1. Diabetes Mellitus
and its
Management
Talk by
Dr Anshu P Gokarn
MBBS, MD(Pharmacology)
2. How My Talk Is Structured
PART - 1
1. Symptoms of Diabetes Mellitus
2. About our body & our pancreas
3. Glucose Metabolism : Role of Insulin
4. When Insulin Does Not Do Its Job - Diabetes
Mellitus
5. Why is Diabetes Mellitus a Silent Killer
Dr Anshu P Gokarn 2
3. How My Talk Is Structured
PART - 2
1. Diagonizing Diabetes Mellitus
2. Management of Diabetes Mellitus :
1. Diet & Excersise
2. Oral Medication
3. Insulin
3. Diabetes Management Algorithm
4. Hypo & Hyper Glycemia
5. Preventing & Controling Diabetes Mellitus - What
you can do ?
Dr Anshu P Gokarn 3
4. Most of us have a close friend or relative
who is suffering from “sugar” or
“diabetes”.
Let us understand a little more about the
disease that suddenly seems to be all
around us….
Dr Anshu P Gokarn 4
5. Diabetes Mellitus
Affects over 300 million people globally.
India leads the world – 50 million
Indians suffer from it.
Incidence increasing rapidly … specially
in the developing world : India & China
– due to lifestyle changes.
Affects the middle class and the rich – is
a lifestyle disease – high caloric diet and
lack of physical excersise.
Dr Anshu P Gokarn 5
6. How My Talk Is Structured
PART - 1
1. Symptoms of Diabetes Mellitus
2. About our body & our pancreas
3. Glucose Metabolism : Role of Insulin
4. When Insulin Does Not Do Its Job - Diabetes
Mellitus
5. Why is Diabetes Mellitus a Silent Killer
Dr Anshu P Gokarn 6
7. PART 1
Symptoms of Diabetes Mellitus
Dr Anshu P Gokarn 7
8. Diabetes Mellitus
Person has high blood sugar,
• either because the pancreas does not
produce enough insulin,
• or because cells do not respond to the
insulin that is produced.
High blood sugar produces classical
symptoms :
• Frequent urination – polyuria
• Increased thirst – polydipsia
• Increased hunger – polyphagia
Dr Anshu P Gokarn 8
12. Pancreas
Is a solid organ lying in the abdomen.
The head of the pancreas fits in the C-shaped
C-
curve of the duodenum
Pancreas is a mixed gland with
• Exocrine part
• Endocrine part
The endocrine part consists of groups of cells
called as Islets of Langerhans
Dr Anshu P Gokarn 12
13. Islets of Langerhans
Consist of different types of cells which
secrete different hormones
-cells : secrete glucagon
-cells : secrete insulin
-cells : secrete somatostatin
F-cells : secrete pancreatic polypeptide
Dr Anshu P Gokarn 13
14. Secretions of Islets of Langerhans
Glucagon
Increases blood glucose levels
Insulin
Decreases blood glucose levels
Somatostatin
Inhibits secretion of glucagon and insulin
Pancreatic polypeptide
Released in response to high protein diet
Dr Anshu P Gokarn 14
16. Normal Body : Glucose/Insulin Self Correction
Dr Anshu P Gokarn 16
17. Insulin
Insulin is a hormone secreted by
the -cells of the islets of
Langerhans of the pancreas
The -cells synthesize a
prehormone called Preproinsulin
Preproinsulin gets processed to
form Proinsulin
Proinsulin splits to form Insulin and
C-peptide
Dr Anshu P Gokarn 17
18. What is C-peptide ?
C-
C-peptide means Connecting
peptide.
It is the portion of proinsulin which
gets split off during formation of
insulin
Levels of C-peptide are measured
C-
to assess -cell function
C-peptide levels are measured
instead of insulin levels because
insulin gets metabolized in the liver
but C-peptide stays in circulation
C-
for a long time
Dr Anshu P Gokarn 18
19. What Are The Actions Of Insulin?
Insulin exerts it’s effects on carbohydrate, fat and
protein metabolism
Effect on Carbohydrate metabolism
• Glucose transport : uptake / entry of glucose into
cells
• Glycogenesis : formation of glycogen from glucose
• Glycolysis : breakdown of glucose to produce
energy
All these actions help in removing glucose from blood
and hence reduce blood glucose levels.
levels.
Dr Anshu P Gokarn 19
20. Actions of Insulin….
Effect on Fat / Lipid metabolism
• Triglyceride synthesis in adipose tissue
• Fatty acid synthesis in liver
• Enhances lipoprotein lipase activity
Increases entry of fatty acids and
triglycerides from lipoproteins into
adipose cells
Adipocytes
Dr Anshu P Gokarn 20
21. Actions of Insulin…
These actions help in removal of fats from
blood and help them to get deposited in
adipocytes.
adipocytes.
Effect on Protein metabolism
• Increased transport of amino acids into cells
• Enhances protein synthesis
Dr Anshu P Gokarn 21
22. How does glucose enters cells?
Insulin acts on Insulin Receptors present on
cell membrane
Glucose Transporters [GLUTs] come to the
[GLUTs]
cell surface
Glucose enters the cells through GLUTs
Dr Anshu P Gokarn 22
24. What are Insulin Receptors
These are the receptors present on cell
membrane which bind the circulating insulin
Actions of insulin are mediated by insulin
receptors
The number and sensitivity of insulin receptors
varies with insulin levels, exercise, food and
other factors
If number and/or sensitivity of
insulin receptors is reduced,
the individual develops
Insulin Resistance
Dr Anshu P Gokarn 24
26. What is Insulin Resistance?
Insulin Resistance is the inability of insulin to act
effectively on peripheral target tissues
[especially muscles and liver]
Resistance to action of insulin impairs glucose
utilization by peripheral cells and increases
hepatic glucose output
This further signals the pancreas to release more
insulin
Hence, excessive levels of insulin build up in the
plasma [Hyperinsulinaemia]
[Hyperinsulinaemia]
Dr Anshu P Gokarn 26
27. Insulin Resistance…..
Insulin Resistance is a
prominent feature of
type 2 diabetes.
Obesity contributes to
insulin resistance.
Insulin resistance is a
part of Syndrome X.
X.
Dr Anshu P Gokarn 27
28. Syndrome X ?
Syndrome X is a condition which includes:
Insulin Resistance
Hypertension
Dyslipidaemia
Central Obesity
Endothelial dysfunction
Accelerated cardiovascular disease
Dr Anshu P Gokarn 28
29. What happens due to lack of Insulin ?
Lack of insulin affects:
Carbohydrate metabolism
Fat metabolism
Protein metabolism
Leading to various biochemical abnormalities….
Dr Anshu P Gokarn 29
30. What happens due to lack of Insulin ?
These biochemical abnormalities include….
Reduced entry of glucose into various peripheral tissues.
tissues.
Glycogenolysis [breakdown of glycogen to glucose]
Increased liberation of glucose into circulation from liver
Gluconeogenesis [synthesis of glucose from fatty acids and amino acids]
Leading to Hyperglycaemia [excessive glucose in blood]
Lipolysis.
Lipolysis.
Reduced entry of fatty acids and triglycerides into adipocytes
Leading to Dyslipidaemia [disturbed lipid profile]
Decreased in entry of amino acids into muscle.
muscle.
Leading to Muscle Wasting
Dr Anshu P Gokarn 30
35. Types of Diabetes?
According to the American Diabetes Association [2000]; diabetes
is classified as follows:
I. Type 1 diabetes
II. Type 2 diabetes
III. Other specific types of diabetes
a. Genetic defects of -cell function
b. Genetic defects in insulin action
c. Diseases of exocrine pancreas
d. Endocrinopathies
e. Drug-
Drug- or chemical-induced
chemical-
f. Infections
g. Uncommon forms of immune-mediated diabetes etc.
immune-
IV. Gestational diabetes [GDM]
Dr Anshu P Gokarn 35
36. What is Type 1 Diabetes?
Type 1 DM is characterized by destruction of -cells,
cells,
usually leading to absolute insulin deficiency
It is further classified as:
Type 1A : results from autoimmune -cell destruction
Type 1B : immunologic markers are not found, hence cause of -
cell destruction is not known
Type 1 was previously known as IDDM or Juvenile Onset of
Diabetes.
However, these terms are now considered obsolete because
type 2 patients eventually require insulin and 5-10% of type 1
5-
DM develops after 30yrs of age
Dr Anshu P Gokarn 36
37. What is Type 2 Diabetes?
Type 2 DM is characterized by
Variable degrees of insulin resistance
Impaired insulin secretion
Increased glucose production
Type 2 DM has a strong genetic component
Obesity, particularly central obesity, is very common in type 2
DM
Type 2 was previously called NIDDM or Maturity onset
diabetes
Now obsolete as :
Type 2 patients eventually require insulin
Type 2 seen even at young age, particularly in obese
adolescents
Dr Anshu P Gokarn 37
38. Gestational diabetes
A form of glucose intolerance that is diagnosed in some women
during pregnancy.
Gestational diabetes occurs more frequently among African
Americans, Hispanic/Latino Americans, and American Indians. It is
also more common among obese women and women with a family
history of diabetes.
During pregnancy, gestational diabetes requires treatment to
normalize maternal blood glucose levels to avoid complications in
the infant.
After pregnancy, 5% to 10% of women with gestational diabetes
are found to have type 2 diabetes.
Women who have had gestational diabetes have a 20% to 50%
chance of developing diabetes in the next 5-10 years.
Dr Anshu P Gokarn 38
39. LADA - Latent Autoimmune Diabetes in Adults
Latent Autoimmune Diabetes in Adults (LADA) is a
form of autoimmune (type 1 diabetes) which is
diagnosed in individuals who are older than the usual
age of onset of type 1 diabetes.
Alternate terms that have been used for "LADA"
include Late-onset Autoimmune Diabetes of
Adulthood, "Slow Onset Type 1" diabetes, and
sometimes also "Type 1.5
Often, patients with LADA are mistakenly thought to
have type 2 diabetes, based on their age at the time of
diagnosis.
Dr Anshu P Gokarn 39
40. LADA - Latent Autoimmune Diabetes in Adults
About 80% of adults apparently with recently
diagnosed Type 2 diabetes but with GAD auto-
antibodies (i.e. LADA) progress to insulin
requirement within 6 years.
The potential value of identifying this group at high
risk of progression to insulin dependence includes:
the avoidance of using metformin treatment
the early introduction of insulin therapy
Dr Anshu P Gokarn 40
41. MODY - Maturity Onset Diabetes of the Young
MODY – Maturity Onset Diabetes of the Young - is a monogenic
form of diabetes with an autosomal dominant mode of
inheritance:
◦ Mutations in any one of several transcription factors or in the
enzyme glucokinase lead to insufficient insulin release from
pancreatic ß-cells, causing MODY.
◦ Different subtypes of MODY are identified based on the
mutated gene.
Originally, diagnosis of MODY was based on presence of non-
ketotic hyperglycemia in adolescents or young adults in
conjunction with a family history of diabetes.
However, genetic testing has shown that MODY can occur at any
age and that a family history of diabetes is not always obvious.
Dr Anshu P Gokarn 41
42. MODY - Maturity Onset Diabetes of the Young
Dr Anshu P Gokarn 42
43. MODY - Maturity Onset Diabetes of the Young
Within MODY, the different subtypes can essentially be divided
into 2 distinct groups: glucokinase MODY and transcription
factor MODY, distinguished by characteristic phenotypic
features and pattern on oral glucose tolerance testing.
Glucokinase MODY requires no treatment, while transcription
factor MODY (i.e. Hepatocyte nuclear factor -1alpha) requires
low-dose sulfonylurea therapy and PNDM (caused by Kir6.2
mutation) requires high-dose sulfonylurea therapy.
Dr Anshu P Gokarn 43
45. Risk Factors for Type 2 DM
Family history of diabetes
Obesity, esp. central
Age > 45 years
Race / ethnicity
Previously identified IFG [impaired fasting glucose]
or IGT [impaired glucose tolerance]
History of GDM or delivery of baby over 9 lbs
Hypertension [BP > 140/90 mm Hg]
HDL-
HDL-c < 35mg/dL and/or TG level > 250mg/dL
35mg/dL 250mg/dL
Dr Anshu P Gokarn 45
46. Why is Diabetes Mellitus a Silent Killer
Dr Anshu P Gokarn 46
47. Complications due to Diabetes?
Complications in diabetes occur due to
• Excessive glucose in blood
• Disturbed lipid profile
• Insulin resistance
• Increased rate of atherosclerosis, etc.
Complications of diabetes can be :
a. Acute
b. Long-term
Long-
Dr Anshu P Gokarn 47
48. Acute Complications of Diabetes
a. Acute Complications
1. Diabetic ketoacidosis :
• Disturbed metabolism of glucose and fats
leads to formation of excessive acetyl CoA
• Excess acetyl CoA gets converted to ketone bodies
• Ketone bodies reduce pH of body fluids
• This leads to the condition called as diabetic ketoacidosis
• Signs include: dehydration, hypertension, tachycardia,
hypothermia.
If untreated, it leads to ketoacidotic coma
Dr Anshu P Gokarn 48
49. Acute Complications
2. Hyperglycaemic coma:
Excessive glucose in blood
disturbs brain functions
Is accompanied by dehydration and uraemia
Management includes insulin and fluid &
electrolyte replacement
3. Lacticacidosis:
Lacticacidosis:
Excessive lactic acid production reduces pH of
body fluids
Occurs due to anaerobic glycolysis
Dr Anshu P Gokarn 49
50. Long-
Long-standing Complications of Diabetes ?
These develop over a period of months to years due to slow
progressive changes occurring in the blood vessels, nerves and
various organs of the body.
body.
Long-
Long-standing complications include:
include:
a) Microvascular Complications
b) Macrovascular Complications
c) Diabetic Neuropathies
d) Diabetic foot
e) Cataract
f) Other complications
Dr Anshu P Gokarn 50
51. Microvascular Complications of Diabetes
These are the complications involving the small
blood vessels
Excessive glucose in blood gets converted to
sorbitol,
sorbitol, which is toxic and damages blood vessel
walls
Excess glucose also binds to proteins in blood
vessel walls by glycation reaction
These complications include
• Diabetic Retinopathy
• Diabetic Nephropathy
Dr Anshu P Gokarn 51
52. Microvascular Complications….
Diabetic Retinopathy Diabetic Nephropathy
Damage to the retinal Damage to renal blood
vessels due to
blood vessels due to
long-
long-standing diabetes
long-
long-standing diabetes
Later on,
on,
nephrons get
damaged too
Dr Anshu P Gokarn 52
53. Macrovascular Complications….
These are the complications involving larger blood vessels due
to long-standing diabetes
long-
Occur due to
• accelerated atherosclerosis
• Dyslipidaemia
These include increased incidence of stroke, CHD [coronary
heart disease, peripheral arterial diseases etc.
disease,
Dr Anshu P Gokarn 53
54. Macrovascular Complications….
CHD [Coronary Heart Disease]
Also called as IHD [ischaemic heart disease]
[ischaemic
Ischaemia = lack of blood supply to a tissue
damage to coronary blood vessels increases
risk of heart attacks
CHD includes:
Angina – pain in chest due to lack of blood
supply to heart muscles
MI [myocardial infarction] – death of cardiac
tissue due to lack of blood supply
Dr Anshu P Gokarn 54
55. Macrovascular Complications….
Stroke Peripheral Arterial
Damage to cerebral Disease
arteries leads to lack of
Damage to arteries of legs
blood supply to brain
leads to pain while walking
tissue
Increasing damage can lead
Resulting neurological
to ischaemic necrosis of
dysfunction [paralysis
tissues and may even
etc.] is called stroke
require amputation of leg
Dr Anshu P Gokarn 55
56. Long standing complications….
Diabetic Neuropathy
Damage to nerves occurs due to
excessive glucose and other factors
Includes:
Peripheral neuropathy – damage occurs to nerves of arms
and legs leading to loss of ability to sense touch, pain,
temperature etc.
Autonomic neuropathy – damage to nerves of autonomic
nervous system leading to GI disturbances, urinary
incontinence, impotence etc.
Dr Anshu P Gokarn 56
57. Long standing complications….
Hypertension
Sustained elevation of blood pressure above
normal limits is called as hypertension.
hypertension.
Hypertension may develop in diabetics due to :
• Increased rate of atherosclerosis
• Insulin resistance
• Endothelial dysfunction
• Diabetic nephropathy, etc.
etc.
Dr Anshu P Gokarn 57
58. Long standing complications….
Diabetic Foot Cataract
Ulcers develop in feet Lens of the eye becomes
These are foul smelling and opaque
become infected with Due to glycation of lens
bacteria proteins
Dr Anshu P Gokarn 58
59. Other Complications …..
Increased incidence of infections like
• UTI
• Skin infections
• Fungal infections
Bone metabolism disorders
Fetal abnormalities in diabetic mothers, etc.
Dr Anshu P Gokarn 59
60. How My Talk Is Structured
PART - 2
1. Diagonizing Diabetes Mellitus
2. Management of Diabetes Mellitus :
1. Diet & Excersise
2. Oral Medication
3. Insulin
3. Diabetes Management Algorithm
4. Hypo & Hyper Glycemia
5. Preventing & Controling Diabetes Mellitus - What
you can do ?
Dr Anshu P Gokarn 60
61. PART 2
Diagonizing Diabetes Mellitus
Dr Anshu P Gokarn 61
62. Tests For Diagnosing Diabetes
Tests involving measurement of glucose levels
include:
Fasting blood glucose [ FBG ]
Post Prandial Blood Glucose [ PPBG ]
Glycosylated Haemoglobin { Hb A1C } levels
Glucose Tolerance Test { in selected cases }
Other tests include:
Urine analysis – for glucose, proteins, ketone bodies
Other tests for screening of complications
Dr Anshu P Gokarn 62
63. Fasting & Post-Prandial Blood Glucose
Post-
FBG [fasting blood glucose] : level of glucose in blood
glucose]
on empty stomach (for at least 8 hours)
hours)
PPBG [post-prandial blood glucose] : blood glucose
post- glucose]
levels at 2 hours after meals
Dr Anshu P Gokarn 63
64. Glycosylated Haemoglobin HbA1C
Glycosylation = enzymatic reaction in which glucose binds with a
protein
Haemoglobin present in the RBCs consists of a pigment ‘haem’
‘haem’
and a protein ‘globin’
‘globin’
Glucose normally binds with the globin of the Hb leading to
formation of a complex called glycosylated Hb
HbAic is the specific portion [1c] of adult haemoglobin [HbA]
HbA]
bound with glucose
Normal levels of HbA1c are <6%
In diabetes, due to high levels of glucose in blood, the levels of
HbA1c are raised
HbA1c is a more sensitive test than plasma glucose measurement
Dr Anshu P Gokarn 64
65. HbA1c formation
HbA1c is the complex formed when glucose
combines with [the globin of] haemoglobin
GLUCOSE
RBC
GLYCOSYLATED Hb
Dr Anshu P Gokarn 65
68. Pre-diabetes: Impaired glucose
tolerance and impaired fasting glucose
Pre-diabetes : people at increased risk of developing
diabetes. People with :
• Impaired fasting glucose (IFG) - fasting blood sugar level
is elevated (100 to 125 milligrams per decilitre or mg/dL)
• Impaired glucose tolerance (IGT) - blood sugar level is
elevated (140 to 199 mg/dL after a 2-hour oral glucose
tolerance test)
Dr Anshu P Gokarn 68
69. Pre-diabetes
People with pre-diabetes are already at increased risk
for other adverse health outcomes such as heart
disease and stroke.
Progression to diabetes among those with pre-diabetes
is not inevitable.
Studies suggest that weight loss and increased
physical activity among people with prediabetes
prevent or delay diabetes and may return blood glucose
levels to normal.
Dr Anshu P Gokarn 69
71. Management of DM
The major components of the treatment of
diabetes are:
A • Diet and Exercise
• Oral hypoglycaemic
B therapy
C • Insulin Therapy
Dr Anshu P Gokarn 71
72. Management of Diabetes
The specific aims of treatment for type 2 diabetes are:
Glycaemic control
• Diet/lifestyle changes
• Exercise
• Medication
Treatment of associated conditions
• Hyperlipidaemia
• Hypertension
• Obesity
• CHD
Screening and management of complications
• Cardiovascular disease
• Nephropathy
• Retinopathy
• Neuropathy
Dr Anshu P Gokarn 72
74. Dietary Guidelines
The following principles are recommended as dietary
guidelines for people with diabetes:
Dietary fat should provide 25-35% of total intake of calories but
saturated fat intake should not exceed 10% of total energy.
Cholesterol consumption should be restricted and limited to 300 mg
or less daily.
Protein intake can range between 10-15% total energy (0.8-1 g/kg
of desirable body weight). Requirements increase for children and
during pregnancy. Protein should be derived from both animal and
vegetable sources.
Carbohydrates provide 50-60% of total caloric content of the diet.
Carbohydrates should be complex and high in fibre.
Excessive salt intake is to be avoided. It should be particularly
restricted in people with hypertension and those with nephropathy.
Dr Anshu P Gokarn 74
75. A. Diet & Lifestyle Management
• Regulating intake of carbohydrates and fat
• Reducing weight if obese
• Exercise
• Dietary adjuncts to reduce absorption of
carbohydrates e.g. guar gum etc.
Dr Anshu P Gokarn 75
76. Goals of eating right :
Weight control & reducing body fat
Blood glucose control
Prevent and manage short-term & long-
term complications of diabetes
Providing nutritional requirements
Dr Anshu P Gokarn 76
77. Slimming tips
Be realistic about your target weight
Aim to lose weight gradually
Eat regular meals
Make small changes you can stick to
Dr Anshu P Gokarn 77
78. Exercise
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.
Dr Anshu P Gokarn 78
79. Foods to Avoid/Reduce intake of :
1. SALT: You get enough salt from vegetables in inorganic form, so reduce the intake
of extra salt.
2. SUGAR: Sucrose, a table sugar, provides nothing but calories and carbohydrates.
Substitute sucrose with natural sugar, like honey, jaggery (gur), etc.
3. FAT: Excessive fat intake is definitely not a good habit. Try and exclude fried items from
the diet But, remember, a small quantity of oil is needed to absorb fat-soluble vitamins,
especially vitamin E.
4. WHOLE MILK AND PRODUCTS: Try to switch to low fat milk and its products like yogurt
(curd).
5. WHITE FLOUR (MAIDA) AND ITS PRODUCTS: Replace these with whole grains, whole
wheat (ATTA) or soya breads and unpolished rice.
6. FOODS WITH A HIGH CARBOHYDRATE (SUGAR) CONTENT: Avoid white rice,
potatoes, carrots, breads and banana – they increase the blood-sugar levels.
Dr Anshu P Gokarn 79
80. Recommended food for diabetics
Bitter gourd (karela)
This vegetable contains a high dosage of 'plant insulin'.
It lowers the blood sugar levels effectively.
Have the juice of three to four karelas early morning on an empty
stomach.
As a vegetable, too, it can be taken on a regular basis.
Powder the seeds of karela (measuring 1 teaspoon), mix with water
and drink it.
Fenugreek (methi)
It is the most common food used to control diabetes.
Gulp a teaspoonful of these seeds with a glass of water daily.
Soak the seeds overnight. Have the water in which the seeds were
soaked.
You can make a chutney with methi seeds. You can also eat them
sprouted, dried and powdered, or mix them in wheat flour to make
chapattis.
Dr Anshu P Gokarn 80
81. Recommended foods for diabetics
Indian blackberry (jamun)
This fruit is very effective in preventing and controlling
diabetes.
Powder the stone of the fruit and eat it -- it contains
glucoside, which prevents the conversion of starch into
sugars.
Garlic
This is used to lower blood-sugar levels. Garlic is rich in
potassium and replaces the potassium which gets
lost in urine. It also contains zinc and sulphur, which are
components of insulin. Take about three to four flakes of
freshly crushed garlic daily.
Onion
Because of its diuretic and digestive properties, onion works
against diabetes. Raw onion is more useful.
Dr Anshu P Gokarn 81
82. Recommended foods for diabetics
Flaxseed
This is the richest source of Omega 3 fatty acids. It
helps control diabetes because it maintains the sensitivity of
the cell membrane, facilitates insulin, and thereby the
uptake of glucose by the cells.
Fibre
Soluble fibre, found in apples, kidney beans (rajma),
oatmeal, soyabean, etc, help control diabetes.
These aid slow digestion and absorption of nutrients,
resulting in a slow and steady release of glucose.
They soak up excess bile acids found in the intestinal tract,
the same acids that are converted to blood cholesterol.
They also help empty the stomach and bring about a feeling of
satisfaction that can help Type 2 diabetics to achieve weight
loss goals.
Dr Anshu P Gokarn 82
83. Recommended foods for diabetics
Cinnamon solution
Water extracts of cinnamon have been found to promote
glucose metabolism and reduce cholesterol. You can boil
cinnamon sticks in water and drink this water.
Antioxidants
Diabetes is often associated with conditions like heart
disease, diabetic retinopathy, immune deficiency and
kidney disease. Many are caused by free radical
damage. Therefore, make sure you include foods containing
antioxidants, like amla, fresh seasonal fruits, pomegranates and
green/black tea in your diet.
Dr Anshu P Gokarn 83
85. B. Oral Anti-Diabetic Agents
Anti-
These drugs depend on endogenous supply of insulin
Include various classes like:
• Sulphonylureas (Insulin Secretagogues)
Secretagogues)
• Biguanides
• -glucosidase inhibitors
• Meglitinides
• Thiazolidinediones
Used as adjunct to dietary and lifestyle modifications
Used as monotherapy or in combination
Dr Anshu P Gokarn 85
86. B. Oral Anti-Diabetic Monotherapy
Anti-
If glycaemic control is not achieved (HbA1c > 6.5%
and/or; FPG > 7.0 mmol/L or; 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
together with lifestyle modification.
Dr Anshu P Gokarn 86
87. B. Oral Anti-Diabetic Monotherapy
Anti-
First line therapy:
Obese type 2 patients, consider use of metformin, acarbose or
TZD.
Non-obese type 2 patients, consider the use of metformin or
insulin secretagogues
Metformin is the drug of choice in overweight/obese patients.
TZDs and acarbose are acceptable alternatives in those who are
intolerant to metformin.
If monotherapy fails, a combination of TZDs, acarbose and
metformin is recommended. If targets are still not achieved,
insulin secretagogues may be added.
Dr Anshu P Gokarn 87
88. B.2 Combination Oral Agents
Combination oral agents is indicated in:
Newly diagnosed symptomatic patients
with HbA1c >10
Patients who are not reaching targets
after 3 months on monotherapy
Dr Anshu P Gokarn 88
89. B.3 Combination Oral & Insulin
If targets have not been reached after optimal dose of combination
therapy for 3 months, consider adding intermediate-acting/long-
acting insulin (BIDS).
Combination of insulin+ oral anti-diabetic agents (BIDS) has been
shown to improve glycaemic control in those not achieving target
despite maximal combination oral anti-diabetic agents.
Combining insulin and the following oral anti-diabetic agents has
been shown to be effective 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)
Insulin dose can be increased until target FPG is achieved.
Dr Anshu P Gokarn 89
90. How do Sulphonyl Ureas act?
SUs stimulate the -cells of the pancreas and
increase the secretion of insulin
In long-term, they also improve insulin-sensitivity
long- insulin-
Useful for management of type 2 DM especially in
non-
non-obese patients
Main adverse effects include:
risk of hypoglycaemia, weight gain
Dr Anshu P Gokarn 90
91. Examples of Sulphonyl Ureas
FIRST GENERATION SECOND GENERATION
Chlorpropamide Glibenclamide
Gliclazide
Tolbutamide
Glipizide
Tolazamide,
Tolazamide, etc. Glipizide extended release
Glimepiride,
Glimepiride, etc.
Second generation sulphonylureas are more potent than first
generation
Glibenclamide should be avoided in elderly and renally
impaired
Gliclazide has beneficial antiplatelet effects
Dr Anshu P Gokarn 91
92. How do Biguanides act ?
Biguanides have peripheral actions only. i.e.,
Reduce hepatic glucose output
Enhance action of insulin on peripheral cells
Increases glucose utilization by peripheral cells
No effect on pancreas or insulin secretion
e.g. Metformin
.g.
Main adverse effects:
GI disturbances, lactoacidosis
Dr Anshu P Gokarn 92
93. What are -Glucosidase Inhibitors?
Agents which inhibit enzyme -glucosidase in the
intestines and prevent absorption of carbohydrates
Help in reducing the post prandial rise in glucose
e.g. Acarbose, Voglibose
.g. Acarbose,
Used as adjunct to diet control
Dr Anshu P Gokarn 93
94. How do Meglitinides act?
Meglitinides stimulate insulin secretion from
pancreas by causing closure of ATP-sensitive K+
ATP-
channels in -cells
Effectiveness depends on number of -cells
present
e.g. Repaglinide, Nateginide
.g. Repaglinide,
Have a fast onset of action
Should be used with caution in patients with liver
dysfunction
Dr Anshu P Gokarn 94
95. How Do Thiazolidinediones Act?
TZDs stimulate PPARs and improve insulin
sensitivity
Improve glycaemic control and also have
beneficial effect on lipid profile
They depend on presence of endogenous insulin
for their action
e.g. Rosiglitazone, Pioglitazone
.g. Rosiglitazone,
Troglitazone was withdrawn because of
hepatotoxicity
Dr Anshu P Gokarn 95
96. What Are PPARs ?
PPARs = Peroxisome Proliferator Activated Receptors
PPARs are a sub-family of nuclear receptors
sub-
Activation of PPARs stimulates the transcription of genes
which are responsible for regulating glucose and fat
metabolism
Rosiglitazone activates PPAR-
PPAR-
Pioglitazone activates PPAR- and PPAR-
PPAR- PPAR-
Dr Anshu P Gokarn 96
98. General Guidelines for Use of Oral
Anti-
Anti-Diabetic Agent in Diabetes
In elderly non-obese patients, short acting insulin secretagogues can
be started but long acting Sulphonylureas are to be avoided. Renal
function should be monitored.
Oral anti-diabetic agents are not recommended for diabetes in
pregnancy
Oral anti-diabetic agents are usually not the first line therapy in
diabetes diagnosed during stress, such as infections. Insulin therapy is
recommended for both the above
Targets for control are applicable for all age groups. However, in
patients with co-morbidities, targets are individualized
When indicated, start with a minimal dose of oral anti-diabetic agent,
while reemphasizing diet and physical activity. An appropriate
duration of time (2-16 weeks depending on agents used) between
increments should be given to allow achievement of steady state
blood glucose control
Dr Anshu P Gokarn 98
100. When is Insulin used?
Exogenous Insulin is
Essential for treatment of type 1 DM
May eventually be required in type 2 DM
where oral antidiabetic agents are not
enough to control glucose levels
Is used during surgery in diabetics when oral
drugs are withheld for sometime
Dr Anshu P Gokarn 100
101. Insulin Sources
Sources
Bovine & Porcine – not used today
Human
Recombinant/synthetic
Depending on duration of action :
Short acting
Intermediate acting
Long acting
Combination
Dr Anshu P Gokarn 101
104. Insulin Therapy
Short-term use:
Acute illness, surgery, stress and emergencies
Pregnancy
Breast-feeding
Insulin may be used as initial therapy in type 2 diabetes
in marked hyperglycaemia
Severe metabolic decompensation (diabetic ketoacidosis, hyperosmolar nonketotic coma,
lactic acidosis, severe hypertriglyceridaemia)
Long-term use:
If targets have not been reached after optimal dose of combination therapy or BIDS,
consider change to multi-dose insulin therapy. When initiating this,insulin secretagogues
should be stopped and insulin sensitisers e.g. Metformin or TZDs, can be continued.
Dr Anshu P Gokarn 104
105. Insulin regimens
The majority of patients will require more than one daily injection if good
glycaemic control is to be achieved. However, a once-daily injection of an
intermediate acting preparation may be effectively used in some patients.
Twice-daily mixtures of short- and intermediate-acting insulin is a commonly
used regimen.
In some cases, a mixture of short- and intermediate-acting insulin
may be given in the morning. Further doses of short-acting insulin are given
before lunch and the evening meal and an evening dose of intermediate-acting
insulin is given at bedtime.
Other regimens based on the same principles may be used.
A regimen of multiple injections of short-acting insulin before the main meals,
with an appropriate dose of an intermediate-acting insulin given at bedtime,
may be used, particularly when strict glycaemic control is mandatory.
Dr Anshu P Gokarn 105
109. Diabetes
Management
Algorithm
Dr Anshu P Gokarn 109
110. Combination Therapy in Diabetes
Diabetes is a progressive disorder
Type 2 diabetics eventually require combinations
of antidiabetic drugs for effective glycaemic
control
The additional agents are added in a stepwise
manner depending upon the quality of control of
diabetic condition
The drugs used in Combinations have additive
action and offer a better glycaemic control
Dr Anshu P Gokarn 110
111. Commonly Used Regimens in Diabetes
Sulphonylurea or Meglitinide +
Metformin or Thiazolidinedione
Sulphonylurea + -glucosidase inhibitor
Insulin + Metformin or Thiazolidinedione
Metformin + Thiazolidinedione
Dr Anshu P Gokarn 111
113. Hyperglycemia Hypoglycemia
• When controlling diabetes, blood sugar can become too high
or too low. These conditions should be taken seriously.
Fortunately, one can easily re-establish control of blood
sugar.
• When there is too much sugar in the blood, this condition is
called hyperglycemia. Hyper is Latin and means "more."
Glycemia is also Latin and means "sugar in the blood."
• Hyperglycemia is caused by eating too much food, eating
sugary foods, or by not taking one’s medication. It can also
occur when one is sick. If not treated, hyperglycemia can lead
to a coma.
Dr Anshu P Gokarn 113
114. Hyperglycemia Hypoglycemia
• Hypoglycemia occurs when too little sugar is present in the
blood. Hypo is Latin and means "less."
• Hypoglycemia usually occurs with patients who take insulin
or other medications.
• Taking too much insulin can cause it. That is why it is also
known as insulin shock.
• Hypoglycemia can also be caused when the food intake is
reduced or a meal is skipped. . Signs of low blood sugar, or
hypoglycemia .
Dr Anshu P Gokarn 114
115. Hyperglycemia Hypoglycemia
• If not treated, low blood sugar can lead to fainting or
seizures. Diabetics experience different signs when their
blood sugar is low and they learn to recognize these signs.
• Some patients do not experience any signs when their blood
sugar is low. These patients must depend on blood sugar
testing to find out if they have hypoglycemia..
Dr Anshu P Gokarn 115
117. Treatment of low blood sugar
If you sugar is 70 or lower you should
treat it with….
½ a glass of juice
¼ glass of soft drink
2 or more glucose tablets if necessary
Dr Anshu P Gokarn 117
119. Treatment of high blood sugar
If your sugar is above 240 you should do the followings:
Drink lots of sugar-free fluids like water or diet drinks
Eat the right food and the right amounts
Check your blood sugars more often
Check keytones if over 240
Call doctor or nurse if you have a positive keytones
Dr Anshu P Gokarn 119
120. Summing Up
Preventing & Controling
Diabetes Mellitus
What you can do ?
Dr Anshu P Gokarn 120
121. B.E.A.T. DIABETES
Be physical active….
Eat a healthy diet
Abcs(know and control) Hb1ac, blood
pressure, cholesterol, and smoking
Take your medication
Dr Anshu P Gokarn 121
122. Getting regular medical care
Schedule for routine medical care
HbA1c 2-4 times/year
Blood pressure At least 2 times/year
Cholesterol At least every other year
Dilated eye exam 1 time/year
Foot exam At least 1 time/year
Dental exam 2 times/year
Urine microalbumin/ 1 time/year
creatinine ratio
Flu shot 1 time/year
Pneumococcal vaccine Once (repeat at age 65)
Dr Anshu P Gokarn 122
123. ABC of Diabetes Care
A – A1c, or hemoglobin A1c test.
ADA goal is 7% or less.
AACE goal is 6.5% or less.
B – Blood pressure
< 130/80 mmHg for non-pregnant adults.
C – Cholesterol
HDL (good) cholesterol – >40 mg/dl (men);
>50 mg/dl (women)
LDL (bad) cholesterol – <100 mg/dl
Triglycerides – <150 mg/dl
Dr Anshu P Gokarn 123
124. Recap - Diabetes can be controlled by
Healthy diet may include changing what one eats, quantities,
and how often.
Exercise helps diabetic patients in many ways - lowers glucose
levels, helps weight loss, maintains a healthy heart and healthy
circulation. In addition, exercising helps relieve stress and
strengthens muscles.
Blood/urine sugar testing is important in order to find out if the
sugar level is where it should be. If the blood/urine sugar is too
low or too high, a change in diabetes medication, diet, or
exercise may be needed. Blood sugar should be checked often.
In cases of very high blood sugar levels that do not respond to
diet and exercise plans, medications may be needed. If insulin is
needed, it can only be injected. Insulin is needed for all patients
with Type 1 diabetes and for some patients with Type 2
diabetes.
Dr Anshu P Gokarn 124
125. Self-
Self-Care
Patients should be educated to practice self-care.
This allows the patient to assume responsibility
and control of his / her own diabetes
management. Self-care should include:
• Blood glucose monitoring
• Body weight monitoring
• Foot-care
• Personal hygiene
• Healthy lifestyle/diet or physical activity
• Identify targets for control
• Stopping smoking
Dr Anshu P Gokarn 125
126. Avoid diabetic products
Cost
Laxative effects
Focus on ‘sugar free’
Still raise blood glucose levels
Still contain same calories
Dr Anshu P Gokarn 126
