Question

Make a scenario of an MCQ Outline the signs and symptoms that you would

expect in a Diabetic patient keeping in mind the actions of Insulin Remember

Diabetes would have the same symptoms as that of Insulin deficiency Give 4 options

for the MCQ question

(EFFECTS OF INSULIN DEFICIENCY)

PATHOPHYSIOLOGY OF DIABETES MELLITUS

1 Hyperglycemia

EFFECTS OF INSULIN DEFICIENCY

2 Glucosuria

EFFECTS OF INSULIN DEFICIENCY

3 Polyuria

EFFECTS OF INSULIN DEFICIENCY

4 Polydipsia amp Polyphagia

(There is an extracellular glucose excess amp an intracellular glucose deficiency-

ldquostarvation in the midst of plentyrdquo)

EFFECTS OF INSULIN DEFICIENCY

5 Weight Loss

(For every gram of glucose excreted 41 kcal is lost from the body Increasing the

caloric intake to cover this loss simply raises the plasma glucose further)

EFFECTS OF INSULIN DEFICIENCY

6 Increase in plasma Cholesterol amp Phospholipid conc

(Role in the accelerated development of atherosclerosis that is a major

complication)

COMPLICATIONS

When Diabetes continues for a long time period (15-20 years) chronic complications occur 1Neuropathies2Peripheral vascular disease3Gangrene 4Atherosclerosis5Ischemic heart disease6Renal disease7Early cataract8Retinopathy9Skin infections10Neuropathies affecting the ANS

Diabetic foot showing ulcer

Gangrene that must be treated with an amputation

KETOSIS AND COMAbull In severe form of Insulin deficiency plasma levels of FFA is more

than doubled darr

bull In the liver and other tissues the fatty acids are catabolized to acetyl Co-A

darrbull Some of the acetyl-CoA enters into the citric acid cycle

darrbull When the supply exceeds the capacity of the citric acid cycle the

excess are converted into acetoacetate and β-hydroxybutyrate darr

These are ketone bodies that lead to progressive metabolic acidosisdarr

Acidosis can depress the brain and if severe enough can lead to coma and death

DIABETES MELLTIUS

DIABETES MELLITUS

Def Diabetes mellitus is a syndrome of impaired

carbohydrate protein amp fat metabolism caused by either lack of insulin secretion or decreased

sensitivity of the tissues to insulin The word ldquoDiabetes Mellitusrdquo literally means

ldquoexcessive secretion of sweet urinerdquo

bull Third leading cause of deathbull Leading cause of blindness bull Diabetes is a very prevalent disease has a huge

economic toll forces individuals to change their lifestyle thus affecting their quality of life amp predisposes the affected to a variety of troublesome amp even life threatening conditions

TYPE I Juvenile Onset Insulin Dependent

It is the more severe from of diabetes and more prevalent in children

DEFINITION

It is a catabolic disorder in which the circulating insulin is virtually absent plasma glucose is elevated amp the pancreatic beta

cells fail to produce any insulin in response to all insulinogenic stimuli

Cause Lack of insulin secretion from the beta cells of the islets of langerhans

bull It is an autoimmune disorder in which there is selective destruction of the pancreatic beta cells by T lymphocytes

bull Mostly it seems to have an immunological basis amp circulating islet cell antibodies amp anti-insulin antibodies may be demonstrated

bull Usually there is a genetic predisposition to this type of diabetes which may be triggered off by

- Viral infections eg rota virus coxsackie virus- Environmental triggers

TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes

It is further classified intobull It is the most common type of diabetes accounting for

about 90 of all cases of diabetes mellitusbull The age of onset is usually after 30 often bw 50 amp 60

years of agebull It develops gradually amp is the less severe form of

diabetes

1 Non-obese type II2 Obese type II

bull Cause Decreased sensitivity of target tissues to the metabolic effects of insulin This reduced sensitivity to insulin is often called INSULIN RESISTANCE

TYPE II DIABETES

Factors that can lead to Insulin resistance include1 Anti-insulin antibodies2 Autoantibodies to the insulin receptor 3 Mutation of insulin receptor4 Down-regulation of insulin receptors by sustained

hyperinsulinism5 Primary hyperinsulinism (Beta cell adenoma)6 Secondary hyperinsulinism (Cushingrsquos syndrome

acromegaly pregnancy or diabetes mellitus)7 Obesityoverweight especially excess fat deposits

around the abdomen8 Insulin resistance in peripheral tissues such as skeletal

muscle brain and liver

PATHOPHYSIOLOGY

bull Diabetes type I is far more rapid in onset occurring over a few days as compared to type II which has a more gradual onset

bull Type I also shows far more complications as compared to Type II which rarely shows complications

bull Type I requires Insulin while Type II can usually be controlled by simple changes in lifestyle as diet exercise amp weight control

bull Type I insulin is more prone to Ketoacidosis while Type II is not

DIAGNOSIS OF DIABETES

1 Blood sugar random ( 80-120 mg100ml)2 Blood sugar fasting (80-90 mg100ml)3 GTT or Glucose Tolerance TestWhen a normal fasting person is given 1g of glucose kg

body weight his plasma glucose levels rise to 120-140 but fall back to normal within 2 hours

In a prediabetic or diabetic not only is the fasting plasma glucose on the higher side but also the post meal plasma glucose rises to as high as 140-200 amp fails to come back to normal within 2 hours of giving conc glucose solution Even after 4-6 hours it rarely comes back to the normal range NORMAL MEAN BLOOD GLUCOSE IS APP 110

Glucose Tolerance Test

POINT TO REMEMBER

WHY IS ORAL GLUCOSE A MORE POWERFUL STIMULANT THAN

INJECTABLE GLUCOSE FOR INSULIN SECRETION

DIAGNOSIS OF DIABETES

4 Presence of glucose in urine (glucosuria)5 Acetone breath6 Lab test for assessing control of diabetes

HbA1c is a minor component of Hb A amp is normally present in small amounts ie up to 6 of normal Hb In the presence of long standing hyperglycemia its concentration rises When plasma glucose is episodically elevated over time small amounts of Hb A are non-enzymatically glycated to form HbA1c

Careful control of diabetes with insulin reduces the amount formed and thus HbA1c levels give an index of diabetic control for past 4-6 weeks

TREATMENT for Type I DIABETES

WHY CANNOT INSULIN BE GIVEN BY MOUTHWHY IS ONLY CHO RESTRICTION NOT VERY EFFECTIVE

Administer enough insulin so that metabolism of fat proteins amp CHO proceed as normally as possible

Insulin is available in various forms1 Insulin preparations are available with rapid (regular) intermediate amp long

durations of action - regular duration of action is 3-8 hours- Intermediate (NPH) not used during- Long duration of action is 10-48 hours

Individualized insulin schedules which consist of one injection of longer acting insulin followed by regular insulin when the glucose level is expected to rise ie at meals

Insulin is administered subcutaneously (sc) except in the case of emergencies when it is given intravenously (iv)

The less soluble an insulin preparation is the longer it acts

INSULIN SYRINGES

Insulin

Human insulin is absorbed more quickly from its site of action than are beef or pork insulins Thus duration of action of human Insulin is shorter amp doses must be adjusted

Hypoglycemia is the most serious amp common side effect of Insulin therapy BC long term diabetics do not produce counteracting hormones of Glucagon EN cortisol etc that normally provide defense against Hypoglycemia

TREATMENT for Type II DIABETES

bull Dietbull Exercise is useful in managing both types of Diabetes

because working muscles are not Insulin dependent Exercising muscles take up some of the excess blood glucose reducing the overall need for insulin

bull Weight lossbull Oral Hypoglycemic Drugs

Oral Hypoglycemic Drugs

There are many types of oral Hypoglycemic drugs some of which are bullSulfonylureas act by stimulating the β- cells to secrete more insulin than they do on their own Eg GlucotrolbullMetformin acts by suppressing liver output of glucose Eg GlucophagebullAlpha-glycosidase Inhibitors act by slowing CHO digestion and absorption from the digestive tract into the blood thus reducing the glucose surge seen after a meal Eg Precose bullByetta (Glucagon-like peptide 1 mimic) mimics the incretin GLP-1 It suppresses glucagon secretion and slows gastric emptying By promoting satiety it decreases food intake and in the long term leads to weight loss Because none of the drugs deliver new insulin to the body they cannot replace insulin therapy for people with Type I Diabetes and later in Type II Diabetics as well

SULFONYLUREAS

NIDDM patients above the age of 40 years amp having ho diabetes of less than 5 years are given Oral Hypoglycemics

Mechanism of Action1 Stimulate release of Insulin from beta cells of

pancreas2 Reduction of serum Glucagon3 Increased binding of Insulin to target tissues amp

receptors Eg Tolbutamide

Glyburide Glipizide

WHO NEEDS INSULIN

bull 1048708 Type 1bull 1048708 Type 2 uncontrolled wmedsbull 1048708 DKAbull 1048708 Hyperosmolar hyperglycemic state (HHS)bull 1048708 Surgerybull 1048708 IllnessInfectionbull 1048708 Stressbull 1048708 Those receiving parental enteral nutritionbull 1048708 Pancreatitis diseases that darr beta cell function

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

(EFFECTS OF INSULIN DEFICIENCY)

PATHOPHYSIOLOGY OF DIABETES MELLITUS

1 Hyperglycemia

EFFECTS OF INSULIN DEFICIENCY

2 Glucosuria

EFFECTS OF INSULIN DEFICIENCY

3 Polyuria

EFFECTS OF INSULIN DEFICIENCY

4 Polydipsia amp Polyphagia

(There is an extracellular glucose excess amp an intracellular glucose deficiency-

ldquostarvation in the midst of plentyrdquo)

EFFECTS OF INSULIN DEFICIENCY

5 Weight Loss

(For every gram of glucose excreted 41 kcal is lost from the body Increasing the

caloric intake to cover this loss simply raises the plasma glucose further)

EFFECTS OF INSULIN DEFICIENCY

6 Increase in plasma Cholesterol amp Phospholipid conc

(Role in the accelerated development of atherosclerosis that is a major

complication)

COMPLICATIONS

When Diabetes continues for a long time period (15-20 years) chronic complications occur 1Neuropathies2Peripheral vascular disease3Gangrene 4Atherosclerosis5Ischemic heart disease6Renal disease7Early cataract8Retinopathy9Skin infections10Neuropathies affecting the ANS

Diabetic foot showing ulcer

Gangrene that must be treated with an amputation

KETOSIS AND COMAbull In severe form of Insulin deficiency plasma levels of FFA is more

than doubled darr

bull In the liver and other tissues the fatty acids are catabolized to acetyl Co-A

darrbull Some of the acetyl-CoA enters into the citric acid cycle

darrbull When the supply exceeds the capacity of the citric acid cycle the

excess are converted into acetoacetate and β-hydroxybutyrate darr

These are ketone bodies that lead to progressive metabolic acidosisdarr

Acidosis can depress the brain and if severe enough can lead to coma and death

DIABETES MELLTIUS

DIABETES MELLITUS

Def Diabetes mellitus is a syndrome of impaired

carbohydrate protein amp fat metabolism caused by either lack of insulin secretion or decreased

sensitivity of the tissues to insulin The word ldquoDiabetes Mellitusrdquo literally means

ldquoexcessive secretion of sweet urinerdquo

bull Third leading cause of deathbull Leading cause of blindness bull Diabetes is a very prevalent disease has a huge

economic toll forces individuals to change their lifestyle thus affecting their quality of life amp predisposes the affected to a variety of troublesome amp even life threatening conditions

TYPE I Juvenile Onset Insulin Dependent

It is the more severe from of diabetes and more prevalent in children

DEFINITION

It is a catabolic disorder in which the circulating insulin is virtually absent plasma glucose is elevated amp the pancreatic beta

cells fail to produce any insulin in response to all insulinogenic stimuli

Cause Lack of insulin secretion from the beta cells of the islets of langerhans

bull It is an autoimmune disorder in which there is selective destruction of the pancreatic beta cells by T lymphocytes

bull Mostly it seems to have an immunological basis amp circulating islet cell antibodies amp anti-insulin antibodies may be demonstrated

bull Usually there is a genetic predisposition to this type of diabetes which may be triggered off by

- Viral infections eg rota virus coxsackie virus- Environmental triggers

TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes

It is further classified intobull It is the most common type of diabetes accounting for

about 90 of all cases of diabetes mellitusbull The age of onset is usually after 30 often bw 50 amp 60

years of agebull It develops gradually amp is the less severe form of

diabetes

1 Non-obese type II2 Obese type II

bull Cause Decreased sensitivity of target tissues to the metabolic effects of insulin This reduced sensitivity to insulin is often called INSULIN RESISTANCE

TYPE II DIABETES

Factors that can lead to Insulin resistance include1 Anti-insulin antibodies2 Autoantibodies to the insulin receptor 3 Mutation of insulin receptor4 Down-regulation of insulin receptors by sustained

hyperinsulinism5 Primary hyperinsulinism (Beta cell adenoma)6 Secondary hyperinsulinism (Cushingrsquos syndrome

acromegaly pregnancy or diabetes mellitus)7 Obesityoverweight especially excess fat deposits

around the abdomen8 Insulin resistance in peripheral tissues such as skeletal

muscle brain and liver

PATHOPHYSIOLOGY

bull Diabetes type I is far more rapid in onset occurring over a few days as compared to type II which has a more gradual onset

bull Type I also shows far more complications as compared to Type II which rarely shows complications

bull Type I requires Insulin while Type II can usually be controlled by simple changes in lifestyle as diet exercise amp weight control

bull Type I insulin is more prone to Ketoacidosis while Type II is not

DIAGNOSIS OF DIABETES

1 Blood sugar random ( 80-120 mg100ml)2 Blood sugar fasting (80-90 mg100ml)3 GTT or Glucose Tolerance TestWhen a normal fasting person is given 1g of glucose kg

body weight his plasma glucose levels rise to 120-140 but fall back to normal within 2 hours

In a prediabetic or diabetic not only is the fasting plasma glucose on the higher side but also the post meal plasma glucose rises to as high as 140-200 amp fails to come back to normal within 2 hours of giving conc glucose solution Even after 4-6 hours it rarely comes back to the normal range NORMAL MEAN BLOOD GLUCOSE IS APP 110

Glucose Tolerance Test

POINT TO REMEMBER

WHY IS ORAL GLUCOSE A MORE POWERFUL STIMULANT THAN

INJECTABLE GLUCOSE FOR INSULIN SECRETION

DIAGNOSIS OF DIABETES

4 Presence of glucose in urine (glucosuria)5 Acetone breath6 Lab test for assessing control of diabetes

HbA1c is a minor component of Hb A amp is normally present in small amounts ie up to 6 of normal Hb In the presence of long standing hyperglycemia its concentration rises When plasma glucose is episodically elevated over time small amounts of Hb A are non-enzymatically glycated to form HbA1c

Careful control of diabetes with insulin reduces the amount formed and thus HbA1c levels give an index of diabetic control for past 4-6 weeks

TREATMENT for Type I DIABETES

WHY CANNOT INSULIN BE GIVEN BY MOUTHWHY IS ONLY CHO RESTRICTION NOT VERY EFFECTIVE

Administer enough insulin so that metabolism of fat proteins amp CHO proceed as normally as possible

Insulin is available in various forms1 Insulin preparations are available with rapid (regular) intermediate amp long

durations of action - regular duration of action is 3-8 hours- Intermediate (NPH) not used during- Long duration of action is 10-48 hours

Individualized insulin schedules which consist of one injection of longer acting insulin followed by regular insulin when the glucose level is expected to rise ie at meals

Insulin is administered subcutaneously (sc) except in the case of emergencies when it is given intravenously (iv)

The less soluble an insulin preparation is the longer it acts

INSULIN SYRINGES

Insulin

Human insulin is absorbed more quickly from its site of action than are beef or pork insulins Thus duration of action of human Insulin is shorter amp doses must be adjusted

Hypoglycemia is the most serious amp common side effect of Insulin therapy BC long term diabetics do not produce counteracting hormones of Glucagon EN cortisol etc that normally provide defense against Hypoglycemia

TREATMENT for Type II DIABETES

bull Dietbull Exercise is useful in managing both types of Diabetes

because working muscles are not Insulin dependent Exercising muscles take up some of the excess blood glucose reducing the overall need for insulin

bull Weight lossbull Oral Hypoglycemic Drugs

Oral Hypoglycemic Drugs

There are many types of oral Hypoglycemic drugs some of which are bullSulfonylureas act by stimulating the β- cells to secrete more insulin than they do on their own Eg GlucotrolbullMetformin acts by suppressing liver output of glucose Eg GlucophagebullAlpha-glycosidase Inhibitors act by slowing CHO digestion and absorption from the digestive tract into the blood thus reducing the glucose surge seen after a meal Eg Precose bullByetta (Glucagon-like peptide 1 mimic) mimics the incretin GLP-1 It suppresses glucagon secretion and slows gastric emptying By promoting satiety it decreases food intake and in the long term leads to weight loss Because none of the drugs deliver new insulin to the body they cannot replace insulin therapy for people with Type I Diabetes and later in Type II Diabetics as well

SULFONYLUREAS

NIDDM patients above the age of 40 years amp having ho diabetes of less than 5 years are given Oral Hypoglycemics

Mechanism of Action1 Stimulate release of Insulin from beta cells of

pancreas2 Reduction of serum Glucagon3 Increased binding of Insulin to target tissues amp

receptors Eg Tolbutamide

Glyburide Glipizide

WHO NEEDS INSULIN

bull 1048708 Type 1bull 1048708 Type 2 uncontrolled wmedsbull 1048708 DKAbull 1048708 Hyperosmolar hyperglycemic state (HHS)bull 1048708 Surgerybull 1048708 IllnessInfectionbull 1048708 Stressbull 1048708 Those receiving parental enteral nutritionbull 1048708 Pancreatitis diseases that darr beta cell function

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

1 Hyperglycemia

EFFECTS OF INSULIN DEFICIENCY

2 Glucosuria

EFFECTS OF INSULIN DEFICIENCY

3 Polyuria

EFFECTS OF INSULIN DEFICIENCY

4 Polydipsia amp Polyphagia

(There is an extracellular glucose excess amp an intracellular glucose deficiency-

ldquostarvation in the midst of plentyrdquo)

EFFECTS OF INSULIN DEFICIENCY

5 Weight Loss

(For every gram of glucose excreted 41 kcal is lost from the body Increasing the

caloric intake to cover this loss simply raises the plasma glucose further)

EFFECTS OF INSULIN DEFICIENCY

6 Increase in plasma Cholesterol amp Phospholipid conc

(Role in the accelerated development of atherosclerosis that is a major

complication)

COMPLICATIONS

When Diabetes continues for a long time period (15-20 years) chronic complications occur 1Neuropathies2Peripheral vascular disease3Gangrene 4Atherosclerosis5Ischemic heart disease6Renal disease7Early cataract8Retinopathy9Skin infections10Neuropathies affecting the ANS

Diabetic foot showing ulcer

Gangrene that must be treated with an amputation

KETOSIS AND COMAbull In severe form of Insulin deficiency plasma levels of FFA is more

than doubled darr

bull In the liver and other tissues the fatty acids are catabolized to acetyl Co-A

darrbull Some of the acetyl-CoA enters into the citric acid cycle

darrbull When the supply exceeds the capacity of the citric acid cycle the

excess are converted into acetoacetate and β-hydroxybutyrate darr

These are ketone bodies that lead to progressive metabolic acidosisdarr

Acidosis can depress the brain and if severe enough can lead to coma and death

DIABETES MELLTIUS

DIABETES MELLITUS

Def Diabetes mellitus is a syndrome of impaired

carbohydrate protein amp fat metabolism caused by either lack of insulin secretion or decreased

sensitivity of the tissues to insulin The word ldquoDiabetes Mellitusrdquo literally means

ldquoexcessive secretion of sweet urinerdquo

bull Third leading cause of deathbull Leading cause of blindness bull Diabetes is a very prevalent disease has a huge

economic toll forces individuals to change their lifestyle thus affecting their quality of life amp predisposes the affected to a variety of troublesome amp even life threatening conditions

TYPE I Juvenile Onset Insulin Dependent

It is the more severe from of diabetes and more prevalent in children

DEFINITION

It is a catabolic disorder in which the circulating insulin is virtually absent plasma glucose is elevated amp the pancreatic beta

cells fail to produce any insulin in response to all insulinogenic stimuli

Cause Lack of insulin secretion from the beta cells of the islets of langerhans

bull It is an autoimmune disorder in which there is selective destruction of the pancreatic beta cells by T lymphocytes

bull Mostly it seems to have an immunological basis amp circulating islet cell antibodies amp anti-insulin antibodies may be demonstrated

bull Usually there is a genetic predisposition to this type of diabetes which may be triggered off by

- Viral infections eg rota virus coxsackie virus- Environmental triggers

TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes

It is further classified intobull It is the most common type of diabetes accounting for

about 90 of all cases of diabetes mellitusbull The age of onset is usually after 30 often bw 50 amp 60

years of agebull It develops gradually amp is the less severe form of

diabetes

1 Non-obese type II2 Obese type II

bull Cause Decreased sensitivity of target tissues to the metabolic effects of insulin This reduced sensitivity to insulin is often called INSULIN RESISTANCE

TYPE II DIABETES

Factors that can lead to Insulin resistance include1 Anti-insulin antibodies2 Autoantibodies to the insulin receptor 3 Mutation of insulin receptor4 Down-regulation of insulin receptors by sustained

hyperinsulinism5 Primary hyperinsulinism (Beta cell adenoma)6 Secondary hyperinsulinism (Cushingrsquos syndrome

acromegaly pregnancy or diabetes mellitus)7 Obesityoverweight especially excess fat deposits

around the abdomen8 Insulin resistance in peripheral tissues such as skeletal

muscle brain and liver

PATHOPHYSIOLOGY

bull Diabetes type I is far more rapid in onset occurring over a few days as compared to type II which has a more gradual onset

bull Type I also shows far more complications as compared to Type II which rarely shows complications

bull Type I requires Insulin while Type II can usually be controlled by simple changes in lifestyle as diet exercise amp weight control

bull Type I insulin is more prone to Ketoacidosis while Type II is not

DIAGNOSIS OF DIABETES

1 Blood sugar random ( 80-120 mg100ml)2 Blood sugar fasting (80-90 mg100ml)3 GTT or Glucose Tolerance TestWhen a normal fasting person is given 1g of glucose kg

body weight his plasma glucose levels rise to 120-140 but fall back to normal within 2 hours

In a prediabetic or diabetic not only is the fasting plasma glucose on the higher side but also the post meal plasma glucose rises to as high as 140-200 amp fails to come back to normal within 2 hours of giving conc glucose solution Even after 4-6 hours it rarely comes back to the normal range NORMAL MEAN BLOOD GLUCOSE IS APP 110

Glucose Tolerance Test

POINT TO REMEMBER

WHY IS ORAL GLUCOSE A MORE POWERFUL STIMULANT THAN

INJECTABLE GLUCOSE FOR INSULIN SECRETION

DIAGNOSIS OF DIABETES

4 Presence of glucose in urine (glucosuria)5 Acetone breath6 Lab test for assessing control of diabetes

HbA1c is a minor component of Hb A amp is normally present in small amounts ie up to 6 of normal Hb In the presence of long standing hyperglycemia its concentration rises When plasma glucose is episodically elevated over time small amounts of Hb A are non-enzymatically glycated to form HbA1c

Careful control of diabetes with insulin reduces the amount formed and thus HbA1c levels give an index of diabetic control for past 4-6 weeks

TREATMENT for Type I DIABETES

WHY CANNOT INSULIN BE GIVEN BY MOUTHWHY IS ONLY CHO RESTRICTION NOT VERY EFFECTIVE

Administer enough insulin so that metabolism of fat proteins amp CHO proceed as normally as possible

Insulin is available in various forms1 Insulin preparations are available with rapid (regular) intermediate amp long

durations of action - regular duration of action is 3-8 hours- Intermediate (NPH) not used during- Long duration of action is 10-48 hours

Individualized insulin schedules which consist of one injection of longer acting insulin followed by regular insulin when the glucose level is expected to rise ie at meals

Insulin is administered subcutaneously (sc) except in the case of emergencies when it is given intravenously (iv)

The less soluble an insulin preparation is the longer it acts

INSULIN SYRINGES

Insulin

Human insulin is absorbed more quickly from its site of action than are beef or pork insulins Thus duration of action of human Insulin is shorter amp doses must be adjusted

Hypoglycemia is the most serious amp common side effect of Insulin therapy BC long term diabetics do not produce counteracting hormones of Glucagon EN cortisol etc that normally provide defense against Hypoglycemia

TREATMENT for Type II DIABETES

bull Dietbull Exercise is useful in managing both types of Diabetes

because working muscles are not Insulin dependent Exercising muscles take up some of the excess blood glucose reducing the overall need for insulin

bull Weight lossbull Oral Hypoglycemic Drugs

Oral Hypoglycemic Drugs

There are many types of oral Hypoglycemic drugs some of which are bullSulfonylureas act by stimulating the β- cells to secrete more insulin than they do on their own Eg GlucotrolbullMetformin acts by suppressing liver output of glucose Eg GlucophagebullAlpha-glycosidase Inhibitors act by slowing CHO digestion and absorption from the digestive tract into the blood thus reducing the glucose surge seen after a meal Eg Precose bullByetta (Glucagon-like peptide 1 mimic) mimics the incretin GLP-1 It suppresses glucagon secretion and slows gastric emptying By promoting satiety it decreases food intake and in the long term leads to weight loss Because none of the drugs deliver new insulin to the body they cannot replace insulin therapy for people with Type I Diabetes and later in Type II Diabetics as well

SULFONYLUREAS

NIDDM patients above the age of 40 years amp having ho diabetes of less than 5 years are given Oral Hypoglycemics

Mechanism of Action1 Stimulate release of Insulin from beta cells of

pancreas2 Reduction of serum Glucagon3 Increased binding of Insulin to target tissues amp

receptors Eg Tolbutamide

Glyburide Glipizide

WHO NEEDS INSULIN

bull 1048708 Type 1bull 1048708 Type 2 uncontrolled wmedsbull 1048708 DKAbull 1048708 Hyperosmolar hyperglycemic state (HHS)bull 1048708 Surgerybull 1048708 IllnessInfectionbull 1048708 Stressbull 1048708 Those receiving parental enteral nutritionbull 1048708 Pancreatitis diseases that darr beta cell function

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

EFFECTS OF INSULIN DEFICIENCY

2 Glucosuria

EFFECTS OF INSULIN DEFICIENCY

3 Polyuria

EFFECTS OF INSULIN DEFICIENCY

4 Polydipsia amp Polyphagia

(There is an extracellular glucose excess amp an intracellular glucose deficiency-

ldquostarvation in the midst of plentyrdquo)

EFFECTS OF INSULIN DEFICIENCY

5 Weight Loss

(For every gram of glucose excreted 41 kcal is lost from the body Increasing the

caloric intake to cover this loss simply raises the plasma glucose further)

EFFECTS OF INSULIN DEFICIENCY

6 Increase in plasma Cholesterol amp Phospholipid conc

(Role in the accelerated development of atherosclerosis that is a major

complication)

COMPLICATIONS

When Diabetes continues for a long time period (15-20 years) chronic complications occur 1Neuropathies2Peripheral vascular disease3Gangrene 4Atherosclerosis5Ischemic heart disease6Renal disease7Early cataract8Retinopathy9Skin infections10Neuropathies affecting the ANS

Diabetic foot showing ulcer

Gangrene that must be treated with an amputation

KETOSIS AND COMAbull In severe form of Insulin deficiency plasma levels of FFA is more

than doubled darr

bull In the liver and other tissues the fatty acids are catabolized to acetyl Co-A

darrbull Some of the acetyl-CoA enters into the citric acid cycle

darrbull When the supply exceeds the capacity of the citric acid cycle the

excess are converted into acetoacetate and β-hydroxybutyrate darr

These are ketone bodies that lead to progressive metabolic acidosisdarr

Acidosis can depress the brain and if severe enough can lead to coma and death

DIABETES MELLTIUS

DIABETES MELLITUS

Def Diabetes mellitus is a syndrome of impaired

carbohydrate protein amp fat metabolism caused by either lack of insulin secretion or decreased

sensitivity of the tissues to insulin The word ldquoDiabetes Mellitusrdquo literally means

ldquoexcessive secretion of sweet urinerdquo

bull Third leading cause of deathbull Leading cause of blindness bull Diabetes is a very prevalent disease has a huge

economic toll forces individuals to change their lifestyle thus affecting their quality of life amp predisposes the affected to a variety of troublesome amp even life threatening conditions

TYPE I Juvenile Onset Insulin Dependent

It is the more severe from of diabetes and more prevalent in children

DEFINITION

It is a catabolic disorder in which the circulating insulin is virtually absent plasma glucose is elevated amp the pancreatic beta

cells fail to produce any insulin in response to all insulinogenic stimuli

Cause Lack of insulin secretion from the beta cells of the islets of langerhans

bull It is an autoimmune disorder in which there is selective destruction of the pancreatic beta cells by T lymphocytes

bull Mostly it seems to have an immunological basis amp circulating islet cell antibodies amp anti-insulin antibodies may be demonstrated

bull Usually there is a genetic predisposition to this type of diabetes which may be triggered off by

- Viral infections eg rota virus coxsackie virus- Environmental triggers

TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes

It is further classified intobull It is the most common type of diabetes accounting for

about 90 of all cases of diabetes mellitusbull The age of onset is usually after 30 often bw 50 amp 60

years of agebull It develops gradually amp is the less severe form of

diabetes

1 Non-obese type II2 Obese type II

bull Cause Decreased sensitivity of target tissues to the metabolic effects of insulin This reduced sensitivity to insulin is often called INSULIN RESISTANCE

TYPE II DIABETES

Factors that can lead to Insulin resistance include1 Anti-insulin antibodies2 Autoantibodies to the insulin receptor 3 Mutation of insulin receptor4 Down-regulation of insulin receptors by sustained

hyperinsulinism5 Primary hyperinsulinism (Beta cell adenoma)6 Secondary hyperinsulinism (Cushingrsquos syndrome

acromegaly pregnancy or diabetes mellitus)7 Obesityoverweight especially excess fat deposits

around the abdomen8 Insulin resistance in peripheral tissues such as skeletal

muscle brain and liver

PATHOPHYSIOLOGY

bull Diabetes type I is far more rapid in onset occurring over a few days as compared to type II which has a more gradual onset

bull Type I also shows far more complications as compared to Type II which rarely shows complications

bull Type I requires Insulin while Type II can usually be controlled by simple changes in lifestyle as diet exercise amp weight control

bull Type I insulin is more prone to Ketoacidosis while Type II is not

DIAGNOSIS OF DIABETES

1 Blood sugar random ( 80-120 mg100ml)2 Blood sugar fasting (80-90 mg100ml)3 GTT or Glucose Tolerance TestWhen a normal fasting person is given 1g of glucose kg

body weight his plasma glucose levels rise to 120-140 but fall back to normal within 2 hours

In a prediabetic or diabetic not only is the fasting plasma glucose on the higher side but also the post meal plasma glucose rises to as high as 140-200 amp fails to come back to normal within 2 hours of giving conc glucose solution Even after 4-6 hours it rarely comes back to the normal range NORMAL MEAN BLOOD GLUCOSE IS APP 110

Glucose Tolerance Test

POINT TO REMEMBER

WHY IS ORAL GLUCOSE A MORE POWERFUL STIMULANT THAN

INJECTABLE GLUCOSE FOR INSULIN SECRETION

DIAGNOSIS OF DIABETES

4 Presence of glucose in urine (glucosuria)5 Acetone breath6 Lab test for assessing control of diabetes

HbA1c is a minor component of Hb A amp is normally present in small amounts ie up to 6 of normal Hb In the presence of long standing hyperglycemia its concentration rises When plasma glucose is episodically elevated over time small amounts of Hb A are non-enzymatically glycated to form HbA1c

Careful control of diabetes with insulin reduces the amount formed and thus HbA1c levels give an index of diabetic control for past 4-6 weeks

TREATMENT for Type I DIABETES

WHY CANNOT INSULIN BE GIVEN BY MOUTHWHY IS ONLY CHO RESTRICTION NOT VERY EFFECTIVE

Administer enough insulin so that metabolism of fat proteins amp CHO proceed as normally as possible

Insulin is available in various forms1 Insulin preparations are available with rapid (regular) intermediate amp long

durations of action - regular duration of action is 3-8 hours- Intermediate (NPH) not used during- Long duration of action is 10-48 hours

Individualized insulin schedules which consist of one injection of longer acting insulin followed by regular insulin when the glucose level is expected to rise ie at meals

Insulin is administered subcutaneously (sc) except in the case of emergencies when it is given intravenously (iv)

The less soluble an insulin preparation is the longer it acts

INSULIN SYRINGES

Insulin

Human insulin is absorbed more quickly from its site of action than are beef or pork insulins Thus duration of action of human Insulin is shorter amp doses must be adjusted

Hypoglycemia is the most serious amp common side effect of Insulin therapy BC long term diabetics do not produce counteracting hormones of Glucagon EN cortisol etc that normally provide defense against Hypoglycemia

TREATMENT for Type II DIABETES

bull Dietbull Exercise is useful in managing both types of Diabetes

because working muscles are not Insulin dependent Exercising muscles take up some of the excess blood glucose reducing the overall need for insulin

bull Weight lossbull Oral Hypoglycemic Drugs

Oral Hypoglycemic Drugs

There are many types of oral Hypoglycemic drugs some of which are bullSulfonylureas act by stimulating the β- cells to secrete more insulin than they do on their own Eg GlucotrolbullMetformin acts by suppressing liver output of glucose Eg GlucophagebullAlpha-glycosidase Inhibitors act by slowing CHO digestion and absorption from the digestive tract into the blood thus reducing the glucose surge seen after a meal Eg Precose bullByetta (Glucagon-like peptide 1 mimic) mimics the incretin GLP-1 It suppresses glucagon secretion and slows gastric emptying By promoting satiety it decreases food intake and in the long term leads to weight loss Because none of the drugs deliver new insulin to the body they cannot replace insulin therapy for people with Type I Diabetes and later in Type II Diabetics as well

SULFONYLUREAS

NIDDM patients above the age of 40 years amp having ho diabetes of less than 5 years are given Oral Hypoglycemics

Mechanism of Action1 Stimulate release of Insulin from beta cells of

pancreas2 Reduction of serum Glucagon3 Increased binding of Insulin to target tissues amp

receptors Eg Tolbutamide

Glyburide Glipizide

WHO NEEDS INSULIN

bull 1048708 Type 1bull 1048708 Type 2 uncontrolled wmedsbull 1048708 DKAbull 1048708 Hyperosmolar hyperglycemic state (HHS)bull 1048708 Surgerybull 1048708 IllnessInfectionbull 1048708 Stressbull 1048708 Those receiving parental enteral nutritionbull 1048708 Pancreatitis diseases that darr beta cell function

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

EFFECTS OF INSULIN DEFICIENCY

3 Polyuria

EFFECTS OF INSULIN DEFICIENCY

4 Polydipsia amp Polyphagia

(There is an extracellular glucose excess amp an intracellular glucose deficiency-

ldquostarvation in the midst of plentyrdquo)

EFFECTS OF INSULIN DEFICIENCY

5 Weight Loss

(For every gram of glucose excreted 41 kcal is lost from the body Increasing the

caloric intake to cover this loss simply raises the plasma glucose further)

EFFECTS OF INSULIN DEFICIENCY

6 Increase in plasma Cholesterol amp Phospholipid conc

(Role in the accelerated development of atherosclerosis that is a major

complication)

COMPLICATIONS

When Diabetes continues for a long time period (15-20 years) chronic complications occur 1Neuropathies2Peripheral vascular disease3Gangrene 4Atherosclerosis5Ischemic heart disease6Renal disease7Early cataract8Retinopathy9Skin infections10Neuropathies affecting the ANS

Diabetic foot showing ulcer

Gangrene that must be treated with an amputation

KETOSIS AND COMAbull In severe form of Insulin deficiency plasma levels of FFA is more

than doubled darr

bull In the liver and other tissues the fatty acids are catabolized to acetyl Co-A

darrbull Some of the acetyl-CoA enters into the citric acid cycle

darrbull When the supply exceeds the capacity of the citric acid cycle the

excess are converted into acetoacetate and β-hydroxybutyrate darr

These are ketone bodies that lead to progressive metabolic acidosisdarr

Acidosis can depress the brain and if severe enough can lead to coma and death

DIABETES MELLTIUS

DIABETES MELLITUS

Def Diabetes mellitus is a syndrome of impaired

carbohydrate protein amp fat metabolism caused by either lack of insulin secretion or decreased

sensitivity of the tissues to insulin The word ldquoDiabetes Mellitusrdquo literally means

ldquoexcessive secretion of sweet urinerdquo

bull Third leading cause of deathbull Leading cause of blindness bull Diabetes is a very prevalent disease has a huge

economic toll forces individuals to change their lifestyle thus affecting their quality of life amp predisposes the affected to a variety of troublesome amp even life threatening conditions

TYPE I Juvenile Onset Insulin Dependent

It is the more severe from of diabetes and more prevalent in children

DEFINITION

It is a catabolic disorder in which the circulating insulin is virtually absent plasma glucose is elevated amp the pancreatic beta

cells fail to produce any insulin in response to all insulinogenic stimuli

Cause Lack of insulin secretion from the beta cells of the islets of langerhans

bull It is an autoimmune disorder in which there is selective destruction of the pancreatic beta cells by T lymphocytes

bull Mostly it seems to have an immunological basis amp circulating islet cell antibodies amp anti-insulin antibodies may be demonstrated

bull Usually there is a genetic predisposition to this type of diabetes which may be triggered off by

- Viral infections eg rota virus coxsackie virus- Environmental triggers

TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes

It is further classified intobull It is the most common type of diabetes accounting for

about 90 of all cases of diabetes mellitusbull The age of onset is usually after 30 often bw 50 amp 60

years of agebull It develops gradually amp is the less severe form of

diabetes

1 Non-obese type II2 Obese type II

bull Cause Decreased sensitivity of target tissues to the metabolic effects of insulin This reduced sensitivity to insulin is often called INSULIN RESISTANCE

TYPE II DIABETES

Factors that can lead to Insulin resistance include1 Anti-insulin antibodies2 Autoantibodies to the insulin receptor 3 Mutation of insulin receptor4 Down-regulation of insulin receptors by sustained

hyperinsulinism5 Primary hyperinsulinism (Beta cell adenoma)6 Secondary hyperinsulinism (Cushingrsquos syndrome

acromegaly pregnancy or diabetes mellitus)7 Obesityoverweight especially excess fat deposits

around the abdomen8 Insulin resistance in peripheral tissues such as skeletal

muscle brain and liver

PATHOPHYSIOLOGY

bull Diabetes type I is far more rapid in onset occurring over a few days as compared to type II which has a more gradual onset

bull Type I also shows far more complications as compared to Type II which rarely shows complications

bull Type I requires Insulin while Type II can usually be controlled by simple changes in lifestyle as diet exercise amp weight control

bull Type I insulin is more prone to Ketoacidosis while Type II is not

DIAGNOSIS OF DIABETES

1 Blood sugar random ( 80-120 mg100ml)2 Blood sugar fasting (80-90 mg100ml)3 GTT or Glucose Tolerance TestWhen a normal fasting person is given 1g of glucose kg

body weight his plasma glucose levels rise to 120-140 but fall back to normal within 2 hours

In a prediabetic or diabetic not only is the fasting plasma glucose on the higher side but also the post meal plasma glucose rises to as high as 140-200 amp fails to come back to normal within 2 hours of giving conc glucose solution Even after 4-6 hours it rarely comes back to the normal range NORMAL MEAN BLOOD GLUCOSE IS APP 110

Glucose Tolerance Test

POINT TO REMEMBER

WHY IS ORAL GLUCOSE A MORE POWERFUL STIMULANT THAN

INJECTABLE GLUCOSE FOR INSULIN SECRETION

DIAGNOSIS OF DIABETES

4 Presence of glucose in urine (glucosuria)5 Acetone breath6 Lab test for assessing control of diabetes

HbA1c is a minor component of Hb A amp is normally present in small amounts ie up to 6 of normal Hb In the presence of long standing hyperglycemia its concentration rises When plasma glucose is episodically elevated over time small amounts of Hb A are non-enzymatically glycated to form HbA1c

Careful control of diabetes with insulin reduces the amount formed and thus HbA1c levels give an index of diabetic control for past 4-6 weeks

TREATMENT for Type I DIABETES

WHY CANNOT INSULIN BE GIVEN BY MOUTHWHY IS ONLY CHO RESTRICTION NOT VERY EFFECTIVE

Administer enough insulin so that metabolism of fat proteins amp CHO proceed as normally as possible

Insulin is available in various forms1 Insulin preparations are available with rapid (regular) intermediate amp long

durations of action - regular duration of action is 3-8 hours- Intermediate (NPH) not used during- Long duration of action is 10-48 hours

Individualized insulin schedules which consist of one injection of longer acting insulin followed by regular insulin when the glucose level is expected to rise ie at meals

Insulin is administered subcutaneously (sc) except in the case of emergencies when it is given intravenously (iv)

The less soluble an insulin preparation is the longer it acts

INSULIN SYRINGES

Insulin

Human insulin is absorbed more quickly from its site of action than are beef or pork insulins Thus duration of action of human Insulin is shorter amp doses must be adjusted

Hypoglycemia is the most serious amp common side effect of Insulin therapy BC long term diabetics do not produce counteracting hormones of Glucagon EN cortisol etc that normally provide defense against Hypoglycemia

TREATMENT for Type II DIABETES

bull Dietbull Exercise is useful in managing both types of Diabetes

because working muscles are not Insulin dependent Exercising muscles take up some of the excess blood glucose reducing the overall need for insulin

bull Weight lossbull Oral Hypoglycemic Drugs

Oral Hypoglycemic Drugs

There are many types of oral Hypoglycemic drugs some of which are bullSulfonylureas act by stimulating the β- cells to secrete more insulin than they do on their own Eg GlucotrolbullMetformin acts by suppressing liver output of glucose Eg GlucophagebullAlpha-glycosidase Inhibitors act by slowing CHO digestion and absorption from the digestive tract into the blood thus reducing the glucose surge seen after a meal Eg Precose bullByetta (Glucagon-like peptide 1 mimic) mimics the incretin GLP-1 It suppresses glucagon secretion and slows gastric emptying By promoting satiety it decreases food intake and in the long term leads to weight loss Because none of the drugs deliver new insulin to the body they cannot replace insulin therapy for people with Type I Diabetes and later in Type II Diabetics as well

SULFONYLUREAS

NIDDM patients above the age of 40 years amp having ho diabetes of less than 5 years are given Oral Hypoglycemics

Mechanism of Action1 Stimulate release of Insulin from beta cells of

pancreas2 Reduction of serum Glucagon3 Increased binding of Insulin to target tissues amp

receptors Eg Tolbutamide

Glyburide Glipizide

WHO NEEDS INSULIN

bull 1048708 Type 1bull 1048708 Type 2 uncontrolled wmedsbull 1048708 DKAbull 1048708 Hyperosmolar hyperglycemic state (HHS)bull 1048708 Surgerybull 1048708 IllnessInfectionbull 1048708 Stressbull 1048708 Those receiving parental enteral nutritionbull 1048708 Pancreatitis diseases that darr beta cell function

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

EFFECTS OF INSULIN DEFICIENCY

4 Polydipsia amp Polyphagia

(There is an extracellular glucose excess amp an intracellular glucose deficiency-

ldquostarvation in the midst of plentyrdquo)

EFFECTS OF INSULIN DEFICIENCY

5 Weight Loss

(For every gram of glucose excreted 41 kcal is lost from the body Increasing the

caloric intake to cover this loss simply raises the plasma glucose further)

EFFECTS OF INSULIN DEFICIENCY

6 Increase in plasma Cholesterol amp Phospholipid conc

(Role in the accelerated development of atherosclerosis that is a major

complication)

COMPLICATIONS

When Diabetes continues for a long time period (15-20 years) chronic complications occur 1Neuropathies2Peripheral vascular disease3Gangrene 4Atherosclerosis5Ischemic heart disease6Renal disease7Early cataract8Retinopathy9Skin infections10Neuropathies affecting the ANS

Diabetic foot showing ulcer

Gangrene that must be treated with an amputation

KETOSIS AND COMAbull In severe form of Insulin deficiency plasma levels of FFA is more

than doubled darr

bull In the liver and other tissues the fatty acids are catabolized to acetyl Co-A

darrbull Some of the acetyl-CoA enters into the citric acid cycle

darrbull When the supply exceeds the capacity of the citric acid cycle the

excess are converted into acetoacetate and β-hydroxybutyrate darr

These are ketone bodies that lead to progressive metabolic acidosisdarr

Acidosis can depress the brain and if severe enough can lead to coma and death

DIABETES MELLTIUS

DIABETES MELLITUS

Def Diabetes mellitus is a syndrome of impaired

carbohydrate protein amp fat metabolism caused by either lack of insulin secretion or decreased

sensitivity of the tissues to insulin The word ldquoDiabetes Mellitusrdquo literally means

ldquoexcessive secretion of sweet urinerdquo

bull Third leading cause of deathbull Leading cause of blindness bull Diabetes is a very prevalent disease has a huge

economic toll forces individuals to change their lifestyle thus affecting their quality of life amp predisposes the affected to a variety of troublesome amp even life threatening conditions

TYPE I Juvenile Onset Insulin Dependent

It is the more severe from of diabetes and more prevalent in children

DEFINITION

It is a catabolic disorder in which the circulating insulin is virtually absent plasma glucose is elevated amp the pancreatic beta

cells fail to produce any insulin in response to all insulinogenic stimuli

Cause Lack of insulin secretion from the beta cells of the islets of langerhans

bull It is an autoimmune disorder in which there is selective destruction of the pancreatic beta cells by T lymphocytes

bull Mostly it seems to have an immunological basis amp circulating islet cell antibodies amp anti-insulin antibodies may be demonstrated

bull Usually there is a genetic predisposition to this type of diabetes which may be triggered off by

- Viral infections eg rota virus coxsackie virus- Environmental triggers

TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes

It is further classified intobull It is the most common type of diabetes accounting for

about 90 of all cases of diabetes mellitusbull The age of onset is usually after 30 often bw 50 amp 60

years of agebull It develops gradually amp is the less severe form of

diabetes

1 Non-obese type II2 Obese type II

bull Cause Decreased sensitivity of target tissues to the metabolic effects of insulin This reduced sensitivity to insulin is often called INSULIN RESISTANCE

TYPE II DIABETES

Factors that can lead to Insulin resistance include1 Anti-insulin antibodies2 Autoantibodies to the insulin receptor 3 Mutation of insulin receptor4 Down-regulation of insulin receptors by sustained

hyperinsulinism5 Primary hyperinsulinism (Beta cell adenoma)6 Secondary hyperinsulinism (Cushingrsquos syndrome

acromegaly pregnancy or diabetes mellitus)7 Obesityoverweight especially excess fat deposits

around the abdomen8 Insulin resistance in peripheral tissues such as skeletal

muscle brain and liver

PATHOPHYSIOLOGY

bull Diabetes type I is far more rapid in onset occurring over a few days as compared to type II which has a more gradual onset

bull Type I also shows far more complications as compared to Type II which rarely shows complications

bull Type I requires Insulin while Type II can usually be controlled by simple changes in lifestyle as diet exercise amp weight control

bull Type I insulin is more prone to Ketoacidosis while Type II is not

DIAGNOSIS OF DIABETES

1 Blood sugar random ( 80-120 mg100ml)2 Blood sugar fasting (80-90 mg100ml)3 GTT or Glucose Tolerance TestWhen a normal fasting person is given 1g of glucose kg

body weight his plasma glucose levels rise to 120-140 but fall back to normal within 2 hours

In a prediabetic or diabetic not only is the fasting plasma glucose on the higher side but also the post meal plasma glucose rises to as high as 140-200 amp fails to come back to normal within 2 hours of giving conc glucose solution Even after 4-6 hours it rarely comes back to the normal range NORMAL MEAN BLOOD GLUCOSE IS APP 110

Glucose Tolerance Test

POINT TO REMEMBER

WHY IS ORAL GLUCOSE A MORE POWERFUL STIMULANT THAN

INJECTABLE GLUCOSE FOR INSULIN SECRETION

DIAGNOSIS OF DIABETES

4 Presence of glucose in urine (glucosuria)5 Acetone breath6 Lab test for assessing control of diabetes

HbA1c is a minor component of Hb A amp is normally present in small amounts ie up to 6 of normal Hb In the presence of long standing hyperglycemia its concentration rises When plasma glucose is episodically elevated over time small amounts of Hb A are non-enzymatically glycated to form HbA1c

Careful control of diabetes with insulin reduces the amount formed and thus HbA1c levels give an index of diabetic control for past 4-6 weeks

TREATMENT for Type I DIABETES

WHY CANNOT INSULIN BE GIVEN BY MOUTHWHY IS ONLY CHO RESTRICTION NOT VERY EFFECTIVE

Administer enough insulin so that metabolism of fat proteins amp CHO proceed as normally as possible

Insulin is available in various forms1 Insulin preparations are available with rapid (regular) intermediate amp long

durations of action - regular duration of action is 3-8 hours- Intermediate (NPH) not used during- Long duration of action is 10-48 hours

Individualized insulin schedules which consist of one injection of longer acting insulin followed by regular insulin when the glucose level is expected to rise ie at meals

Insulin is administered subcutaneously (sc) except in the case of emergencies when it is given intravenously (iv)

The less soluble an insulin preparation is the longer it acts

INSULIN SYRINGES

Insulin

Human insulin is absorbed more quickly from its site of action than are beef or pork insulins Thus duration of action of human Insulin is shorter amp doses must be adjusted

Hypoglycemia is the most serious amp common side effect of Insulin therapy BC long term diabetics do not produce counteracting hormones of Glucagon EN cortisol etc that normally provide defense against Hypoglycemia

TREATMENT for Type II DIABETES

bull Dietbull Exercise is useful in managing both types of Diabetes

because working muscles are not Insulin dependent Exercising muscles take up some of the excess blood glucose reducing the overall need for insulin

bull Weight lossbull Oral Hypoglycemic Drugs

Oral Hypoglycemic Drugs

There are many types of oral Hypoglycemic drugs some of which are bullSulfonylureas act by stimulating the β- cells to secrete more insulin than they do on their own Eg GlucotrolbullMetformin acts by suppressing liver output of glucose Eg GlucophagebullAlpha-glycosidase Inhibitors act by slowing CHO digestion and absorption from the digestive tract into the blood thus reducing the glucose surge seen after a meal Eg Precose bullByetta (Glucagon-like peptide 1 mimic) mimics the incretin GLP-1 It suppresses glucagon secretion and slows gastric emptying By promoting satiety it decreases food intake and in the long term leads to weight loss Because none of the drugs deliver new insulin to the body they cannot replace insulin therapy for people with Type I Diabetes and later in Type II Diabetics as well

SULFONYLUREAS

NIDDM patients above the age of 40 years amp having ho diabetes of less than 5 years are given Oral Hypoglycemics

Mechanism of Action1 Stimulate release of Insulin from beta cells of

pancreas2 Reduction of serum Glucagon3 Increased binding of Insulin to target tissues amp

receptors Eg Tolbutamide

Glyburide Glipizide

WHO NEEDS INSULIN

bull 1048708 Type 1bull 1048708 Type 2 uncontrolled wmedsbull 1048708 DKAbull 1048708 Hyperosmolar hyperglycemic state (HHS)bull 1048708 Surgerybull 1048708 IllnessInfectionbull 1048708 Stressbull 1048708 Those receiving parental enteral nutritionbull 1048708 Pancreatitis diseases that darr beta cell function

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

EFFECTS OF INSULIN DEFICIENCY

5 Weight Loss

(For every gram of glucose excreted 41 kcal is lost from the body Increasing the

caloric intake to cover this loss simply raises the plasma glucose further)

EFFECTS OF INSULIN DEFICIENCY

6 Increase in plasma Cholesterol amp Phospholipid conc

(Role in the accelerated development of atherosclerosis that is a major

complication)

COMPLICATIONS

When Diabetes continues for a long time period (15-20 years) chronic complications occur 1Neuropathies2Peripheral vascular disease3Gangrene 4Atherosclerosis5Ischemic heart disease6Renal disease7Early cataract8Retinopathy9Skin infections10Neuropathies affecting the ANS

Diabetic foot showing ulcer

Gangrene that must be treated with an amputation

KETOSIS AND COMAbull In severe form of Insulin deficiency plasma levels of FFA is more

than doubled darr

bull In the liver and other tissues the fatty acids are catabolized to acetyl Co-A

darrbull Some of the acetyl-CoA enters into the citric acid cycle

darrbull When the supply exceeds the capacity of the citric acid cycle the

excess are converted into acetoacetate and β-hydroxybutyrate darr

These are ketone bodies that lead to progressive metabolic acidosisdarr

Acidosis can depress the brain and if severe enough can lead to coma and death

DIABETES MELLTIUS

DIABETES MELLITUS

Def Diabetes mellitus is a syndrome of impaired

carbohydrate protein amp fat metabolism caused by either lack of insulin secretion or decreased

sensitivity of the tissues to insulin The word ldquoDiabetes Mellitusrdquo literally means

ldquoexcessive secretion of sweet urinerdquo

bull Third leading cause of deathbull Leading cause of blindness bull Diabetes is a very prevalent disease has a huge

economic toll forces individuals to change their lifestyle thus affecting their quality of life amp predisposes the affected to a variety of troublesome amp even life threatening conditions

TYPE I Juvenile Onset Insulin Dependent

It is the more severe from of diabetes and more prevalent in children

DEFINITION

It is a catabolic disorder in which the circulating insulin is virtually absent plasma glucose is elevated amp the pancreatic beta

cells fail to produce any insulin in response to all insulinogenic stimuli

Cause Lack of insulin secretion from the beta cells of the islets of langerhans

bull It is an autoimmune disorder in which there is selective destruction of the pancreatic beta cells by T lymphocytes

bull Mostly it seems to have an immunological basis amp circulating islet cell antibodies amp anti-insulin antibodies may be demonstrated

bull Usually there is a genetic predisposition to this type of diabetes which may be triggered off by

- Viral infections eg rota virus coxsackie virus- Environmental triggers

TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes

It is further classified intobull It is the most common type of diabetes accounting for

about 90 of all cases of diabetes mellitusbull The age of onset is usually after 30 often bw 50 amp 60

years of agebull It develops gradually amp is the less severe form of

diabetes

1 Non-obese type II2 Obese type II

bull Cause Decreased sensitivity of target tissues to the metabolic effects of insulin This reduced sensitivity to insulin is often called INSULIN RESISTANCE

TYPE II DIABETES

Factors that can lead to Insulin resistance include1 Anti-insulin antibodies2 Autoantibodies to the insulin receptor 3 Mutation of insulin receptor4 Down-regulation of insulin receptors by sustained

hyperinsulinism5 Primary hyperinsulinism (Beta cell adenoma)6 Secondary hyperinsulinism (Cushingrsquos syndrome

acromegaly pregnancy or diabetes mellitus)7 Obesityoverweight especially excess fat deposits

around the abdomen8 Insulin resistance in peripheral tissues such as skeletal

muscle brain and liver

PATHOPHYSIOLOGY

bull Diabetes type I is far more rapid in onset occurring over a few days as compared to type II which has a more gradual onset

bull Type I also shows far more complications as compared to Type II which rarely shows complications

bull Type I requires Insulin while Type II can usually be controlled by simple changes in lifestyle as diet exercise amp weight control

bull Type I insulin is more prone to Ketoacidosis while Type II is not

DIAGNOSIS OF DIABETES

1 Blood sugar random ( 80-120 mg100ml)2 Blood sugar fasting (80-90 mg100ml)3 GTT or Glucose Tolerance TestWhen a normal fasting person is given 1g of glucose kg

body weight his plasma glucose levels rise to 120-140 but fall back to normal within 2 hours

In a prediabetic or diabetic not only is the fasting plasma glucose on the higher side but also the post meal plasma glucose rises to as high as 140-200 amp fails to come back to normal within 2 hours of giving conc glucose solution Even after 4-6 hours it rarely comes back to the normal range NORMAL MEAN BLOOD GLUCOSE IS APP 110

Glucose Tolerance Test

POINT TO REMEMBER

WHY IS ORAL GLUCOSE A MORE POWERFUL STIMULANT THAN

INJECTABLE GLUCOSE FOR INSULIN SECRETION

DIAGNOSIS OF DIABETES

4 Presence of glucose in urine (glucosuria)5 Acetone breath6 Lab test for assessing control of diabetes

HbA1c is a minor component of Hb A amp is normally present in small amounts ie up to 6 of normal Hb In the presence of long standing hyperglycemia its concentration rises When plasma glucose is episodically elevated over time small amounts of Hb A are non-enzymatically glycated to form HbA1c

Careful control of diabetes with insulin reduces the amount formed and thus HbA1c levels give an index of diabetic control for past 4-6 weeks

TREATMENT for Type I DIABETES

WHY CANNOT INSULIN BE GIVEN BY MOUTHWHY IS ONLY CHO RESTRICTION NOT VERY EFFECTIVE

Administer enough insulin so that metabolism of fat proteins amp CHO proceed as normally as possible

Insulin is available in various forms1 Insulin preparations are available with rapid (regular) intermediate amp long

durations of action - regular duration of action is 3-8 hours- Intermediate (NPH) not used during- Long duration of action is 10-48 hours

Individualized insulin schedules which consist of one injection of longer acting insulin followed by regular insulin when the glucose level is expected to rise ie at meals

Insulin is administered subcutaneously (sc) except in the case of emergencies when it is given intravenously (iv)

The less soluble an insulin preparation is the longer it acts

INSULIN SYRINGES

Insulin

Human insulin is absorbed more quickly from its site of action than are beef or pork insulins Thus duration of action of human Insulin is shorter amp doses must be adjusted

Hypoglycemia is the most serious amp common side effect of Insulin therapy BC long term diabetics do not produce counteracting hormones of Glucagon EN cortisol etc that normally provide defense against Hypoglycemia

TREATMENT for Type II DIABETES

bull Dietbull Exercise is useful in managing both types of Diabetes

because working muscles are not Insulin dependent Exercising muscles take up some of the excess blood glucose reducing the overall need for insulin

bull Weight lossbull Oral Hypoglycemic Drugs

Oral Hypoglycemic Drugs

There are many types of oral Hypoglycemic drugs some of which are bullSulfonylureas act by stimulating the β- cells to secrete more insulin than they do on their own Eg GlucotrolbullMetformin acts by suppressing liver output of glucose Eg GlucophagebullAlpha-glycosidase Inhibitors act by slowing CHO digestion and absorption from the digestive tract into the blood thus reducing the glucose surge seen after a meal Eg Precose bullByetta (Glucagon-like peptide 1 mimic) mimics the incretin GLP-1 It suppresses glucagon secretion and slows gastric emptying By promoting satiety it decreases food intake and in the long term leads to weight loss Because none of the drugs deliver new insulin to the body they cannot replace insulin therapy for people with Type I Diabetes and later in Type II Diabetics as well

SULFONYLUREAS

NIDDM patients above the age of 40 years amp having ho diabetes of less than 5 years are given Oral Hypoglycemics

Mechanism of Action1 Stimulate release of Insulin from beta cells of

pancreas2 Reduction of serum Glucagon3 Increased binding of Insulin to target tissues amp

receptors Eg Tolbutamide

Glyburide Glipizide

WHO NEEDS INSULIN

bull 1048708 Type 1bull 1048708 Type 2 uncontrolled wmedsbull 1048708 DKAbull 1048708 Hyperosmolar hyperglycemic state (HHS)bull 1048708 Surgerybull 1048708 IllnessInfectionbull 1048708 Stressbull 1048708 Those receiving parental enteral nutritionbull 1048708 Pancreatitis diseases that darr beta cell function

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

EFFECTS OF INSULIN DEFICIENCY

6 Increase in plasma Cholesterol amp Phospholipid conc

(Role in the accelerated development of atherosclerosis that is a major

complication)

COMPLICATIONS

When Diabetes continues for a long time period (15-20 years) chronic complications occur 1Neuropathies2Peripheral vascular disease3Gangrene 4Atherosclerosis5Ischemic heart disease6Renal disease7Early cataract8Retinopathy9Skin infections10Neuropathies affecting the ANS

Diabetic foot showing ulcer

Gangrene that must be treated with an amputation

KETOSIS AND COMAbull In severe form of Insulin deficiency plasma levels of FFA is more

than doubled darr

bull In the liver and other tissues the fatty acids are catabolized to acetyl Co-A

darrbull Some of the acetyl-CoA enters into the citric acid cycle

darrbull When the supply exceeds the capacity of the citric acid cycle the

excess are converted into acetoacetate and β-hydroxybutyrate darr

These are ketone bodies that lead to progressive metabolic acidosisdarr

Acidosis can depress the brain and if severe enough can lead to coma and death

DIABETES MELLTIUS

DIABETES MELLITUS

Def Diabetes mellitus is a syndrome of impaired

carbohydrate protein amp fat metabolism caused by either lack of insulin secretion or decreased

sensitivity of the tissues to insulin The word ldquoDiabetes Mellitusrdquo literally means

ldquoexcessive secretion of sweet urinerdquo

bull Third leading cause of deathbull Leading cause of blindness bull Diabetes is a very prevalent disease has a huge

economic toll forces individuals to change their lifestyle thus affecting their quality of life amp predisposes the affected to a variety of troublesome amp even life threatening conditions

TYPE I Juvenile Onset Insulin Dependent

It is the more severe from of diabetes and more prevalent in children

DEFINITION

It is a catabolic disorder in which the circulating insulin is virtually absent plasma glucose is elevated amp the pancreatic beta

cells fail to produce any insulin in response to all insulinogenic stimuli

Cause Lack of insulin secretion from the beta cells of the islets of langerhans

bull It is an autoimmune disorder in which there is selective destruction of the pancreatic beta cells by T lymphocytes

bull Mostly it seems to have an immunological basis amp circulating islet cell antibodies amp anti-insulin antibodies may be demonstrated

bull Usually there is a genetic predisposition to this type of diabetes which may be triggered off by

- Viral infections eg rota virus coxsackie virus- Environmental triggers

TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes

It is further classified intobull It is the most common type of diabetes accounting for

about 90 of all cases of diabetes mellitusbull The age of onset is usually after 30 often bw 50 amp 60

years of agebull It develops gradually amp is the less severe form of

diabetes

1 Non-obese type II2 Obese type II

bull Cause Decreased sensitivity of target tissues to the metabolic effects of insulin This reduced sensitivity to insulin is often called INSULIN RESISTANCE

TYPE II DIABETES

Factors that can lead to Insulin resistance include1 Anti-insulin antibodies2 Autoantibodies to the insulin receptor 3 Mutation of insulin receptor4 Down-regulation of insulin receptors by sustained

hyperinsulinism5 Primary hyperinsulinism (Beta cell adenoma)6 Secondary hyperinsulinism (Cushingrsquos syndrome

acromegaly pregnancy or diabetes mellitus)7 Obesityoverweight especially excess fat deposits

around the abdomen8 Insulin resistance in peripheral tissues such as skeletal

muscle brain and liver

PATHOPHYSIOLOGY

bull Diabetes type I is far more rapid in onset occurring over a few days as compared to type II which has a more gradual onset

bull Type I also shows far more complications as compared to Type II which rarely shows complications

bull Type I requires Insulin while Type II can usually be controlled by simple changes in lifestyle as diet exercise amp weight control

bull Type I insulin is more prone to Ketoacidosis while Type II is not

DIAGNOSIS OF DIABETES

1 Blood sugar random ( 80-120 mg100ml)2 Blood sugar fasting (80-90 mg100ml)3 GTT or Glucose Tolerance TestWhen a normal fasting person is given 1g of glucose kg

body weight his plasma glucose levels rise to 120-140 but fall back to normal within 2 hours

In a prediabetic or diabetic not only is the fasting plasma glucose on the higher side but also the post meal plasma glucose rises to as high as 140-200 amp fails to come back to normal within 2 hours of giving conc glucose solution Even after 4-6 hours it rarely comes back to the normal range NORMAL MEAN BLOOD GLUCOSE IS APP 110

Glucose Tolerance Test

POINT TO REMEMBER

WHY IS ORAL GLUCOSE A MORE POWERFUL STIMULANT THAN

INJECTABLE GLUCOSE FOR INSULIN SECRETION

DIAGNOSIS OF DIABETES

4 Presence of glucose in urine (glucosuria)5 Acetone breath6 Lab test for assessing control of diabetes

HbA1c is a minor component of Hb A amp is normally present in small amounts ie up to 6 of normal Hb In the presence of long standing hyperglycemia its concentration rises When plasma glucose is episodically elevated over time small amounts of Hb A are non-enzymatically glycated to form HbA1c

Careful control of diabetes with insulin reduces the amount formed and thus HbA1c levels give an index of diabetic control for past 4-6 weeks

TREATMENT for Type I DIABETES

WHY CANNOT INSULIN BE GIVEN BY MOUTHWHY IS ONLY CHO RESTRICTION NOT VERY EFFECTIVE

Administer enough insulin so that metabolism of fat proteins amp CHO proceed as normally as possible

Insulin is available in various forms1 Insulin preparations are available with rapid (regular) intermediate amp long

durations of action - regular duration of action is 3-8 hours- Intermediate (NPH) not used during- Long duration of action is 10-48 hours

Individualized insulin schedules which consist of one injection of longer acting insulin followed by regular insulin when the glucose level is expected to rise ie at meals

Insulin is administered subcutaneously (sc) except in the case of emergencies when it is given intravenously (iv)

The less soluble an insulin preparation is the longer it acts

INSULIN SYRINGES

Insulin

Human insulin is absorbed more quickly from its site of action than are beef or pork insulins Thus duration of action of human Insulin is shorter amp doses must be adjusted

Hypoglycemia is the most serious amp common side effect of Insulin therapy BC long term diabetics do not produce counteracting hormones of Glucagon EN cortisol etc that normally provide defense against Hypoglycemia

TREATMENT for Type II DIABETES

bull Dietbull Exercise is useful in managing both types of Diabetes

because working muscles are not Insulin dependent Exercising muscles take up some of the excess blood glucose reducing the overall need for insulin

bull Weight lossbull Oral Hypoglycemic Drugs

Oral Hypoglycemic Drugs

There are many types of oral Hypoglycemic drugs some of which are bullSulfonylureas act by stimulating the β- cells to secrete more insulin than they do on their own Eg GlucotrolbullMetformin acts by suppressing liver output of glucose Eg GlucophagebullAlpha-glycosidase Inhibitors act by slowing CHO digestion and absorption from the digestive tract into the blood thus reducing the glucose surge seen after a meal Eg Precose bullByetta (Glucagon-like peptide 1 mimic) mimics the incretin GLP-1 It suppresses glucagon secretion and slows gastric emptying By promoting satiety it decreases food intake and in the long term leads to weight loss Because none of the drugs deliver new insulin to the body they cannot replace insulin therapy for people with Type I Diabetes and later in Type II Diabetics as well

SULFONYLUREAS

NIDDM patients above the age of 40 years amp having ho diabetes of less than 5 years are given Oral Hypoglycemics

Mechanism of Action1 Stimulate release of Insulin from beta cells of

pancreas2 Reduction of serum Glucagon3 Increased binding of Insulin to target tissues amp

receptors Eg Tolbutamide

Glyburide Glipizide

WHO NEEDS INSULIN

bull 1048708 Type 1bull 1048708 Type 2 uncontrolled wmedsbull 1048708 DKAbull 1048708 Hyperosmolar hyperglycemic state (HHS)bull 1048708 Surgerybull 1048708 IllnessInfectionbull 1048708 Stressbull 1048708 Those receiving parental enteral nutritionbull 1048708 Pancreatitis diseases that darr beta cell function

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

COMPLICATIONS

When Diabetes continues for a long time period (15-20 years) chronic complications occur 1Neuropathies2Peripheral vascular disease3Gangrene 4Atherosclerosis5Ischemic heart disease6Renal disease7Early cataract8Retinopathy9Skin infections10Neuropathies affecting the ANS

Diabetic foot showing ulcer

Gangrene that must be treated with an amputation

KETOSIS AND COMAbull In severe form of Insulin deficiency plasma levels of FFA is more

than doubled darr

bull In the liver and other tissues the fatty acids are catabolized to acetyl Co-A

darrbull Some of the acetyl-CoA enters into the citric acid cycle

darrbull When the supply exceeds the capacity of the citric acid cycle the

excess are converted into acetoacetate and β-hydroxybutyrate darr

These are ketone bodies that lead to progressive metabolic acidosisdarr

Acidosis can depress the brain and if severe enough can lead to coma and death

DIABETES MELLTIUS

DIABETES MELLITUS

Def Diabetes mellitus is a syndrome of impaired

carbohydrate protein amp fat metabolism caused by either lack of insulin secretion or decreased

sensitivity of the tissues to insulin The word ldquoDiabetes Mellitusrdquo literally means

ldquoexcessive secretion of sweet urinerdquo

bull Third leading cause of deathbull Leading cause of blindness bull Diabetes is a very prevalent disease has a huge

economic toll forces individuals to change their lifestyle thus affecting their quality of life amp predisposes the affected to a variety of troublesome amp even life threatening conditions

TYPE I Juvenile Onset Insulin Dependent

It is the more severe from of diabetes and more prevalent in children

DEFINITION

It is a catabolic disorder in which the circulating insulin is virtually absent plasma glucose is elevated amp the pancreatic beta

cells fail to produce any insulin in response to all insulinogenic stimuli

Cause Lack of insulin secretion from the beta cells of the islets of langerhans

bull It is an autoimmune disorder in which there is selective destruction of the pancreatic beta cells by T lymphocytes

bull Mostly it seems to have an immunological basis amp circulating islet cell antibodies amp anti-insulin antibodies may be demonstrated

bull Usually there is a genetic predisposition to this type of diabetes which may be triggered off by

- Viral infections eg rota virus coxsackie virus- Environmental triggers

TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes

It is further classified intobull It is the most common type of diabetes accounting for

about 90 of all cases of diabetes mellitusbull The age of onset is usually after 30 often bw 50 amp 60

years of agebull It develops gradually amp is the less severe form of

diabetes

1 Non-obese type II2 Obese type II

bull Cause Decreased sensitivity of target tissues to the metabolic effects of insulin This reduced sensitivity to insulin is often called INSULIN RESISTANCE

TYPE II DIABETES

Factors that can lead to Insulin resistance include1 Anti-insulin antibodies2 Autoantibodies to the insulin receptor 3 Mutation of insulin receptor4 Down-regulation of insulin receptors by sustained

hyperinsulinism5 Primary hyperinsulinism (Beta cell adenoma)6 Secondary hyperinsulinism (Cushingrsquos syndrome

acromegaly pregnancy or diabetes mellitus)7 Obesityoverweight especially excess fat deposits

around the abdomen8 Insulin resistance in peripheral tissues such as skeletal

muscle brain and liver

PATHOPHYSIOLOGY

bull Diabetes type I is far more rapid in onset occurring over a few days as compared to type II which has a more gradual onset

bull Type I also shows far more complications as compared to Type II which rarely shows complications

bull Type I requires Insulin while Type II can usually be controlled by simple changes in lifestyle as diet exercise amp weight control

bull Type I insulin is more prone to Ketoacidosis while Type II is not

DIAGNOSIS OF DIABETES

1 Blood sugar random ( 80-120 mg100ml)2 Blood sugar fasting (80-90 mg100ml)3 GTT or Glucose Tolerance TestWhen a normal fasting person is given 1g of glucose kg

body weight his plasma glucose levels rise to 120-140 but fall back to normal within 2 hours

In a prediabetic or diabetic not only is the fasting plasma glucose on the higher side but also the post meal plasma glucose rises to as high as 140-200 amp fails to come back to normal within 2 hours of giving conc glucose solution Even after 4-6 hours it rarely comes back to the normal range NORMAL MEAN BLOOD GLUCOSE IS APP 110

Glucose Tolerance Test

POINT TO REMEMBER

WHY IS ORAL GLUCOSE A MORE POWERFUL STIMULANT THAN

INJECTABLE GLUCOSE FOR INSULIN SECRETION

DIAGNOSIS OF DIABETES

4 Presence of glucose in urine (glucosuria)5 Acetone breath6 Lab test for assessing control of diabetes

HbA1c is a minor component of Hb A amp is normally present in small amounts ie up to 6 of normal Hb In the presence of long standing hyperglycemia its concentration rises When plasma glucose is episodically elevated over time small amounts of Hb A are non-enzymatically glycated to form HbA1c

Careful control of diabetes with insulin reduces the amount formed and thus HbA1c levels give an index of diabetic control for past 4-6 weeks

TREATMENT for Type I DIABETES

WHY CANNOT INSULIN BE GIVEN BY MOUTHWHY IS ONLY CHO RESTRICTION NOT VERY EFFECTIVE

Administer enough insulin so that metabolism of fat proteins amp CHO proceed as normally as possible

Insulin is available in various forms1 Insulin preparations are available with rapid (regular) intermediate amp long

durations of action - regular duration of action is 3-8 hours- Intermediate (NPH) not used during- Long duration of action is 10-48 hours

Individualized insulin schedules which consist of one injection of longer acting insulin followed by regular insulin when the glucose level is expected to rise ie at meals

Insulin is administered subcutaneously (sc) except in the case of emergencies when it is given intravenously (iv)

The less soluble an insulin preparation is the longer it acts

INSULIN SYRINGES

Insulin

Human insulin is absorbed more quickly from its site of action than are beef or pork insulins Thus duration of action of human Insulin is shorter amp doses must be adjusted

Hypoglycemia is the most serious amp common side effect of Insulin therapy BC long term diabetics do not produce counteracting hormones of Glucagon EN cortisol etc that normally provide defense against Hypoglycemia

TREATMENT for Type II DIABETES

bull Dietbull Exercise is useful in managing both types of Diabetes

because working muscles are not Insulin dependent Exercising muscles take up some of the excess blood glucose reducing the overall need for insulin

bull Weight lossbull Oral Hypoglycemic Drugs

Oral Hypoglycemic Drugs

There are many types of oral Hypoglycemic drugs some of which are bullSulfonylureas act by stimulating the β- cells to secrete more insulin than they do on their own Eg GlucotrolbullMetformin acts by suppressing liver output of glucose Eg GlucophagebullAlpha-glycosidase Inhibitors act by slowing CHO digestion and absorption from the digestive tract into the blood thus reducing the glucose surge seen after a meal Eg Precose bullByetta (Glucagon-like peptide 1 mimic) mimics the incretin GLP-1 It suppresses glucagon secretion and slows gastric emptying By promoting satiety it decreases food intake and in the long term leads to weight loss Because none of the drugs deliver new insulin to the body they cannot replace insulin therapy for people with Type I Diabetes and later in Type II Diabetics as well

SULFONYLUREAS

NIDDM patients above the age of 40 years amp having ho diabetes of less than 5 years are given Oral Hypoglycemics

Mechanism of Action1 Stimulate release of Insulin from beta cells of

pancreas2 Reduction of serum Glucagon3 Increased binding of Insulin to target tissues amp

receptors Eg Tolbutamide

Glyburide Glipizide

WHO NEEDS INSULIN

bull 1048708 Type 1bull 1048708 Type 2 uncontrolled wmedsbull 1048708 DKAbull 1048708 Hyperosmolar hyperglycemic state (HHS)bull 1048708 Surgerybull 1048708 IllnessInfectionbull 1048708 Stressbull 1048708 Those receiving parental enteral nutritionbull 1048708 Pancreatitis diseases that darr beta cell function

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

Diabetic foot showing ulcer

Gangrene that must be treated with an amputation

KETOSIS AND COMAbull In severe form of Insulin deficiency plasma levels of FFA is more

than doubled darr

bull In the liver and other tissues the fatty acids are catabolized to acetyl Co-A

darrbull Some of the acetyl-CoA enters into the citric acid cycle

darrbull When the supply exceeds the capacity of the citric acid cycle the

excess are converted into acetoacetate and β-hydroxybutyrate darr

These are ketone bodies that lead to progressive metabolic acidosisdarr

Acidosis can depress the brain and if severe enough can lead to coma and death

DIABETES MELLTIUS

DIABETES MELLITUS

Def Diabetes mellitus is a syndrome of impaired

carbohydrate protein amp fat metabolism caused by either lack of insulin secretion or decreased

sensitivity of the tissues to insulin The word ldquoDiabetes Mellitusrdquo literally means

ldquoexcessive secretion of sweet urinerdquo

bull Third leading cause of deathbull Leading cause of blindness bull Diabetes is a very prevalent disease has a huge

economic toll forces individuals to change their lifestyle thus affecting their quality of life amp predisposes the affected to a variety of troublesome amp even life threatening conditions

TYPE I Juvenile Onset Insulin Dependent

It is the more severe from of diabetes and more prevalent in children

DEFINITION

It is a catabolic disorder in which the circulating insulin is virtually absent plasma glucose is elevated amp the pancreatic beta

cells fail to produce any insulin in response to all insulinogenic stimuli

Cause Lack of insulin secretion from the beta cells of the islets of langerhans

bull It is an autoimmune disorder in which there is selective destruction of the pancreatic beta cells by T lymphocytes

bull Mostly it seems to have an immunological basis amp circulating islet cell antibodies amp anti-insulin antibodies may be demonstrated

bull Usually there is a genetic predisposition to this type of diabetes which may be triggered off by

- Viral infections eg rota virus coxsackie virus- Environmental triggers

TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes

It is further classified intobull It is the most common type of diabetes accounting for

about 90 of all cases of diabetes mellitusbull The age of onset is usually after 30 often bw 50 amp 60

years of agebull It develops gradually amp is the less severe form of

diabetes

1 Non-obese type II2 Obese type II

bull Cause Decreased sensitivity of target tissues to the metabolic effects of insulin This reduced sensitivity to insulin is often called INSULIN RESISTANCE

TYPE II DIABETES

Factors that can lead to Insulin resistance include1 Anti-insulin antibodies2 Autoantibodies to the insulin receptor 3 Mutation of insulin receptor4 Down-regulation of insulin receptors by sustained

hyperinsulinism5 Primary hyperinsulinism (Beta cell adenoma)6 Secondary hyperinsulinism (Cushingrsquos syndrome

acromegaly pregnancy or diabetes mellitus)7 Obesityoverweight especially excess fat deposits

around the abdomen8 Insulin resistance in peripheral tissues such as skeletal

muscle brain and liver

PATHOPHYSIOLOGY

bull Diabetes type I is far more rapid in onset occurring over a few days as compared to type II which has a more gradual onset

bull Type I also shows far more complications as compared to Type II which rarely shows complications

bull Type I requires Insulin while Type II can usually be controlled by simple changes in lifestyle as diet exercise amp weight control

bull Type I insulin is more prone to Ketoacidosis while Type II is not

DIAGNOSIS OF DIABETES

1 Blood sugar random ( 80-120 mg100ml)2 Blood sugar fasting (80-90 mg100ml)3 GTT or Glucose Tolerance TestWhen a normal fasting person is given 1g of glucose kg

body weight his plasma glucose levels rise to 120-140 but fall back to normal within 2 hours

In a prediabetic or diabetic not only is the fasting plasma glucose on the higher side but also the post meal plasma glucose rises to as high as 140-200 amp fails to come back to normal within 2 hours of giving conc glucose solution Even after 4-6 hours it rarely comes back to the normal range NORMAL MEAN BLOOD GLUCOSE IS APP 110

Glucose Tolerance Test

POINT TO REMEMBER

WHY IS ORAL GLUCOSE A MORE POWERFUL STIMULANT THAN

INJECTABLE GLUCOSE FOR INSULIN SECRETION

DIAGNOSIS OF DIABETES

4 Presence of glucose in urine (glucosuria)5 Acetone breath6 Lab test for assessing control of diabetes

HbA1c is a minor component of Hb A amp is normally present in small amounts ie up to 6 of normal Hb In the presence of long standing hyperglycemia its concentration rises When plasma glucose is episodically elevated over time small amounts of Hb A are non-enzymatically glycated to form HbA1c

Careful control of diabetes with insulin reduces the amount formed and thus HbA1c levels give an index of diabetic control for past 4-6 weeks

TREATMENT for Type I DIABETES

WHY CANNOT INSULIN BE GIVEN BY MOUTHWHY IS ONLY CHO RESTRICTION NOT VERY EFFECTIVE

Administer enough insulin so that metabolism of fat proteins amp CHO proceed as normally as possible

Insulin is available in various forms1 Insulin preparations are available with rapid (regular) intermediate amp long

durations of action - regular duration of action is 3-8 hours- Intermediate (NPH) not used during- Long duration of action is 10-48 hours

Individualized insulin schedules which consist of one injection of longer acting insulin followed by regular insulin when the glucose level is expected to rise ie at meals

Insulin is administered subcutaneously (sc) except in the case of emergencies when it is given intravenously (iv)

The less soluble an insulin preparation is the longer it acts

INSULIN SYRINGES

Insulin

Human insulin is absorbed more quickly from its site of action than are beef or pork insulins Thus duration of action of human Insulin is shorter amp doses must be adjusted

Hypoglycemia is the most serious amp common side effect of Insulin therapy BC long term diabetics do not produce counteracting hormones of Glucagon EN cortisol etc that normally provide defense against Hypoglycemia

TREATMENT for Type II DIABETES

bull Dietbull Exercise is useful in managing both types of Diabetes

because working muscles are not Insulin dependent Exercising muscles take up some of the excess blood glucose reducing the overall need for insulin

bull Weight lossbull Oral Hypoglycemic Drugs

Oral Hypoglycemic Drugs

There are many types of oral Hypoglycemic drugs some of which are bullSulfonylureas act by stimulating the β- cells to secrete more insulin than they do on their own Eg GlucotrolbullMetformin acts by suppressing liver output of glucose Eg GlucophagebullAlpha-glycosidase Inhibitors act by slowing CHO digestion and absorption from the digestive tract into the blood thus reducing the glucose surge seen after a meal Eg Precose bullByetta (Glucagon-like peptide 1 mimic) mimics the incretin GLP-1 It suppresses glucagon secretion and slows gastric emptying By promoting satiety it decreases food intake and in the long term leads to weight loss Because none of the drugs deliver new insulin to the body they cannot replace insulin therapy for people with Type I Diabetes and later in Type II Diabetics as well

SULFONYLUREAS

NIDDM patients above the age of 40 years amp having ho diabetes of less than 5 years are given Oral Hypoglycemics

Mechanism of Action1 Stimulate release of Insulin from beta cells of

pancreas2 Reduction of serum Glucagon3 Increased binding of Insulin to target tissues amp

receptors Eg Tolbutamide

Glyburide Glipizide

WHO NEEDS INSULIN

bull 1048708 Type 1bull 1048708 Type 2 uncontrolled wmedsbull 1048708 DKAbull 1048708 Hyperosmolar hyperglycemic state (HHS)bull 1048708 Surgerybull 1048708 IllnessInfectionbull 1048708 Stressbull 1048708 Those receiving parental enteral nutritionbull 1048708 Pancreatitis diseases that darr beta cell function

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

Gangrene that must be treated with an amputation

KETOSIS AND COMAbull In severe form of Insulin deficiency plasma levels of FFA is more

than doubled darr

bull In the liver and other tissues the fatty acids are catabolized to acetyl Co-A

darrbull Some of the acetyl-CoA enters into the citric acid cycle

darrbull When the supply exceeds the capacity of the citric acid cycle the

excess are converted into acetoacetate and β-hydroxybutyrate darr

These are ketone bodies that lead to progressive metabolic acidosisdarr

Acidosis can depress the brain and if severe enough can lead to coma and death

DIABETES MELLTIUS

DIABETES MELLITUS

Def Diabetes mellitus is a syndrome of impaired

carbohydrate protein amp fat metabolism caused by either lack of insulin secretion or decreased

sensitivity of the tissues to insulin The word ldquoDiabetes Mellitusrdquo literally means

ldquoexcessive secretion of sweet urinerdquo

bull Third leading cause of deathbull Leading cause of blindness bull Diabetes is a very prevalent disease has a huge

economic toll forces individuals to change their lifestyle thus affecting their quality of life amp predisposes the affected to a variety of troublesome amp even life threatening conditions

TYPE I Juvenile Onset Insulin Dependent

It is the more severe from of diabetes and more prevalent in children

DEFINITION

It is a catabolic disorder in which the circulating insulin is virtually absent plasma glucose is elevated amp the pancreatic beta

cells fail to produce any insulin in response to all insulinogenic stimuli

Cause Lack of insulin secretion from the beta cells of the islets of langerhans

bull It is an autoimmune disorder in which there is selective destruction of the pancreatic beta cells by T lymphocytes

bull Mostly it seems to have an immunological basis amp circulating islet cell antibodies amp anti-insulin antibodies may be demonstrated

bull Usually there is a genetic predisposition to this type of diabetes which may be triggered off by

- Viral infections eg rota virus coxsackie virus- Environmental triggers

TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes

It is further classified intobull It is the most common type of diabetes accounting for

about 90 of all cases of diabetes mellitusbull The age of onset is usually after 30 often bw 50 amp 60

years of agebull It develops gradually amp is the less severe form of

diabetes

1 Non-obese type II2 Obese type II

bull Cause Decreased sensitivity of target tissues to the metabolic effects of insulin This reduced sensitivity to insulin is often called INSULIN RESISTANCE

TYPE II DIABETES

Factors that can lead to Insulin resistance include1 Anti-insulin antibodies2 Autoantibodies to the insulin receptor 3 Mutation of insulin receptor4 Down-regulation of insulin receptors by sustained

hyperinsulinism5 Primary hyperinsulinism (Beta cell adenoma)6 Secondary hyperinsulinism (Cushingrsquos syndrome

acromegaly pregnancy or diabetes mellitus)7 Obesityoverweight especially excess fat deposits

around the abdomen8 Insulin resistance in peripheral tissues such as skeletal

muscle brain and liver

PATHOPHYSIOLOGY

bull Diabetes type I is far more rapid in onset occurring over a few days as compared to type II which has a more gradual onset

bull Type I also shows far more complications as compared to Type II which rarely shows complications

bull Type I requires Insulin while Type II can usually be controlled by simple changes in lifestyle as diet exercise amp weight control

bull Type I insulin is more prone to Ketoacidosis while Type II is not

DIAGNOSIS OF DIABETES

1 Blood sugar random ( 80-120 mg100ml)2 Blood sugar fasting (80-90 mg100ml)3 GTT or Glucose Tolerance TestWhen a normal fasting person is given 1g of glucose kg

body weight his plasma glucose levels rise to 120-140 but fall back to normal within 2 hours

In a prediabetic or diabetic not only is the fasting plasma glucose on the higher side but also the post meal plasma glucose rises to as high as 140-200 amp fails to come back to normal within 2 hours of giving conc glucose solution Even after 4-6 hours it rarely comes back to the normal range NORMAL MEAN BLOOD GLUCOSE IS APP 110

Glucose Tolerance Test

POINT TO REMEMBER

WHY IS ORAL GLUCOSE A MORE POWERFUL STIMULANT THAN

INJECTABLE GLUCOSE FOR INSULIN SECRETION

DIAGNOSIS OF DIABETES

4 Presence of glucose in urine (glucosuria)5 Acetone breath6 Lab test for assessing control of diabetes

HbA1c is a minor component of Hb A amp is normally present in small amounts ie up to 6 of normal Hb In the presence of long standing hyperglycemia its concentration rises When plasma glucose is episodically elevated over time small amounts of Hb A are non-enzymatically glycated to form HbA1c

Careful control of diabetes with insulin reduces the amount formed and thus HbA1c levels give an index of diabetic control for past 4-6 weeks

TREATMENT for Type I DIABETES

WHY CANNOT INSULIN BE GIVEN BY MOUTHWHY IS ONLY CHO RESTRICTION NOT VERY EFFECTIVE

Administer enough insulin so that metabolism of fat proteins amp CHO proceed as normally as possible

Insulin is available in various forms1 Insulin preparations are available with rapid (regular) intermediate amp long

durations of action - regular duration of action is 3-8 hours- Intermediate (NPH) not used during- Long duration of action is 10-48 hours

Individualized insulin schedules which consist of one injection of longer acting insulin followed by regular insulin when the glucose level is expected to rise ie at meals

Insulin is administered subcutaneously (sc) except in the case of emergencies when it is given intravenously (iv)

The less soluble an insulin preparation is the longer it acts

INSULIN SYRINGES

Insulin

Human insulin is absorbed more quickly from its site of action than are beef or pork insulins Thus duration of action of human Insulin is shorter amp doses must be adjusted

Hypoglycemia is the most serious amp common side effect of Insulin therapy BC long term diabetics do not produce counteracting hormones of Glucagon EN cortisol etc that normally provide defense against Hypoglycemia

TREATMENT for Type II DIABETES

bull Dietbull Exercise is useful in managing both types of Diabetes

because working muscles are not Insulin dependent Exercising muscles take up some of the excess blood glucose reducing the overall need for insulin

bull Weight lossbull Oral Hypoglycemic Drugs

Oral Hypoglycemic Drugs

There are many types of oral Hypoglycemic drugs some of which are bullSulfonylureas act by stimulating the β- cells to secrete more insulin than they do on their own Eg GlucotrolbullMetformin acts by suppressing liver output of glucose Eg GlucophagebullAlpha-glycosidase Inhibitors act by slowing CHO digestion and absorption from the digestive tract into the blood thus reducing the glucose surge seen after a meal Eg Precose bullByetta (Glucagon-like peptide 1 mimic) mimics the incretin GLP-1 It suppresses glucagon secretion and slows gastric emptying By promoting satiety it decreases food intake and in the long term leads to weight loss Because none of the drugs deliver new insulin to the body they cannot replace insulin therapy for people with Type I Diabetes and later in Type II Diabetics as well

SULFONYLUREAS

NIDDM patients above the age of 40 years amp having ho diabetes of less than 5 years are given Oral Hypoglycemics

Mechanism of Action1 Stimulate release of Insulin from beta cells of

pancreas2 Reduction of serum Glucagon3 Increased binding of Insulin to target tissues amp

receptors Eg Tolbutamide

Glyburide Glipizide

WHO NEEDS INSULIN

bull 1048708 Type 1bull 1048708 Type 2 uncontrolled wmedsbull 1048708 DKAbull 1048708 Hyperosmolar hyperglycemic state (HHS)bull 1048708 Surgerybull 1048708 IllnessInfectionbull 1048708 Stressbull 1048708 Those receiving parental enteral nutritionbull 1048708 Pancreatitis diseases that darr beta cell function

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

KETOSIS AND COMAbull In severe form of Insulin deficiency plasma levels of FFA is more

than doubled darr

bull In the liver and other tissues the fatty acids are catabolized to acetyl Co-A

darrbull Some of the acetyl-CoA enters into the citric acid cycle

darrbull When the supply exceeds the capacity of the citric acid cycle the

excess are converted into acetoacetate and β-hydroxybutyrate darr

These are ketone bodies that lead to progressive metabolic acidosisdarr

Acidosis can depress the brain and if severe enough can lead to coma and death

DIABETES MELLTIUS

DIABETES MELLITUS

Def Diabetes mellitus is a syndrome of impaired

carbohydrate protein amp fat metabolism caused by either lack of insulin secretion or decreased

sensitivity of the tissues to insulin The word ldquoDiabetes Mellitusrdquo literally means

ldquoexcessive secretion of sweet urinerdquo

bull Third leading cause of deathbull Leading cause of blindness bull Diabetes is a very prevalent disease has a huge

economic toll forces individuals to change their lifestyle thus affecting their quality of life amp predisposes the affected to a variety of troublesome amp even life threatening conditions

TYPE I Juvenile Onset Insulin Dependent

It is the more severe from of diabetes and more prevalent in children

DEFINITION

It is a catabolic disorder in which the circulating insulin is virtually absent plasma glucose is elevated amp the pancreatic beta

cells fail to produce any insulin in response to all insulinogenic stimuli

Cause Lack of insulin secretion from the beta cells of the islets of langerhans

bull It is an autoimmune disorder in which there is selective destruction of the pancreatic beta cells by T lymphocytes

bull Mostly it seems to have an immunological basis amp circulating islet cell antibodies amp anti-insulin antibodies may be demonstrated

bull Usually there is a genetic predisposition to this type of diabetes which may be triggered off by

- Viral infections eg rota virus coxsackie virus- Environmental triggers

TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes

It is further classified intobull It is the most common type of diabetes accounting for

about 90 of all cases of diabetes mellitusbull The age of onset is usually after 30 often bw 50 amp 60

years of agebull It develops gradually amp is the less severe form of

diabetes

1 Non-obese type II2 Obese type II

bull Cause Decreased sensitivity of target tissues to the metabolic effects of insulin This reduced sensitivity to insulin is often called INSULIN RESISTANCE

TYPE II DIABETES

Factors that can lead to Insulin resistance include1 Anti-insulin antibodies2 Autoantibodies to the insulin receptor 3 Mutation of insulin receptor4 Down-regulation of insulin receptors by sustained

hyperinsulinism5 Primary hyperinsulinism (Beta cell adenoma)6 Secondary hyperinsulinism (Cushingrsquos syndrome

acromegaly pregnancy or diabetes mellitus)7 Obesityoverweight especially excess fat deposits

around the abdomen8 Insulin resistance in peripheral tissues such as skeletal

muscle brain and liver

PATHOPHYSIOLOGY

bull Diabetes type I is far more rapid in onset occurring over a few days as compared to type II which has a more gradual onset

bull Type I also shows far more complications as compared to Type II which rarely shows complications

bull Type I requires Insulin while Type II can usually be controlled by simple changes in lifestyle as diet exercise amp weight control

bull Type I insulin is more prone to Ketoacidosis while Type II is not

DIAGNOSIS OF DIABETES

1 Blood sugar random ( 80-120 mg100ml)2 Blood sugar fasting (80-90 mg100ml)3 GTT or Glucose Tolerance TestWhen a normal fasting person is given 1g of glucose kg

body weight his plasma glucose levels rise to 120-140 but fall back to normal within 2 hours

In a prediabetic or diabetic not only is the fasting plasma glucose on the higher side but also the post meal plasma glucose rises to as high as 140-200 amp fails to come back to normal within 2 hours of giving conc glucose solution Even after 4-6 hours it rarely comes back to the normal range NORMAL MEAN BLOOD GLUCOSE IS APP 110

Glucose Tolerance Test

POINT TO REMEMBER

WHY IS ORAL GLUCOSE A MORE POWERFUL STIMULANT THAN

INJECTABLE GLUCOSE FOR INSULIN SECRETION

DIAGNOSIS OF DIABETES

4 Presence of glucose in urine (glucosuria)5 Acetone breath6 Lab test for assessing control of diabetes

HbA1c is a minor component of Hb A amp is normally present in small amounts ie up to 6 of normal Hb In the presence of long standing hyperglycemia its concentration rises When plasma glucose is episodically elevated over time small amounts of Hb A are non-enzymatically glycated to form HbA1c

Careful control of diabetes with insulin reduces the amount formed and thus HbA1c levels give an index of diabetic control for past 4-6 weeks

TREATMENT for Type I DIABETES

WHY CANNOT INSULIN BE GIVEN BY MOUTHWHY IS ONLY CHO RESTRICTION NOT VERY EFFECTIVE

Administer enough insulin so that metabolism of fat proteins amp CHO proceed as normally as possible

Insulin is available in various forms1 Insulin preparations are available with rapid (regular) intermediate amp long

durations of action - regular duration of action is 3-8 hours- Intermediate (NPH) not used during- Long duration of action is 10-48 hours

Individualized insulin schedules which consist of one injection of longer acting insulin followed by regular insulin when the glucose level is expected to rise ie at meals

Insulin is administered subcutaneously (sc) except in the case of emergencies when it is given intravenously (iv)

The less soluble an insulin preparation is the longer it acts

INSULIN SYRINGES

Insulin

Human insulin is absorbed more quickly from its site of action than are beef or pork insulins Thus duration of action of human Insulin is shorter amp doses must be adjusted

Hypoglycemia is the most serious amp common side effect of Insulin therapy BC long term diabetics do not produce counteracting hormones of Glucagon EN cortisol etc that normally provide defense against Hypoglycemia

TREATMENT for Type II DIABETES

bull Dietbull Exercise is useful in managing both types of Diabetes

because working muscles are not Insulin dependent Exercising muscles take up some of the excess blood glucose reducing the overall need for insulin

bull Weight lossbull Oral Hypoglycemic Drugs

Oral Hypoglycemic Drugs

There are many types of oral Hypoglycemic drugs some of which are bullSulfonylureas act by stimulating the β- cells to secrete more insulin than they do on their own Eg GlucotrolbullMetformin acts by suppressing liver output of glucose Eg GlucophagebullAlpha-glycosidase Inhibitors act by slowing CHO digestion and absorption from the digestive tract into the blood thus reducing the glucose surge seen after a meal Eg Precose bullByetta (Glucagon-like peptide 1 mimic) mimics the incretin GLP-1 It suppresses glucagon secretion and slows gastric emptying By promoting satiety it decreases food intake and in the long term leads to weight loss Because none of the drugs deliver new insulin to the body they cannot replace insulin therapy for people with Type I Diabetes and later in Type II Diabetics as well

SULFONYLUREAS

NIDDM patients above the age of 40 years amp having ho diabetes of less than 5 years are given Oral Hypoglycemics

Mechanism of Action1 Stimulate release of Insulin from beta cells of

pancreas2 Reduction of serum Glucagon3 Increased binding of Insulin to target tissues amp

receptors Eg Tolbutamide

Glyburide Glipizide

WHO NEEDS INSULIN

bull 1048708 Type 1bull 1048708 Type 2 uncontrolled wmedsbull 1048708 DKAbull 1048708 Hyperosmolar hyperglycemic state (HHS)bull 1048708 Surgerybull 1048708 IllnessInfectionbull 1048708 Stressbull 1048708 Those receiving parental enteral nutritionbull 1048708 Pancreatitis diseases that darr beta cell function

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

DIABETES MELLTIUS

DIABETES MELLITUS

Def Diabetes mellitus is a syndrome of impaired

carbohydrate protein amp fat metabolism caused by either lack of insulin secretion or decreased

sensitivity of the tissues to insulin The word ldquoDiabetes Mellitusrdquo literally means

ldquoexcessive secretion of sweet urinerdquo

bull Third leading cause of deathbull Leading cause of blindness bull Diabetes is a very prevalent disease has a huge

economic toll forces individuals to change their lifestyle thus affecting their quality of life amp predisposes the affected to a variety of troublesome amp even life threatening conditions

TYPE I Juvenile Onset Insulin Dependent

It is the more severe from of diabetes and more prevalent in children

DEFINITION

It is a catabolic disorder in which the circulating insulin is virtually absent plasma glucose is elevated amp the pancreatic beta

cells fail to produce any insulin in response to all insulinogenic stimuli

Cause Lack of insulin secretion from the beta cells of the islets of langerhans

bull It is an autoimmune disorder in which there is selective destruction of the pancreatic beta cells by T lymphocytes

bull Mostly it seems to have an immunological basis amp circulating islet cell antibodies amp anti-insulin antibodies may be demonstrated

bull Usually there is a genetic predisposition to this type of diabetes which may be triggered off by

- Viral infections eg rota virus coxsackie virus- Environmental triggers

TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes

It is further classified intobull It is the most common type of diabetes accounting for

about 90 of all cases of diabetes mellitusbull The age of onset is usually after 30 often bw 50 amp 60

years of agebull It develops gradually amp is the less severe form of

diabetes

1 Non-obese type II2 Obese type II

bull Cause Decreased sensitivity of target tissues to the metabolic effects of insulin This reduced sensitivity to insulin is often called INSULIN RESISTANCE

TYPE II DIABETES

Factors that can lead to Insulin resistance include1 Anti-insulin antibodies2 Autoantibodies to the insulin receptor 3 Mutation of insulin receptor4 Down-regulation of insulin receptors by sustained

hyperinsulinism5 Primary hyperinsulinism (Beta cell adenoma)6 Secondary hyperinsulinism (Cushingrsquos syndrome

acromegaly pregnancy or diabetes mellitus)7 Obesityoverweight especially excess fat deposits

around the abdomen8 Insulin resistance in peripheral tissues such as skeletal

muscle brain and liver

PATHOPHYSIOLOGY

bull Diabetes type I is far more rapid in onset occurring over a few days as compared to type II which has a more gradual onset

bull Type I also shows far more complications as compared to Type II which rarely shows complications

bull Type I requires Insulin while Type II can usually be controlled by simple changes in lifestyle as diet exercise amp weight control

bull Type I insulin is more prone to Ketoacidosis while Type II is not

DIAGNOSIS OF DIABETES

1 Blood sugar random ( 80-120 mg100ml)2 Blood sugar fasting (80-90 mg100ml)3 GTT or Glucose Tolerance TestWhen a normal fasting person is given 1g of glucose kg

body weight his plasma glucose levels rise to 120-140 but fall back to normal within 2 hours

In a prediabetic or diabetic not only is the fasting plasma glucose on the higher side but also the post meal plasma glucose rises to as high as 140-200 amp fails to come back to normal within 2 hours of giving conc glucose solution Even after 4-6 hours it rarely comes back to the normal range NORMAL MEAN BLOOD GLUCOSE IS APP 110

Glucose Tolerance Test

POINT TO REMEMBER

WHY IS ORAL GLUCOSE A MORE POWERFUL STIMULANT THAN

INJECTABLE GLUCOSE FOR INSULIN SECRETION

DIAGNOSIS OF DIABETES

4 Presence of glucose in urine (glucosuria)5 Acetone breath6 Lab test for assessing control of diabetes

HbA1c is a minor component of Hb A amp is normally present in small amounts ie up to 6 of normal Hb In the presence of long standing hyperglycemia its concentration rises When plasma glucose is episodically elevated over time small amounts of Hb A are non-enzymatically glycated to form HbA1c

Careful control of diabetes with insulin reduces the amount formed and thus HbA1c levels give an index of diabetic control for past 4-6 weeks

TREATMENT for Type I DIABETES

WHY CANNOT INSULIN BE GIVEN BY MOUTHWHY IS ONLY CHO RESTRICTION NOT VERY EFFECTIVE

Administer enough insulin so that metabolism of fat proteins amp CHO proceed as normally as possible

Insulin is available in various forms1 Insulin preparations are available with rapid (regular) intermediate amp long

durations of action - regular duration of action is 3-8 hours- Intermediate (NPH) not used during- Long duration of action is 10-48 hours

Individualized insulin schedules which consist of one injection of longer acting insulin followed by regular insulin when the glucose level is expected to rise ie at meals

Insulin is administered subcutaneously (sc) except in the case of emergencies when it is given intravenously (iv)

The less soluble an insulin preparation is the longer it acts

INSULIN SYRINGES

Insulin

Human insulin is absorbed more quickly from its site of action than are beef or pork insulins Thus duration of action of human Insulin is shorter amp doses must be adjusted

Hypoglycemia is the most serious amp common side effect of Insulin therapy BC long term diabetics do not produce counteracting hormones of Glucagon EN cortisol etc that normally provide defense against Hypoglycemia

TREATMENT for Type II DIABETES

bull Dietbull Exercise is useful in managing both types of Diabetes

because working muscles are not Insulin dependent Exercising muscles take up some of the excess blood glucose reducing the overall need for insulin

bull Weight lossbull Oral Hypoglycemic Drugs

Oral Hypoglycemic Drugs

There are many types of oral Hypoglycemic drugs some of which are bullSulfonylureas act by stimulating the β- cells to secrete more insulin than they do on their own Eg GlucotrolbullMetformin acts by suppressing liver output of glucose Eg GlucophagebullAlpha-glycosidase Inhibitors act by slowing CHO digestion and absorption from the digestive tract into the blood thus reducing the glucose surge seen after a meal Eg Precose bullByetta (Glucagon-like peptide 1 mimic) mimics the incretin GLP-1 It suppresses glucagon secretion and slows gastric emptying By promoting satiety it decreases food intake and in the long term leads to weight loss Because none of the drugs deliver new insulin to the body they cannot replace insulin therapy for people with Type I Diabetes and later in Type II Diabetics as well

SULFONYLUREAS

NIDDM patients above the age of 40 years amp having ho diabetes of less than 5 years are given Oral Hypoglycemics

Mechanism of Action1 Stimulate release of Insulin from beta cells of

pancreas2 Reduction of serum Glucagon3 Increased binding of Insulin to target tissues amp

receptors Eg Tolbutamide

Glyburide Glipizide

WHO NEEDS INSULIN

bull 1048708 Type 1bull 1048708 Type 2 uncontrolled wmedsbull 1048708 DKAbull 1048708 Hyperosmolar hyperglycemic state (HHS)bull 1048708 Surgerybull 1048708 IllnessInfectionbull 1048708 Stressbull 1048708 Those receiving parental enteral nutritionbull 1048708 Pancreatitis diseases that darr beta cell function

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

DIABETES MELLITUS

Def Diabetes mellitus is a syndrome of impaired

carbohydrate protein amp fat metabolism caused by either lack of insulin secretion or decreased

sensitivity of the tissues to insulin The word ldquoDiabetes Mellitusrdquo literally means

ldquoexcessive secretion of sweet urinerdquo

bull Third leading cause of deathbull Leading cause of blindness bull Diabetes is a very prevalent disease has a huge

economic toll forces individuals to change their lifestyle thus affecting their quality of life amp predisposes the affected to a variety of troublesome amp even life threatening conditions

TYPE I Juvenile Onset Insulin Dependent

It is the more severe from of diabetes and more prevalent in children

DEFINITION

It is a catabolic disorder in which the circulating insulin is virtually absent plasma glucose is elevated amp the pancreatic beta

cells fail to produce any insulin in response to all insulinogenic stimuli

Cause Lack of insulin secretion from the beta cells of the islets of langerhans

bull It is an autoimmune disorder in which there is selective destruction of the pancreatic beta cells by T lymphocytes

bull Mostly it seems to have an immunological basis amp circulating islet cell antibodies amp anti-insulin antibodies may be demonstrated

bull Usually there is a genetic predisposition to this type of diabetes which may be triggered off by

- Viral infections eg rota virus coxsackie virus- Environmental triggers

TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes

It is further classified intobull It is the most common type of diabetes accounting for

about 90 of all cases of diabetes mellitusbull The age of onset is usually after 30 often bw 50 amp 60

years of agebull It develops gradually amp is the less severe form of

diabetes

1 Non-obese type II2 Obese type II

bull Cause Decreased sensitivity of target tissues to the metabolic effects of insulin This reduced sensitivity to insulin is often called INSULIN RESISTANCE

TYPE II DIABETES

Factors that can lead to Insulin resistance include1 Anti-insulin antibodies2 Autoantibodies to the insulin receptor 3 Mutation of insulin receptor4 Down-regulation of insulin receptors by sustained

hyperinsulinism5 Primary hyperinsulinism (Beta cell adenoma)6 Secondary hyperinsulinism (Cushingrsquos syndrome

acromegaly pregnancy or diabetes mellitus)7 Obesityoverweight especially excess fat deposits

around the abdomen8 Insulin resistance in peripheral tissues such as skeletal

muscle brain and liver

PATHOPHYSIOLOGY

bull Diabetes type I is far more rapid in onset occurring over a few days as compared to type II which has a more gradual onset

bull Type I also shows far more complications as compared to Type II which rarely shows complications

bull Type I requires Insulin while Type II can usually be controlled by simple changes in lifestyle as diet exercise amp weight control

bull Type I insulin is more prone to Ketoacidosis while Type II is not

DIAGNOSIS OF DIABETES

1 Blood sugar random ( 80-120 mg100ml)2 Blood sugar fasting (80-90 mg100ml)3 GTT or Glucose Tolerance TestWhen a normal fasting person is given 1g of glucose kg

body weight his plasma glucose levels rise to 120-140 but fall back to normal within 2 hours

In a prediabetic or diabetic not only is the fasting plasma glucose on the higher side but also the post meal plasma glucose rises to as high as 140-200 amp fails to come back to normal within 2 hours of giving conc glucose solution Even after 4-6 hours it rarely comes back to the normal range NORMAL MEAN BLOOD GLUCOSE IS APP 110

Glucose Tolerance Test

POINT TO REMEMBER

WHY IS ORAL GLUCOSE A MORE POWERFUL STIMULANT THAN

INJECTABLE GLUCOSE FOR INSULIN SECRETION

DIAGNOSIS OF DIABETES

4 Presence of glucose in urine (glucosuria)5 Acetone breath6 Lab test for assessing control of diabetes

HbA1c is a minor component of Hb A amp is normally present in small amounts ie up to 6 of normal Hb In the presence of long standing hyperglycemia its concentration rises When plasma glucose is episodically elevated over time small amounts of Hb A are non-enzymatically glycated to form HbA1c

Careful control of diabetes with insulin reduces the amount formed and thus HbA1c levels give an index of diabetic control for past 4-6 weeks

TREATMENT for Type I DIABETES

WHY CANNOT INSULIN BE GIVEN BY MOUTHWHY IS ONLY CHO RESTRICTION NOT VERY EFFECTIVE

Administer enough insulin so that metabolism of fat proteins amp CHO proceed as normally as possible

Insulin is available in various forms1 Insulin preparations are available with rapid (regular) intermediate amp long

durations of action - regular duration of action is 3-8 hours- Intermediate (NPH) not used during- Long duration of action is 10-48 hours

Individualized insulin schedules which consist of one injection of longer acting insulin followed by regular insulin when the glucose level is expected to rise ie at meals

Insulin is administered subcutaneously (sc) except in the case of emergencies when it is given intravenously (iv)

The less soluble an insulin preparation is the longer it acts

INSULIN SYRINGES

Insulin

Human insulin is absorbed more quickly from its site of action than are beef or pork insulins Thus duration of action of human Insulin is shorter amp doses must be adjusted

Hypoglycemia is the most serious amp common side effect of Insulin therapy BC long term diabetics do not produce counteracting hormones of Glucagon EN cortisol etc that normally provide defense against Hypoglycemia

TREATMENT for Type II DIABETES

bull Dietbull Exercise is useful in managing both types of Diabetes

because working muscles are not Insulin dependent Exercising muscles take up some of the excess blood glucose reducing the overall need for insulin

bull Weight lossbull Oral Hypoglycemic Drugs

Oral Hypoglycemic Drugs

There are many types of oral Hypoglycemic drugs some of which are bullSulfonylureas act by stimulating the β- cells to secrete more insulin than they do on their own Eg GlucotrolbullMetformin acts by suppressing liver output of glucose Eg GlucophagebullAlpha-glycosidase Inhibitors act by slowing CHO digestion and absorption from the digestive tract into the blood thus reducing the glucose surge seen after a meal Eg Precose bullByetta (Glucagon-like peptide 1 mimic) mimics the incretin GLP-1 It suppresses glucagon secretion and slows gastric emptying By promoting satiety it decreases food intake and in the long term leads to weight loss Because none of the drugs deliver new insulin to the body they cannot replace insulin therapy for people with Type I Diabetes and later in Type II Diabetics as well

SULFONYLUREAS

NIDDM patients above the age of 40 years amp having ho diabetes of less than 5 years are given Oral Hypoglycemics

Mechanism of Action1 Stimulate release of Insulin from beta cells of

pancreas2 Reduction of serum Glucagon3 Increased binding of Insulin to target tissues amp

receptors Eg Tolbutamide

Glyburide Glipizide

WHO NEEDS INSULIN

bull 1048708 Type 1bull 1048708 Type 2 uncontrolled wmedsbull 1048708 DKAbull 1048708 Hyperosmolar hyperglycemic state (HHS)bull 1048708 Surgerybull 1048708 IllnessInfectionbull 1048708 Stressbull 1048708 Those receiving parental enteral nutritionbull 1048708 Pancreatitis diseases that darr beta cell function

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

TYPE I Juvenile Onset Insulin Dependent

It is the more severe from of diabetes and more prevalent in children

DEFINITION

It is a catabolic disorder in which the circulating insulin is virtually absent plasma glucose is elevated amp the pancreatic beta

cells fail to produce any insulin in response to all insulinogenic stimuli

Cause Lack of insulin secretion from the beta cells of the islets of langerhans

bull It is an autoimmune disorder in which there is selective destruction of the pancreatic beta cells by T lymphocytes

bull Mostly it seems to have an immunological basis amp circulating islet cell antibodies amp anti-insulin antibodies may be demonstrated

bull Usually there is a genetic predisposition to this type of diabetes which may be triggered off by

- Viral infections eg rota virus coxsackie virus- Environmental triggers

TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes

It is further classified intobull It is the most common type of diabetes accounting for

about 90 of all cases of diabetes mellitusbull The age of onset is usually after 30 often bw 50 amp 60

years of agebull It develops gradually amp is the less severe form of

diabetes

1 Non-obese type II2 Obese type II

bull Cause Decreased sensitivity of target tissues to the metabolic effects of insulin This reduced sensitivity to insulin is often called INSULIN RESISTANCE

TYPE II DIABETES

Factors that can lead to Insulin resistance include1 Anti-insulin antibodies2 Autoantibodies to the insulin receptor 3 Mutation of insulin receptor4 Down-regulation of insulin receptors by sustained

hyperinsulinism5 Primary hyperinsulinism (Beta cell adenoma)6 Secondary hyperinsulinism (Cushingrsquos syndrome

acromegaly pregnancy or diabetes mellitus)7 Obesityoverweight especially excess fat deposits

around the abdomen8 Insulin resistance in peripheral tissues such as skeletal

muscle brain and liver

PATHOPHYSIOLOGY

bull Diabetes type I is far more rapid in onset occurring over a few days as compared to type II which has a more gradual onset

bull Type I also shows far more complications as compared to Type II which rarely shows complications

bull Type I requires Insulin while Type II can usually be controlled by simple changes in lifestyle as diet exercise amp weight control

bull Type I insulin is more prone to Ketoacidosis while Type II is not

DIAGNOSIS OF DIABETES

1 Blood sugar random ( 80-120 mg100ml)2 Blood sugar fasting (80-90 mg100ml)3 GTT or Glucose Tolerance TestWhen a normal fasting person is given 1g of glucose kg

body weight his plasma glucose levels rise to 120-140 but fall back to normal within 2 hours

In a prediabetic or diabetic not only is the fasting plasma glucose on the higher side but also the post meal plasma glucose rises to as high as 140-200 amp fails to come back to normal within 2 hours of giving conc glucose solution Even after 4-6 hours it rarely comes back to the normal range NORMAL MEAN BLOOD GLUCOSE IS APP 110

Glucose Tolerance Test

POINT TO REMEMBER

WHY IS ORAL GLUCOSE A MORE POWERFUL STIMULANT THAN

INJECTABLE GLUCOSE FOR INSULIN SECRETION

DIAGNOSIS OF DIABETES

4 Presence of glucose in urine (glucosuria)5 Acetone breath6 Lab test for assessing control of diabetes

HbA1c is a minor component of Hb A amp is normally present in small amounts ie up to 6 of normal Hb In the presence of long standing hyperglycemia its concentration rises When plasma glucose is episodically elevated over time small amounts of Hb A are non-enzymatically glycated to form HbA1c

Careful control of diabetes with insulin reduces the amount formed and thus HbA1c levels give an index of diabetic control for past 4-6 weeks

TREATMENT for Type I DIABETES

WHY CANNOT INSULIN BE GIVEN BY MOUTHWHY IS ONLY CHO RESTRICTION NOT VERY EFFECTIVE

Administer enough insulin so that metabolism of fat proteins amp CHO proceed as normally as possible

Insulin is available in various forms1 Insulin preparations are available with rapid (regular) intermediate amp long

durations of action - regular duration of action is 3-8 hours- Intermediate (NPH) not used during- Long duration of action is 10-48 hours

Individualized insulin schedules which consist of one injection of longer acting insulin followed by regular insulin when the glucose level is expected to rise ie at meals

Insulin is administered subcutaneously (sc) except in the case of emergencies when it is given intravenously (iv)

The less soluble an insulin preparation is the longer it acts

INSULIN SYRINGES

Insulin

Human insulin is absorbed more quickly from its site of action than are beef or pork insulins Thus duration of action of human Insulin is shorter amp doses must be adjusted

Hypoglycemia is the most serious amp common side effect of Insulin therapy BC long term diabetics do not produce counteracting hormones of Glucagon EN cortisol etc that normally provide defense against Hypoglycemia

TREATMENT for Type II DIABETES

bull Dietbull Exercise is useful in managing both types of Diabetes

because working muscles are not Insulin dependent Exercising muscles take up some of the excess blood glucose reducing the overall need for insulin

bull Weight lossbull Oral Hypoglycemic Drugs

Oral Hypoglycemic Drugs

There are many types of oral Hypoglycemic drugs some of which are bullSulfonylureas act by stimulating the β- cells to secrete more insulin than they do on their own Eg GlucotrolbullMetformin acts by suppressing liver output of glucose Eg GlucophagebullAlpha-glycosidase Inhibitors act by slowing CHO digestion and absorption from the digestive tract into the blood thus reducing the glucose surge seen after a meal Eg Precose bullByetta (Glucagon-like peptide 1 mimic) mimics the incretin GLP-1 It suppresses glucagon secretion and slows gastric emptying By promoting satiety it decreases food intake and in the long term leads to weight loss Because none of the drugs deliver new insulin to the body they cannot replace insulin therapy for people with Type I Diabetes and later in Type II Diabetics as well

SULFONYLUREAS

NIDDM patients above the age of 40 years amp having ho diabetes of less than 5 years are given Oral Hypoglycemics

Mechanism of Action1 Stimulate release of Insulin from beta cells of

pancreas2 Reduction of serum Glucagon3 Increased binding of Insulin to target tissues amp

receptors Eg Tolbutamide

Glyburide Glipizide

WHO NEEDS INSULIN

bull 1048708 Type 1bull 1048708 Type 2 uncontrolled wmedsbull 1048708 DKAbull 1048708 Hyperosmolar hyperglycemic state (HHS)bull 1048708 Surgerybull 1048708 IllnessInfectionbull 1048708 Stressbull 1048708 Those receiving parental enteral nutritionbull 1048708 Pancreatitis diseases that darr beta cell function

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes

It is further classified intobull It is the most common type of diabetes accounting for

about 90 of all cases of diabetes mellitusbull The age of onset is usually after 30 often bw 50 amp 60

years of agebull It develops gradually amp is the less severe form of

diabetes

1 Non-obese type II2 Obese type II

bull Cause Decreased sensitivity of target tissues to the metabolic effects of insulin This reduced sensitivity to insulin is often called INSULIN RESISTANCE

TYPE II DIABETES

Factors that can lead to Insulin resistance include1 Anti-insulin antibodies2 Autoantibodies to the insulin receptor 3 Mutation of insulin receptor4 Down-regulation of insulin receptors by sustained

hyperinsulinism5 Primary hyperinsulinism (Beta cell adenoma)6 Secondary hyperinsulinism (Cushingrsquos syndrome

acromegaly pregnancy or diabetes mellitus)7 Obesityoverweight especially excess fat deposits

around the abdomen8 Insulin resistance in peripheral tissues such as skeletal

muscle brain and liver

PATHOPHYSIOLOGY

bull Diabetes type I is far more rapid in onset occurring over a few days as compared to type II which has a more gradual onset

bull Type I also shows far more complications as compared to Type II which rarely shows complications

bull Type I requires Insulin while Type II can usually be controlled by simple changes in lifestyle as diet exercise amp weight control

bull Type I insulin is more prone to Ketoacidosis while Type II is not

DIAGNOSIS OF DIABETES

1 Blood sugar random ( 80-120 mg100ml)2 Blood sugar fasting (80-90 mg100ml)3 GTT or Glucose Tolerance TestWhen a normal fasting person is given 1g of glucose kg

body weight his plasma glucose levels rise to 120-140 but fall back to normal within 2 hours

In a prediabetic or diabetic not only is the fasting plasma glucose on the higher side but also the post meal plasma glucose rises to as high as 140-200 amp fails to come back to normal within 2 hours of giving conc glucose solution Even after 4-6 hours it rarely comes back to the normal range NORMAL MEAN BLOOD GLUCOSE IS APP 110

Glucose Tolerance Test

POINT TO REMEMBER

WHY IS ORAL GLUCOSE A MORE POWERFUL STIMULANT THAN

INJECTABLE GLUCOSE FOR INSULIN SECRETION

DIAGNOSIS OF DIABETES

4 Presence of glucose in urine (glucosuria)5 Acetone breath6 Lab test for assessing control of diabetes

HbA1c is a minor component of Hb A amp is normally present in small amounts ie up to 6 of normal Hb In the presence of long standing hyperglycemia its concentration rises When plasma glucose is episodically elevated over time small amounts of Hb A are non-enzymatically glycated to form HbA1c

Careful control of diabetes with insulin reduces the amount formed and thus HbA1c levels give an index of diabetic control for past 4-6 weeks

TREATMENT for Type I DIABETES

WHY CANNOT INSULIN BE GIVEN BY MOUTHWHY IS ONLY CHO RESTRICTION NOT VERY EFFECTIVE

Administer enough insulin so that metabolism of fat proteins amp CHO proceed as normally as possible

Insulin is available in various forms1 Insulin preparations are available with rapid (regular) intermediate amp long

durations of action - regular duration of action is 3-8 hours- Intermediate (NPH) not used during- Long duration of action is 10-48 hours

Individualized insulin schedules which consist of one injection of longer acting insulin followed by regular insulin when the glucose level is expected to rise ie at meals

Insulin is administered subcutaneously (sc) except in the case of emergencies when it is given intravenously (iv)

The less soluble an insulin preparation is the longer it acts

INSULIN SYRINGES

Insulin

Human insulin is absorbed more quickly from its site of action than are beef or pork insulins Thus duration of action of human Insulin is shorter amp doses must be adjusted

Hypoglycemia is the most serious amp common side effect of Insulin therapy BC long term diabetics do not produce counteracting hormones of Glucagon EN cortisol etc that normally provide defense against Hypoglycemia

TREATMENT for Type II DIABETES

bull Dietbull Exercise is useful in managing both types of Diabetes

because working muscles are not Insulin dependent Exercising muscles take up some of the excess blood glucose reducing the overall need for insulin

bull Weight lossbull Oral Hypoglycemic Drugs

Oral Hypoglycemic Drugs

There are many types of oral Hypoglycemic drugs some of which are bullSulfonylureas act by stimulating the β- cells to secrete more insulin than they do on their own Eg GlucotrolbullMetformin acts by suppressing liver output of glucose Eg GlucophagebullAlpha-glycosidase Inhibitors act by slowing CHO digestion and absorption from the digestive tract into the blood thus reducing the glucose surge seen after a meal Eg Precose bullByetta (Glucagon-like peptide 1 mimic) mimics the incretin GLP-1 It suppresses glucagon secretion and slows gastric emptying By promoting satiety it decreases food intake and in the long term leads to weight loss Because none of the drugs deliver new insulin to the body they cannot replace insulin therapy for people with Type I Diabetes and later in Type II Diabetics as well

SULFONYLUREAS

NIDDM patients above the age of 40 years amp having ho diabetes of less than 5 years are given Oral Hypoglycemics

Mechanism of Action1 Stimulate release of Insulin from beta cells of

pancreas2 Reduction of serum Glucagon3 Increased binding of Insulin to target tissues amp

receptors Eg Tolbutamide

Glyburide Glipizide

WHO NEEDS INSULIN

bull 1048708 Type 1bull 1048708 Type 2 uncontrolled wmedsbull 1048708 DKAbull 1048708 Hyperosmolar hyperglycemic state (HHS)bull 1048708 Surgerybull 1048708 IllnessInfectionbull 1048708 Stressbull 1048708 Those receiving parental enteral nutritionbull 1048708 Pancreatitis diseases that darr beta cell function

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

TYPE II DIABETES

Factors that can lead to Insulin resistance include1 Anti-insulin antibodies2 Autoantibodies to the insulin receptor 3 Mutation of insulin receptor4 Down-regulation of insulin receptors by sustained

hyperinsulinism5 Primary hyperinsulinism (Beta cell adenoma)6 Secondary hyperinsulinism (Cushingrsquos syndrome

acromegaly pregnancy or diabetes mellitus)7 Obesityoverweight especially excess fat deposits

around the abdomen8 Insulin resistance in peripheral tissues such as skeletal

muscle brain and liver

PATHOPHYSIOLOGY

bull Diabetes type I is far more rapid in onset occurring over a few days as compared to type II which has a more gradual onset

bull Type I also shows far more complications as compared to Type II which rarely shows complications

bull Type I requires Insulin while Type II can usually be controlled by simple changes in lifestyle as diet exercise amp weight control

bull Type I insulin is more prone to Ketoacidosis while Type II is not

DIAGNOSIS OF DIABETES

1 Blood sugar random ( 80-120 mg100ml)2 Blood sugar fasting (80-90 mg100ml)3 GTT or Glucose Tolerance TestWhen a normal fasting person is given 1g of glucose kg

body weight his plasma glucose levels rise to 120-140 but fall back to normal within 2 hours

In a prediabetic or diabetic not only is the fasting plasma glucose on the higher side but also the post meal plasma glucose rises to as high as 140-200 amp fails to come back to normal within 2 hours of giving conc glucose solution Even after 4-6 hours it rarely comes back to the normal range NORMAL MEAN BLOOD GLUCOSE IS APP 110

Glucose Tolerance Test

POINT TO REMEMBER

WHY IS ORAL GLUCOSE A MORE POWERFUL STIMULANT THAN

INJECTABLE GLUCOSE FOR INSULIN SECRETION

DIAGNOSIS OF DIABETES

4 Presence of glucose in urine (glucosuria)5 Acetone breath6 Lab test for assessing control of diabetes

HbA1c is a minor component of Hb A amp is normally present in small amounts ie up to 6 of normal Hb In the presence of long standing hyperglycemia its concentration rises When plasma glucose is episodically elevated over time small amounts of Hb A are non-enzymatically glycated to form HbA1c

Careful control of diabetes with insulin reduces the amount formed and thus HbA1c levels give an index of diabetic control for past 4-6 weeks

TREATMENT for Type I DIABETES

WHY CANNOT INSULIN BE GIVEN BY MOUTHWHY IS ONLY CHO RESTRICTION NOT VERY EFFECTIVE

Administer enough insulin so that metabolism of fat proteins amp CHO proceed as normally as possible

Insulin is available in various forms1 Insulin preparations are available with rapid (regular) intermediate amp long

durations of action - regular duration of action is 3-8 hours- Intermediate (NPH) not used during- Long duration of action is 10-48 hours

Individualized insulin schedules which consist of one injection of longer acting insulin followed by regular insulin when the glucose level is expected to rise ie at meals

Insulin is administered subcutaneously (sc) except in the case of emergencies when it is given intravenously (iv)

The less soluble an insulin preparation is the longer it acts

INSULIN SYRINGES

Insulin

Human insulin is absorbed more quickly from its site of action than are beef or pork insulins Thus duration of action of human Insulin is shorter amp doses must be adjusted

Hypoglycemia is the most serious amp common side effect of Insulin therapy BC long term diabetics do not produce counteracting hormones of Glucagon EN cortisol etc that normally provide defense against Hypoglycemia

TREATMENT for Type II DIABETES

bull Dietbull Exercise is useful in managing both types of Diabetes

because working muscles are not Insulin dependent Exercising muscles take up some of the excess blood glucose reducing the overall need for insulin

bull Weight lossbull Oral Hypoglycemic Drugs

Oral Hypoglycemic Drugs

There are many types of oral Hypoglycemic drugs some of which are bullSulfonylureas act by stimulating the β- cells to secrete more insulin than they do on their own Eg GlucotrolbullMetformin acts by suppressing liver output of glucose Eg GlucophagebullAlpha-glycosidase Inhibitors act by slowing CHO digestion and absorption from the digestive tract into the blood thus reducing the glucose surge seen after a meal Eg Precose bullByetta (Glucagon-like peptide 1 mimic) mimics the incretin GLP-1 It suppresses glucagon secretion and slows gastric emptying By promoting satiety it decreases food intake and in the long term leads to weight loss Because none of the drugs deliver new insulin to the body they cannot replace insulin therapy for people with Type I Diabetes and later in Type II Diabetics as well

SULFONYLUREAS

NIDDM patients above the age of 40 years amp having ho diabetes of less than 5 years are given Oral Hypoglycemics

Mechanism of Action1 Stimulate release of Insulin from beta cells of

pancreas2 Reduction of serum Glucagon3 Increased binding of Insulin to target tissues amp

receptors Eg Tolbutamide

Glyburide Glipizide

WHO NEEDS INSULIN

bull 1048708 Type 1bull 1048708 Type 2 uncontrolled wmedsbull 1048708 DKAbull 1048708 Hyperosmolar hyperglycemic state (HHS)bull 1048708 Surgerybull 1048708 IllnessInfectionbull 1048708 Stressbull 1048708 Those receiving parental enteral nutritionbull 1048708 Pancreatitis diseases that darr beta cell function

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

PATHOPHYSIOLOGY

bull Diabetes type I is far more rapid in onset occurring over a few days as compared to type II which has a more gradual onset

bull Type I also shows far more complications as compared to Type II which rarely shows complications

bull Type I requires Insulin while Type II can usually be controlled by simple changes in lifestyle as diet exercise amp weight control

bull Type I insulin is more prone to Ketoacidosis while Type II is not

DIAGNOSIS OF DIABETES

1 Blood sugar random ( 80-120 mg100ml)2 Blood sugar fasting (80-90 mg100ml)3 GTT or Glucose Tolerance TestWhen a normal fasting person is given 1g of glucose kg

body weight his plasma glucose levels rise to 120-140 but fall back to normal within 2 hours

In a prediabetic or diabetic not only is the fasting plasma glucose on the higher side but also the post meal plasma glucose rises to as high as 140-200 amp fails to come back to normal within 2 hours of giving conc glucose solution Even after 4-6 hours it rarely comes back to the normal range NORMAL MEAN BLOOD GLUCOSE IS APP 110

Glucose Tolerance Test

POINT TO REMEMBER

WHY IS ORAL GLUCOSE A MORE POWERFUL STIMULANT THAN

INJECTABLE GLUCOSE FOR INSULIN SECRETION

DIAGNOSIS OF DIABETES

4 Presence of glucose in urine (glucosuria)5 Acetone breath6 Lab test for assessing control of diabetes

HbA1c is a minor component of Hb A amp is normally present in small amounts ie up to 6 of normal Hb In the presence of long standing hyperglycemia its concentration rises When plasma glucose is episodically elevated over time small amounts of Hb A are non-enzymatically glycated to form HbA1c

Careful control of diabetes with insulin reduces the amount formed and thus HbA1c levels give an index of diabetic control for past 4-6 weeks

TREATMENT for Type I DIABETES

WHY CANNOT INSULIN BE GIVEN BY MOUTHWHY IS ONLY CHO RESTRICTION NOT VERY EFFECTIVE

Administer enough insulin so that metabolism of fat proteins amp CHO proceed as normally as possible

Insulin is available in various forms1 Insulin preparations are available with rapid (regular) intermediate amp long

durations of action - regular duration of action is 3-8 hours- Intermediate (NPH) not used during- Long duration of action is 10-48 hours

Individualized insulin schedules which consist of one injection of longer acting insulin followed by regular insulin when the glucose level is expected to rise ie at meals

Insulin is administered subcutaneously (sc) except in the case of emergencies when it is given intravenously (iv)

The less soluble an insulin preparation is the longer it acts

INSULIN SYRINGES

Insulin

Human insulin is absorbed more quickly from its site of action than are beef or pork insulins Thus duration of action of human Insulin is shorter amp doses must be adjusted

Hypoglycemia is the most serious amp common side effect of Insulin therapy BC long term diabetics do not produce counteracting hormones of Glucagon EN cortisol etc that normally provide defense against Hypoglycemia

TREATMENT for Type II DIABETES

bull Dietbull Exercise is useful in managing both types of Diabetes

because working muscles are not Insulin dependent Exercising muscles take up some of the excess blood glucose reducing the overall need for insulin

bull Weight lossbull Oral Hypoglycemic Drugs

Oral Hypoglycemic Drugs

There are many types of oral Hypoglycemic drugs some of which are bullSulfonylureas act by stimulating the β- cells to secrete more insulin than they do on their own Eg GlucotrolbullMetformin acts by suppressing liver output of glucose Eg GlucophagebullAlpha-glycosidase Inhibitors act by slowing CHO digestion and absorption from the digestive tract into the blood thus reducing the glucose surge seen after a meal Eg Precose bullByetta (Glucagon-like peptide 1 mimic) mimics the incretin GLP-1 It suppresses glucagon secretion and slows gastric emptying By promoting satiety it decreases food intake and in the long term leads to weight loss Because none of the drugs deliver new insulin to the body they cannot replace insulin therapy for people with Type I Diabetes and later in Type II Diabetics as well

SULFONYLUREAS

NIDDM patients above the age of 40 years amp having ho diabetes of less than 5 years are given Oral Hypoglycemics

Mechanism of Action1 Stimulate release of Insulin from beta cells of

pancreas2 Reduction of serum Glucagon3 Increased binding of Insulin to target tissues amp

receptors Eg Tolbutamide

Glyburide Glipizide

WHO NEEDS INSULIN

bull 1048708 Type 1bull 1048708 Type 2 uncontrolled wmedsbull 1048708 DKAbull 1048708 Hyperosmolar hyperglycemic state (HHS)bull 1048708 Surgerybull 1048708 IllnessInfectionbull 1048708 Stressbull 1048708 Those receiving parental enteral nutritionbull 1048708 Pancreatitis diseases that darr beta cell function

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

DIAGNOSIS OF DIABETES

1 Blood sugar random ( 80-120 mg100ml)2 Blood sugar fasting (80-90 mg100ml)3 GTT or Glucose Tolerance TestWhen a normal fasting person is given 1g of glucose kg

body weight his plasma glucose levels rise to 120-140 but fall back to normal within 2 hours

In a prediabetic or diabetic not only is the fasting plasma glucose on the higher side but also the post meal plasma glucose rises to as high as 140-200 amp fails to come back to normal within 2 hours of giving conc glucose solution Even after 4-6 hours it rarely comes back to the normal range NORMAL MEAN BLOOD GLUCOSE IS APP 110

Glucose Tolerance Test

POINT TO REMEMBER

WHY IS ORAL GLUCOSE A MORE POWERFUL STIMULANT THAN

INJECTABLE GLUCOSE FOR INSULIN SECRETION

DIAGNOSIS OF DIABETES

4 Presence of glucose in urine (glucosuria)5 Acetone breath6 Lab test for assessing control of diabetes

HbA1c is a minor component of Hb A amp is normally present in small amounts ie up to 6 of normal Hb In the presence of long standing hyperglycemia its concentration rises When plasma glucose is episodically elevated over time small amounts of Hb A are non-enzymatically glycated to form HbA1c

Careful control of diabetes with insulin reduces the amount formed and thus HbA1c levels give an index of diabetic control for past 4-6 weeks

TREATMENT for Type I DIABETES

WHY CANNOT INSULIN BE GIVEN BY MOUTHWHY IS ONLY CHO RESTRICTION NOT VERY EFFECTIVE

Administer enough insulin so that metabolism of fat proteins amp CHO proceed as normally as possible

Insulin is available in various forms1 Insulin preparations are available with rapid (regular) intermediate amp long

durations of action - regular duration of action is 3-8 hours- Intermediate (NPH) not used during- Long duration of action is 10-48 hours

Individualized insulin schedules which consist of one injection of longer acting insulin followed by regular insulin when the glucose level is expected to rise ie at meals

Insulin is administered subcutaneously (sc) except in the case of emergencies when it is given intravenously (iv)

The less soluble an insulin preparation is the longer it acts

INSULIN SYRINGES

Insulin

Human insulin is absorbed more quickly from its site of action than are beef or pork insulins Thus duration of action of human Insulin is shorter amp doses must be adjusted

Hypoglycemia is the most serious amp common side effect of Insulin therapy BC long term diabetics do not produce counteracting hormones of Glucagon EN cortisol etc that normally provide defense against Hypoglycemia

TREATMENT for Type II DIABETES

bull Dietbull Exercise is useful in managing both types of Diabetes

because working muscles are not Insulin dependent Exercising muscles take up some of the excess blood glucose reducing the overall need for insulin

bull Weight lossbull Oral Hypoglycemic Drugs

Oral Hypoglycemic Drugs

There are many types of oral Hypoglycemic drugs some of which are bullSulfonylureas act by stimulating the β- cells to secrete more insulin than they do on their own Eg GlucotrolbullMetformin acts by suppressing liver output of glucose Eg GlucophagebullAlpha-glycosidase Inhibitors act by slowing CHO digestion and absorption from the digestive tract into the blood thus reducing the glucose surge seen after a meal Eg Precose bullByetta (Glucagon-like peptide 1 mimic) mimics the incretin GLP-1 It suppresses glucagon secretion and slows gastric emptying By promoting satiety it decreases food intake and in the long term leads to weight loss Because none of the drugs deliver new insulin to the body they cannot replace insulin therapy for people with Type I Diabetes and later in Type II Diabetics as well

SULFONYLUREAS

NIDDM patients above the age of 40 years amp having ho diabetes of less than 5 years are given Oral Hypoglycemics

Mechanism of Action1 Stimulate release of Insulin from beta cells of

pancreas2 Reduction of serum Glucagon3 Increased binding of Insulin to target tissues amp

receptors Eg Tolbutamide

Glyburide Glipizide

WHO NEEDS INSULIN

bull 1048708 Type 1bull 1048708 Type 2 uncontrolled wmedsbull 1048708 DKAbull 1048708 Hyperosmolar hyperglycemic state (HHS)bull 1048708 Surgerybull 1048708 IllnessInfectionbull 1048708 Stressbull 1048708 Those receiving parental enteral nutritionbull 1048708 Pancreatitis diseases that darr beta cell function

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

Glucose Tolerance Test

POINT TO REMEMBER

WHY IS ORAL GLUCOSE A MORE POWERFUL STIMULANT THAN

INJECTABLE GLUCOSE FOR INSULIN SECRETION

DIAGNOSIS OF DIABETES

4 Presence of glucose in urine (glucosuria)5 Acetone breath6 Lab test for assessing control of diabetes

HbA1c is a minor component of Hb A amp is normally present in small amounts ie up to 6 of normal Hb In the presence of long standing hyperglycemia its concentration rises When plasma glucose is episodically elevated over time small amounts of Hb A are non-enzymatically glycated to form HbA1c

Careful control of diabetes with insulin reduces the amount formed and thus HbA1c levels give an index of diabetic control for past 4-6 weeks

TREATMENT for Type I DIABETES

WHY CANNOT INSULIN BE GIVEN BY MOUTHWHY IS ONLY CHO RESTRICTION NOT VERY EFFECTIVE

Administer enough insulin so that metabolism of fat proteins amp CHO proceed as normally as possible

Insulin is available in various forms1 Insulin preparations are available with rapid (regular) intermediate amp long

durations of action - regular duration of action is 3-8 hours- Intermediate (NPH) not used during- Long duration of action is 10-48 hours

Individualized insulin schedules which consist of one injection of longer acting insulin followed by regular insulin when the glucose level is expected to rise ie at meals

Insulin is administered subcutaneously (sc) except in the case of emergencies when it is given intravenously (iv)

The less soluble an insulin preparation is the longer it acts

INSULIN SYRINGES

Insulin

Human insulin is absorbed more quickly from its site of action than are beef or pork insulins Thus duration of action of human Insulin is shorter amp doses must be adjusted

Hypoglycemia is the most serious amp common side effect of Insulin therapy BC long term diabetics do not produce counteracting hormones of Glucagon EN cortisol etc that normally provide defense against Hypoglycemia

TREATMENT for Type II DIABETES

bull Dietbull Exercise is useful in managing both types of Diabetes

because working muscles are not Insulin dependent Exercising muscles take up some of the excess blood glucose reducing the overall need for insulin

bull Weight lossbull Oral Hypoglycemic Drugs

Oral Hypoglycemic Drugs

There are many types of oral Hypoglycemic drugs some of which are bullSulfonylureas act by stimulating the β- cells to secrete more insulin than they do on their own Eg GlucotrolbullMetformin acts by suppressing liver output of glucose Eg GlucophagebullAlpha-glycosidase Inhibitors act by slowing CHO digestion and absorption from the digestive tract into the blood thus reducing the glucose surge seen after a meal Eg Precose bullByetta (Glucagon-like peptide 1 mimic) mimics the incretin GLP-1 It suppresses glucagon secretion and slows gastric emptying By promoting satiety it decreases food intake and in the long term leads to weight loss Because none of the drugs deliver new insulin to the body they cannot replace insulin therapy for people with Type I Diabetes and later in Type II Diabetics as well

SULFONYLUREAS

NIDDM patients above the age of 40 years amp having ho diabetes of less than 5 years are given Oral Hypoglycemics

Mechanism of Action1 Stimulate release of Insulin from beta cells of

pancreas2 Reduction of serum Glucagon3 Increased binding of Insulin to target tissues amp

receptors Eg Tolbutamide

Glyburide Glipizide

WHO NEEDS INSULIN

bull 1048708 Type 1bull 1048708 Type 2 uncontrolled wmedsbull 1048708 DKAbull 1048708 Hyperosmolar hyperglycemic state (HHS)bull 1048708 Surgerybull 1048708 IllnessInfectionbull 1048708 Stressbull 1048708 Those receiving parental enteral nutritionbull 1048708 Pancreatitis diseases that darr beta cell function

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

POINT TO REMEMBER

WHY IS ORAL GLUCOSE A MORE POWERFUL STIMULANT THAN

INJECTABLE GLUCOSE FOR INSULIN SECRETION

DIAGNOSIS OF DIABETES

4 Presence of glucose in urine (glucosuria)5 Acetone breath6 Lab test for assessing control of diabetes

HbA1c is a minor component of Hb A amp is normally present in small amounts ie up to 6 of normal Hb In the presence of long standing hyperglycemia its concentration rises When plasma glucose is episodically elevated over time small amounts of Hb A are non-enzymatically glycated to form HbA1c

Careful control of diabetes with insulin reduces the amount formed and thus HbA1c levels give an index of diabetic control for past 4-6 weeks

TREATMENT for Type I DIABETES

WHY CANNOT INSULIN BE GIVEN BY MOUTHWHY IS ONLY CHO RESTRICTION NOT VERY EFFECTIVE

Administer enough insulin so that metabolism of fat proteins amp CHO proceed as normally as possible

Insulin is available in various forms1 Insulin preparations are available with rapid (regular) intermediate amp long

durations of action - regular duration of action is 3-8 hours- Intermediate (NPH) not used during- Long duration of action is 10-48 hours

Individualized insulin schedules which consist of one injection of longer acting insulin followed by regular insulin when the glucose level is expected to rise ie at meals

Insulin is administered subcutaneously (sc) except in the case of emergencies when it is given intravenously (iv)

The less soluble an insulin preparation is the longer it acts

INSULIN SYRINGES

Insulin

Human insulin is absorbed more quickly from its site of action than are beef or pork insulins Thus duration of action of human Insulin is shorter amp doses must be adjusted

Hypoglycemia is the most serious amp common side effect of Insulin therapy BC long term diabetics do not produce counteracting hormones of Glucagon EN cortisol etc that normally provide defense against Hypoglycemia

TREATMENT for Type II DIABETES

bull Dietbull Exercise is useful in managing both types of Diabetes

because working muscles are not Insulin dependent Exercising muscles take up some of the excess blood glucose reducing the overall need for insulin

bull Weight lossbull Oral Hypoglycemic Drugs

Oral Hypoglycemic Drugs

There are many types of oral Hypoglycemic drugs some of which are bullSulfonylureas act by stimulating the β- cells to secrete more insulin than they do on their own Eg GlucotrolbullMetformin acts by suppressing liver output of glucose Eg GlucophagebullAlpha-glycosidase Inhibitors act by slowing CHO digestion and absorption from the digestive tract into the blood thus reducing the glucose surge seen after a meal Eg Precose bullByetta (Glucagon-like peptide 1 mimic) mimics the incretin GLP-1 It suppresses glucagon secretion and slows gastric emptying By promoting satiety it decreases food intake and in the long term leads to weight loss Because none of the drugs deliver new insulin to the body they cannot replace insulin therapy for people with Type I Diabetes and later in Type II Diabetics as well

SULFONYLUREAS

NIDDM patients above the age of 40 years amp having ho diabetes of less than 5 years are given Oral Hypoglycemics

Mechanism of Action1 Stimulate release of Insulin from beta cells of

pancreas2 Reduction of serum Glucagon3 Increased binding of Insulin to target tissues amp

receptors Eg Tolbutamide

Glyburide Glipizide

WHO NEEDS INSULIN

bull 1048708 Type 1bull 1048708 Type 2 uncontrolled wmedsbull 1048708 DKAbull 1048708 Hyperosmolar hyperglycemic state (HHS)bull 1048708 Surgerybull 1048708 IllnessInfectionbull 1048708 Stressbull 1048708 Those receiving parental enteral nutritionbull 1048708 Pancreatitis diseases that darr beta cell function

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

DIAGNOSIS OF DIABETES

4 Presence of glucose in urine (glucosuria)5 Acetone breath6 Lab test for assessing control of diabetes

HbA1c is a minor component of Hb A amp is normally present in small amounts ie up to 6 of normal Hb In the presence of long standing hyperglycemia its concentration rises When plasma glucose is episodically elevated over time small amounts of Hb A are non-enzymatically glycated to form HbA1c

Careful control of diabetes with insulin reduces the amount formed and thus HbA1c levels give an index of diabetic control for past 4-6 weeks

TREATMENT for Type I DIABETES

WHY CANNOT INSULIN BE GIVEN BY MOUTHWHY IS ONLY CHO RESTRICTION NOT VERY EFFECTIVE

Administer enough insulin so that metabolism of fat proteins amp CHO proceed as normally as possible

Insulin is available in various forms1 Insulin preparations are available with rapid (regular) intermediate amp long

durations of action - regular duration of action is 3-8 hours- Intermediate (NPH) not used during- Long duration of action is 10-48 hours

Individualized insulin schedules which consist of one injection of longer acting insulin followed by regular insulin when the glucose level is expected to rise ie at meals

Insulin is administered subcutaneously (sc) except in the case of emergencies when it is given intravenously (iv)

The less soluble an insulin preparation is the longer it acts

INSULIN SYRINGES

Insulin

Human insulin is absorbed more quickly from its site of action than are beef or pork insulins Thus duration of action of human Insulin is shorter amp doses must be adjusted

Hypoglycemia is the most serious amp common side effect of Insulin therapy BC long term diabetics do not produce counteracting hormones of Glucagon EN cortisol etc that normally provide defense against Hypoglycemia

TREATMENT for Type II DIABETES

bull Dietbull Exercise is useful in managing both types of Diabetes

because working muscles are not Insulin dependent Exercising muscles take up some of the excess blood glucose reducing the overall need for insulin

bull Weight lossbull Oral Hypoglycemic Drugs

Oral Hypoglycemic Drugs

There are many types of oral Hypoglycemic drugs some of which are bullSulfonylureas act by stimulating the β- cells to secrete more insulin than they do on their own Eg GlucotrolbullMetformin acts by suppressing liver output of glucose Eg GlucophagebullAlpha-glycosidase Inhibitors act by slowing CHO digestion and absorption from the digestive tract into the blood thus reducing the glucose surge seen after a meal Eg Precose bullByetta (Glucagon-like peptide 1 mimic) mimics the incretin GLP-1 It suppresses glucagon secretion and slows gastric emptying By promoting satiety it decreases food intake and in the long term leads to weight loss Because none of the drugs deliver new insulin to the body they cannot replace insulin therapy for people with Type I Diabetes and later in Type II Diabetics as well

SULFONYLUREAS

NIDDM patients above the age of 40 years amp having ho diabetes of less than 5 years are given Oral Hypoglycemics

Mechanism of Action1 Stimulate release of Insulin from beta cells of

pancreas2 Reduction of serum Glucagon3 Increased binding of Insulin to target tissues amp

receptors Eg Tolbutamide

Glyburide Glipizide

WHO NEEDS INSULIN

bull 1048708 Type 1bull 1048708 Type 2 uncontrolled wmedsbull 1048708 DKAbull 1048708 Hyperosmolar hyperglycemic state (HHS)bull 1048708 Surgerybull 1048708 IllnessInfectionbull 1048708 Stressbull 1048708 Those receiving parental enteral nutritionbull 1048708 Pancreatitis diseases that darr beta cell function

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

TREATMENT for Type I DIABETES

WHY CANNOT INSULIN BE GIVEN BY MOUTHWHY IS ONLY CHO RESTRICTION NOT VERY EFFECTIVE

Administer enough insulin so that metabolism of fat proteins amp CHO proceed as normally as possible

Insulin is available in various forms1 Insulin preparations are available with rapid (regular) intermediate amp long

durations of action - regular duration of action is 3-8 hours- Intermediate (NPH) not used during- Long duration of action is 10-48 hours

Individualized insulin schedules which consist of one injection of longer acting insulin followed by regular insulin when the glucose level is expected to rise ie at meals

Insulin is administered subcutaneously (sc) except in the case of emergencies when it is given intravenously (iv)

The less soluble an insulin preparation is the longer it acts

INSULIN SYRINGES

Insulin

Human insulin is absorbed more quickly from its site of action than are beef or pork insulins Thus duration of action of human Insulin is shorter amp doses must be adjusted

Hypoglycemia is the most serious amp common side effect of Insulin therapy BC long term diabetics do not produce counteracting hormones of Glucagon EN cortisol etc that normally provide defense against Hypoglycemia

TREATMENT for Type II DIABETES

bull Dietbull Exercise is useful in managing both types of Diabetes

because working muscles are not Insulin dependent Exercising muscles take up some of the excess blood glucose reducing the overall need for insulin

bull Weight lossbull Oral Hypoglycemic Drugs

Oral Hypoglycemic Drugs

There are many types of oral Hypoglycemic drugs some of which are bullSulfonylureas act by stimulating the β- cells to secrete more insulin than they do on their own Eg GlucotrolbullMetformin acts by suppressing liver output of glucose Eg GlucophagebullAlpha-glycosidase Inhibitors act by slowing CHO digestion and absorption from the digestive tract into the blood thus reducing the glucose surge seen after a meal Eg Precose bullByetta (Glucagon-like peptide 1 mimic) mimics the incretin GLP-1 It suppresses glucagon secretion and slows gastric emptying By promoting satiety it decreases food intake and in the long term leads to weight loss Because none of the drugs deliver new insulin to the body they cannot replace insulin therapy for people with Type I Diabetes and later in Type II Diabetics as well

SULFONYLUREAS

NIDDM patients above the age of 40 years amp having ho diabetes of less than 5 years are given Oral Hypoglycemics

Mechanism of Action1 Stimulate release of Insulin from beta cells of

pancreas2 Reduction of serum Glucagon3 Increased binding of Insulin to target tissues amp

receptors Eg Tolbutamide

Glyburide Glipizide

WHO NEEDS INSULIN

bull 1048708 Type 1bull 1048708 Type 2 uncontrolled wmedsbull 1048708 DKAbull 1048708 Hyperosmolar hyperglycemic state (HHS)bull 1048708 Surgerybull 1048708 IllnessInfectionbull 1048708 Stressbull 1048708 Those receiving parental enteral nutritionbull 1048708 Pancreatitis diseases that darr beta cell function

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

INSULIN SYRINGES

Insulin

Human insulin is absorbed more quickly from its site of action than are beef or pork insulins Thus duration of action of human Insulin is shorter amp doses must be adjusted

Hypoglycemia is the most serious amp common side effect of Insulin therapy BC long term diabetics do not produce counteracting hormones of Glucagon EN cortisol etc that normally provide defense against Hypoglycemia

TREATMENT for Type II DIABETES

bull Dietbull Exercise is useful in managing both types of Diabetes

because working muscles are not Insulin dependent Exercising muscles take up some of the excess blood glucose reducing the overall need for insulin

bull Weight lossbull Oral Hypoglycemic Drugs

Oral Hypoglycemic Drugs

There are many types of oral Hypoglycemic drugs some of which are bullSulfonylureas act by stimulating the β- cells to secrete more insulin than they do on their own Eg GlucotrolbullMetformin acts by suppressing liver output of glucose Eg GlucophagebullAlpha-glycosidase Inhibitors act by slowing CHO digestion and absorption from the digestive tract into the blood thus reducing the glucose surge seen after a meal Eg Precose bullByetta (Glucagon-like peptide 1 mimic) mimics the incretin GLP-1 It suppresses glucagon secretion and slows gastric emptying By promoting satiety it decreases food intake and in the long term leads to weight loss Because none of the drugs deliver new insulin to the body they cannot replace insulin therapy for people with Type I Diabetes and later in Type II Diabetics as well

SULFONYLUREAS

NIDDM patients above the age of 40 years amp having ho diabetes of less than 5 years are given Oral Hypoglycemics

Mechanism of Action1 Stimulate release of Insulin from beta cells of

pancreas2 Reduction of serum Glucagon3 Increased binding of Insulin to target tissues amp

receptors Eg Tolbutamide

Glyburide Glipizide

WHO NEEDS INSULIN

bull 1048708 Type 1bull 1048708 Type 2 uncontrolled wmedsbull 1048708 DKAbull 1048708 Hyperosmolar hyperglycemic state (HHS)bull 1048708 Surgerybull 1048708 IllnessInfectionbull 1048708 Stressbull 1048708 Those receiving parental enteral nutritionbull 1048708 Pancreatitis diseases that darr beta cell function

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

Insulin

Human insulin is absorbed more quickly from its site of action than are beef or pork insulins Thus duration of action of human Insulin is shorter amp doses must be adjusted

Hypoglycemia is the most serious amp common side effect of Insulin therapy BC long term diabetics do not produce counteracting hormones of Glucagon EN cortisol etc that normally provide defense against Hypoglycemia

TREATMENT for Type II DIABETES

bull Dietbull Exercise is useful in managing both types of Diabetes

because working muscles are not Insulin dependent Exercising muscles take up some of the excess blood glucose reducing the overall need for insulin

bull Weight lossbull Oral Hypoglycemic Drugs

Oral Hypoglycemic Drugs

There are many types of oral Hypoglycemic drugs some of which are bullSulfonylureas act by stimulating the β- cells to secrete more insulin than they do on their own Eg GlucotrolbullMetformin acts by suppressing liver output of glucose Eg GlucophagebullAlpha-glycosidase Inhibitors act by slowing CHO digestion and absorption from the digestive tract into the blood thus reducing the glucose surge seen after a meal Eg Precose bullByetta (Glucagon-like peptide 1 mimic) mimics the incretin GLP-1 It suppresses glucagon secretion and slows gastric emptying By promoting satiety it decreases food intake and in the long term leads to weight loss Because none of the drugs deliver new insulin to the body they cannot replace insulin therapy for people with Type I Diabetes and later in Type II Diabetics as well

SULFONYLUREAS

NIDDM patients above the age of 40 years amp having ho diabetes of less than 5 years are given Oral Hypoglycemics

Mechanism of Action1 Stimulate release of Insulin from beta cells of

pancreas2 Reduction of serum Glucagon3 Increased binding of Insulin to target tissues amp

receptors Eg Tolbutamide

Glyburide Glipizide

WHO NEEDS INSULIN

bull 1048708 Type 1bull 1048708 Type 2 uncontrolled wmedsbull 1048708 DKAbull 1048708 Hyperosmolar hyperglycemic state (HHS)bull 1048708 Surgerybull 1048708 IllnessInfectionbull 1048708 Stressbull 1048708 Those receiving parental enteral nutritionbull 1048708 Pancreatitis diseases that darr beta cell function

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

TREATMENT for Type II DIABETES

bull Dietbull Exercise is useful in managing both types of Diabetes

because working muscles are not Insulin dependent Exercising muscles take up some of the excess blood glucose reducing the overall need for insulin

bull Weight lossbull Oral Hypoglycemic Drugs

Oral Hypoglycemic Drugs

There are many types of oral Hypoglycemic drugs some of which are bullSulfonylureas act by stimulating the β- cells to secrete more insulin than they do on their own Eg GlucotrolbullMetformin acts by suppressing liver output of glucose Eg GlucophagebullAlpha-glycosidase Inhibitors act by slowing CHO digestion and absorption from the digestive tract into the blood thus reducing the glucose surge seen after a meal Eg Precose bullByetta (Glucagon-like peptide 1 mimic) mimics the incretin GLP-1 It suppresses glucagon secretion and slows gastric emptying By promoting satiety it decreases food intake and in the long term leads to weight loss Because none of the drugs deliver new insulin to the body they cannot replace insulin therapy for people with Type I Diabetes and later in Type II Diabetics as well

SULFONYLUREAS

NIDDM patients above the age of 40 years amp having ho diabetes of less than 5 years are given Oral Hypoglycemics

Mechanism of Action1 Stimulate release of Insulin from beta cells of

pancreas2 Reduction of serum Glucagon3 Increased binding of Insulin to target tissues amp

receptors Eg Tolbutamide

Glyburide Glipizide

WHO NEEDS INSULIN

bull 1048708 Type 1bull 1048708 Type 2 uncontrolled wmedsbull 1048708 DKAbull 1048708 Hyperosmolar hyperglycemic state (HHS)bull 1048708 Surgerybull 1048708 IllnessInfectionbull 1048708 Stressbull 1048708 Those receiving parental enteral nutritionbull 1048708 Pancreatitis diseases that darr beta cell function

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

Oral Hypoglycemic Drugs

There are many types of oral Hypoglycemic drugs some of which are bullSulfonylureas act by stimulating the β- cells to secrete more insulin than they do on their own Eg GlucotrolbullMetformin acts by suppressing liver output of glucose Eg GlucophagebullAlpha-glycosidase Inhibitors act by slowing CHO digestion and absorption from the digestive tract into the blood thus reducing the glucose surge seen after a meal Eg Precose bullByetta (Glucagon-like peptide 1 mimic) mimics the incretin GLP-1 It suppresses glucagon secretion and slows gastric emptying By promoting satiety it decreases food intake and in the long term leads to weight loss Because none of the drugs deliver new insulin to the body they cannot replace insulin therapy for people with Type I Diabetes and later in Type II Diabetics as well

SULFONYLUREAS

NIDDM patients above the age of 40 years amp having ho diabetes of less than 5 years are given Oral Hypoglycemics

Mechanism of Action1 Stimulate release of Insulin from beta cells of

pancreas2 Reduction of serum Glucagon3 Increased binding of Insulin to target tissues amp

receptors Eg Tolbutamide

Glyburide Glipizide

WHO NEEDS INSULIN

bull 1048708 Type 1bull 1048708 Type 2 uncontrolled wmedsbull 1048708 DKAbull 1048708 Hyperosmolar hyperglycemic state (HHS)bull 1048708 Surgerybull 1048708 IllnessInfectionbull 1048708 Stressbull 1048708 Those receiving parental enteral nutritionbull 1048708 Pancreatitis diseases that darr beta cell function

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

SULFONYLUREAS

NIDDM patients above the age of 40 years amp having ho diabetes of less than 5 years are given Oral Hypoglycemics

Mechanism of Action1 Stimulate release of Insulin from beta cells of

pancreas2 Reduction of serum Glucagon3 Increased binding of Insulin to target tissues amp

receptors Eg Tolbutamide

Glyburide Glipizide

WHO NEEDS INSULIN

bull 1048708 Type 1bull 1048708 Type 2 uncontrolled wmedsbull 1048708 DKAbull 1048708 Hyperosmolar hyperglycemic state (HHS)bull 1048708 Surgerybull 1048708 IllnessInfectionbull 1048708 Stressbull 1048708 Those receiving parental enteral nutritionbull 1048708 Pancreatitis diseases that darr beta cell function

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

WHO NEEDS INSULIN

bull 1048708 Type 1bull 1048708 Type 2 uncontrolled wmedsbull 1048708 DKAbull 1048708 Hyperosmolar hyperglycemic state (HHS)bull 1048708 Surgerybull 1048708 IllnessInfectionbull 1048708 Stressbull 1048708 Those receiving parental enteral nutritionbull 1048708 Pancreatitis diseases that darr beta cell function

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

WHAT HAPPENS WHEN THERE IS INSULIN EXCESS

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

Symptoms

bull Decreased blood supply to the brain as the brain literally starves

bull Tremors

bull Fatigue

bull Sleepiness

bull Inability to concentrate

bull Unconsciousness

bull Death

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE

NOTE

A diabetic can lose consciousness and die from either diabetic ketoacidotic coma

caused by prolonged Insulin deficiency or acute hypoglycemia caused by Insulin

excess

How do you differentiate between the two if a diabetic patient is brought to you unconscious

• Question
• (Effects of insulin deficiency)
• Slide 3
• EFFECTS OF INSULIN DEFICIENCY
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• COMPLICATIONS
• Diabetic foot showing ulcer
• Gangrene that must be treated with an amputation
• Slide 13
• KETOSIS AND COMA
• Slide 15
• DIABETES MELLTIUS
• DIABETES MELLITUS
• Slide 18
• TYPE I Juvenile Onset Insulin Dependent
• Slide 20
• TYPE II DIABETES Non-Insulin Dependant Adult Onset Diabetes
• Slide 22
• TYPE II DIABETES
• PATHOPHYSIOLOGY
• DIAGNOSIS OF DIABETES
• Glucose Tolerance Test
• POINT TO REMEMBER
• Slide 28
• Slide 29
• DIAGNOSIS OF DIABETES
• TREATMENT for Type I DIABETES
• INSULIN SYRINGES
• Insulin
• TREATMENT for Type II DIABETES
• Oral Hypoglycemic Drugs
• SULFONYLUREAS
• WHO NEEDS INSULIN
• What happens when there is insulin excess
• Slide 39
• Symptoms
• NOTE