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Diabetes MellitusIntroduction to Diabetes Epidemiology

Definition:A metabolic disorder of multiple aetiology characterized by chronic hyperglycaemia with disturbances of carbohydrate, fat and protein metabolism resulting from one or more of the following:1. Defects in insulin secretion (lack or absence).2. Defects in insulin formation (structure or action).3. Defects in insulin receptors (lack or abnormal).

Diabetes mellitus Diabetes mellitus was well known in ancient times, long before scientists and doctor began to investigate itThe main features of the disease were recognized at that time, and may still be listed as:1. Severe thirst2. Excessive drinking3. Frequent urination4. Bodily wasting

Classification:1. Diabetes Mellitus (DM): i-Insulin dependant diabetes Mellitus (IDDM, Type 1) ii- Non - insulin dependant diabetes Mellitus (NIDDM, Type 2) iii- Malnutrition – related diabetes mellitus (MRDM) iv- Other types (secondary to pancreatic, hormonal , drug induced, genetics and other abnormalities)2. Impaired glucose tolerance (IGT)3. Gestational diabetes mellitus (GDM)4. Metabolic syndrome.

Epidemiology of diabetes

Prevalence worldwide is increasing* 2.8% in 2000; 4.4% in 2030 worldwide 171 million in 2000; 366 million in 2030 Greatest rise in developing world

Global Prevalence Estimates, 2000 and 2030

4.4 %
2.8 %
Reference: Wild S, Roglic G, Green A, Sicree R, King H. Global prevalence of diabetes. Diabetes Care. 2004; 27(5): 1047-1053.

Prevalence of Diabetes - 2025

380 Million
380 Million



Natural history of DiabetesI- Agent:1. Pancreatic disorders.2. Defects in the formation of insulin.3. Destruction of Beta cells of the pancreas.4. Decreased insulin sensitivity.5. Genetic defects.6. Autoimmunity.


Natural history of DiabetesII- Host factors:1. Age.2. Sex.3. Genetic factors (twins).4. Genetic markers ( only IDDM, HLA- B8, B15, DR3, DR4)5. Immune mechanisms.6. Obesity.


Natural history of DiabetesIII- Environmental risk factors:1. Sedentary life.2. Diets.3. Malnutrition ( PEM )4. Alcohol.5. Viral infection ( rubella, mumps and HCV, HBV)6. Chemical agents (Alloxan, Streptozotocin and Valcor)7. Stress.8. Others ( social class, before 50 years > in upper , now the reverse occur)

TYPE I AND TYPE II DIABETES

Characteristic
Type I
Type II
Other Names
IDDM (Insulin-Dependent Diabetes Mellitus). Previously, juvenile – onset diabetes mellitus NIDDM (Non insulin Dependent Diabetes Mellitus). Previously, adult onset diabetes mellitus
Percent of Diabetic Population
5% - 10%
90%
Age at Onset
younger than 30 years; peaks at 10 – 14 years; rare before 6 months Usually over 40 years
Pancreatic Function
None
Insulin present in low, “normal’ or high amounts


Pathogenesis
Associated with certain HLA types; presence of islet cell antibodies suggests autoimmune process
Defect in insulin secretion. Tissue resistance to insulin. Increased hepatic glucose output
Family History
Generally not strong
Strong
Obesity
Uncommon unless “over-insulinized” Common (60% to 90%)
History of Ketacidosis
Often present
Rare, except in circumstances of unusual stress
Clinical Presentation
Moderate to severe symptoms which progress relatively rapidly (days to weeks): polyuria, polydipsia, fatigue, weight loss, ketoacidosis
Mild polyuria, fatigue. Often diagnosed on physical examination
Treatment
Insulin Diet Exercise
Diet Exercise Sulfonylureas Biguanides Insulin

SIGNS AND SYMPTOMS

1. As a result of the loss of calories and water, patients experience symptoms of polyuria, polydipsia, fatigue, and profound weight loss.
2. Since high glucose levels provide an excellent medium for microorganisms, patients with diabetes may also present with recurrent respiratory, vaginal, and other infections.


3. Muscle begins to metabolize glycogen for fuel.
4. Liver begins to metabolize free fatty acids which are released in response to epinephrine and low insulin concentrations.
5. An absolute lack of insulin may cause excessive mobilization of free fatty acids to the liver where they are metabolized to ketones.

6. This can result in ketonemia, ketonuria, and ultimately, ketoacidosis

7. Patients with high blood glucose concentrations may also experience blurred vision secondary to osmotically-induced changes in the lens.
8. It should be emphasized that weight loss and ketoacidosis primarily occur in poorly – controlled Type I (IDDM) diabetic individuals. 9. Persons with NIDDM frequently have mild symptoms related to elevated blood glucose concentrations (fatigue, polyuria, polydipsia, vaginal infections) but rarely develop ketoacidosis bec insulin is present in sufficient amount to suppress lipolysis.
10. Furthermore, weight loss is uncommon in these individuals because relatively high endogenous insulin levels promote lipogenesis.

DIAGNOSIS

For non-pregnant individuals of any age, a diagnosis of diabetes can be made if at least one of the following is present:
1. The patient presents with classical signs and symptoms of diabetes ( and has FBS ≥ 140 mg/dL or RBS ≥ 200 mg/dL 2. A fasting plasma glucose concentration is ≥ 140 mg/dL on two or more occasions. 3. Following a standard oral glucose challenge (75 gms glucose for an adult or 1.75 gms/kg for a child), the venous plasma glucose concentration is ≥ 200 mg/dL at 2 hours and > 200 mg/dL at least one other time at Ѕ, 1, 1 Ѕ hours. 4. Individuals with fasting plasma glucose values or OGTT values that are intermediate between normal and those considered diagnostic of diabetes are considered to have “impaired glucose to tolerances”.

Many factors can impair glucose tolerance without being diabetic:

1. An individual who has not fasted for a minimum of ten hours.
2. One who has fasted too long (greater than 16 hours).
3. Has ingested insufficient carbohydrates before testing.
4. During or soon after an acute illness such as a myocardial infarction.
5. Pregnancy, other forms of stress.
6. Lack of physical activity.
7. Many drugs may alter glucose tolerance.


Urine Glucose
1. Its presence is not diagnostic because glucosuria may occur when the renal threshold for glucose is decreased (as in pregnancy) or when there are other sugars and interfering substances in the urine.
2. Conversely, the absence of glucose in the urine does not rule -out diabetes in individuals with elevated renal thresholds.
Glycosylated Hemoglobin (HbA1C).
1. Glycosylated hemoglobin concentrations generally reflect the mean blood glucose concentrations over the past one to two months and are almost always elevated in patients with diabetes.
2. Glycosylated hemoglobin levels cannot be used to diagnose diabetes is that there is little standardization of the testing procedure from one laboratory to the next; but it is a good predictor for complications.


LONG –TERM COMPLICATIONS •Large blood vessels (macro-vascular)Arterial disease, coronary heart disease (heart attacks),Stroke, reduced blood supply to legs •Small blood vessels (micro-vascular)Eye (retinopathy)Kidney (nephropathy)Nerve (neuropathy)

LONG –TERM COMPLICATIONS Some other diabetic complications •Skin disorders (necrobiosis, diabetic dermopathy). •Sexual dysfunction Male impotence (due to neuropathy, impaired circulation, psychological problems)

Prone to autoimmune diseases. (Grave’s, Addison, Hashimoto’s thyroiditis). LONG –TERM COMPLICATIONS

Screening of diabetes:1. Urine examination.2. Blood sugar testing.Target population (high-risk population):1. > 40 years.2. +ve family history.3. Obese.4. Women who have had a baby > 4.5 Kg.5. Women who show excess weight gain during pregnancy.6. Premature atherosclerosis.


Management of Diabetes: 1. Maintain blood glucose as close as possible to normal values (drug therapy).2. To maintain ideal body weight: A- Diets. B- Exercise. 3. Self care.4. Blood glucose monitoring: A- Glycosylated hemoglobin. B- Home blood glucose monitoring. C- Routine lab. 6. Having a pocket card.


By managing the ABCs of diabetes, people with diabetes can reduce their risk for heart disease and stroke. A stands for A1C B stands for Blood pressure C stands for Cholesterol D stands for diet and lifestyle change E stands for exercise



Prevention of diabetes:I- Primordial prevention (population strategy).II- High-risk strategy (primary prevention).III- Secondary prevention:Maintain blood glucose as close as possible to normal values (treatment).To maintain ideal body weight (eating and exercise).Glycosylated hemoglobin.Self care.Home blood glucose monitoring.Having a pocket card.IV- Tertiary prevention: as diabetic clinic, epidemiological surveillance and studies.