DIABETES MELLITUS BY Dr. HUSSEIN SAAD, MRCP (UK) Consultant Family Medicine Assistant Clinical Professor KKUH.

DIABETES MELLITUSDIABETES MELLITUS

BYBY

Dr. HUSSEIN SAAD, Dr. HUSSEIN SAAD, MRCP (UK)MRCP (UK)

Consultant Family MedicineConsultant Family Medicine

Assistant Clinical ProfessorAssistant Clinical Professor

KKUHKKUH

DEFINITIONDEFINITION

A group of metabolic disorders A group of metabolic disorders characterized bycharacterized by hyperglycemiahyperglycemia resulting from defects in insulin resulting from defects in insulin secretion, insulin action or both.secretion, insulin action or both.

CLASSIFICATIONCLASSIFICATION Type 1 diabetesType 1 diabetes (absolute insulin deficiency) (absolute insulin deficiency) Type 2 diabetesType 2 diabetes (insulin resistance with (insulin resistance with

relative insulin def.)relative insulin def.) Gestational diabetes mellitusGestational diabetes mellitus Other typesOther types (genetic or secondary types) (genetic or secondary types)

Prevalence of DM in Saudi ArabiaPrevalence of DM in Saudi Arabia      

A community based study of A community based study of 1723217232 subjects subjects conducted between 1995 and 2000 in KSA. conducted between 1995 and 2000 in KSA.

The examining age group, The examining age group, 30-70 years30-70 years of selected of selected households during 5-year periodhouseholds during 5-year period

Mansour M. Al-Nozha et al,The prevalence of CAD among Saudis of both sexes, in rural as Mansour M. Al-Nozha et al,The prevalence of CAD among Saudis of both sexes, in rural as well as urban communities, as well as modifiable risk factors for CAD.well as urban communities, as well as modifiable risk factors for CAD.

Saudi Medical Journal 2004;Saudi Medical Journal 2004;  Vol.Vol.  2525  (9):(9):  1165-11711165-1171

Prevalence of DM in Saudi ArabiaPrevalence of DM in Saudi Arabia

The overall prevalence of DM obtained The overall prevalence of DM obtained from this study is from this study is 23.7%23.7% in KSA. in KSA.

The prevalence in males and females were The prevalence in males and females were 26.2%26.2% and and 21.5%21.5% respectively respectively (p<0.00001). (p<0.00001).

A large number of diabetics 1116 (A large number of diabetics 1116 (27.9%27.9%) ) were unaware of having DM.were unaware of having DM.

Mansour M. Al-Nozha et al,The prevalence of CAD among Saudis of both sexes, in Mansour M. Al-Nozha et al,The prevalence of CAD among Saudis of both sexes, in rural as well as urban communities, as well as modifiable risk factors for CAD.rural as well as urban communities, as well as modifiable risk factors for CAD.

Saudi Medical Journal 2004;Saudi Medical Journal 2004;  Vol.Vol.  2525  (9):(9):  1165-1171 1165-1171

DIAGNOSISDIAGNOSIS A symptomatic patient plus casual plasma A symptomatic patient plus casual plasma

glucose glucose ≥ 11.1 mmol/L≥ 11.1 mmol/L or FPG or FPG ≥ 7.0 ≥ 7.0 mmol/L.mmol/L.

During an OGTT 2-hr post 75 gm-glucose During an OGTT 2-hr post 75 gm-glucose

≥ ≥ 11.1 mmol/L.11.1 mmol/L.

● ● In the absence of symptoms suggestive of In the absence of symptoms suggestive of DM, these criteria should be confirmed by DM, these criteria should be confirmed by repeat testing on a different day.repeat testing on a different day.

DIAGNOSISDIAGNOSIS FPG FPG ≤ 5.5 mmol/L≤ 5.5 mmol/L = normal = normal

FPG FPG ≥ 5.6 mmol/L≥ 5.6 mmol/L to to 6.9 mmol/L6.9 mmol/L= IFG= IFG

FPG FPG ≥ 7.0 mmol/L≥ 7.0 mmol/L = provisional = provisional diagnosis of DM and must be diagnosis of DM and must be confirmedconfirmed

in asymptomatic person.in asymptomatic person.

Diagnosis Diagnosis based onbased on: Glucose Tolerance : Glucose Tolerance TestTest

2 hr post 75 gm 2 hr post 75 gm glucoseglucose

If If << 7.8 7.8 mmol/Lmmol/L = normal GTT = normal GTT

IfIf ≥≥ 7.8 mmol/L 7.8 mmol/L andand < 11.1 mmol/L < 11.1 mmol/L = =

Impaired Impaired GTTGTT

IfIf ≥≥ 11.1 mmol/L 11.1 mmol/L = provisional diagnosis of = provisional diagnosis of

DiabetesDiabetes

Screening FOR DM IN Screening FOR DM IN ASYMPTOMATICASYMPTOMATIC

All individuals at age 45 years or above.All individuals at age 45 years or above. At younger age or more frequently in whom:At younger age or more frequently in whom:

■ ■ Are ObeseAre Obese

■ ■ Have a first degree relative with diabetesHave a first degree relative with diabetes

■ ■ Are Hypertensive ≥ 140/90Are Hypertensive ≥ 140/90

■ ■ Have been diagnosed with GDMHave been diagnosed with GDM

■ ■ Have DyslipidaemiaHave Dyslipidaemia

■ ■ Had IGT or IFGHad IGT or IFG

Impaired Glucose Impaired Glucose ToleranceTolerance

● ● There is growing evidence that at There is growing evidence that at glucoseglucose levels levels

above normal but below the diabetes thresholdabove normal but below the diabetes threshold

diagnostic now referred to as diagnostic now referred to as pre-diabetes.pre-diabetes.

●● There is a substantially increased risk ofThere is a substantially increased risk of

cardiovascular disease (CVD) and death.cardiovascular disease (CVD) and death.

1- The DECODE Study Group: Glucose tolerance and cardiovascular mortality: comparison of 1- The DECODE Study Group: Glucose tolerance and cardiovascular mortality: comparison of fasting and 2-hour diagnostic criteria. fasting and 2-hour diagnostic criteria. Arch Intern MedArch Intern Med 161:397–405, 2001 161:397–405, 2001

2- Saydah SH, Loria CM, Eberhardt MS, Brancati FL: Subclinical states of glucose intolerance 2- Saydah SH, Loria CM, Eberhardt MS, Brancati FL: Subclinical states of glucose intolerance and risk of death in the U.S. and risk of death in the U.S. Diabetes CareDiabetes Care 24:447–453, 2001 24:447–453, 2001

Impaired Glucose ToleranceImpaired Glucose Tolerance

■■ In the Finnish studyIn the Finnish study, 522 middle-aged obese (mean , 522 middle-aged obese (mean BMI 31 kg/mBMI 31 kg/m22) subjects with IGT were randomized to ) subjects with IGT were randomized to receive either brief diet and exercise counseling receive either brief diet and exercise counseling (control group)(control group) or intensive individualized instruction or intensive individualized instruction on weight reduction, food intake, and guidance on on weight reduction, food intake, and guidance on increasing physical activity increasing physical activity (intervention group).(intervention group).

After an average follow-up of After an average follow-up of 3.2 years3.2 years, there was a , there was a 58%58% relative reduction in the incidence of diabetes relative reduction in the incidence of diabetes in the intervention group compared with the control in the intervention group compared with the control subjects.subjects.

Tuomilehto J et alTuomilehto J et al Prevention of type 2 diabetes mellitus by changes in lifestyle among Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with subjects with impairedimpaired glucoseglucose tolerancetolerance. . N Engl J MedN Engl J Med 344:1343 344:1343––1350, 20011350, 2001

Impaired Glucose ToleranceImpaired Glucose Tolerance

■ ■ Three diabetes prevention trials used pharmacological therapy, Three diabetes prevention trials used pharmacological therapy, and all have reported a significant lowering of the incidence of and all have reported a significant lowering of the incidence of diabetesdiabetes. .

1-1- The Biguanide The Biguanide MetforminMetformin reduced the risk of diabetes by 31% reduced the risk of diabetes by 31% in in

the DPPthe DPP (1)(1)

2-2- The -Glucosidase Inhibitor The -Glucosidase Inhibitor AcarboseAcarbose reduced the risk by 32% in reduced the risk by 32% in thethe

STOP-NIDDM trial STOP-NIDDM trial (2)(2)

3- 3- The Thiazolidinedione The Thiazolidinedione TroglitazoneTroglitazone reduced the risk by 56% in reduced the risk by 56% in thethe

TRIPOD study TRIPOD study (3)(3)

1- 1- Diabetes Prevention Research Group: Reduction in the evidence of type 2 diabetes with life-style intervention Diabetes Prevention Research Group: Reduction in the evidence of type 2 diabetes with life-style intervention

or or metforminmetformin. . N Engl J MedN Engl J Med 346:393 346:393––403, 2002403, 2002 2- 2- Chiasson JL et alChiasson JL et al for the STOP-NIDDM Trial Research Group: Acarbose for prevention of type 2 diabetes mellitus: for the STOP-NIDDM Trial Research Group: Acarbose for prevention of type 2 diabetes mellitus:

the STOP-NIDDM randomised trial. the STOP-NIDDM randomised trial. LancetLancet 359:2072 359:2072––2077, 20022077, 2002 3-3- DiabetesDiabetes 51:2796 51:2796––2803, 2002 2803, 2002

Oral medication for type 2 DMOral medication for type 2 DM 11 - -Sulphonylurea groupSulphonylurea group::

• •GlibenclamideGlibenclamide • • GliclazideGliclazide

• • GlipizideGlipizide

Action:Action: stimulate the pancreace to secretestimulate the pancreace to secrete insulininsulin..

Note:Note: GliclazideGliclazide is suitable for is suitable for patientspatients

with impaired hepatic and renalwith impaired hepatic and renal functionsfunctions..

Oral Medication for type 2 Oral Medication for type 2 DMDM

22 - -Biguanide Group (METFORMIN)Biguanide Group (METFORMIN)

ActionAction: : ▪▪ Inhibit the process of Gluconeogenesis Inhibit the process of Gluconeogenesis..

▪▪ Increasing the peripheral utilization ofIncreasing the peripheral utilization of GlucoseGlucose..

▪▪ It acts only in the presence of insulinIt acts only in the presence of insulin..

PrecautionPrecaution:: Not given in patients with impairedNot given in patients with impaired liver or renal functions liver or renal functions (Hold if creatinine(Hold if creatinine

> > 160160 in males and > 150 mmol/l inin males and > 150 mmol/l in females)females), severe infections, severe infections,,

..

Oral Medication for type Oral Medication for type 2 DM2 DM

33 - -Alpha Glucosidase Inhibitors (Alpha Glucosidase Inhibitors (ACARBOSEACARBOSE))

■■ Used for Post Prandial Used for Post Prandial HyperglycaemiaHyperglycaemia

ActionAction: inhibit the absorption of : inhibit the absorption of carbohydratecarbohydrate..

Side effectsSide effects: flatulance, distension, soft: flatulance, distension, soft

stoolstool..,..,

Oral Medication for type 2 Oral Medication for type 2 DMDM

44 - -MeglitinidesMeglitinides ( REPAGLINIDE )( REPAGLINIDE )

■■ Used for Post Prandial HyperglycaemiaUsed for Post Prandial Hyperglycaemia

ActionAction: : •• Similar in action to Sulphonylurea Similar in action to Sulphonylurea

•• Rapid onset of actionRapid onset of action

••Taken immediately before mealsTaken immediately before meals

■■ Used as Monotherapy or in combination withUsed as Monotherapy or in combination with MetforminMetformin

Oral Medication for type 2 DMOral Medication for type 2 DM

4- 4- Thiozolidinediones:Thiozolidinediones: ● ● ROSIGLITAZONE ROSIGLITAZONE ● ● PIOGLITAZONEPIOGLITAZONE Reduce insulin resistanceReduce insulin resistance Promotes glucose uptake by skeletal muscles Promotes glucose uptake by skeletal muscles

and adipose tissueand adipose tissue Inhibits hepatic gluconeogenesisInhibits hepatic gluconeogenesis Used in combination with metformin and Used in combination with metformin and

sulphonylureasulphonylurea Periodic monitoring of liver enzymesPeriodic monitoring of liver enzymes Not given in patients with heart failure Not given in patients with heart failure

INCRETINSINCRETINS

Glucagon-like Peptide-1Glucagon-like Peptide-1• GLP-1 is secreted throughout the day by intestinal GLP-1 is secreted throughout the day by intestinal mucosa in response to oral glucose in the gut. mucosa in response to oral glucose in the gut. • GLP-1 causes anabolic actions on the synthesis of GLP-1 causes anabolic actions on the synthesis of insulin in beta cells by stimulating all steps of insulin insulin in beta cells by stimulating all steps of insulin biosynthesis. biosynthesis. • GLP-1 provides continued and augmented release of GLP-1 provides continued and augmented release of insulin for secretion in response to glucose without insulin for secretion in response to glucose without overproduction that could lead to hypoglycemia.overproduction that could lead to hypoglycemia.• GLP-1 also acts on islet alpha cells, causing strong GLP-1 also acts on islet alpha cells, causing strong inhibition of postprandial glucagon secretion.inhibition of postprandial glucagon secretion.• GLP-1 slows gastric emptying and promotes early GLP-1 slows gastric emptying and promotes early satiety with reduced food intakesatiety with reduced food intake

Dipeptidyl Peptidase-4Dipeptidyl Peptidase-4

• Within minutes of secretion or Within minutes of secretion or exogenous exogenous administration, GLP-1 is rapidly administration, GLP-1 is rapidly degraded bydegraded by dipeptidyl peptidase-4 (DPP-4).dipeptidyl peptidase-4 (DPP-4).

• DPP-4 is found in many body tissues,DPP-4 is found in many body tissues, including liver, renal, and intestinal including liver, renal, and intestinal brush-brush- border membranes; lymphocytes; and border membranes; lymphocytes; and endothelial cells.endothelial cells.

INCRETINSINCRETINS

The incretin system is impaired in The incretin system is impaired in patients with T2DM, which, as a patients with T2DM, which, as a consequence of its insulinotropic consequence of its insulinotropic actions, contributes to fasting and actions, contributes to fasting and postprandial hyperglycemia. postprandial hyperglycemia.

The impairment of GLP-1 secretion The impairment of GLP-1 secretion varies directly with the degree of insulin varies directly with the degree of insulin resistance; those who are more insulin resistance; those who are more insulin resistant have a lower rise in GLP-1 in resistant have a lower rise in GLP-1 in response to a meal. response to a meal.

The American Association of Clinical The American Association of Clinical Endocrinologists (AACE) guidelines Endocrinologists (AACE) guidelines make it clear that make it clear that IncretinsIncretins can be can be used early and are not limited to used early and are not limited to third- or fourth-line therapy for third- or fourth-line therapy for T2DM T2DM

Medication:Medication:Two agents are currently available in the Two agents are currently available in the US that act upon the US that act upon the Incretin hormone Incretin hormone system system ––● ● ExenatideExenatide ( (ByettaByetta),), a twice-daily a twice-daily glucagon-like peptide-1 (GLP-1) receptor glucagon-like peptide-1 (GLP-1) receptor agonist. agonist. ● ● SitagliptinSitagliptin ( (JanuviaJanuvia),), a dipeptidyl a dipeptidyl peptidase-4 (DPP-4) inhibitor. peptidase-4 (DPP-4) inhibitor. ● ● Agents are currently under review by Agents are currently under review by (FDA). These include the once-daily (FDA). These include the once-daily human GLP-1 analog human GLP-1 analog liraglutideliraglutide and the and the DPP-4 inhibitors DPP-4 inhibitors AlogliptinAlogliptin, , SaxagliptinSaxagliptin,, and and VildagliptinVildagliptin. .

C au ses o f D ea th

Adapted from Geiss LS et al. In Diabetes in Am erica . 2nd ed. 1995: chap 11.

M o rta lity in P eo p le w ith D iab etes

Ischemicheart

disease

Otherheart

disease

Diabetes Cancer Stroke Infection Other

%o

fd

eath

s

50

40

30

20

10

0

C H D M o rta lity in Ty p e 2 D ia b etics w ith a n d w ith o u t P r io r M I

Adapted from Haffner SM et al New Engl J Med 1998;339:229-234.

%S

urv

ival

100

80

60

40

20

0

Non-diabetic, no MI (n=1304)Type 2, no MI (n=890)Non-diabetic, MI (n=69)

Type 2, MI (n=169)

0 1 2 3 4 5 6 7 8

Years

UKPDSUKPDS

Aim:Aim:To determine whether intensified blood To determine whether intensified blood glucose control with either sulfonylurea or glucose control with either sulfonylurea or insulin reduces the risk of Macrovascular or insulin reduces the risk of Macrovascular or Microvascular complications in type 2 diabetMicrovascular complications in type 2 diabet

UKPDS ResultsUKPDS ResultsCauseIntensive

rateConventional

rateP% decrease

Any Diabetes related

40.9460.02912

MI14.717.40.05216

Stroke 5.650.52-

PVD1.1 1.60.15-

Microvascular8.611.40.002925

Lancet 1998;352:837-853

M a jo r C o ro n a ry E v en ts in 4 S :D ia b etics v s . N o n -D ia b etics

Adapted from Pyörälä K et al Diabetes Care 1997;20:614-620.

C oron ary D ea th an d N on -fa ta l M I

Pro

po

rtio

no

fp

atie

nts

wit

ho

ut

eve

nts

Years since randomization0 1 2 3 4 5 6

Diabetic–simvastatin (n=105)Diabetic–placebo (n=97)

Non-diabetic–simvastatin (n=2116)Non-diabetic–placebo (n=2126)

55%risk

reductionP=0.002

Diabetic–simvastatin

Diabetic–placebo

100

90

80

70

60

50

0

Pro

po

rtio

no

fp

atie

nts

wit

ho

ut

eve

nts

Years since randomization0 1 2 3 4 5 6

Diabetic–simvastatin (n=105)Diabetic–placebo (n=97)

Non-diabetic–simvastatin (n=2116)Non-diabetic–placebo (n=2126)

55%risk

reductionP=0.002

Diabetic–simvastatin

Diabetic–placebo

100

90

80

70

60

50

0

Adapted from Pyörälä K et al Diabetes Care 1997;20:614-620.

D ia b etic v s . N o n -D ia b etic P a tien ts in 4 S

Simvastatin better

0 0.2 0.4 0.6 0.8 1.0 1.2 1.4

P=0.001P=0.087

P<0.0001P=0.242

P<0.0001P=0.002

P=0.097P=0.071

P <0.0001P=0.018

Relative risk (95% CI)

Placebo better

Reduced IncreasedNon-diabetic

Diabetic

Total mortality

CHD mortality

Major CHD event

Cerebrovascular event

Any atherosclerotic event

Simvastatin better

0 0.2 0.4 0.6 0.8 1.0 1.2 1.4

P=0.001P=0.087

P<0.0001P=0.242

P<0.0001P=0.002

P=0.097P=0.071

P <0.0001P=0.018

Relative risk (95% CI)

Placebo better

Reduced IncreasedNon-diabetic

Diabetic

Simvastatin better

0 0.2 0.4 0.6 0.8 1.0 1.2 1.4

P=0.001P=0.087

P<0.0001P=0.242

P<0.0001P=0.002

P=0.097P=0.071

P <0.0001P=0.018

Relative risk (95% CI)

Placebo better

Reduced IncreasedNon-diabetic

Diabetic

Total mortality

CHD mortality

Major CHD event

Cerebrovascular event

Any atherosclerotic event

MANAGEMENT OF TYPE 2 MANAGEMENT OF TYPE 2 DMDM

DietDiet and and ExerciseExercise should be offered should be offered for all patients for 2 months.for all patients for 2 months.

Obese patients:Obese patients: ■ ■ METFORMINMETFORMIN is the drug of choice is the drug of choice Start with 500 mg PO three times a day up Start with 500 mg PO three times a day up

up to 850 mg or 1 gm PO TDS.up to 850 mg or 1 gm PO TDS. ■ ■ If not controlled add If not controlled add SulphonylureaSulphonylurea or or GlitazonesGlitazones

MANAGEMENT OF TYPE 2 MANAGEMENT OF TYPE 2 DMDM

Non-Obese patientsNon-Obese patients DietDiet and and ExerciseExercise MetforminMetformin Add Add Sulphonylurea Sulphonylurea (e.g. (e.g.

Glibenclamide or Gliclazide)Glibenclamide or Gliclazide) In secondary failure, consider shifting In secondary failure, consider shifting

to Insulinto Insulin

PHYSICAL EXAMINATIONPHYSICAL EXAMINATION Height and WeightHeight and Weight Blood PressureBlood Pressure Fundus ExaminationFundus Examination Cardiac examinationCardiac examination Lower Limbs:Lower Limbs:

■ ■ Skin ExaminationSkin Examination

■ ■ Evaluation of pulsesEvaluation of pulses

■ ■ Foot ExaminationFoot Examination

■ ■ Neurologic ExaminationNeurologic Examination

LABORATORY LABORATORY EVALUATIONEVALUATION FPG and 2 hr PPFPG and 2 hr PP

Midstream UrineMidstream Urine Urea and CreatinineUrea and Creatinine Lipid Profile (Lipid Profile (total cholesterol, LDLc, total cholesterol, LDLc,

HDLc and triglyceridesHDLc and triglycerides)) HbA1cHbA1c 24 hr urine collection for protein24 hr urine collection for protein ECGECG Chest X-RayChest X-Ray

TREATMENT REGIMENS OF TYPE TREATMENT REGIMENS OF TYPE 1 DM1 DM

Conventional Insulin TherapyConventional Insulin Therapy

Two injections of NPH and Regular InsulinTwo injections of NPH and Regular Insulin Mixed InsulinMixed Insulin

Two injections of 70/30 or 60/40 Two injections of 70/30 or 60/40 Multiple Insulin InjectionsMultiple Insulin Injections

►►1 or 2 injections of 1 or 2 injections of NPHNPH plus 3 injections of plus 3 injections of

RegularRegular or or Lispro InsulinLispro Insulin

►►One injection of One injection of GlargineGlargine or or Detemir Detemir plus 3plus 3

injections injections of of RegularRegular or or Lispro InsulinLispro Insulin

INSULIN GLARGINE INSULIN GLARGINE (LANTUS)(LANTUS)

The first clear long-acting insulinThe first clear long-acting insulin Acidic Acidic (pH of 4)(pH of 4) when injected it is neutralized when injected it is neutralized

by the body, causing by the body, causing Glargine crystalsGlargine crystals to be to be precipitated and slowly absorbed.precipitated and slowly absorbed.

It is taken once a dayIt is taken once a day Being acidic, cannot be mixed with other Being acidic, cannot be mixed with other

insulin insulin

Insulin administrationInsulin administration

• Do not mix Glargine with other insulin products. Do not mix Glargine with other insulin products. • Insulin site should be clean, but wiping with alcohol is not Insulin site should be clean, but wiping with alcohol is not

needed.needed.• Syringe reuse acceptable but meticulous attention to Syringe reuse acceptable but meticulous attention to

cleanliness is needed.cleanliness is needed.• Insulin pens improve the dose accuracy.Insulin pens improve the dose accuracy.• Injection site rotation reduces the lipoatrophy.Injection site rotation reduces the lipoatrophy.• Abdomen region has a faster absorption rate than the Arm,Abdomen region has a faster absorption rate than the Arm,

which is faster than the leg.which is faster than the leg.

Targets in DMTargets in DM

Bp Bp < 130 / 80< 130 / 80

HbA1C HbA1C ≤ 7 % (≤ 7 % (European Diab. Soc. European Diab. Soc. ≤ 6.5 %) ≤ 6.5 %)

LDL-C LDL-C < 100 mg/dl < 100 mg/dl (2.6 mmol/L)(2.6 mmol/L)

HDL-C HDL-C > 40 mg/dl > 40 mg/dl (males)(males)

> 50 mg/dl > 50 mg/dl (females)(females)

Trig. Trig. < 150 mg/dl < 150 mg/dl (1.7 mmol/L)(1.7 mmol/L)

CASE 1CASE 1

A 50-year-old man presents to your A 50-year-old man presents to your office to check the results of some office to check the results of some routine investigations.routine investigations.

FPG : 6.6 mmol/LFPG : 6.6 mmol/L

In another occasion FPG: 6.2 n another occasion FPG: 6.2

what is your diagnosis ?what is your diagnosis ?

what further investigations are you what further investigations are you going to do ?going to do ?

CASE 2CASE 2

A 48-year-old man presents to your office for A 48-year-old man presents to your office for routine checkup for hypertension. routine checkup for hypertension. Asymptomatic .Asymptomatic .

On Atenolol 50 mg a day.On Atenolol 50 mg a day.

FH FH : his father is diabetic: his father is diabetic

BMI 38 Bp: 150/94BMI 38 Bp: 150/94

FPGFPG: 14.6 mmol/L U and E: normal: 14.6 mmol/L U and E: normal

Cholesterol: 5.7 mmol/LCholesterol: 5.7 mmol/L

Trig. 2.86 mmol/LTrig. 2.86 mmol/L

How are you going to deal with him?How are you going to deal with him?

CASE 3CASE 3 A 44-year-old woman presents to A 44-year-old woman presents to

your office with 2 month H/O loss of your office with 2 month H/O loss of weight and polyurea.weight and polyurea.

BMI 20BMI 20 RBS : 24.4 mmol/LRBS : 24.4 mmol/L Urine dipstick : glucose: 4+ Urine dipstick : glucose: 4+ ketones : nilketones : nil Protein : ++Protein : ++

what is your diagnosis ?what is your diagnosis ? what is your management ?what is your management ?

Case 4Case 4

A 22-year-old university student, A 22-year-old university student, presents to your office with one presents to your office with one week H/O fatigue and nocturia. week H/O fatigue and nocturia.

He lost 6 kg per last month.He lost 6 kg per last month.

RBS : 24.6 mmol/LRBS : 24.6 mmol/L

What is the most important next What is the most important next step to do ?step to do ?

CASE 5CASE 5 A 52-year-old man is known case of DM A 52-year-old man is known case of DM

presents to your office for follow up.presents to your office for follow up. He is on : glibenclamide 10 mg po bidHe is on : glibenclamide 10 mg po bid Metformin 1 gm po tidMetformin 1 gm po tid FBS : 16.2 mmol/L Cholesterol : FBS : 16.2 mmol/L Cholesterol : 7.3 mmo/L7.3 mmo/L

2hPP: 21.4 mmol/L LDL-C : 4.8 mmol/L2hPP: 21.4 mmol/L LDL-C : 4.8 mmol/L HDL-C : 0.88 mmol/L HDL-C : 0.88 mmol/L Trig. 4.6 mmol/LTrig. 4.6 mmol/L U& E : norm.U& E : norm. BMI 33BMI 33 ? :? : How are you going to manage this patient ?How are you going to manage this patient ?