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Oral glucose Tolerance Test

and Factors Influencing Blood


Glucose Level.
Done By
Abdulaziz Massoud Alfaydi
Blood Glucose Homeostasis

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

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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 for test

 The 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 3.9-
6.7mmol/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 , anti-
inflammatories
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%), 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  28
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
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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

10/18/09 32
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)
Pancreaticdiseases-
pancreatitis,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 38
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. 41
GTT

10/18/09 42
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.

10/18/09 44
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

10/18/09 47
Drug therapy for DKA
Insulin
therapy: lower BG by 75-
150mg/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 protocol
1. 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 All CHD events
Incidence (%) in 3 . 5 Incidence (%) in 3 . 5
years years
25 25
20 20
15 15
10 10
5 5
0 0
Low Middle High Low Middle High
<6% 6-7.9% >7.9 <6% 6-7.9% >7.9
% %
HbA 1c HbA 1c
ADA Treatment Goals
Hgb A1C maintained at 7% or below
 . Premeal blood glucose level 70 to
110mg/dl
 Blood glucose at bedtime 100-
140mg/Dl
Values for HbA1c

Non-diabetic <6 %

Diabetic with good control <7 %

Diabetic out of control >8 %
Hemoglobin A1c
A blood test
that shows Hb A1c
glucose levels
for the past 3
months
No preparation
needed i.e.
fasting, etc.
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% are obese
10% non-obese
10% 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 Insulin
Process: Beta resistance has
cells some insulin
destroyed Insul Obesity is risk factor
in deficiency Physical inactivity
Has no insulin
Genetic
Idiopathic predisposition
Genetic Adult onset
predisposition
< Age 30