Blood Glucose Oki Aziz894180

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

Blood Glucose Homeostasis Blood

Glucose Level Normal:70-110 mg% Abnormal: ◦ A.Hyperglycemia,glycosuria-diebetes ◦ B.Hypoglycemia ◦

2

Oral glucose tolerance test (OGTT) Definition. Aim. Procedure. Curves. Different Types Explain. Merits. Demerits.

Definition .The

glucose tolerance test (GTT) Consists of drinking (75 to 100 )grams of glucose solution .  .Measuring the blood glucose values every hour to get a cerve . .A 2 hour GTT is used to diagnosis diabetes , but a 6 hour test might also diagnosis diabetes plus hypoglycemia. .Symptoms of hypoglycemia occur after the 5 th hour. .In healthy individual the insuline 

Tndication  The

for test

GTT/OGTT is done on certain patients , with the following indications .  1- Family history of diabetes.  2-Obesity.  3-Unexplained episodes of hypoglycemia.  4- History of recurrent infectons (boils and abscesses).  5- In women, history of delivery of large infants ,stillbirth ,neonatal death, premature labor, and spontaaneous

Referance values Normal

/FPG: Adults: 110mg/dl or 6.1 mmol/L. 30-minute Adults 110-170 mg/dl or 6.1-9.4 mmol/L. 60- minute PG after glucose load : Adults <184mg/dl or <10.2 mmol/L. 120-minute GTT PG after glucose load : 







.3- hours PG after glucose load: Adults b70-120 mg/dl or 3.96.7mmol/L. All four blood values must be within normal limits to be considered normal.

Procedure This

is timed test for glucose tolerance . A-2 hour plasma glucose test is done after glucose load to detect diabetes in individuals other than pregnant women . The 3- hour test is done for pregnant women .The 4- hour test evaluates possible hypoglycemia. 1- Have patiant eat a diet with

Ensure

that the following drugs are discontinued 3 dayes before the test because they may influence test results: a) Hormones , oral contraceptives , steroids. b)Salicylates, anti inflammatory drugs. C)Diuretic agents d) Hypoglycemic agents. .e)Antihypertensive drugs

F)Anti

convulsants . 3-Insuline and oral hypoglycemics should be with held until the test completed . 4- Record the patient s weight a)Pediatric doses of glucose are based on body weight. Calculated as 1.75g/kg not to exceed a total of 75g. b)Pregnant women 100g glucose. C) Non pregnant adults 75g glucose.

5-A

5ml sample of venous blood is drawn. The patient should fast 12 to 16 hours before testing . 6-Bbood samples are obtained 30 menutes , 1 hr, 2hrs, 3hrs after glucose ingestion. 7- Specimens taken 4 hrs after ingestion are significants for detecting hypoglycemia . 8-Tolerance tests can also be performed for pentose ,lactose

a)

Persistent fasting hyperglycemia >140mg/dl or >7.8mmol/l. b) persistent fasting normal plasma glucose . c)Patient with overt diabetes mellitus. d)Persistent 2-hour plasma glucose >200mg/dl or >11.1mmol/l.

Interfering factors 1-

Smoking increases glucose levels. 2-Altered diets (weight reduction) before testing can diminish carbohydrate tolerance and suggest ,false diabetes. Glucose levels normally tend to increase with aging. 3-Prolonged oral contraceptive use causes significantly higher glucose levels in the second

5-Infections

disease illnesses and operative procedures affect glucose tolerance. 6- Certain drugs impair glucose tolerance levels . a) Insulin . b) Oral hypoglycemics. c)Large doses of salicylates , antiinflammatories d) Thiazide diuretics. e) Oral contraceptives.

1a. Normal Minimum curve according to Seale Harris Time [hours]

0

0.5

1

2

3

4

5

6

Blood glucose [mg/dl]

80

90

105

90

80

80

80

80

1b. Normal Maximum curve Time [hours]

0

0.5

1

2

3

4

5

6

Blood glucose [mg/dl]

120

135

160

130

110

100

110

105

2. Curve with mild diabetes Time [hours]

0

0.5

1

2

3

4

5

6

Blood glucose[mg/dl]

115

145

180

160

120

130

130

130

3. Curve with severe diabetes

Time [hours]

0

0.5

1

2

3

4

5

6

Blood glucose[mg/dl]

200

235

265

280

300

295

280

270

4. Diabetes and hypoglycemia

Time [hours]

0

0.5

1

2

3

4

5

6

Blood glucose[mg/dl]

100

160

220

160

85

60

50

85

 5. Continuous low values Time [hours]

0

0.5

1

2

3

4

5

6

Blood glucose[mg/dl]

60

80

100

60

60

60

60

55

6. Pre-hypoglycemia Time [hours]

0

0.5

1

2

3

4

5

6

Blood glucose [mg/dl]

90

115

140

100

85

80

70

75

7. Mild hypoglycemia Time [hours]

0

0.5 1

2

3

4

5

6

Blood glucose [mg/dl]

80

120 80

60

80

75

80

80

8. Severe hypoglycemia I Time [hours]

0

0.5

1

2

3

4

5

6

Blood glucose[mg/dl]

95

110

120

105

100

60

40

60

9. Severe hypoglycemia II Time [hours]

00.5

1

2

3

4

5

6

7

Blood glucose [mg/dl]

100

170

110

130

170

125

100

100

10. Flat curve

Time [hours]

0

0.5

1

2

3

4

5

6

Blood glucose [mg/dl]

90

90

90

100

90

100

80

90

f)

Corticosteroids. g) Estrogens. h) Heparin. i) Nicotinic acid . j) Phenothiazines. k) Lithium . l) Metryrapone(metopirone).

HOMEOSTASIS NORMAL 3

Mechanisms: 1.Metabolic 2.Hormonal 3.Renal

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Metabolic .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 Pyruvate  ◦ Lactate 

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Hormonal Insulin-

β cell of Langerhans favours uptake into cell Glucagon, epinephrine,glucocorticoids,GH,thyr oxin-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 30

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 34

IIry (Unknown causes) Pancreatic

diseasespancreatitis,cystic fibrosis Endocrinopathies-cushing syndrome,thyrotoxicosis,acrome galy 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. 10/18/09

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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 effectscomplications,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 10/18/09

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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 





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Drug therapy for DKA Insulin

therapy: lower BG by 75150mg/dl/hr

1.Regular insulin IV bolus dose of .1u/kg followed by IV drip of .1u/kg/hr. 2.SQ insulin when client can eat and ketosis has ended. Electrolyte

replacement

1.Potassium 2.Bicarbonate

Treatment for DKA Frequent

assessment of client: LOC, V/S, blood glucose levels, fluid and electrolyte status Correct fluid volume deficit 1.1 liter of hypertonic solution (D51/2NS) over 8 to 12 hrs. 2.1 liter of isotonic saline over 1 hour 3.1 liter of hypotonic saline over 6 to 8 hrs 

Management of Hypoglycemia Hypoglycemic

1.

protocol

Mild hypoglycemia (BG < 60 and symptomatic)  - 10 to 15g of carbohydrate  - Recheck BG in 15minutes 2.Moderate (BG < 40 and symptomatic)  -15 to 30g of rapidly absorbed CHO 3. Severe (BG < 20 and unable to swallow) - 1mg of glucagon IM/SQ or amp of D50 IVP

HbA1c Predicts CHD in Type 2 CHD mortality Incidence (%) in 3 . 5 years 25 20 15 10 5 0

Low <6%

Middle High 6-7.9% >7.9 % HbA 1c

All CHD events Incidence (%) in 3 . 5 years 25 20 15 10 5 0

Low <6%

Middle 6-7.9% HbA 1c

High >7.9 %

ADA Treatment Goals Hgb

A1C maintained at 7% or below  . Premeal blood glucose level 70 to 110mg/dl  Blood glucose at bedtime 100140mg/Dl

Values for HbA1c Non-diabetic

<6 %

 Diabetic

with good control <7 %

 Diabetic

out of control

>8 %

Hemoglobin A1c A

blood test that shows glucose levels for the past 3 months No preparation needed i.e. fasting, etc.

Hb A1c

Checking Blood Glucose CBGs AccuChecks Glucometer Glucoscan

Lab Assessment for All Diabetic Clients Blood tests            

1. Fasting Blood Glucose Test (Cavenaugh pg. 105) 2. Blood Glucose Monitor Systems 2. Oral Glucose Tolerance Test (Cavenaugh pg. 109) 3. Glycosylated Hemoglobin Assays (Cavenaugh pg. 112) 4. Glycosylated Serum Proteins and Albumin (Cavenaugh pg. 114) 

Type 2 Diabetes 80% 10% 10%

are obese non-obese unstable: may look more like a Type 1 Diabetic



Type 2 Diabetes Signs and Symptoms Hyperglycemia Polyuria Polydipsia Blurred

vision

Fatigue Paresthesias Skin

infections 

Type 2 Diabetes Etiology There

is abnormally high level of glucose Pancreas does produce insulin Body resists the insulin’s effects

DIABETES COMPARISON TYPE 1 TYPE 2 Autoimmune

Process: Beta cells destroyed Insul in deficiency Has no insulin Idiopathic Genetic predisposition < Age 30

Insulin

resistance has some insulin Obesity is risk factor Physical inactivity Genetic predisposition Adult onset