Download Introduction to diabetes mellitus

Introduction
to diabetes
mellitus
What is diabetes?
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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
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Previous classification:
1. Juvenile onset diabetes/insulin dependent diabetes mellitus
2. 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 resistant
3. 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.
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Diagnosis of
diabetes mellitus
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Classical symptoms of hyperglycaemia - polyuria (excessive
urination); polydipsia (thirst); nocturia (nocturnal urination);
lethargy; weight loss
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Criteria for diagnosis:
1. Classical symptoms plus a random plasma glucose
concentration > 11.1mmol/l
or
2. Fasting plasma glucose > 7.0mmol/l (fasting is no food for
> 8 hours)
or
3. 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
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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 - Environment
Environmental - 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
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Hypothetical Stages of Type 1
1. Genetic susceptibility
2. Triggering of immune response by
environmental agent
3. Autoimmunity develops - antibodies detectable
include ICA (islet cell antibodies), IAA (insulin
autoantibodies) and anti-GAD.
4. Clinical diabetes
5. 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
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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
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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 diabetes
ii) 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
development
iii) Age
iv) Ethnicity
Type 2
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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.
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Insulin resistance is of two types - insulin insensitivity & insulin
unresponsiveness
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Can be due to:
1) Abnormality in insulin molecule
2) Defects in target cells/tissues (most common cause)
3) Excessive amounts of antagonists
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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
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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
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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
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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
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Complications of
DM
Complications of Diabetes
 Acute complications:
- ketoacidosis, hypoglycaemia,
hyperosmolar non-ketotic coma,
intercurrent illness
Chronic complications:
- retinopathy, nephropathy,
neuropathy, macrovascular disease,
other
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Hypoglycemia
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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
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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
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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
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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
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Treatment for
Diabetes control
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General procedures
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Diet and exercise
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MethodsSelf-care
Fundamentals of the diabetic diet
Eating habits
Medication
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Insulin
Oral anti diabetic agent
Diabetes
Oral 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
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Diabetes
Oral relationships/
findings
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Periodontal Involvement
Diabetes is a risk factor for periodontal infections
Clinical findings
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Marked periodontal disease
Alveolar bone resorption
Loss of attachment
Deep pockets
Tooth mobility +/- migration
Signs of trauma from occlusion
Sometimes periodontal abscess formation
Diabetes
Oral relationships/
findings
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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.
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Diabetes
Oral relationships
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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
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Patient history
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Consultation with physician
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Type, medication, diet requirements and frequency, whether its
controlled and medications.
Familial diabetes
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
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Appointment planning
Antibiotic premedication
 Time: morning 1 ½ -3 hours after breakfast
and medication
 Precautions:
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• 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
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Clinical procedures
Instrumentation:
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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
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Influence of diabetes instructions –relate control of
oral tissue infection and control of diabetes
Bacterial plaque control
Diets
Dental hygiene care
for DM patients
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Maintenance phase
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Appointments for examination at least on 2-3
months basis
Probe carefully to detect early periodontal disease
Routine scaling and root planning