Blood Glucose Aziz666

Oral glucose Tolerance Test and Factors Influencing Blood Glucose Level. Done By Abdulaziz Massoud Alfaydi

2 10/18/09

• Blood Glucose Level • Normal:70-110 mg% • Abnormal: ▫ A.Hyperglycemia,glycosuria-diebetes ▫ B.Hypoglycemia

3 10/18/09

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

Metabolic

4 10/18/09

• Dietary-Primary source of all body components • Glycogen-Initial-liver(92%), latermuscle(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 

6 10/18/09

Hormonal • Insulin- β cell of Langerhans favours uptake into cell • Glucagon, epinephrine,glucocorticoids,GH,thyroxinantagonists to insulin,favours excessive glycogenolysis and release of more glucose in blood • Cooperative action of both types of hormones help maintaining the blood glucose

7 10/18/09

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

8 10/18/09

ABNORMAL • HYPERGLYCEMIA • HYPOGLYCEMIA

9 10/18/09

HYPERGLYCEMIA: 

DIABETES: 



10 % population worldwide affected, 2 %>50 y

10 10/18/09

: 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

11 10/18/09

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

•

12 10/18/09

GLYCOSURIA 

GFR-NC,KT & TMG ↓ A. HYPERGLYCEMIC: • Alimentary-IFG • Emotional-sympathetic and splanic nerve excitation↑ • Endocrinal • Experimental-alloxan 

13 10/18/09

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

14 10/18/09

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

15 10/18/09

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)

16 10/18/09

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 )

17 10/18/09

Factors affecting GTT • Concerned with the blood glucose regulation • 1.Metabolic-diet-thiamine -starvation • -excretion • -liver diseases, infection • • 2.Hormones-insulin • -antagonistsepinephrine,glucagon,glucocorticoids,GH,thyroxin

18 10/18/09

GTT

19 10/18/09

STATE

NORMAL

IMPAIRED

DIABETES

Fasting

70-110

110-126 (IFG)

>126

2 Hr(mini GTT)

140

140-200(IGT)

>200

20 10/18/09

MANAGEMENT OF DIEBETES • Organs involved-side effectscomplications,acute,chronic-multiple organs

21 10/18/09

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

22 10/18/09

• 7.Ketone bodies • 8.altered lipid profile

23 10/18/09

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 