Oral glucose Tolerance Test and

Factors Influencing Blood Glucose

Level.
Done By
Abdulaziz Massoud Alfaydi
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10/18/09

• Blood Glucose Level

• Normal:70-110 mg%
• Abnormal:
▫ A.Hyperglycemia,glycosuria-diebetes
▫ B.Hypoglycemia
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HOMEOSTASIS NORMAL

• 3Mechanisms:
1. Metabolic
2. Hormonal
3. Renal
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Metabolic 10/18/09

• 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-PropionicAcid  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 Glomerularfiltration 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 risk mortality↑,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, βblockers

•
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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 profile

 4.Microalbuminuria- >300 mg%/D excretion

 5.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) Adult
 Diet Under nourished Over nourished
 Prevalence 10-20%% 80—90%
 Genetics Weak Strong
 Defect βCells β Cells-Normal
 Ketosis Common Rare
 Insulin ↓ No change
 O.Hypogly.agent Unresponsive Unresponsive
 Insulin Always required Not required