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1
PRESENTED BY:
ABDUL RICHARD CONTEH
S.C.S.
MAGBURAKA TEAM
SECOND YEAR STUDENT
2
Diabetes Mellitus
 Diabetes mellitus (DM) is a chronic condition
that is characterised by raised blood glucose
levels (Hyperglycemia).
3
Regulation of Plasma
Glucose Level
4
How Insuline Decrease
Plasma Glucose Level?
5
Classification of DM
1. Type 1 DM
• It is due to insulin deficiency and is formerly known as.
• Type I
• Insulin Dependent DM (IDDM)
• Juvenile onset DM
2. Type 2 DM
• It is a combined insulin resistance and relative deficiency in
insulin secretion and is frequently known as.
• Type II
• Noninsulin Dependent DM (NIDDM)
• Adult onset DM
6
3. Gestational Diabetes Mellitus (GDM):
 Gestational Diabetes Mellitus (GDM) developing during some
cases of pregnancy but usually disappears after pregnancy.
4. Other types:
 Secondary DM
• Congenital
• Neonatal
7
Etiology
1. Etiology of Type 1 Diabetes
8
9
2. Etiology of Type 2 Diabetes
10
a
11
12
13
14
Risk Factors
• Type 1 DM
– Genetic predisposition
• In an individual with a genetic
predisposition, an event such as virus
or toxin triggers autoimmune
destruction of b-cells probably over a
period of several years.
15
Risk Factors
• Type 2 DM
– Family History
– Obesity
– Habitual physical inactivity
– Previously identified impaired glucose tolerance
– Impaired fasting glucose (IFG)
– Hypertension
– Hyperlipidemia
16
Pathophysiology
• Type 1 DM
– Type 1 DM is characterized by an absolute
deficiency of insulin due to immune- mediated
destruction of the pancreatic b-cells
– In rare cases the b-cell destruction is not due to
immune mediated reaction (idiopathic type 1 DM)
17
18
Pathophysiology
• Type 1 DM
 There are four stages in the development of
Type 1 DM:
1. Preclinical period with positive b-cell antibodies
2. Hyperglycemia when 80-90% of the
β- cells are destroyed.
3. Transient remission (honeymoon phase).
3. Establishment of the disease
19
Pathophysiology
• Type 2 DM
– Type 2 DM is characterized by the presence of both insulin
resistance (tissue insensitivity) and some degree of insulin
deficiency or b- cell dysfunction
– Type 2 DM occurs when a diabetogenic lifestyle (excessive
calories, inadequate caloric expenditure and obesity) is
superimposed upon a susceptible genotype
20
Laboratory Tests
1. Glucosuria
– To detect glucose in urine by a paper strip
• Semi-quantitative
• Normal kidney threshold for glucose is essential
2. Ketonuria
– To detect ketonbodies in urine by a paper strip
• Semi-quantitative
21
Laboratory Tests (Cont’d)
3. Fasting blood glucose
– Glucose blood concentration in samples obtained after at
least 8 hours of the last meal
4. Random Blood glucose
– Glucose blood concentration in samples obtained at any
time regardless the time of the last meal
22
Laboratory Tests (Cont’d)
5. Glucose tolerance test
– 75 gm of glucose are given to the patient with 300 ml of
water after an overnight fast
– Blood samples are drawn 1, 2, and 3 hours after taking the
glucose
– This is a more accurate test for glucose utilization if the
fasting glucose is borderline
23
Laboratory Tests (Cont’d)
6. Glycosylated hemoglobin (HbA1C)
– HbA1C is formed by condensation of glucose with free
amino groups of the globin component of hemoglobin
– Normally it comprises 4-6% of the total hemoglobin.
– Increase in the glucose blood concentration increases the
glycated hemoglobin fraction.
– HbA1C reflects the glycemic state during the preceding 8-
12 weeks.
24
Laboratory Findings (Cont’d)
7. Serum Fructosamine
– Formed by glycosylation of serum protein (mainly albumin)
– Since serum albumin has shorter half life than hemoglobin,
serum fructosamine reflects the glycemic state in the
preceding 2 weeks
– Normal is 1.5 - 2.4 mmole/L when serum albumin is 5 gm/dL.
25
Diagnostic Criteria
• Any one test should be confirmed with a second test, most
often fasting plasma glucose (FPG).
• This criteria for diagnosis should be confirmed by
repeating the test on a different day.
26
27
Clinical Presentation
• Type 1 DM
- Polyuria
- Polydipsia
- Polyphagia
- Weight loss
- Weakness
- Dry skin
- Ketoacidosis
• Type 2 DM
- Patients can be asymptomatic
- Polyuria
- Polydipsia
- Polyphagia
- Fatigue
- Weight loss
- Most patients are discovered
while performing urine glucose
screening
28
Treatment
- Relieve symptoms
- Reduce mortality
- Improve quality of life
- Reduce the risk of microvascular and macrovascular
disease complications
- Macrovascular complications:
Coronary heart disease, stroke and peripheral vascular disease
- Microvascular Complications:
Retinopathy, nephropathy and neuropathy
Desired outcome
29
How to achieve the goals ?
- Near normal glycemic control reduce the risk
of developing microvascular disease
complications
- Control of the traditional CV risk factors such
as smoking, management of dyslipidemia,
intensive BP control and antiplatelet therapy.
Treatment
30
Treatment
General approaches
- Medications
- Dietary and exercise modification
- Regular complication monitoring
- Self monitoring of blood glucose
- Control of BP and lipid level
31
Treatment
Complication monitoring
- Annual eye examination
- Annual microalbuminuria
- Feet examination
- BP monitoring
- Lipid profile
32
Treatment
Self-monitoring of blood glucose
- Frequent self monitoring of blood glucose to
achieve near normal level
- More intense insulin regimen require more
frequent monitoring
33
Treatment
Nonpharmacological therapy
- For type 1 the goal is to regulate insulin
administration with a balanced diet
- In most cases, high carbohydrate, low fat, and low
cholesterol diet is appropriate
- Type 2 DM patients need caloric restriction
Diet
34
Treatment
Nonpharmacological therapy
- Artificial sweeteners:
- e.g. Aspartame, saccharin, sucralose, and acesulfame
- Safe for use by all people with diabetes
- Nutritive sweeteners:
- e.g. fructose and sorbitol
- Their use is increasing except for acute diarrhea in
some patients
Diet (Cont’d)
35
Treatment
Nonpharmacological therapy
- Exercise improves insulin resistance and achieving glycemic
control.
- Exercise should start slowly for patients with limited activity.
- Patients with CV diseases should be evaluated before
starting any exercise
Activity
36
37
Treatment
Pharmacological therapy
- Insulin (Type 1 and Type 2 DM)
- Sulfonylurea (Type 2 DM)
- Biguanides (Type 2 DM)
- Meglitinides (Type 2 DM)
- Thiazolidinediones Glitazones (Type 2 DM)
 a-Glucosidase inhibitors (Type 2 DM)
38
Pharmacotherapy :Type 1 DM
The choice of therapy is simple
All patients need Insulin
39
Pharmacotherapy :Type 1 DM
The goal is:
To balance the caloric intake with the
glucose lowering processes (insulin and
exercise), and allowing the patient to live
as normal a life as possible
40
II. Surgery
• Islet transplantation has been investigated as a
treatment for type 1 diabetes mellitus in selected
patients with inadequate glucose control despite
insulin therapy.
• Observations in patients with type 1 diabetes
indicate that islet transplantation can result in
insulin independence with excellent metabolic
control
Ref. Shapiro A.M. J., et al. N Engl J Med 2000; 343:230-238, Jul 27, 2000
41
Diabetes Mellitus Complications
1. Hypoglycemia
- Cause: Missing meals or excessive exercise or too
much insulin
- Symptoms: Tachycardia, palpitation, sweating,
nausea, and vomiting. Progress to mental confusion,
bizarre behavior and coma
- Treatment: Candy or sugar
IV glucose
Glucagon 1 gm IM
- Identification: MedicAler bracelet
42
Diabetes Mellitus Complications
2. Diabetes retinopathy
- Microaneurysm
- Hemorrhage
- Exudates
- Retinal edema
- other
43
Diabetes Mellitus Complications
3. Diabetes nephropathy
- 30-40 % of all type 1 DM patients develop
nephropathy in 20 years
- 15-20 % of type 2 DM patients develop nephropathy
- Manifested as:
- Microalbuminuria
- Progressive diabetic nephropathy leading to end-
stage renal disease
44
Diabetes Mellitus Complications
Diabetes nephropathy (Cont’d)
- All diabetic patients should be screened annually for
microalbuminurea to detect patients at high risk of
developing progressive diabetic nephropathy
- Tight glycemic control and management of the blood
pressure can significantly decrease the risk of
developing diabetic nephropathy.
- ACE-inhibitors are recommended to decrease the
progression of nephropathy
45
Diabetes Mellitus Complications
4. Diabetes neuropathy
Autonomic neuropathy:
- Manifested by orthostatic hypotension, diabetic
diarrhea, erectile dysfunction, and difficulty in
urination.
46
Diabetes Mellitus Complications
5. Peripheral vascular disease and foot ulcer
Incidence of gangrene
of the feet in DM is 20
fold higher than control
group due to:
- Ischemia
- Peripheral neuropathy
- Secondary infection
47
Special Patient Population
1. Adolescent Type 2 DM
- Type 2 DM is increasing in adolescent
- Lifestyle modification is essential in these patients
- If lifestyle modification alone is not effective,
metformin the only labeled oral agent for use in
children (10-16 years)
48
Special Patient Population
2. Gestational DM
- Dietary control
- If blood glucose is not controlled by dietary control,
insulin therapy is initiated
- One dose of NPH or NPH + regular insulin (2:1) given
before breakfast. Adjust regimen according to SMBG.
- Sulfonylureas: Effective, but require further studies to
demonstrate safety.
49
Special Situations
3. Diabetic ketoacidosis
- It is a true emergency
- Usually results from omitting insulin in type 1 DM or
increase insulin requirements in other illness (e.g.
infection, trauma) in type 1 DM and type 2 DM
50
THANK YOU FOR LISTENING

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5 DIABETES MELLITUS.power point presentation

  • 1. 1 PRESENTED BY: ABDUL RICHARD CONTEH S.C.S. MAGBURAKA TEAM SECOND YEAR STUDENT
  • 2. 2 Diabetes Mellitus  Diabetes mellitus (DM) is a chronic condition that is characterised by raised blood glucose levels (Hyperglycemia).
  • 5. 5 Classification of DM 1. Type 1 DM • It is due to insulin deficiency and is formerly known as. • Type I • Insulin Dependent DM (IDDM) • Juvenile onset DM 2. Type 2 DM • It is a combined insulin resistance and relative deficiency in insulin secretion and is frequently known as. • Type II • Noninsulin Dependent DM (NIDDM) • Adult onset DM
  • 6. 6 3. Gestational Diabetes Mellitus (GDM):  Gestational Diabetes Mellitus (GDM) developing during some cases of pregnancy but usually disappears after pregnancy. 4. Other types:  Secondary DM • Congenital • Neonatal
  • 7. 7 Etiology 1. Etiology of Type 1 Diabetes
  • 8. 8
  • 9. 9 2. Etiology of Type 2 Diabetes
  • 10. 10 a
  • 11. 11
  • 12. 12
  • 13. 13
  • 14. 14 Risk Factors • Type 1 DM – Genetic predisposition • In an individual with a genetic predisposition, an event such as virus or toxin triggers autoimmune destruction of b-cells probably over a period of several years.
  • 15. 15 Risk Factors • Type 2 DM – Family History – Obesity – Habitual physical inactivity – Previously identified impaired glucose tolerance – Impaired fasting glucose (IFG) – Hypertension – Hyperlipidemia
  • 16. 16 Pathophysiology • Type 1 DM – Type 1 DM is characterized by an absolute deficiency of insulin due to immune- mediated destruction of the pancreatic b-cells – In rare cases the b-cell destruction is not due to immune mediated reaction (idiopathic type 1 DM)
  • 17. 17
  • 18. 18 Pathophysiology • Type 1 DM  There are four stages in the development of Type 1 DM: 1. Preclinical period with positive b-cell antibodies 2. Hyperglycemia when 80-90% of the β- cells are destroyed. 3. Transient remission (honeymoon phase). 3. Establishment of the disease
  • 19. 19 Pathophysiology • Type 2 DM – Type 2 DM is characterized by the presence of both insulin resistance (tissue insensitivity) and some degree of insulin deficiency or b- cell dysfunction – Type 2 DM occurs when a diabetogenic lifestyle (excessive calories, inadequate caloric expenditure and obesity) is superimposed upon a susceptible genotype
  • 20. 20 Laboratory Tests 1. Glucosuria – To detect glucose in urine by a paper strip • Semi-quantitative • Normal kidney threshold for glucose is essential 2. Ketonuria – To detect ketonbodies in urine by a paper strip • Semi-quantitative
  • 21. 21 Laboratory Tests (Cont’d) 3. Fasting blood glucose – Glucose blood concentration in samples obtained after at least 8 hours of the last meal 4. Random Blood glucose – Glucose blood concentration in samples obtained at any time regardless the time of the last meal
  • 22. 22 Laboratory Tests (Cont’d) 5. Glucose tolerance test – 75 gm of glucose are given to the patient with 300 ml of water after an overnight fast – Blood samples are drawn 1, 2, and 3 hours after taking the glucose – This is a more accurate test for glucose utilization if the fasting glucose is borderline
  • 23. 23 Laboratory Tests (Cont’d) 6. Glycosylated hemoglobin (HbA1C) – HbA1C is formed by condensation of glucose with free amino groups of the globin component of hemoglobin – Normally it comprises 4-6% of the total hemoglobin. – Increase in the glucose blood concentration increases the glycated hemoglobin fraction. – HbA1C reflects the glycemic state during the preceding 8- 12 weeks.
  • 24. 24 Laboratory Findings (Cont’d) 7. Serum Fructosamine – Formed by glycosylation of serum protein (mainly albumin) – Since serum albumin has shorter half life than hemoglobin, serum fructosamine reflects the glycemic state in the preceding 2 weeks – Normal is 1.5 - 2.4 mmole/L when serum albumin is 5 gm/dL.
  • 25. 25 Diagnostic Criteria • Any one test should be confirmed with a second test, most often fasting plasma glucose (FPG). • This criteria for diagnosis should be confirmed by repeating the test on a different day.
  • 26. 26
  • 27. 27 Clinical Presentation • Type 1 DM - Polyuria - Polydipsia - Polyphagia - Weight loss - Weakness - Dry skin - Ketoacidosis • Type 2 DM - Patients can be asymptomatic - Polyuria - Polydipsia - Polyphagia - Fatigue - Weight loss - Most patients are discovered while performing urine glucose screening
  • 28. 28 Treatment - Relieve symptoms - Reduce mortality - Improve quality of life - Reduce the risk of microvascular and macrovascular disease complications - Macrovascular complications: Coronary heart disease, stroke and peripheral vascular disease - Microvascular Complications: Retinopathy, nephropathy and neuropathy Desired outcome
  • 29. 29 How to achieve the goals ? - Near normal glycemic control reduce the risk of developing microvascular disease complications - Control of the traditional CV risk factors such as smoking, management of dyslipidemia, intensive BP control and antiplatelet therapy. Treatment
  • 30. 30 Treatment General approaches - Medications - Dietary and exercise modification - Regular complication monitoring - Self monitoring of blood glucose - Control of BP and lipid level
  • 31. 31 Treatment Complication monitoring - Annual eye examination - Annual microalbuminuria - Feet examination - BP monitoring - Lipid profile
  • 32. 32 Treatment Self-monitoring of blood glucose - Frequent self monitoring of blood glucose to achieve near normal level - More intense insulin regimen require more frequent monitoring
  • 33. 33 Treatment Nonpharmacological therapy - For type 1 the goal is to regulate insulin administration with a balanced diet - In most cases, high carbohydrate, low fat, and low cholesterol diet is appropriate - Type 2 DM patients need caloric restriction Diet
  • 34. 34 Treatment Nonpharmacological therapy - Artificial sweeteners: - e.g. Aspartame, saccharin, sucralose, and acesulfame - Safe for use by all people with diabetes - Nutritive sweeteners: - e.g. fructose and sorbitol - Their use is increasing except for acute diarrhea in some patients Diet (Cont’d)
  • 35. 35 Treatment Nonpharmacological therapy - Exercise improves insulin resistance and achieving glycemic control. - Exercise should start slowly for patients with limited activity. - Patients with CV diseases should be evaluated before starting any exercise Activity
  • 36. 36
  • 37. 37 Treatment Pharmacological therapy - Insulin (Type 1 and Type 2 DM) - Sulfonylurea (Type 2 DM) - Biguanides (Type 2 DM) - Meglitinides (Type 2 DM) - Thiazolidinediones Glitazones (Type 2 DM)  a-Glucosidase inhibitors (Type 2 DM)
  • 38. 38 Pharmacotherapy :Type 1 DM The choice of therapy is simple All patients need Insulin
  • 39. 39 Pharmacotherapy :Type 1 DM The goal is: To balance the caloric intake with the glucose lowering processes (insulin and exercise), and allowing the patient to live as normal a life as possible
  • 40. 40 II. Surgery • Islet transplantation has been investigated as a treatment for type 1 diabetes mellitus in selected patients with inadequate glucose control despite insulin therapy. • Observations in patients with type 1 diabetes indicate that islet transplantation can result in insulin independence with excellent metabolic control Ref. Shapiro A.M. J., et al. N Engl J Med 2000; 343:230-238, Jul 27, 2000
  • 41. 41 Diabetes Mellitus Complications 1. Hypoglycemia - Cause: Missing meals or excessive exercise or too much insulin - Symptoms: Tachycardia, palpitation, sweating, nausea, and vomiting. Progress to mental confusion, bizarre behavior and coma - Treatment: Candy or sugar IV glucose Glucagon 1 gm IM - Identification: MedicAler bracelet
  • 42. 42 Diabetes Mellitus Complications 2. Diabetes retinopathy - Microaneurysm - Hemorrhage - Exudates - Retinal edema - other
  • 43. 43 Diabetes Mellitus Complications 3. Diabetes nephropathy - 30-40 % of all type 1 DM patients develop nephropathy in 20 years - 15-20 % of type 2 DM patients develop nephropathy - Manifested as: - Microalbuminuria - Progressive diabetic nephropathy leading to end- stage renal disease
  • 44. 44 Diabetes Mellitus Complications Diabetes nephropathy (Cont’d) - All diabetic patients should be screened annually for microalbuminurea to detect patients at high risk of developing progressive diabetic nephropathy - Tight glycemic control and management of the blood pressure can significantly decrease the risk of developing diabetic nephropathy. - ACE-inhibitors are recommended to decrease the progression of nephropathy
  • 45. 45 Diabetes Mellitus Complications 4. Diabetes neuropathy Autonomic neuropathy: - Manifested by orthostatic hypotension, diabetic diarrhea, erectile dysfunction, and difficulty in urination.
  • 46. 46 Diabetes Mellitus Complications 5. Peripheral vascular disease and foot ulcer Incidence of gangrene of the feet in DM is 20 fold higher than control group due to: - Ischemia - Peripheral neuropathy - Secondary infection
  • 47. 47 Special Patient Population 1. Adolescent Type 2 DM - Type 2 DM is increasing in adolescent - Lifestyle modification is essential in these patients - If lifestyle modification alone is not effective, metformin the only labeled oral agent for use in children (10-16 years)
  • 48. 48 Special Patient Population 2. Gestational DM - Dietary control - If blood glucose is not controlled by dietary control, insulin therapy is initiated - One dose of NPH or NPH + regular insulin (2:1) given before breakfast. Adjust regimen according to SMBG. - Sulfonylureas: Effective, but require further studies to demonstrate safety.
  • 49. 49 Special Situations 3. Diabetic ketoacidosis - It is a true emergency - Usually results from omitting insulin in type 1 DM or increase insulin requirements in other illness (e.g. infection, trauma) in type 1 DM and type 2 DM
  • 50. 50 THANK YOU FOR LISTENING