Diabetes mellitus is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both.

2. History & epidemiology
Anatomy of PancreasAnatomy of Pancreas
Biochemistry & Physiology Of InsulinBiochemistry & Physiology Of Insulin
PathogenesisPathogenesis
Clinical Features & Lab diagnosisClinical Features & Lab diagnosis
Treatment & Management
Complications
Case presentationCase presentation
Prevention, Control & Recent Advances

3. Case PresentationCase Presentation

4. Manipal Teaching HospitalManipal Teaching Hospital
OPD RecordOPD Record
● Name of the Patient :Sharmila Gharti Magar
● Age/sex : 55 yrs/F
● Weight : 79 Kg
● Height : 152 cm
BMI : 34 kg/m2
(Obese)

5. Presents to Department of Medicine with symptoms of:
● Fatigue
● Increased hunger
● Frequent urination
● Weight loss
● Exercise intolerance with shortness of breath for many
months
● Tingling sensation in extremities
● Blurred vision

6. FAMILY HISTORYFAMILY HISTORY
Obesity
Diabetes
HTN
● No history of Medications, Nutritional
supplements or Herbal remedies.
} In both parents and siblings

7. PHYSICAL EXAMINATIONPHYSICAL EXAMINATION
● BMI: 34 kg/m2
(obese)
● BP:150/90 mmHg
● Mild Peripheral neuropathy

8. LAB INVESTIGATIONSLAB INVESTIGATIONS
Random blood glucose level: 260 mg/dL
Fasting Plasma glucose: 190 mg/dL
Fasting lipid panel:
Total Cholesterol: 264 mg/dL
TG: 255 mg/dL
LDL: 170 mg/dL
HDL: 43 mg/dL
Urine test:Urine test:
● Urine sugar (value +++)

9.  Case was diagnosed as:Case was diagnosed as: Type 2 Diabetes MellitusType 2 Diabetes Mellitus
 Rx:
 Tab Metformin 500mg PO, Twice a day
 Adv- Regular physical exercise and life style
modification.
 Follow up- after 1 week

10. Diabetes MellitusDiabetes Mellitus
SURENDRA KSHETRI

11. What is diabetes mellitus?
● It is a chronic metabolic disease in which high level of
glucose (sugar) build up in the bloodstream either due to
● Insulin Deficiency
● Insulin Resistance
● The high blood sugar produces the classical symptoms:
● Polyuria
● Polydipsia
● Polyphagia

12. TYPES OF DIABETESTYPES OF DIABETES
MELLITUSMELLITUS
● Diabetes Mellitus Type 1: There is deficiency
of insulin .
● Diabetes Mellitus Type 2: There is enough
insulin but cells are resistant to insulin.
● Gestational Diabetes: Develops during
pregnancy.

13. Other types of Diabetes MellitusOther types of Diabetes Mellitus
● LADA (Latent-Autoimmune Diabetes in
Adults)
● MODY (maturity-Onset Diabetes of youths)
● Other secondary diabetes mellitus

14. HISTORY &
EPIDEMIOLOGY

15. ● The term DIABETES :Greek word for siphon, “to go
through” or “excess discharge of urine”
● MELLITUS: Latin word for “sweet as honey”
HISTORY OF DIABETESHISTORY OF DIABETES
MELLITUSMELLITUS

16. ●Banting and Best - Isolated insulin 1st
time from
dog’s pancreas - on July 30,1921.
●Sanger et al- Discovered the structure of insulin for
the 1st
time in 1951 A.D.

17. 1922 – Banting, Mc Leod, Best, Collip
shared the Nobel prize
Banting
Mc Leod
Best
Collip

18. ● Recombinant human insulin was developed
in 1976 .

19. EPIDEMIOLOGY

20.  Diabetes Mellitus is an iceberg diseaseDiabetes Mellitus is an iceberg disease

21. Fastest growing chronic disease that affects millions
of people worldwide.
Diabetes is a huge and growing problem.
50-80% don’t know they have it !!

22. Type 1 diabetes: 10-20% cases
Type 2 diabetes: 80-90% cases

23. GLOBAL SCENARIO
Currently number of estimated cases- around 387 million.
(IDF 2014)
The expected increase in number is +205 million by
2035.
77% people with diabetes live in low and middle income
country
In every 7 seconds 1 person dies from diabetes.
People death per year- 4.9 million.
50% of deaths - under age of 60 years.

24. PREVALENCE
● Male >female
● The global diabetes prevalence rate is 8.3%.
● People with DM live 7-8 years less than their non
diabetic peers.

25. Global Diabetes PrevalenceGlobal Diabetes Prevalence

26. MORTALITY FROM DIABETESMORTALITY FROM DIABETES
MELLITUSMELLITUS
J. Olefsky, JAMA
2001:285:628-632

27. According to the IDF (data publishedAccording to the IDF (data published
in April 2014)in April 2014)
In NepalIn Nepal
•Diabetes cases are 700 thousand.
•Diabetes related death (20-70 years age) are 14778.
In IndiaIn India
•Diabetes cases are 66,846,880.
•Diabetes related death (20-70 years age) are 1,039,980

28. WORLD DIABETES DAYWORLD DIABETES DAY
14th
November
Birthday of the man who co-
discovered insulin: Frederick
Banting
Blue circle : Universal symbol for
diabetes
The color blue reflects the sky that
unites all nations.
Recent theme :
2014-2016:Healthy Living and Diabetes

29. ANATOMY OF
PANCREAS

30. PANCREASPANCREAS
INTRODUCTION:
 French word: Pan-all and kreas –
flesh
 Retroperitoneal, soft, lobulated,
elongated
 Extension: Concavity of
duodenum to hilum of spleen
 Consists:
Exocrine and Endocrine parts

31. SITUATIONSITUATION
 Epigastrium & left hypo-
chondrium
SHAPE
 J or retort shaped
 Wt=90 g

32. PARTSPARTS
Head, Neck, Body and Tail
 Head:
● Enlarged towards right and
occupies the concavity of
duodenum
Parts-
 Surfaces - anterior & posterior
 Borders-Upper ,lower,
right/lateral
 Process – Uncinate process

33. Head- RelationsHead- Relations
● Anterior Surface:
o Gastroduodenal artery, transverse
colon, and jejunum
● Posterior surface:
o IVC, bile duct, Rt. crus of
diaphragm
● Upper border: 1st
part of duodenum, sup. Pancreatico duodenal
artery
● Lower border: 3rd
part of duodenum, inf pancreatico duodenal
artery
● Right lateral: 2nd
part of duodenum, bile duct, anastomosis of
pancreatico duodenal arteries

34. NeckNeck
● Constricted part of pancreas between head
and body
L = 2cm
● Parts:
Surfaces- anterior and posterior
Borders- upper and lower
● Relations:
Anterior surface:
Lesser sac
Pylorus
Posterior surface:
Termination of superior mesenteric vein
Beginning of portal vein

35. NeckNeck
Relations:
 Upper border:
 1st
part of duodenum
 Lower border:
 Root of transverse
mesocolon

36. Body of pancreasBody of pancreas
Prismoid in appearance,Triangular
on CS
Extends from neck to tail i.e. aorta
to lt. kidney
Parts-
3 surfaces- antero- superior ,
antero-inferior and posterior
Borders - superior, anterior &
inferior

37. Body- RelationsBody- Relations
 Anterio- Superior surface
 Lesser sac and Stomach
 Anterio-Inferior surface:
 Duodenojejunal flexure
 Coils of jejunum and Lt. colic flexure
• Posterior surface:
 Abdominal aorta
 Lt. crus of diaphragm
 Lt. psoas major
 Lt. sympathetic trunk
 Lt. suprarenal gland
 Lt. kidney across its hilum
 Lt. renal vessels
 Pelvis of lt. ureter
 Lt. suprarenal vein

38. Tail of pancreasTail of pancreas
 Narrow left end of pancreas
 Lies in lienorenal ligament ,
opposite to T12, together with
splenic vessels
 Comes in contact with spleen

39. DUCTS OF PANCREASDUCTS OF PANCREAS
Main duct of Wirsung
Duct of Santorini

40. BLOOD SUPPLYBLOOD SUPPLY

41. LYMPHATICSLYMPHATICS
Coeliac and sup. Mesenteric
 Pancreaticosplenic lymph nodes
NERVESNERVES
 Sympathetic – Vasomotor
Parasympathetic – Vagus nerve
control
pancreatic secretion.

42. Endocrine part/ islets ofEndocrine part/ islets of
LangerhansLangerhans
● Cells of islets of Langerhans –
 Alpha cells( A- cells) – 20% usually in peripheryperiphery
- secretes glucagon.
 Beta cells ( B- cells) – 70% seen in centralcentral region
- secretes insulin.
 Delta cells (D- cells) – 10% , peripheral (variable in
position,
-secretes somatostatin.
 PP cell( F cell) - secretes pancreatic polypeptide

43. Biochemistry & PhysiologyBiochemistry & Physiology
Of InsulinOf Insulin

44. INSULININSULIN
● A Polypeptide hormone
● M.Wt-5808
● Composed up of 51 AA
● 2 chains i.e chain A (21)
chain B (30)
● Connected to each other by
disulphide linkages

45. SYNTHESIS OF INSULINSYNTHESIS OF INSULIN
● Synthesized in beta cell of islets of langerhans
● Translation of insulin RNA
(By Ribosomes attached to ER)
Preproinsulin(m.wt-11500)
Cleaving in ER
Proinsulin (m.wt-9000)

46. ● Proinsulin = Peptide A + Peptide B + Peptide C
● Most of the Proinsulin cleaved in Golgi
apparatus to form Insulin and C Peptide
(Insulin=Peptide A -s-s- Peptide B)
● 5-10% released as Proinsulin.

47. Secretion of InsulinSecretion of Insulin

48. Secretion of InsulinSecretion of Insulin
 1st
Phase
o Within 2-3 mins of acute elevation in blood
glucose concentration, increases almost 10 times
 2nd
Phase
o Decreases for sometime
o Again increases about 15 times and maintained
till blood glucose is high

49. TRANSPORT AND DISTRIBUTIONTRANSPORT AND DISTRIBUTION
● Binds with plasma protein: Synalbumin
● Half life=5-10min
● Plasma concentration=20-30microU/ML
● Fixed to many tissues but RBC and many of brain
cells do not bind to it
● Large amounts are bound to liver and kidney
● Exerts effect without entering cell on which it acts.

50. MOA- InsulinMOA- Insulin

51. REGULATION OF INSULINREGULATION OF INSULIN
SECRETIONSECRETION
Somatostatin Somatostatin
Insulin
D-cells
Alpha cells Beta cellsGlucagon
●GIP, increased glucose, AA ,PNS, β Adrenergic activities :-
Stimulate Beta cells
( -)( -)

52. REGULATION OF INSULINREGULATION OF INSULIN
SECRETIONSECRETION
STIMULATORS INHIBITORS
GLUCOSE SOMATOSTATIN
MANNOSE 2- DEOXYGLUCOSE
AMINO ACIDS
[LEUCINE,ARGININE,OTHERS ]
MANNOHEPTULOSE
INTESTINALHORMONES
[GASTRIN,SECRETIN CCK,GIP]
ALPHAADRENERGICSTIMULATORS
[EPINEPHRINE,NOREPINEPHRINE]
BETA KETO ACIDS BETA ADRENERGIC BLOCKERS’
[PROPRANOLOL]
ACETYLCHOLINE GELANIN
GLUCAGON DIAZOXIDE
CYCLIC AMP & VARIOUS c AMP
GENERATING SUBSTANCE
THIAZIDE DIURETICS
BETA ADRENERGIC STIMULATORS
THEOPHYLLINE
K+ DEPLETION
PHENYTOIN

53. ACTIONS OF INSULINACTIONS OF INSULIN
● Carbohydrate Metabolism:
● Increase glucose uptake and utilization by muscle and
adipose tissue
● Increase hepatic uptake of glucose
● Increase Glycogenesis
● Inhibit Glycogenolysis
● Inhibit Gluconeogenesis and stimulate Glycolysis

54. ● Fat Metabolism:
● Increase fatty acid synthesis , glycerol
phosphate and TGs
● Inhibit lipolysis
● Protein Metabolism:
● Increase protein synthesis
● promotes amino acid transport to cell

55. Blood glucose HomeostasisBlood glucose Homeostasis
● Two types of mutually antagonistic metabolic hormones
regulate blood glucose levels:
● Anabolic hormone :Insulin
● Catabolic hormones :
● Early response
● Glucagon
● Epinephrine
● Delayed response
● Cortisol
● Growth hormone

56. Catabolic hormonesCatabolic hormones
● Glucagon:
●Primary hyperglycemic hormone
●Released when blood glucose <70 mg/dl
●Epinephrine:
●Secondary early response hyperglycemic hormone
●Mediated through hypothalamus
●Cortisol and GH:
●Long term hyperglycemic hormone
●Activation takes hours to days
●Effect mediated through hypothalamus
●Decrease glucose utilization in most of the cells

57. PathogenesisPathogenesis OfOf
Diabetes MellitusDiabetes Mellitus

58. Pathogenesis of Type I DMPathogenesis of Type I DM
 An autoimmune disease
 T cell-mediated progressive destruction of pancreatic β-cells
 Manifest clinically – after loss of 80/90 % of β-cell mass
βCellMass
Time
Development of type 1 diabetes

59.  1/3rd
of the susceptibility
 20 different regions of human genome show some linkage
 Polymorphism in HLA region - accounts for 40-50 % risk
 Other genes,
• CD25, PTPN22, IL-2RA and IL-10
Genetic Factors

60.  Have not been conclusively linked
 Possible candidates include;
 Virus - Mumps, Coxsackie B4, retroviruses, rubella
(in utero), CMV & EBV
“MOLECULAR MIMICRY “
 Diet - Dietary nitrosamine, coffee
Environmental ConsiderationsEnvironmental Considerations

61.  Bovine Serum Albumin (BSA)Bovine Serum Albumin (BSA)
 cross neonatal gut
 raise Ab
 cross-react with heat-shock protein
expressed by β cells.

62.  HygieneHygiene HypothesisHypothesis
 reduced exposure to microbes
 limits immunity maturation
 Increase susceptibility to autoimmune
diseases

63. Mechanisms of β - Cell Destruction
 Failure of self--tolerance in T cells specific for islet
Ag
 Initial activation - Peri-pancreatic lymph nodes
 Activated T cells - traffic to pancreas
 TH1 cells - secrete cytokines - injure β cells
 CD8+ cells - kill β cells directly

64.  Heterogeneous group of
disorders
 interplay of genetic &
environmental factors
 Absence of an
autoimmune basis
Genetic
susceptibility,
obesity, Sedentary
lifestyle
TYPE 2 DIABETES
IR β
Insulin
resistance
β-cell
dysfunction
Pathogenesis of Type II DMPathogenesis of Type II DM

65. EtiopathogenesisEtiopathogenesis
• Obesity
• Sedentary lifestyle
• Functional defects - tyrosine
phosphorylation, serine
phosphorylation
• β cell mass, islet degeneration
• Secretory defect - loss of normal
oscillating pattern of insulin
secretion
INSULIN RESISTANCE β - CELL DYSFUNCTION
TYPE II DIABETES MELLITUS

66. DEVELOPMENT OF TYPE 2 DMDEVELOPMENT OF TYPE 2 DM

67. CLINICAL FEATURESCLINICAL FEATURES
&&
LAB DIAGNOSISLAB DIAGNOSIS

69. Mental apathy
TACHYCARDIA
Dry & itchy skin

70. ON CLINICALON CLINICAL
EXAMINATION (SIGNS)EXAMINATION (SIGNS)
Delayed tendon jerk reflex

72. DifferencesDifferences:
Features Type 1
(IDDM)
Type 2
(NIDDM)
Age at onset <40 yrs >50 yrs
onset acute gradual
Body weight Normal or low Obese
Ketonuria common uncommon
Rapid death without
T/t with insulin
Yes No
Family history No Yes

73. Lab DiagnosisLab Diagnosis
CATEGORIES:
1)Test performed in blood/serum
A. Estimation of glucose by
GOD/POD
method:FPS,RBS,PPBS test.
B. Estimation of glycosylated
HbA1c
C. C peptide test

74. Fasting plasma glucose (FPG) testFasting plasma glucose (FPG) test
 Preferred method for diagnosing children, men, and
non pregnant women.
 The test measures blood glucose levels after an
overnight fast (no food intake for at least eight
hours).

75. Random blood glucose testRandom blood glucose test
 Measures blood glucose levels at any time of
day.
 Used in people with classic diabetes
symptoms such as excessive thirst, frequent
urination and unexplained weight loss.

76. GLYCOSYLATED HAEMOGLOBIN TESTGLYCOSYLATED HAEMOGLOBIN TEST
((HbA1c blood carrier)HbA1c blood carrier)
 Determines Blood Glucose Level over past
90-120 days

77. Oral Glucose Tolerance TestOral Glucose Tolerance Test
(OGTT)(OGTT)
Procedure
1. A fasting blood sample is drawn
2. Subject is given 75 g glucose is dissolved in 300ml
of water
3. Blood sample are collected at interval for at least
2hrs.

78. WHO diabetes diagnostic criteriaWHO diabetes diagnostic criteria
Condition
2 hour
glucose
Fasting glucose HbA1c
Unit mg/dl mg/dl DCCT %
Normal
<140(7.8mmo
l)
<110 <6.0
Impaired
fasting
glycaemia
<140 ≥110 & <126 6.0–6.4
Impaired
glucose
tolerance
≥140 <126 6.0–6.4
Diabetes
mellitus
≥200(11.1mm
ol)
≥126(7.0mmol) ≥6.5

79. C peptide TestC peptide Test
 Distinguishes between type1and type 2 DM
 Pancreas of patients with type 1 is unable to
produce insulin so have a decreased level of C-
peptide
 Whereas C-peptide levels in type 2 patients are
normal or higher than normal.
 Interpretation
Normal range for a c-peptide test:
0.51-2.72 nanograms per millilitre (ng/mL)

80. 2) Test performed in urine2) Test performed in urine
A. BENEDICT TEST-Color reaction test
B. ROTHERA’S TEST: Purple ring – presence of ketone
bodies
C. Microalbumin /Albumin protein- Nephropathy
D.DIPSTICK TEST:
•Sensitive to as little as 0.1% glucose in urine
•Result: Different colour response of indicator strip
reflect glucose concentration

81. TREATMENT &TREATMENT &
MANAGEMENT OFMANAGEMENT OF
DIABETES MELLITUSDIABETES MELLITUS

82. Antidiabetic agentsAntidiabetic agents
 Insulin
 Oral hypoglycemic drugs

83. TYPES OF INSULINTYPES OF INSULIN
Bovine Insulin (more antigenic)
Porcine Insulin (less antigenic)
Human insulin : Made by rDNA technology
(BASED ON SOURCES)

84. Insulin PreparationsInsulin Preparations

85. INSULIN DELIVERYINSULIN DELIVERY
SYSTEMSYSTEM
 Insulin Syringes
 Direct subcutaneous insulin injection remains the
most common form of delivery, using a needle
and syringe.
 Site of injection:
Abdomen>Arm>Buttock>Thigh
 Other delivery system-
Insulin Pump,Transdermal Patch,
Nasal spray ,Insulin pen

86. Complications of InsulinComplications of Insulin
TherapyTherapy
1) Hypoglycemia :Symptoms include sweating, slurring
of speech, palpitations, tachycardia,restlessness
2) Insulin allergy : rare condition
Utricaria results from Histamine release from mast cells.
3) Immune Insulin resistance : Low titer of circulating IgG
anti-insulin antibodies that neutralize action of insulin
4) Lipodystrophy at injection sites : There is atrophy of
subcutaneous fatty tissues at site of injection

87. Oral Anti-diabetic Agents:Oral Anti-diabetic Agents:
Group Drugs
1. Sulphonylurea
• 1st
generation
• 2nd
generation
•Tolbutamide
•Chlorpropamide
•Glibenclamide
•Gliclazide, Glipizide
2. Meglitinide Nateglinide, Repaglinide
3. Biguanides Metformin, Phenformin
4. Thiazolidinediones Rosiglitazone, Pioglitazone
5. Alpha glucosidase
inhibitors
Acarbose

88. SULFONYLUREASULFONYLUREA
●Tolbutamide Glibenclamide
●Insulin secretagogue
●Requires at least 30% functional beta cells

89. BIGUANIDESBIGUANIDES
 Metformin
 Suppresses hepatic gluconeogenesis and glucose output
from liver
 Enhance insulin mediated glucose disposal in muscle and
fat via GLUT-4, enhance GLUT-1 transport from
intracellular site to plasma membrane
 Retards intestinal absorption of glucose
 Promotes peripheral glucose utilization
 FIRST LINE THERAPY FOR TYPE 2 DM

91. MANAGEMENT OFMANAGEMENT OF
DIABETES MELLITUSDIABETES MELLITUS
 Nutritional
 Exercise
 Stress management
 Monitoring
 Pharmacologic measures
 Education

92. Dietary ManagementDietary Management
 Carbohydrate 45-65% total daily calories
 Protein-15-20% total daily calories
 Fats—less than 30% total calories,
saturated fats only 10% of total calories
 Fiber—lowers cholesterol, so preferred
 Consistent, well-balanced small meals
several times per day.
 Salt intake less than 6 gm per day
A Plate Model for Meal
Planning

93. Exercise and DiabetesExercise and Diabetes
 Exercise increases uptake of glucose by
muscles and improves utilization and alters
lipid levels.
 Check BS before, during and after
exercising if the exercise is prolonged

94. Stress ManagementStress Management
 Stress leads to increase in cortisol level
 Prolonged cortisol level antagonize action of insulin

95. Stress ManagementStress Management
 Behavioral modification
 Positive thinking
 Meditation
 Satisfactory treatment plans and special
attention
 Optimal family support and counseling

96. Glucose monitoringGlucose monitoring
 Patients on insulin should
check sugars 2-4 times per day.
 Not on insulin, two or three
times a week.
 Should check before meals and 2
hours after meals.
 HbA1 C measures blood glucose over
2-3 months.

97. Pharmacological management approaches in DMPharmacological management approaches in DM
 Fig: Flow chart of management approach in diabetes mellitus
 BG: Biguanide SU: Sulfonylureas TZD: Thiazolidinedione PP : Postprandial

98. Targets for Glycemic (blood sugar) ControlTargets for Glycemic (blood sugar) Control
In Most Non-Pregnant Adults:In Most Non-Pregnant Adults:
Factors ADA Guidlines
A1c (%)
<7*
Fasting (preprandial) plasma
glucose 70-130 mg/dL
Postprandial (after meal)
plasma glucose <180 mg/dL
*<6 for certain individuals

99. Teaching Plan to patientsTeaching Plan to patients
Foot care, eye care, general hygiene, risk factor
management
Recognition, treatment and prevention of acute
complications
When to call the doctor

100. Diabetes Mellitus: “Not So Sweet”

101. Complications Of Diabetes Mellitus:Complications Of Diabetes Mellitus:
● Acute complications
● Chronic complications

102. Acute complicationsAcute complications
 Diabetic ketoacidosis
 Non- ketotic hyperosmolar diabetic coma
 Hypoglycemia

103. Diabetic ketoacidosis (DKA)Diabetic ketoacidosis (DKA)
 MEDICAL EMERGENCY!!!
 Characterized by:
• Hyperglycemia
• Ketosis
• Metabolic acidosis
 Most often seen in Type 1 DM

104. Non- ketotic hyperosmolarNon- ketotic hyperosmolar
diabetic coma (HHS)diabetic coma (HHS)
Characterized by:
Hyperglycemia
Hyperosmolarity
Dehydration without ketosis
Seen in Type 2 DM

105. Pathogenesis of DKA and HHSPathogenesis of DKA and HHS

107. Diabetic ketoacidosis Non- ketotic hyperosmolar
diabetic coma (HHS)
Polyuria Polyuria
Tachycardia Tachycardia
Hypotension Orthostatic hypotension
Tachypnea / Kussmaul
respirations
Neurological symptoms :
Altered level of conciousness
(when sOsm > 350mosm/kg)
Nausea / vomiting
Abdominal pain
Nausea ,vomiting , abdominal
pain and kussmaul respirations
are absent
Clinical Manifestations :Clinical Manifestations :

108. HypoglycemiaHypoglycemia
 Most commonly in Type 1 DM patients treated
with insulin injections.
 Signs/Symptoms :
 Anxiety
 Tachycardia , Palpitation
 Sweating
 Weakness, lethargy
 Blurred vision

109. Treatment of Acute complicationsTreatment of Acute complications
 Hypoglycemia:
• If patient is conscious : 15 gm of sugar and wait for 15 minutes
• If patient is not concious: 25 %– 50% glucose IV, followed by
infusion of 5% dextrose in water
 Diabetic ketoacidosis:
• Administration of short acting insulin
• Fluid replacement
• Potassium replacement
 Non- ketotic hyperosmolar diabetic coma
• Similar to ketoacidosis except:
• Faster fluid replacement
• NaHCO3 usually not required
• Heparin (subcutaneous)

110. Chronic complicationsChronic complications
 Vascular complications:
 Macrovascular Complications:
 Coronary heart disease
 Cerebrovascular disease
 Peripheral vascular disease
 Microvascular Complications:
 Retinopathy
 Nephropathy
 Neuropathy
 Non vascular complications:
 Gastrointestinal
 Genitourinary ( erectile dysfunction in males)
 Infections
 Periodontal disease
 Hearing loss

111. Pathogenesis of ChronicPathogenesis of Chronic
complications:complications:

112. Macrovascular diseasesMacrovascular diseases
 Ischemic Heart Disease :
 4 times increased risk of MI compared to
general population.
 Greater incidence of “Silent MI”
Likely due to sensory neuropathy
May present as CHF
 Cerebro-vascular disease
 Peripheral vascular disease

113. Microvascular ComplicationsMicrovascular Complications

114. Diabetic RetinopathyDiabetic Retinopathy
 Diabetes is the leading cause of blindness in the working population of the
Western world.
 Diabetic retinopathy is characterized by:
 Abnormal retinal vascular permeability
 Microaneurysm
 Neovascularization
 Hemorrhage & Scarring
 Types:
 Non proliferative:
 Proliferative:

115. Diabetic NephropathyDiabetic Nephropathy
 Most common cause of end stage renal disease
 First indicator: microalbuminuria
 Glomerular changes that occur are:
 Capillary basement membrane thickening
 Diffuse Glomerularsclerosis
 Nodular Glomerulosclerosis
 Also known as Kimmelstiel-Wilson syndrome

116. Diabetic NeuropathyDiabetic Neuropathy
Types:
Peripheral neuropathy:
May manifest as Polyneuropathy or Mononeuropathy
Autonomic neuropathy:
May cause hypoglycemia unawareness subjecting the
patient to the risk of severe hypoglycemia.

117. Lower extremity complicationsLower extremity complications
• Diabetic foot ulcers are leading cause of
non traumatic lower extremity amputation
in US.
•Diabetic foot ulcers are due to:
•Loss of protective sensation due to
Peripheral neuropathy
•Poor blood flow or ischemia due to
Peripheral vascular disease

118. Glycemic Control and Complications:Glycemic Control and Complications:
Long term complications depend upon the
duration of diabetes and state of glycemic
control.
Diabetic retinopathy , nephropathy and
neuropathy are irreversible.
Glycemic control can only reduce the rate of
progression of retinopathy and nephropathy.

119. Are Diabetic complications
Preventable ??
● Aim of treatment should be:
● ‘Near normal’ glycemia
● Avoid severe hypoglycemic episodes.

120. Prevention and
Control

121. Why Should we prevent
Diabetes?
 To reduce human suffering.
 To alleviate the economic burden.
 To prevent morbidity and mortality from
diabetes-related chronic vascular diseases

122. Levels of prevention
 Primary prevention
 Secondary prevention
 Tertiary prevention

123. Primary PreventionPrimary Prevention
•Health Promotion & Specific Protection
•Two strategies suggested:
 Population Strategy
 High Risk Strategy
• High risk Group :
 Age group of 40 and above
 Family history of DM
 Obese
 Women with excess weight gain during pregnancy
 Patient with premature atherosclerosis

124. Population StrategyPopulation Strategy
 Scope for Primary prevention in Type1 limited.
 More important in Type 2 DM.
 Measures include:
 Life style Interventions
 Weight reduction
 Physical Exercise
 Nutrition
 Education

125. Nutritional HabitsNutritional Habits
 Adequate protein intake
 Dietary fibers
 Avoidance of sweet food
 Limit meals away from home

126. Physical ExercisePhysical Exercise
• Helps to increase insulin sensitivity and aids in
weight loss.
• Insulin sensitivity persists hours after exercise

127. High Risk StrategyHigh Risk Strategy
 No special high risk strategy for type 1 DM
 More concerned with type 2 DM since it is related to:
• Sedentary life style
• Over nutrition and obesity
 Avoid use of alcohol
 Diabetogenic drugs like OCPs should be avoided.
 Control atherosclerosis inducing factors:
Smoking
High BP
Elevated cholesterol and TGs levels

128. Secondary PreventionSecondary Prevention
 Early diagnosis and treatment
 Aims of treatment:
 Maintain blood glucose levels
 Maintain ideal body weight
 Treatment based on:
 Diet alone
 Diet and oral antidiabetic drugs
 Diet and insulin

129.  Proper management
 Routine check up: Every 3 months
Blood sugar
Serum Creatinine
Urine for proteins and ketones : Yearly
Blood pressure : Every 3 months
Visual acuity : Yearly
Foot examination
Skin examination : Every 3 months
 Glycosylated Haemoglobin estimation :
Every 6 months

130.  Self care
 Home blood glucose monitoring:

131. Tertiary PreventionTertiary Prevention
 Disability limitation and rehabilitation
 Complications
 Blindness
 Kidney failure
 Coronary thrombosis
 Gangrene of lower extremities.

132. RECENTRECENT
ADVANCESADVANCES

133. New drugs for the treatment of
diabetes….
1.GLP (Glucagon like peptide)– 1 mimetic
 Exenatide
 Liraglutide
1.DPP (Dipeptidyl peptidase) – 4 inhibitors
 Sitagliptin
 Saxagliptin

134. NNewew insulin delivery system
•Jet Injector
•Insulin Pump
•Transdermal
Patch
• Nasal spray
•Insulin pen

135. New monitoring systems
 Continuous blood glucose monitoring.

136. FUTURE PROSPECTFUTURE PROSPECT
 Tolrestat has been recently approved for the prevention of
diabetes complication.
e.g: Diabetes retinopathy, neuropathy, nephropathy.

137. Beta cell transplantation and incorporation of insulin
gene :
 Which have tremendous potential in treatment of DM
 Provide long lasting endogenous source of insulin in
both Type-1 and Type -2 patient.

138. CONCLUSIONCONCLUSION
 What an irony!!
“Cells are swimming in glucose but are starving
to death because of impairment in uptake”

139. Can diabetes be cured?

140. Cause if u don’t…..

141. Q & A

142. THAT’S ALL!!THAT’S ALL!!
THANK