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DIABETES MELLITUS
⚫It is a metabolicdisorderof multipleetiology
characterized by chronic Hyperglycaemia with
disturbances of Carbohydrates, Fats and Protein
metabolism resulting from defects in Insulin secretion,
Insulin action or Both.
Clinical Features
⚫Easy Fatigability
⚫Polyuria
⚫Polydipsia
⚫Wasting
⚫Weight loss
⚫Air hunger
⚫Blurred vision
⚫Poor wound healing
Complications
Acute :- Diabetic ketoacidosis.
Hyperglycemic Hyperosmolar state.
Chronic :-
A. Microvascular
B. Macrovascular
C. Others
A. Microvascular complications :- Retinopathy,
Macular edema, Sensory & motor neuropathy,
Autonomic neuropathy.
B. Macrovascularcomplications :- Coronary
heart disease, Peripheral arterial disease,
Cerebrovasculardisease.
C. Others :- Cataract, Glaucoma, Periodontal disease,
Hearing loss, Gastroparesis, Diarrhea, Uropathy,
Sexual dysfunction, Acanthosis nigricans,
Necrobiosis lipoidica, Vitiligoetc….
Retinopathy Macularedema
Glaucoma Cataract
Acanthosisnigricans
Necrobiosis lipoidica
Vitiligo Neuropathic foot ulcer
Lipohypertrophy
Types
 Type 1 :- IDDM alsocalled Juvenile Diabetes
 Type2 :- NIDDM
 Type3 :- Gestational Diabetes
 Type4 :- Other Specific Types
Type 1
⚫Insulin Dependent Diabetes Mellitus.
⚫Alsocalled Juvenile Diabetes
⚫Commonamong 10-14 yrsof age group.
⚫Accounts for 5%-10% of all diagnosed casesof Diabetes
Mellitus.
⚫90% is Autoimmune mediated.
10% is Idiopathic.
Type 2
⚫Non Insulin Dependent Diabetes Mellitus.
⚫Commonamong adultsand elderly people.
⚫Accounts forabout 90-95% of all thediagnosed cases
of Diabetes.
⚫Beginsas Insulin resistance, as the need for insulin
rises, the pancreas gradually loses it’s ability to
produce insulin.
Type 3
⚫Gestational Diabetes.
⚫It is a condition of Glucose Intolerance diagnosed in
somewomen during pregnancy.
⚫Common in African americans, Latino americans,
American Indians, Obese and women with family
historyof Diabetes.
⚫After pregnancy, 5-10% of women with Gestational
Diabetesare found todevelopType 2 Diabetes.
Other Specific Types
⚫Geneticdefectsof Beta-cell function.
⚫Geneticdefect in insulinaction.
⚫Pancreaticdiseases.
⚫Excessendogenous production of hormonal
antagonist to Insulin.
⚫Drug- Induced.
⚫Viral infections.
⚫Latent Autoimmune Diabetes in Adults (LADA).
⚫Modified Onsetof Diabetes in Young (MODY).
Risk Factors
Host Factors
 Age
 Sex
 Genetic Factors
 Genetic Markers:- HLA-B8, HLA-B15, HLA-DR3 and HLA-
DR4
 Immune mechanism
 Maternal Diabetes
 Obesity
Environmental Factors
 Sedentary life style
 Diet rich in Saturated Fattyacids
 Decreased consumption of Diatary
Fibers
 Malnutrition
 Alcohol
 Chemical agents
 Stress
 Otherfactors
Diagnosis of Diabetes Mellitus
Values of Diagnosis of Diabetes Mellitus
Screening
Urineexamination:- LAck of Sensitivity
Gives too many “False Negatives”
Blood SugarTesting:-
RBS - >200mg/dl with symptoms & signsof diabetes.
FBS - >126mg/dl
PPBS - >200mg/dl
Glycated Haemoglobin - >6.5%
Target Population:-
More than 40yrs
Family historyof Diabetes
Obese
HDL <35mg/dl and Triglycerides >250mg/dl
Women who had babyweighing >4.0kg
Women who show excessweightgain during pregnancy
Patientswith Premature Atherosclerosis
⚫The majorcomponentsof the treatmentof diabetes
are:
Management of DM
• Dietand Exercise
A
• Oral hypoglycaemic
therapy
B
• InsulinTherapy
C
⦁ Diet is a basic part of management in every case.
Treatment cannot be effective unless adequate
attention is given toensuring appropriate nutrition.
⦁ Dietary treatmentshould aim at:
◦ ensuring weight control
◦ providing nutritional requirements
◦ allowing good glycaemiccontrol with blood glucose
levels as close to normal as possible
◦ correcting anyassociated blood lipid abnormalities
A. Diet
⦁ Physical activity promotes weight reduction and improves
insulin sensitivity, thus lowering blood glucose levels.
⦁ Together with dietary treatment, a programme of regular
physical activity and exercise should be considered for
each person. Such a programme must be tailored to the
individual’s health status and fitness.
⦁ People should, however, be educated about the potential
risk of hypoglycaemia and how to avoid it.
Exercise
⚫There are currently fourclassesof oral anti-diabetic
agents:
i. Biguanides
ii. Insulin Secretagogues – Sulphonylureas
iii. Insulin Secretagogues – Non-sulphonylureas
iv.α-glucosidase inhibitors
v.Thiazolidinediones (TZDs)
B. Oral Anti-Diabetic Agents
⦁ If glycaemic control is not achieved (HbA1c > 6.5%
and/or; FPG > 7.0 mmol/Lor; RPG >11.0mmol/L) with
lifestyle modification within 1 –3 months, ORAL
ANTI-DIABETIC AGENT should be initiated.
⦁ In the presence of marked hyperglycaemia in newly
diagnosed symptomatic type 2 diabetes (HbA1c > 8%,
FPG > 11.1 mmol/L, or RPG > 14 mmol/L), oral anti-
diabetic agents can be considered at the outset
togetherwith lifestyle modification.
B.1 Oral Agent Monotherapy
⦁ Obese type 2 patients, consideruseof metformin, acarbose orTZD.
⦁ Non-obese type 2 patients, considerthe useof metforminor insulin
secretagogues
⦁ Metformin is the drug of choice in overweight/obese patients. TZDs
and acarboseareacceptable alternatives in thosewhoare intolerant to
metformin.
⦁ If monotherapy fails, acombinationof TZDs, acarboseand metformin
is recommended. If targets are still not achieved, insulin
secretagogues may beadded
B.1 Oral Agent Monotherapy (cont.)
As first line therapy:
Combinationoral agents is indicated in:
⚫Newlydiagnosed symptomaticpatientswith HbA1c
>10
⚫Patientswhoare not reaching targetsafter 3 months
on monotherapy
B.2 Combination Oral Agents
⦁ If targets have not been reached afteroptimal doseof combination
therapy for 3 months, consideradding intermediate-acting/long-
acting insulin (BIDS).
⦁ Combinationof insulin+ oral anti-diabeticagents (BIDS) has been
shown to improveglycaemiccontrol in those notachieving target
despite maximal combinationoral anti-diabeticagents.
⦁ Combining insulinand the following oral anti-diabeticagents has
been shown to beeffective in people with type 2 diabetes:
◦ Biguanide (metformin)
◦ Insulin secretagogues (sulphonylureas)
◦ Insulin sensitizers (TZDs)(the combination of a TZD plus insulin is not
an approved indication)
◦ α-glucosidase inhibitor (acarbose)
⦁ Insulindosecan be increased until target FPG is achieved.
B.3 Combination Oral Agents and Insulin
Diabetes
Management
Algorithm
Oral Hypoglycaemic Medications
Short-term use:
⦁ Acute illness, surgery, stressand emergencies
⦁ Pregnancy
⦁ Breast-feeding
⦁ Insulin may be used as initial therapy in type 2 diabetes
⦁ in marked hyperglycaemia
⦁ Severe metabolicdecompensation (diabetic ketoacidosis,
hyperosmolar nonketotic coma, lactic acidosis, severe
hypertriglyceridaemia)
Long-term use:
⦁ If targets have not been reached after optimal dose of combination
therapyor BIDS, considerchange to multi-dose insulin therapy. When
initiating this,insulin secretagogues should be stopped and insulin
sensitiserse.g. MetforminorTZDs, can becontinued.
C. Insulin Therapy
Self-Care
⦁ Patients should be educated to practice self-care. This
allows the patient toassume responsibilityand control of
his / her own diabetes management. Self-care should
include:
◦ Blood glucose monitoring
◦ Bodyweight monitoring
◦ Foot-care
◦ Personal hygiene
◦ Healthy lifestyle/dietorphysical activity
◦ Identifytargets forcontrol
◦ Stopping smoking
◦ Carrying Diabetic Identitycard
Prevention
PRIMARY PREVENTION
 Population Strategy
 High-Risk Strategy
SECONDARY PREVENTION
TERTIARY PREVENTION
Primary Prevention
POPULATION STRATEGY
 The scope forprimary preventionof IDDM is limited.
 Based on Elimination of environmental risk factors ,
developmentof prevention programmes for NIDDM is
possible.
HIGH-RISK STRATEGY
 Effectivelydirected at TARGET POPULATION groups.
 No special high risk strategy for IDDM.
 Risk of Diabetes in NIDDM can be reduced bycorrecting
sedentary lifestyle, over nutrition, obesity, and avoiding
alcohol, smoking & OCPs.
Secondary Prevention
Aims :-
To maintain blood glucose levels as close within
normal limits.
To maintain ideal body weight.
Treatment :-
Dietalone – small balanced meals more frequently.
Dietand Oral Antidiabeticdrugs.
Dietand Insulin.
Combination of Oral Antidiabeticdrugs and Insulin.
Oral Hypoglycaemic Medications
Tertiary Prevention
Aim:- Prevention of complications from occurring.
The main objectiveat the tertiary level is toorganize
specialized clinics and units capable of providing
diagnosticand management skillsat high order.
Alsoto be involved in Epidemiological research.
⚫ National Diabetes Fact Sheet2003, DEPARTMENT OF HEALTH AND
HUMAN SERVICES Centres for Disease Control and Prevention
⚫ World Health Organization. Definition, Diagnosis and Classification of
Diabetes Mellitus and its Complications. Reportof WHO. Departmentof
Non-communicable Disease Surveillance. Geneva 1999
⚫ Academy of Medicine. Clinical Practice Guidelines. Management of type 2
diabetes mellitus. MOH/P/PAK/87.04(GU), 2004
⚫ NHS. Diabetes - insulin initiation - University Hospitalsof Leicester
NHS Trust Working in partnershipwith PCTs across Leicestershireand
Rutland, May 2008.
References
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  • 1.
  • 2. DIABETES MELLITUS ⚫It is a metabolicdisorderof multipleetiology characterized by chronic Hyperglycaemia with disturbances of Carbohydrates, Fats and Protein metabolism resulting from defects in Insulin secretion, Insulin action or Both.
  • 3. Clinical Features ⚫Easy Fatigability ⚫Polyuria ⚫Polydipsia ⚫Wasting ⚫Weight loss ⚫Air hunger ⚫Blurred vision ⚫Poor wound healing
  • 4. Complications Acute :- Diabetic ketoacidosis. Hyperglycemic Hyperosmolar state. Chronic :- A. Microvascular B. Macrovascular C. Others
  • 5. A. Microvascular complications :- Retinopathy, Macular edema, Sensory & motor neuropathy, Autonomic neuropathy. B. Macrovascularcomplications :- Coronary heart disease, Peripheral arterial disease, Cerebrovasculardisease. C. Others :- Cataract, Glaucoma, Periodontal disease, Hearing loss, Gastroparesis, Diarrhea, Uropathy, Sexual dysfunction, Acanthosis nigricans, Necrobiosis lipoidica, Vitiligoetc….
  • 8. Types  Type 1 :- IDDM alsocalled Juvenile Diabetes  Type2 :- NIDDM  Type3 :- Gestational Diabetes  Type4 :- Other Specific Types
  • 9. Type 1 ⚫Insulin Dependent Diabetes Mellitus. ⚫Alsocalled Juvenile Diabetes ⚫Commonamong 10-14 yrsof age group. ⚫Accounts for 5%-10% of all diagnosed casesof Diabetes Mellitus. ⚫90% is Autoimmune mediated. 10% is Idiopathic.
  • 10. Type 2 ⚫Non Insulin Dependent Diabetes Mellitus. ⚫Commonamong adultsand elderly people. ⚫Accounts forabout 90-95% of all thediagnosed cases of Diabetes. ⚫Beginsas Insulin resistance, as the need for insulin rises, the pancreas gradually loses it’s ability to produce insulin.
  • 11. Type 3 ⚫Gestational Diabetes. ⚫It is a condition of Glucose Intolerance diagnosed in somewomen during pregnancy. ⚫Common in African americans, Latino americans, American Indians, Obese and women with family historyof Diabetes. ⚫After pregnancy, 5-10% of women with Gestational Diabetesare found todevelopType 2 Diabetes.
  • 12. Other Specific Types ⚫Geneticdefectsof Beta-cell function. ⚫Geneticdefect in insulinaction. ⚫Pancreaticdiseases. ⚫Excessendogenous production of hormonal antagonist to Insulin. ⚫Drug- Induced. ⚫Viral infections. ⚫Latent Autoimmune Diabetes in Adults (LADA). ⚫Modified Onsetof Diabetes in Young (MODY).
  • 13. Risk Factors Host Factors  Age  Sex  Genetic Factors  Genetic Markers:- HLA-B8, HLA-B15, HLA-DR3 and HLA- DR4  Immune mechanism  Maternal Diabetes  Obesity
  • 14. Environmental Factors  Sedentary life style  Diet rich in Saturated Fattyacids  Decreased consumption of Diatary Fibers  Malnutrition  Alcohol  Chemical agents  Stress  Otherfactors
  • 16. Values of Diagnosis of Diabetes Mellitus
  • 17. Screening Urineexamination:- LAck of Sensitivity Gives too many “False Negatives” Blood SugarTesting:- RBS - >200mg/dl with symptoms & signsof diabetes. FBS - >126mg/dl PPBS - >200mg/dl Glycated Haemoglobin - >6.5%
  • 18. Target Population:- More than 40yrs Family historyof Diabetes Obese HDL <35mg/dl and Triglycerides >250mg/dl Women who had babyweighing >4.0kg Women who show excessweightgain during pregnancy Patientswith Premature Atherosclerosis
  • 19. ⚫The majorcomponentsof the treatmentof diabetes are: Management of DM • Dietand Exercise A • Oral hypoglycaemic therapy B • InsulinTherapy C
  • 20. ⦁ Diet is a basic part of management in every case. Treatment cannot be effective unless adequate attention is given toensuring appropriate nutrition. ⦁ Dietary treatmentshould aim at: ◦ ensuring weight control ◦ providing nutritional requirements ◦ allowing good glycaemiccontrol with blood glucose levels as close to normal as possible ◦ correcting anyassociated blood lipid abnormalities A. Diet
  • 21. ⦁ Physical activity promotes weight reduction and improves insulin sensitivity, thus lowering blood glucose levels. ⦁ Together with dietary treatment, a programme of regular physical activity and exercise should be considered for each person. Such a programme must be tailored to the individual’s health status and fitness. ⦁ People should, however, be educated about the potential risk of hypoglycaemia and how to avoid it. Exercise
  • 22. ⚫There are currently fourclassesof oral anti-diabetic agents: i. Biguanides ii. Insulin Secretagogues – Sulphonylureas iii. Insulin Secretagogues – Non-sulphonylureas iv.α-glucosidase inhibitors v.Thiazolidinediones (TZDs) B. Oral Anti-Diabetic Agents
  • 23. ⦁ If glycaemic control is not achieved (HbA1c > 6.5% and/or; FPG > 7.0 mmol/Lor; RPG >11.0mmol/L) with lifestyle modification within 1 –3 months, ORAL ANTI-DIABETIC AGENT should be initiated. ⦁ In the presence of marked hyperglycaemia in newly diagnosed symptomatic type 2 diabetes (HbA1c > 8%, FPG > 11.1 mmol/L, or RPG > 14 mmol/L), oral anti- diabetic agents can be considered at the outset togetherwith lifestyle modification. B.1 Oral Agent Monotherapy
  • 24. ⦁ Obese type 2 patients, consideruseof metformin, acarbose orTZD. ⦁ Non-obese type 2 patients, considerthe useof metforminor insulin secretagogues ⦁ Metformin is the drug of choice in overweight/obese patients. TZDs and acarboseareacceptable alternatives in thosewhoare intolerant to metformin. ⦁ If monotherapy fails, acombinationof TZDs, acarboseand metformin is recommended. If targets are still not achieved, insulin secretagogues may beadded B.1 Oral Agent Monotherapy (cont.) As first line therapy:
  • 25. Combinationoral agents is indicated in: ⚫Newlydiagnosed symptomaticpatientswith HbA1c >10 ⚫Patientswhoare not reaching targetsafter 3 months on monotherapy B.2 Combination Oral Agents
  • 26. ⦁ If targets have not been reached afteroptimal doseof combination therapy for 3 months, consideradding intermediate-acting/long- acting insulin (BIDS). ⦁ Combinationof insulin+ oral anti-diabeticagents (BIDS) has been shown to improveglycaemiccontrol in those notachieving target despite maximal combinationoral anti-diabeticagents. ⦁ Combining insulinand the following oral anti-diabeticagents has been shown to beeffective in people with type 2 diabetes: ◦ Biguanide (metformin) ◦ Insulin secretagogues (sulphonylureas) ◦ Insulin sensitizers (TZDs)(the combination of a TZD plus insulin is not an approved indication) ◦ α-glucosidase inhibitor (acarbose) ⦁ Insulindosecan be increased until target FPG is achieved. B.3 Combination Oral Agents and Insulin
  • 29. Short-term use: ⦁ Acute illness, surgery, stressand emergencies ⦁ Pregnancy ⦁ Breast-feeding ⦁ Insulin may be used as initial therapy in type 2 diabetes ⦁ in marked hyperglycaemia ⦁ Severe metabolicdecompensation (diabetic ketoacidosis, hyperosmolar nonketotic coma, lactic acidosis, severe hypertriglyceridaemia) Long-term use: ⦁ If targets have not been reached after optimal dose of combination therapyor BIDS, considerchange to multi-dose insulin therapy. When initiating this,insulin secretagogues should be stopped and insulin sensitiserse.g. MetforminorTZDs, can becontinued. C. Insulin Therapy
  • 30. Self-Care ⦁ Patients should be educated to practice self-care. This allows the patient toassume responsibilityand control of his / her own diabetes management. Self-care should include: ◦ Blood glucose monitoring ◦ Bodyweight monitoring ◦ Foot-care ◦ Personal hygiene ◦ Healthy lifestyle/dietorphysical activity ◦ Identifytargets forcontrol ◦ Stopping smoking ◦ Carrying Diabetic Identitycard
  • 31. Prevention PRIMARY PREVENTION  Population Strategy  High-Risk Strategy SECONDARY PREVENTION TERTIARY PREVENTION
  • 32. Primary Prevention POPULATION STRATEGY  The scope forprimary preventionof IDDM is limited.  Based on Elimination of environmental risk factors , developmentof prevention programmes for NIDDM is possible. HIGH-RISK STRATEGY  Effectivelydirected at TARGET POPULATION groups.  No special high risk strategy for IDDM.  Risk of Diabetes in NIDDM can be reduced bycorrecting sedentary lifestyle, over nutrition, obesity, and avoiding alcohol, smoking & OCPs.
  • 33. Secondary Prevention Aims :- To maintain blood glucose levels as close within normal limits. To maintain ideal body weight. Treatment :- Dietalone – small balanced meals more frequently. Dietand Oral Antidiabeticdrugs. Dietand Insulin. Combination of Oral Antidiabeticdrugs and Insulin.
  • 35. Tertiary Prevention Aim:- Prevention of complications from occurring. The main objectiveat the tertiary level is toorganize specialized clinics and units capable of providing diagnosticand management skillsat high order. Alsoto be involved in Epidemiological research.
  • 36. ⚫ National Diabetes Fact Sheet2003, DEPARTMENT OF HEALTH AND HUMAN SERVICES Centres for Disease Control and Prevention ⚫ World Health Organization. Definition, Diagnosis and Classification of Diabetes Mellitus and its Complications. Reportof WHO. Departmentof Non-communicable Disease Surveillance. Geneva 1999 ⚫ Academy of Medicine. Clinical Practice Guidelines. Management of type 2 diabetes mellitus. MOH/P/PAK/87.04(GU), 2004 ⚫ NHS. Diabetes - insulin initiation - University Hospitalsof Leicester NHS Trust Working in partnershipwith PCTs across Leicestershireand Rutland, May 2008. References