Diabetes mellitus/endodontic courses

INDIAN DENTAL ACADEMY
Leader in continuing Dental Education

CONTENTS
• Introduction
• Classification
• Epidemiology & prevalence
• Etiology & pathogenesis
• Pathophysiology
• Clinical features
• Diagnosis & Management
• Metabolic control & assessment
• Complications & management
• Special problems and management
• Prevention & future prospects
www.indiandentalacademy.com

Definition
Group of metabolic disorders having a common
phenotypic expression of hyperglycemia.
Complex interaction of genetics,
environmental factors & lifestyle influences
the course & outcome.The metabolic
dysregulation associated with DM causes
multitude of secondary pathophysiologic
changes in multiple organs leading to macro
& micro vascular complications.

PREVALENCE-Growing menace in India
• 300 million diabetics in world by 2025
• India-World’s largest diabetic population.
• Every 4th
diabetic in the world is an Indian
• 30-33 million diabetics in India will go up to 40
million by 2010 & 72 million by 2025.

Why increased prevalence in India?
• Ethnic susceptibility
• Central obesity
• Sedentary lifestyle
• Hypertension
• Atypical tubercular presentation
• GDM-baby weighing more than 4.5 kg
• Stress hyperglycemia
• Premature atherosclerosis
More in urban high income group populations.

NORMAL PHYSIOLOGY

NORMAL GLUCOSE METABOLISM &
HOMEOSTASIS

REGULATION OF INSULIN SECRETION

INSULIN ACTIONS
stimulus for insulin release
hypoglycemia
ketone bodies
B2 stimulation
Stimulus to inhibit release
A1 stimulation
glucocarticoids
glucagon
Thyroid harmonewww.indiandentalacademy.com

Insulin is a potent anabolic hormone,known with
multiple synthetic & growth promoting effects
Its principle metabolic function is increase in
rate of glucose uptake by tissues (skeletal
muscle,adipose tissue)
• muscle-glucose stored as glycogen-ATP
• adipose tissue-promotes lipogenesis
• Stimulates protein synthesis

Etiology & pathogenesis
Type 1 diabetes
a. Immune mediated-cellular mediated
autoimmune destruction of B- cells of
pancreas
b. Idiopathic-no etiology,suffer from episodic
ketoacidosis,lack immunological evidence
of B-cell autoimmunity & is not HLA
associated.

Genetics
-1/3rd
susceptibility-HLA DR3/DR4 are more
susceptible.
-40% prevalence in monozygotic twins
Environmental factors
-Viruses-mumps,rubella,retro virus, CMV,EBR
-Diet-bovine serum albumin implicated in
triggering disease.
-Stress-progress the development of disease
by secretion of counter regulatory hormones.

Type 1 diabetes
-Cell mediated autoimmune disease.
• HLA linked genetic predisposition
• Association with other autoimmune diseases
• Circulating islet cell antibodies in new cases
• Mononuclear cell infiltration of pancreatic
islets
• Recurrence of insulitis & selective destruction
of B-cells in pancreatic grafts
• Induction of remission by immunosuppressive
drugs such as cyclosporin

Type-2 diabetes
The two metabolic pathways that characterize
type 2 diabetes are
• Insulin resistance -Decrease ability of
peripheral tissues to respond to insulin
• B-cell dysfunction-manifested as inadequate
insulin secretion in face of insulin resistance
THUS RESULTING IN
HYPERGLYCEMIA

Insulin resistance
• Defined as resistance to effects of insulin on
glucose uptake, metabolism & storage.
• Three causes:
a. an abnormal insulin molecule
b. excessive amounts of circulatory
antagonists
c. target tissue defects.(common)
• Resistance in diabetics is due to
Genetic susceptibility,sedentary life style,
obesity, TNF alpha, glucotoxicity, drugs like
glucocarticoids, B-blockers & adrenergic
agonists.

Obesity
• Insulin resistance is present in simple
obesity unaccompanied by hyperglycemia
• In diabetes the resistance is further
increased.
• The mechanisms are
1. Role of free fatty acids-inverse
correlations exist b/w FFA & insulin
sensitivity.Further intercellular triglcerides is
increased in liver & muscles in obese
persons(more FFA).This results in potent
inhibition of insulin signalling
Acquired insulin resistance.

2. Role of adipokines
• Adipokines are proteins released by
adipocytes in systemic circulation
• Dysregulation of adipokine
secretion(increase or decrease) is one of
mechanism insulin resistance is tied to
obesity.
decrease in leptin, & increase in resistin.
• Thus obesity is central factor in insulin
resistance-diabetogenic.

Tumour necrosis factor alpha
cytokine produced by adipocytes & if in
excess, it exerts inhibitory effects on insulin
signaling mechanisms,exacerbating insulin
resistance.
furthermore acute infections increase
secretion of TNF, thus worsening insulin
resistance.
Glucotoxicity
severe hyperglycemia aids in production of
glucosamine which directly influences
glucose transport functions-thus insulin
resistance.

B-cell dysfunction
1.Qualitative-initially secretion is subtle,followed
by loss of normal oscillating pattern of
secretion,finally affecting all phases of
secretion.
2. Quantitative-decrease in B-cell mass,islet cell
degeneration & deposition of amyloid.
it is uncertain if amyloid is involved in or as a
consequence of reduction in B-cell mass.

PATHOPHYSIOLOGY
Type 1 diabetes

TYPE 2 DIABETES

Clinical features-type 1

CLINICAL FEATURES

SECONDARY DIABETES
Maturity onset diabetes of young(MODY)
• Primary defect in B-cell function, that occurs
without B-cell loss affecting either B-cell mass
or insulin production.
• Is the outcome of heterogenous group of
genetic defects characterised by
-autosomal dominant inheritance
-early onset usually before 25 years
-absence of obesity.
-lack of islet cell antibody & insulin
resistance syndrome

DIAGNOSIS
OGTT not recommended for routine clinical use as
it is poorly reproducible,difficult to use & rarely
performed in practice.(though more sensitive & modestly
specific than FPG).But required in evaluation of IFG or when
diabetes is stilL suspected despite normal FPGwww.indiandentalacademy.com

TESTING FOR TYPE 2 DIABETES IN
CHILDREN
CRITERIA
Weight (BMI>85th
percentile for that age & sex or >120%
of ideal for weight)
ANY TWO OF FOLLOWING RISK FACTORS
• Family history in first or second degree relative
• Race-native American,African American.
• Signs or conditions associated with insulin resistance
(acanthosis nigricans, hypertension, dyslipidemia,
polycystic ovary syndrome.
• Puberty occurs at young age
TEST PREFERRED-FPGwww.indiandentalacademy.com

VALUE OF SCREENING
RECOMMENDATIONS
• Evaluation should be performed within the health
care setting,for particularly those with
BMI>25kg/m2
.They should be screened at 3 yr
interval beginning at age 45.Testing considered early
& frequently if additional risk factors are present.
• FPG is recommended screening test.
• Diagnostic screening performed in any clinical
situation that warrants testing
• Community screening-not beneficial

DIABETES CONTROL & ASSESMENT
TESTS OF GLYCEMIA
TESTS USED TO MONITER THE GLYCEMIC
STATUS OF DIABETICS ARE
• Urine sugar
-urine glucose & ketones
• Blood glucose testing- SMBG
• Glycated proteins
-Glycated hemoglobin &
-Glycated serum proteins

URINE SUGARS-GLUCOSE TESTING
THE TEST IS NOT RECOMMENDED BECAUSE
• There is wide individual variation in renal
threshold esp in long standing adult diabetics
(underestimation) ,pregnant women & children
(overestimation)
• Fluid intake & urine concentration affects results
• It reflects an average level of blood glucose since
the last voiding & not the level at time of test.
• Negative results does not distinguish
hypoglycemia, euglycemia or even mild
hyperglycemia-hence limited in preventing
complications

• Errors in interpreting the results
• Some drugs interfere with urine glucose
determinations
• Alimentary glycosuria after gastric surgery
and in pts with hyperthyroidism,peptic ulcer &
hepatic disease.
Hence presently it is recommended that all
diabetics esp those who are on insulin should
monitor blood & not urine glucose levels.
Urine testing should be considered only if pts
are unable or unwilling to perform Self
monitoring of blood glucose(SMBG).

KETONE TESTS
Ketone testing is very important,esp in type I diabetics.
• Frequent urine ketone tests are important in the first
few days after diagnosis to determine if enough insulin
is being given to turn off ketone production. Turning
off ketone production is the first goal in the treatment
of newly diagnosed diabetes managed in the
outpatient setting. This usually takes one or two days
after starting insulin.
• It is important to test for urine or blood ketones
because they can build up in the body. This can result
in one of the two emergencies of diabetes-
ketoacidosis

• Recommended that all pts test for ketones
during acute illness,stress (blood glucose
constantly>300),pregnancy & anytime the
person feels sick or nauseated (especially if
he/she vomits, even once). If the person is
sick, ketones can be present even when the
sugar is not high.
• False positive values-in normal individuals
during fasting,in pts with captopril, & 30%of
pregnant women.
• False negative values-when strips are
exposed to air & in acidic urine specimens.

The Precision Xtra™ meter is now available to do a home
fingerstick test for blood ketones

SELF MONITORING BLOOD GLUCOSE
TESTING
• Allows patient to evaluate their individual response to
therapy & assess if glycemic targets are being
achieved.
• Results can be used to prevent hypoglycemia,to
adjust medications & physical activity.
• Daily SMBG for pts on insulin is recommended. For
type 1 diabetics & pregnant women,it recommended
3-4 times daily.
• Technically sensitive & interpretation of data is
difficult.
• ? Stable diet treated patients.

GLYCATED PROTEIN TESTING
GLYCATED HEMOGLOBIN
This test helps to provide the pts average glycemia over
past 2-3 months & thus to assess treatment efficacy.

Varied results in
Conditions reducing RBC LIFE SPAN, Vit C & Vit E lowers test
values.Iron deficiency anemia increases test values.
Hyperbilirubenemia,anemia,chronic alcoholism,ingestion of
salicylates, & hypertriglyceridemia interfere with assay.www.indiandentalacademy.com

ADA RECOMMENDATIONS
• Test to be performed at initial patient visit, & atleast
twice a year in pts who meet the treatment goals &
quarterly in pts whose therapy has changed or who is
not meeting glycemic controls.
• Develop the management plan to achieve AIC values
to 7%.More stringent (6%) in high risk groups.
• Lowering AIC lowers the risk of micro &
macrovascular complications
• Less stringent goals for pts with h/o severe
hypoglycemia,limited life expectancy, very young
children & older adults.

Fructosamine (or Glycosylated Albumin)
Test
• This test measures the amount of sugar
attached to the main serum protein, albumin.
It reflects the blood sugars every second of
the day for the past 2-3 weeks (whereas the
HbA1c reflects the past two or three months).
• It is often helpful to know how someone is
doing more recently (in contrast to the past
three months).
• The test is also helpful for someone who is
changing treatment (more shots, an insulin
pump, etc.).

• A commercial meter, the In Charge™, is
available and measures either blood sugar or
fructosamine in the home setting.
• This home meter may be particularly helpful
to families who are unable to have an HbA1c
determined every three months when
attending a diabetes clinic.

MANAGEMENT
1.Diet alone
2.Diet+OAD
3.Diet+OAD+insulin

DIETARY MANAGEMENT
Medical nutrition therapy describes optimal
coordination of calorie intake with other
aspects of diabetes(insulin, exercise,weight
loss & drugs)
Nutritional recommendations(ADA-1998 & 02)
• Protein-15-20%
• Saturated fat<10%
• 60-70% of calories divided b/w carbohydrates
& unsaturated fats.

• Use of caloric sweetners ,including sucrose is
acceptable.much emphasis on risk factors
like hypertension & dyslipidemia.(increased
dietary fibre, & decreased fat)
• Fibre-20-35g/d & sodium< 3000mg/d are
recommended
• Cholesterol-</= 300mg/d.
For alcohol users
• Alcohol to be taken with food as it increases
the risk of hypoglycemia
• Tendency for lactic acidosis with biguanides
• Similarity b/w its effects & hypoglycemia.

IMPORTANCE OF EXERCISE

ORAL HYPOGLYCEMIC AGENTS
Classification
-
According to mechanism of action.
1.Drugs that stimulate insulin secretion
- Sulfonylureas & Meglitide analogs.
2.Drugs that alter insulin action.(decrease
gluconeogenesis & increase insulin
sensitivity.
- Biguanides & Thiazolidines
3.Drugs that affect absorption of glucose.
- Acarbose & Miglitol.

INSULIN
• Exogenous insulin is the most physiologic ,
most rapid & most effective treatment
available for enabling pts to reach
normoglycemia.(Rosentock & Riddle)
• Anabolic hormone that helps in utilization of
glucose, in lipogenesis & storage of proteins.
• No fixed upper dose of insulin.(Nathan- 2002)
• No insulin failure described, always works,
though higher doses are required in those
with insulin resistance (obesity)
• Longest established safety.

Advantages of Insulin Aspart over Actrapid.
•Superior postprandial control in diabetics due to
twice as fast onset & a high peak.
•Lower risk of noctural hypoglycemia (duration
remains for 4 hrs.
•Freedom from meal time constrints
•Can be given just before or after
meals.
•Less need to snack b/w meals to
avoid hypoglycemia.

Advantages of Actrapid (regular) over
Aspart / Lispro (ultrashort)
• Intravenous infusions are particularly helpful
in treatment of ketoacidosis & during
perioperative management.
• In case of pump failure, users of ultrashort
acting insulins will have more rapid onset of
hyperglycemia & ketosis when compared to
regular insulin users.
• Also indicated when subcutaneous insulin
requirements change rapidly.(post surgery &
during acute infections).

MIXTURES OF INSULIN
1. Intermediate+ Regular/Lispro
• Given preprandially,as require several
hours to reach therapeutic levels.
• NPH is preferred to Lente as zinc binds to
soluble insulin's & partially blunts its action.
• Premixed preparations of Lispro/Aspart &
NPH are unstable because of exchange of
human insulin with Protamine complex,hence
Neutral Protamine Lispro was developed.
2.Long acting +Regular/lispro

Different Insulin Regimens
1.Basal Bolus
2.Split Mix or Self Mix Regimen
3.Premixed Insulins.
ADVANTAGES OF PREMIXED INSULINS
(Novomox 30(30%insulin Aspart + 70% Protamined
insulin Aspart.)
• Simple convenient meal time regimen
• Better 24 hr physiological basal control
• Controls FPG, PPG, & HbAic.
• High safety-low risk of hypoglycemia
• Once a day regimen

• Different methods of insulin administration
are Insulin syringes & needles,Insulin pen
injection devices, Insulin pumps, & inhaled
Insulins.
• Most important complication of Insulin
administration is Hypoglycemia.Human
Insulins have less immunogenic reactions.
• Should not be given with Carticosteroids &
B-blockers.
• Pancreas transplantation & Asprin therapy
are other treatment modalities to treat
diabetes

NEW THERAPEUTIC STRATEGIES IN TYPE 2
DIABETICS
1.Three thresholds for AIC
Monotherapy- If AIC remains b/w 6-6.5,its
necessary to introduce an OAD after 6
months without any hypoglycemia-metformin
Bitherapy-AIC exceeds 6.5 with max dose of
metformin, then bitherapy not delayed.
metformin+Glitazones/insulin secretor.
Tritherapy- AIC>7%.then choose tritherapy
b/w metformin+ glitazones+ insulin secretor
or insulin therapy.

2.Target Goal for Blood pressure
130/80 with as many hypertensives as
necessary.
3.Target goals for lipids
LDL Cholesterol < 1g/L in pts with increased
CVS risk for primary & secondary prevention
LDL Cholesterol b/w 1.3-1.6g/L for other type 2
diabetics.

HYPOGLYCEMIA
Lab diagnosis-plasma glucose<2.5-2.8nmol/L or
<45-50 mg/dl(individual variation)
Whipple triad
symptoms consistent with hypoglycemia
a low plasma glucose concentration
relief of symptoms after plasma glucose conc is
raised.
Causes -a. Fasting-underproduction or over utilization
of glucose
b. Post Prandial /reactive-post gastric surgery &
rare enzymatic defects.www.indiandentalacademy.com

clinical features
Autonomic-sweating,tremors, pounding heart,
hunger & anxiety.
Neuroglycopenia-confusion,drowsiness,speech
difficulty & disorientation
Non specific-nausea, tiredness & headache.
Management
Acute therapy-oral glucose or 25g of 50% soln of
dextrose(I.V) with constant infusion of 5-10%
dextrose.
Glucagon-1mg IM-effective in pts who do not respond
to IV glucose.
Dose of insulin is reduced by 20% unless cause is
known. www.indiandentalacademy.com

DIABETIC KETOACIDOSIS
DKA is the acute complication of diabetes
mellitus associated with relative or absolute
deficiency of insulin.
Causes: inadequate insulin administration,
infection, surgery, drugs and pregnancy.
Signs: dehydration, hypotension, tachycardia,
air hunger, hypothermia, confusion,
drowsiness and coma.
Symptoms: polyurea, weight loss, weakness,
nausea, vomiting, blurred vision and
abdominal pain.

LATE COMPLICATIONS
The morbidity associated with long standing
diabetics result from number of serious
complications involving both large & medium
sized muscular arteries (macrovascular
disease) as well as capillary dysfunction in
target organs (microvascular disease).

GESTATIONAL DIABETES MELLITUS
GDM is defined as any degree of glucose
tolerance with first onset of pregnancy.This
definition applies regardless of whether
insulin or dietary modification is used for
treatment & whether condition persists after
treatment.
It is a prodromal form of type 2 diabetes ,being
unmasked by pregnancy.
Pregnancy is associated with increased insulin
resistance thus necessitating increased
production.

Foetal complications
• Congenital malformations are atypical since
glucose tolerance occurs late in pregnancy.
• Macrosomia-20% (gestational age.maternal
weight)
• Neonatal hypoglycemia
Other complications include
respiratory distress syndrome,polycythemia,
hypocalcimia, hyperbilirubenemia.
Maternal surveillance should include B.P &
urine protein monitoring.

Management
• All women with GDM should receive
nutritional counseling which includes
provision of adequate calories & nutrients to
meet demands of pregnancy.(200kc/day)
• For obese –calories is reduced
• If target values not achieved with diet, human
insulin should be initiated.OHA not approved.
• GDM is not in itself an indication for cesarean
delivery.(before 38 weeks) but prolongation
beyond time will increase the risk of
macrosomia without decreasing cesarean
rates.

Management during pregnancy
• Maintain good glycemic control –AIC within
range of 6.5-8% by use of 3-4 injections daily.
• Do not strive for normoglycemia at the
expense of hypoglycemia.
• Check overnight sample of urine for ketones
regularly.increase intake of glucose & dose
of insulin to abolish ketonuria.
• Insulin stopped during delivery & resumed 12
hours after pregnancy.

SURGERY AND DIABETES
WHY IS GOOD DIABETIC CONTROL
NECESSARY IN SURGERY???

PRE OPERATIVE ASSESSMENT
 Assess CVS and renal function.
 Check signs of neuropathy
 Assess diabetic control
 Review treatment of diabetes
- replace long acting insulin with
intermediate insulins
- stop OADs and replace with insulins

CONCLUSION
DIABETES CAN ONLY BE PREVENTED
AND NEVER CURED.

Diabetes mellitus/endodontic courses

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