Introduction to diabetes mellitus. What is diabetes? Heterogenous clinical syndrome in which the central feature is a chronic elevation of the blood glucose.

Introduction to diabetes mellitus

What is diabetes?

Heterogenous clinical syndrome in which the central feature is a chronic elevation of the blood glucose concentration - this results in a range of pathologies.

Due to a deficiency of insulin (absolute) or a resistance to insulin (relative).

The chronic hyperglycaemia is associated with long term tissue damage, especially the blood vessels, nerves, heart, kidneys and eyes.

Normal blood glucose levels Normal homeostatic mechanisms

maintain blood glucose levels within a narrow range of 3.5-6.5 mmol/l

Classification of diabetes mellitus Previous classification:

1. Juvenile onset diabetes/insulin dependent diabetes mellitus2. Adult onset diabetes/non-insulin dependent diabetes mellitus

Now classified as:1. Type 1: Immune mediated (could be in children with a more rapid onset (classic) or adults with a slower onset – LADA, ‘late autoimmune diabetes of adults’)2. Type 2: Insulin resistant3. Other specific types (eg certain genetic defects; drug induced; etc)4. Gestational diabetes mellitus

The epidemiology and diagnosis of diabetes mellitus Affects generally around 7% of

the population in developed countries with large geographic and ethnic variations in incidence.

Type 2 accounts for up to 85%-95% of cases of diabetes mellitus.

Diagnosis of diabetes mellitus Classical symptoms of hyperglycaemia -

polyuria (excessive urination); polydipsia (thirst); nocturia (nocturnal urination); lethargy; weight loss

Criteria for diagnosis:1. Classical symptoms plus a random plasma glucose concentration > 11.1mmol/lor2. Fasting plasma glucose > 7.0mmol/l (fasting is no food for > 8 hours)or3. 2 hour plasma glucose greater than 11.1mmol/l during oral glucose tolerance test (OGTT)

Diagnosis of diabetes mellitus Impaired glucose tolerance (IGT):

• represents an intermediate category between normal and diabetes – an area of uncertainty• at higher risk of developing type 2 diabetes and macrovascular disease (sometimes called ‘dysglycaemic macroangiopathy’)• usually clinically asymptomatic• not at increased risk for microvascular complications• a small percent with IGT revert to normal glucose tolerance on subsequent tests• the diagnostic levels for fasting blood glucose are considered to be at a level that there is an increased risk for microvascular disease and not at the assumed lower levels when there may be an increased risk for macrovascular disease

The aetiology and pathophysiology of diabetes mellitus Etiology of Type 1

Due to selective destruction of pancreatic beta cells by an autoimmune process - assumed to occur following an environmental trigger in genetically susceptible individuals absolute insulin deficiency.

The aetiology and pathophysiology of diabetes mellitus Aetiology - Type 1 - Genetics

Genetic susceptibility - HLA-DR3, -DR4, B8 and B15 predispose to diabetes (account for 40% of the genetic susceptibility). However, the majority of those who are genetically predisposed do not develop diabetes. Risk of developing diabetes when close relative has diabetes are 30% for identical twins, 5% for siblings and 6% for offspring.

Aetiology - Type 1 - EnvironmentEnvironmental - could be viral (several have been implicated - Coxsackie B4, retroviruses, rubella, cytomegalovirus, Epstein-Barr); diet (cow's milk has been implicated); stress Viruses may initiate immune mediated damage to beta cells by direct destruction, by the generation of cytokines that can damage the beta cells or by molecular mimicry

The aetiology and pathophysiology of diabetes mellitus Hypothetical Stages of Type 1

1. Genetic susceptibility2. Triggering of immune response by environmental agent3. Autoimmunity develops - antibodies detectable include ICA (islet cell antibodies), IAA (insulin autoantibodies) and anti-GAD.4. Clinical diabetes5. Remission (honeymoon phase)6. Relapse - need insulin for survival

The aetiology and pathophysiology of diabetes mellitus Aetiology - Type 2

- Insulin resistance creates a relative insulin deficiency. Insulin resistance can be due to a number of reasons - tends to occur in those that are obese. - Consensus is that the aetiology is a multifactorial interaction of environmental and genetic factors

Aetiology - Type 2 - Genetics- genetic predisposition for Type 2 diabetes is stronger than for Type 1- concordance rates in monozygotic twins is almost 100%- magnitude of genetic contribution is unknown- probably involves several genes

The aetiology and pathophysiology of diabetes mellitus Aetiology - Type 2 - Environment

i) Lifestyle:- overeating, obesity and inactivity are a high risk for type 2- most of type 2 patients are obese, but only a few obese people develop diabetesii) Malnutrition in utero- retrospective analysis has shown an inverse relationship between weight at birth and type 2 diabetes in late adulthood- suggested that malnutrition in utero may damage beta cell developmentiii) Age iv) Ethnicity

Type 2 Insulin resistance

- Insulin resistance plays a central role - "the insulin resistance syndrome" (syndrome X, plurimetabolic syndrome, metabolic syndrome)- clustering of conditions - type 2 diabetes, central obesity, hypertension & dyslipidaemia.

Insulin resistance is of two types - insulin insensitivity & insulin unresponsiveness

Can be due to:1) Abnormality in insulin molecule2) Defects in target cells/tissues (most common cause)3) Excessive amounts of antagonists

  Other aspects of type 2 pathophysiology

- No initial decrease in mass of beta cells, but later get amyloid deposits - role in pathogenesis is unclear.- Eventually get failure of beta cell secretion of insulin.- Endothelial dysfunction and leptin physiology also plays important roles in Type 2 diabetes.

Gestational Diabetes

During pregnancy, sensitivity to insulin decreases (placental hormones affect glucose tolerance)

beta cells may not be able to meet this increased need for insulin gestational diabetes

Occurs in up to 14% of pregnancies This increases subsequent risk of

developing type 2 diabetes Increased risk for perinatal mortality and

neonatal morbidity.

Clinical features - Type 1 Onset is variable. Classically, in younger age groups, the

onset is acute and insulin is needed for survival - generally present with a history of polyuria, polydipsia, lethargy and weight loss over a period of up to two weeks - many may present with ketoacidosis.

Ketoacidosis - salt and water depletion; loss of skin turgor; tachycardia; hypotension; deep and sighing breath (usually smells of acetone).

In older age groups onset is more insidious - residual beta cell function lessens risk of ketoacidosis at time of presentation.

Clinical features - type 2 Usually occur in older age groups -

especially obese (in 70%) (however, incidence in child is assumed to be increasing due to increased prevalence of childhood obesity).

- 50% have hypertension.- Classical signs of thirst, polyuria, nocturia and weight loss are not always present in Type 2 - often start with fatigue and malaise- Symptoms of hyperglycaemia are long standing and generally mild.

Up to 20% may have one/some of the complications of diabetes present at time of diagnosis.

Functional consequences of hyperglycaemia

Haemodynamic disturbances (eg increased capillary pressure)

Haemorrheological abnormalities (eg increased blood viscosity; increased coagubility)

Microvascular dysfunction Endothelial dysfunction  

Complications of DM

Complications of Diabetes Acute complications:

- ketoacidosis, hypoglycaemia, hyperosmolar non-ketotic coma, intercurrent illnessChronic complications:- retinopathy, nephropathy, neuropathy, macrovascular disease, other

Hypoglycemia

Hypoglycemia- Most "hypo's" are minor and easily treated- Prolonged and repeated attacks can result in permanent damage. - Symptoms occur when blood glucose level drops to about 3.00mmol/l.- Commonly precipitated by diet changes (eg missed meals, delayed meals, not eating enough), exercise, inappropriate insulin doses.

- More common in those on insulin than sulphonylurea drugs. - Fictitious or deliberately induced hypoglycaemic attacks may occur for psychological reasons.

Risk factors - older person; change in hypoglycaemic treatment; type of sulphonylurea; male; tight glycaemic control; polypharmacy; renal disease; high alcohol consumption

Hypoglycaemia

Clinical features of hypoglycaemia:Most patients recognise the symptoms (except during sleep) - sweating, tremor/trembling, palpitations/pounding heart, anxiety, tiredness, pallor, headache, hunger, dizziness, irritability, blurred vision, irritability, aggressive behaviour, slurred speech, confusion, drowsiness, convulsions, coma

In longstanding cases - develop a hypoglycaemic unawareness (especially in presence of autonomic neuropathy) and have difficulty recognising the symptoms.

Consequences of serious and/or repeated hypoglycaemic attacks:Coma, convulsions, impaired cognitive function, intellectual decline, cardiac arrythmias, eye damage, hypothermia, accidents (eg motor vehicle)

Management:Give food containing glucose (soft drink; honey; jelly beans etc); nothing by mouth if unconscious - use glucagon or IV dextrose; determine cause

Diabetic ketoacidosis (DKA

Life threatening - result of severe insulin deficiency - leading to a release of free fatty acids into the circulation and hepatic fatty acid oxidation à forms ketone bodies.Biochemical features - hyperglycaemia, hyperketonaemia and metabolic acidosis

Aetiology:New presentation; intercurrent infection (loose appetite - stop taking insulin); illness (eg stroke); withdrawal of insulin; major dietary indiscretion; significant emotional stress.

Clinical features:Develops over a few days; polyuria; thirst; weight loss; weakness; leg cramps; hypotension; tachycardia; nausea; vomiting; abdominal pain and tenderness; dehydration; kussmaul respiration; blurred vision; ketotic breath; hypothermia; confusion; coma

Consequences of ketoacidosis - cerebral oedema; acute respiratory distress syndrome; thromboembolism; disseminated intravascular coagulation

Management:Hospitalisation; fluids; insulin (IV infusion); electrolyte balance (especially potassium); determine cause; antibiotics if infection

Treatment for Diabetes control General procedures

Methods- Self-care

Diet and exercise Fundamentals of the diabetic diet Eating habits

Medication Insulin Oral anti diabetic agent

DiabetesOral relationships/

findings The oral mucosa, tongue and

periodontal tissues may show unusual susceptibility and a tendency toward more marked reactions to injury, infections, and all local irritants

Such response is related to generally lowered resistance and delay healing processes

DiabetesOral relationships/

findings Periodontal Involvement Diabetes is a risk factor for periodontal

infections Clinical findings

Marked periodontal disease Alveolar bone resorption Loss of attachment Deep pockets Tooth mobility +/- migration Signs of trauma from occlusion Sometimes periodontal abscess

formation

DiabetesOral relationships/

findings Dental Caries

Dental caries rate is generally consistent patient’s own age group or may be slightly higher due to diminished saliva and dry mouth or to high carbohydrate diet in the obese

Control: with a well-regulated diet, low in or free of sugar containing foods – high caries rate is controlled.

DiabetesOral relationships

Other oral findings: common in poorly controlled DM

Lips: Drying, cracking, angular cheilitis

Xerostomia: Alternation in micro flora, increased plaque formation

Mucosa: Edematous, red possibly ulcerated; burning sensations, poor tolerance for removable prostheses

Dental hygiene care for DM patients Patient history-

Type, medication, diet requirements and frequency, whether its controlled and medications.

Familial diabetes Consultation with physician

Degree of control, stability, severity and susceptibility to emergency

Advice about prescriptions and prophylactic antibiotics

Other instructions to be given postoperatively Use of information

Appointment planning Antiboitic premdeicatin Time: mornig 1 ½ -3 hours after breakfast and

medication precautions

Dental hygiene care for DM patients

Appointment planningAntibiotic premedicationTime: morning 1 ½ -3 hours after

breakfast and medicationPrecautions:

• Patients should not be kept waiting unduly

• Do not interfere with patients regular meal and between meal eating schedule

• Avoid long periods of stressful procedures• Prepare for diabetic emergency if history

reveal diabetic instability

Dental hygiene care for DM patients Clinical procedures Instrumentation:

quadrant scaling or area scaling especially when patient has a healing problem

Avoid undue trauma to tissues to encourage postoperative healing

Fluoride application Patient instruction

Influence of diabetes instructions –relate control of oral tissue infection and control of diabetes

Bacterial plaque control Diets

Dental hygiene care for DM patients

Maintenance phaseAppointments for examination at

least on 2-3 months basisProbe carefully to detect early

periodontal diseaseRoutine scaling and root planning