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Oral glucose Tolerance TestOral glucose Tolerance Testand Factors Influencing Bloodand Factors Influencing Blood
Glucose Level.Glucose Level. one By bdulaziz Massoud Alfaydi
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DefinitionDefinition. The glucose tolerance test (GTT)
Consists of drinking (75 to 100 )gramsof glucose solution ..Measuring the blood glucose values
every hour toget a cerve ..A 2 hour GTT is used to diagnosis
diabetes , but a 6 hour test might alsodiagnosis diabetes plus hypoglycemia..Symptoms of hypoglycemia occur after
the 5 th hour..In healthy individual the insuline
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Referance valuesReferance values
Normal /FPG:Adults: 110mg/dl or 6.1 mmol/L.30-minute
Adults 110-170 mg/dl or 6.1-9.4mmol/L.60- minute PG after glucose load :
Adults
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.3- hours PG afterglucose load:
Adults b70-120
mg/dl or 3.9-6.7mmol/L.All four blood
values must bewithin normallimits to beconsidered normal.
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ProcedureProcedure
This is timed test for glucosetolerance . A-2 hourplasma glucose test is done
after glucose load to detectdiabetes in individuals otherthan pregnant women .
The 3- hour test is done forpregnant women .The 4- hourtest evaluates possiblehypoglycemia.
1- Have patiant eat a diet with
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Ensure that the following drugsare discontinued 3 dayes beforethe test because they mayinfluence test results:
a) Hormones , oralcontraceptives , steroids.
b)Salicylates, anti inflammatory
drugs.C)Diuretic agentsd) Hypoglycemic agents.
.e)Antihypertensive drugs
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F)Anti convulsants .3-Insuline and oral hypoglycemics
should be with held until the testcompleted .
4- Record the patient s weighta)Pediatric doses of glucose are
based on body weight. Calculated
as 1.75g/kg not to exceed a totalof 75g.b)Pregnant women 100g glucose.C) Non pregnant adults 75g
glucose.
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5-A 5ml sample of venous blood isdrawn. The patient should fast 12to 16 hours before testing .
6-Bbood samples are obtained 30menutes , 1 hr, 2hrs, 3hrs afterglucose ingestion.
7- Specimens taken 4 hrs afteringestion are significants fordetecting hypoglycemia .
8-Tolerance tests can also be
performed for pentose ,lactose-
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a) Persistent fastinghyperglycemia >140mg/dl or>7.8mmol/l.
b) persistent fasting normalplasma glucose .
c)Patient with overt diabetes
mellitus.d)Persistent 2-hour plasmaglucose >200mg/dl or>11.1mmol/l.
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Interfering factorsInterfering factors
1- Smoking increases glucoselevels.
2-Altered diets (weight reduction)
before testing can diminishcarbohydrate tolerance andsuggest ,false diabetes.
Glucose levels normally tend toincrease with aging.3-Prolonged oral contraceptive
use causes significantly higherlucose levels in the second
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5-Infections disease illnesses andoperative procedures affectglucose tolerance.
6- Certain drugs impair glucosetolerance levels .a) Insulin .b) Oral hypoglycemics.c)Large doses of salicylates , anti-
inflammatoriesd) Thiazide diuretics.e) Oral contraceptives.
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1a. Normal Minimum curve1a. Normal Minimum curveaccording to Seale Harrisaccording 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
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1b. Normal Maximum1b. Normal Maximumcurvecurve
Time [hours] 0 0.5 1 2 3 4 5 6
Blood glucose [mg/dl] 120 135 160 130 110 100 110 105
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..diabetesdiabetesTime [hours] 0 0.5 1 2 3 4 5 6
Blood glucose[mg/dl] 115 145 180 160 120 130 130 130
h3 C i h
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3. Curve with severe3. Curve with severediabetesdiabetesTime [hours] 0 0.5 1 2 3 4 5 6
Blood glucose[mg/dl] 200 235 265 280 300 295 280 270
b d4 Di b d
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4. Diabetes and4. Diabetes andhypoglycemiahypoglycemia
Time [hours] 0 0.5 1 2 3 4 5 6
Blood glucose[mg/dl] 100 160 220 160 85 60 50 85
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5. Continuous low values5. 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
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6. Pre-hypoglycemia6. 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
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7. Mild hypoglycemia7. Mild hypoglycemiaTime [hours] 0 0.5 1 2 3 4 5 6
Blood glucose [mg/dl] 80 120 80 60 80 75 80 80
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8. Severe hypoglycemia I8. Severe hypoglycemia ITime [hours] 0 0.5 1 2 3 4 5 6
Blood glucose[mg/dl] 95 110 120 105 100 60 40 60
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10. Flat curve10. 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
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f) Corticosteroids.g) Estrogens.h) Heparin.
i) Nicotinic acid . j) Phenothiazines.k) Lithium .l) Metryrapone(metopirone).
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HOMEOSTASIS NORMALHOMEOSTASIS NORMAL
3 Mechanisms:
1.Metabolic2.Hormonal3.Renal
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MetabolicMetabolic.Dietary-Primary
source of all bodycomponents
Glycogen-Initial-liver(92%), later-
muscle(8%),sufficient for 18 hrsGluconeogenesis:Non-cabohydrates Glucogenic amino acids all except ,lys,
leu TG Glycerol DHAP Odd chain FA-PropionicAcid
Succinyl CoA Lactate Pyruvate
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HormonalHormonal
Insulin- cell of Langerhans favoursuptake into cell
Glucagon,
epinephrine,glucocorticoids,GH,thyroxin-antagonists to insulin,favoursexcessive glycogenolysis andrelease of more glucose in blood
Cooperative action of both types of hormones help maintaining theblood glucose
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RenalRenal
Rates of Glomerularfiltration and Tubular absorption maintain bloodglucose
Kidney threshold for glucose-180 mg%, more than this spillover in urine glycosuria
TMG-375 mg/min,more accurate indexthan kidney threshold
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ABNORMALABNORMAL
HYPERGLYCEMIAHYPOGLYCEMIA
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HYPERGLYCEMIA:HYPERGLYCEMIA:
DIABETES:10 % population worldwide affected, 2
%>50 y
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:: Iry (Known causes)Iry (Known causes)
I.IDDM- Insulin deficiencyI.IDDM- Insulin deficiencyAutoimmune -Immunity mediated(Antibodies to
insulin 50%,antibodies to islet cell cytoplasmicproteins 80%), idiopathic( damage of cell of islet of Langerhans or viral infection)
II.NIDDM- Normal insulin but unavailable(insulinresistance)-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, Childrisk mortality ,BWt ,ii)IFG, iii)IGT
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IIry (Unknown causes)IIry (Unknown causes)
Pancreatic diseases-pancreatitis,cystic fibrosis
Endocrinopathies-cushing
syndrome,thyrotoxicosis,acromegalyDrug induced-steroids, blockers
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GLYCOSURIAGLYCOSURIA
GFR-NC,KT & TMG A. HYPERGLYCEMIC:
Alimentary-IFG
Emotional-sympathetic and splanicnerve excitation
Endocrinal
Experimental-alloxan
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GLYCOSURIAGLYCOSURIA
B.RENAL:HereditaryAcquired
Threshold ( 180 mg%) Tubular reabsorption Experimental-phloridzine
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II.HYPOGLYCEMIAII.HYPOGLYCEMIA
Risk-50 mg%,fatal < 30 mg%Insulin
Thyroid Liver diseasesSevere exerciseGlycogen storage diseasesAlcohol ingestion.
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DIEBETES STATUSDIEBETES STATUS
MONITORINGA.Conventional:
Glucose-Blood (GOD-POD)-Urine
Benedict reagent
G Y O R0.5% 1% 1.5% 2->2%
GTT: 1.Lab-Oral GTT (OGTT)
2.Clinic-Post-prandial (meal)
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B. Modern investigationsB. 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 GTTFactors affecting GTT
Concerned with the blood glucoseregulation
1.Metabolic-diet-thiamine
-starvation-excretion-liver diseases, infection
2.Hormones-insulin-antagonists
epinephrine,glucagon,glucocorticoids,
GH,thyroxin.
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GTTGTT
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MANAGEMENT OFMANAGEMENT OFDIEBETESDIEBETES
Organs involved-side effects-complications,acute,chronic-multipleorgans.
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CLINICAL PRESENTATION INCLINICAL PRESENTATION INDMDM
Cardinal Symptoms:Complications1.Poly-urea-Urine (wt.loss)
-dypsea-thirst-water intake -phagia-Food intake
2.Chronic skin infection-Boils-Celluloitis-Absesses
3.Plaques-CVD:CHD+CADMyocardial infarction4.Retinopathy5.Nephropathy6.Fatty liver
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7.Ketone bodies8.altered lipid profile
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Drug therapy for DKADrug therapy for DKAInsulin therapy: lower BG by 75-
150mg/dl/hr1. 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. Potassium2. Bicarbonate
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Treatment for DKATreatment for DKA
Frequent assessment of client: LOC,V/S, blood glucose levels, fluid andelectrolyte status
Correct fluid volume deficit1. 1 liter of hypertonic solution (D51/2NS)
over 8 to 12 hrs.2. 1 liter of isotonic saline over 1 hour3. 1 liter of hypotonic saline over 6 to 8 hrs
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Management ofManag
ement of
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Management of Manag ement of HypoglycemiaHypoglycemia
Hypoglycemic protocol1. 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
HbAHbA Predicts CHD in TypePredicts CHD in Type
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0
5
10
1520
25
0
5
10
1520
25
HD mortali ty(%) .ncidence in 3 5
years
l l CHD events(%) .ncidence in 3 5
years
HbA1c HbA1c
Low< %
Middle- . %7 9
High> .9
%
Low< %
Middle- . %7 9
High> .9
%
HbAHbA 1c1c Predicts CHD in TypePredicts CHD in Type22
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ADA Treatment GoalsADA Treatment Goals
Hgb A1C maintained at 7% or below. Premeal blood glucose level 70 to
110mg/dl
Blood glucose at bedtime 100-140mg/Dl
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Values for HbAValues for HbA 1c1c
Non-diabetic
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Hemoglobin AHemoglobin A 1c1c
A blood testthat showsglucose levelsfor the past 3months
No preparationneeded i.e.fasting, etc.
H b A 1 cH b A 1 c
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Checking Blood GlucoseChecking Blood Glucose
CBGs
AccuChecksGlucometerGlucoscan
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Lab Assessment for AllLab Assessment for All
Diabetic ClientsDiabetic ClientsBlood tests
1. Fasting Blood GlucoseTest (Cavenaugh pg. 105)
2. Blood GlucoseMonitor Systems2. Oral Glucose
Tolerance Test(Cavenaugh pg. 109)
3. Glycosylated Hemoglobin
Assays (Cavenaugh pg. 112)4. Glycosylated Serum
Proteins and Albumin(Cavenaugh pg. 114)
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Type 2 DiabetesTyp e 2 Diabetes
80% are obese10% non-obese10% unstable:may look morelike a Type 1Diabetic
Type 2 DiabetesType 2 Diabetes
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Type 2 Diabetes Type 2 DiabetesSigns and SymptomsSig ns and Symptoms
HyperglycemiaPolyuriaPolydipsiaBlurred visionFatigueParesthesiasSkin infections
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Type 2 DiabetesType 2 DiabetesEtiologyEtiology
There isabnormallyhigh level of glucose
Pancreas does produce insulin
Body resists theinsulinseffects
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DIABETES COMPARISONDIABETES COMPARISONTYPE 1TYPE 1 TYPE 2TYPE 2
AutoimmuneProcess: Betacellsdestroyed Insulin deficiency
Has no insulin
IdiopathicGeneticpredisposition
< Age 30
Insulinresistance hassome insulin
Obesity is risk factorPhysical inactivityGenetic
predispositionAdult onset