metabolic-diet-thiamine•- starvation•- excretion•- liver diseases, infection•2.Hormones-insulin•- antagonists-

epinephrine,glucagon,glucocorticoids,GH,thyroxin

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GTT

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STATE NORMAL IMPAIRED DIABETES

Fasting 70-110 110-126( IFG) >126

2 Hr(mini GTT) 140 140-200(IGT) >200

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MANAGEMENT OF DIEBETES

•Organs involved-side effects-complications,acute,chronic-multiple

organs

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CLINICAL PRESENTATION IN DM•Cardinal Symptoms:Complications•1.Poly-urea-Urine↑ (wt.loss)•- dypsea-thirst-water intake ↑•- phagia-Food intake↑•2.Chronic skin infection-Boils•- Celluloitis•- Absesses•3.Plaques-CVD:CHD+CAD→Myocardial infarction•4.Retinopathy•5.Nephropathy•6.Fatty liver

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•7.Ketone bodies•8.altered lipid profile

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Differentiation of DM Parameter Type I Type II

Features Juvenile(Puberty) AdultDiet Under nourished Over nourished

Prevalence 10-20%% 80—90%Genetics Weak Strong

Defect β Cells β Cells-NormalKetosis Common RareInsulin ↓ No change

O.Hypogly.agent Unresponsive UnresponsiveInsulin Always required Not required