1. Presented By-
Kamini Singh

2. o Introduction - What Is Diabetes Mellitus ?
o Classification of Diabetes Mellitus .
o Clinical features of various types of Diabetes
Mellitus .
o Complications from Diabetes Mellitus .
o Diagnosis of Diabetes Mellitus .
o Management of Diabetes Mellitus .
o Diabetes and its importance in Oral & Dental
Surgery.

3.  Diabetes Mellitus – Diabetes Mellitus is a
clinical syndrome of hyperglycaemia with
glycosuria due to lack of insulin or insulin
resistance.
 It is a chronic disorder of carbohydrate, fat
and protein metabolism.
 The condition of Glycosuria or high blood
sugar produces the classical symptoms of
polyuria(frequent
urination), polydipsia(increased thirst) and
polyphagia(increased hunger).

5.  Primary Diabetes Or Idiopathic  Secondary Diabetes
Diabetes:
 I. Type – 1 IDDM (INSULIN  Pancreatic diabetes due to
DEPENDENT DIABETES MELLITUS) pancreatitis
 Its Sub-divided into:  Diabetes due to endocrinal or
hormonal disturbances i.e.
 A. Immune Mediated (Islet cell Acromegaly , Cushing’s
antibodies) syndrome
, Phaeochromocytoma
 B. Non immune (No antibodies
 Drug Induced Diabetes or
Iatrogenic Diabetes - Due to
 II. Type – 2 NIDDM (NON INSULIN steroids and Thiazides (medium
DEPENDENT DIABETES MELLITUS) efficacy diuretics)
 Diabetes caused by insulin
 Its sub-divided into: receptor antibodies
 A. Obese (Insulin resistance with  Diabetes caused by Genetic
relative insulin deficiency) Syndrome i.e.
Lipodystrophies, muscular
 B. Non- Obese (Insulin secretory dystrophy, Klinefelter’s
defect with insulin resistance syndrome,Turner’s
 C. Maturity Onset Diabetes of the Syndrome, Down’s
Young (MODY) Syndrome, and DIDMOAD (
Diabetes Insipidus , Diabetes
 D. Gestational Onset Diabetes Mellitus , Optic Atrophy and

6.  Type 1 diabetes or Insulin Dependent Diabetes Mellitus is
also known as childhood-onset diabetes & juvenile
diabetes.
 Type 1 Diabetes Mellitus usually occurs in childhood or
early adulthood i.e. usually begins below the age of 30
yrs. And manifests itself in two ways:
 Classic Triad Of Type 1 Diabetes Mellitus : Polydipsia, Polyuria
and Polyphagia.
 Ketoacidosis: Patient present with Diabetic Ketoacidosis
following an acute infection or surgery as an first episode
without any apparent cause. In severe cases, patient may
develop mental apathy, confusion and may lapse into coma.
This accounts for 10 % cases of Diabetes Mellitus.

7.  Type 1 diabetes is caused due to failure of Beta
cells of islets of langerhans. This occurs due to
multifactorial causes such as genetic
predisposition, viral and auto-immune attack on
the beta cells of islets of langerhans of pancreas.
 The abrupt onset of symptoms with
polyuria, polydipsia and polyphagia and weight
loss developing over days or over weeks.
 Some cases may present as Ketoacidosis. It is
followed by a symptom free period during which
no treatment is required .
 Characteristically, the plasma insulin is low or
immeasurable .
 Glucagon intervals are elevated but suppressible
with insulin.

8.  Type 2 diabetes mellitus or Non insulin
dependent diabetes mellitus, usually begins
after the age of 40 years and 60 % of the
patients are obese. However young patients
of type 2DM are also seen nowadays.
 Type 2 DM occurs with intact beta cells of
islets of langerhans, but there is peripheral
tissue resistance to insulin.
 There may be some decrease in insulin
production or a hyper insulin state. These
patients are not ketosis prone, but may
develop it under conditions of stress.

9.  The symptoms begin gradually over a period of
months to years. Frequently, hyperglycaemia is
detected in an asymptomatic person on a routine
examination.
 These patients usually does not develop
Ketoacidosis.
 In the decompensated state, they are susceptible to
the syndrome of Hyperosmolar Hypoglycaemic state
i.e. Hyperosmolar Non Ketotic Coma due to polyuria
and increased osmotic concentration.
 The plasma insulin levels are normal to high.
 Glucagon levels are high but resistant to insulin.

10.  Gestational type of diabetes occur when diabetes
onset is during pregnancy and resolves with
pregnancy and resolves with delivery.
 These patients are at a higher risk of developing
Diabetes mellitus at a later stage.
 Age: The occurence of Type 2 DM after 30 years of
age, indicates the age as an important factor.
 Environmental factor: Physical inactivity and
inactivity acts an diabetogenic factor who are
genetically susceptible to develop type 2 DM.

11.  They include diseases of exocrine pancreas, various
endocrinopathies(cushings syndrome(increased level
of cortisol), phaeocromocytoma(increased level of
catecholamines), drug or chemical induced
Diabetes Mellitus (beta blockers, oral
contraceptives) or genetic
syndromes(lipodystrophies), associated with
Diabetes.

12.  ACUTE METABOLIC  CHRONIC METABOLIC
COMPLICATIONS COMPLICATIONS
(OR IMMEDIATE METABOLIC (OR LATE ONSET
COMPLICATIONS) COMPLICATION )

13. A. Diabetic Ketoacidosis or Diabetic Coma - It results from a
shortage of insulin , in response to which the body starts
lipolysis and breakdown of fatty acids, producing Acidic
Ketone bodies, namely acetone, Aceto-acetic acid and beta
Hydroxy Butryic acid. Presence of these Ketone bodies
results in acidosis known as Diabetic Ketoacidosis.
B. Features :
C. Ketoacidosis ; Kussmaul hyperventilation: deep, rapid
breathing ; Confusion or a decreased level of consciousness;
Dehydration due to glycosuria and osmotic diuresis ; Acute
hunger and/or thirst 'Fruity' smelling breath odor Impairment
of cognitive function, along with increased sadness and
anxiety.

14. B. Hypoglycemia or Hypoglycemic Coma – It may develop in
Type 1 Diabetes patient, due to hypoglycemia caused by
excessive administration of insulin, missing a meal or due
to stress.
Hypogycemic episodes may produce:
Permanent brain damage or worsening of diabetic control
and rebound hyperglycaemia. This condition is called
Somogyi’s effect.

15.  C. Non- Ketotic Hyperosmolar Diabetic Coma : Its usually a
complication of Type 2 Diabetes Mellitus. Its caused due to
severe dehydration resulting from sustained hyperglycaemic
diuresis.
 D. Lactic Acidosis: Lactic acidosis is a physiological condition
characterized by low pH in body tissues and blood (acidosis)
accompanied by the buildup of lactate especially D-
lactate, and is considered a distinct form of metabolic
acidosis. The condition typically occurs when cells receive
too little oxygen (hypoxia), In this situation, impaired
cellular respiration leads to lower pH levels.
Simultaneously, cells are forced to metabolize glucose
anaerobically, which leads to lactate formation.
Therefore, elevated lactate is indicative of tissue
hypoxia, hypoperfusion, and possible damage.

16. MICROVASCULAR MACROVASCULAR
COMPLICATIONS COMPLICATIONS
 1. Diabetic Retinopathy  1. Atherosclerosis
 2. Diabetic Neuropathy  2. Hypertension
 3. Diabetic Nephropathy  3. Peripheral Vascular
 4. Miscellaneous Disease
Infections  4. Foot Ulcer

17.  Microvascular complictions :
 1. Diabetic Retinopathy – Diabetic
Retinopathy is a leading cause of blindness.
 Characterstic features are:
 Microaneurysms .
 Hard and soft exudates.
 Retinal Hemorrhage.
 Neovascularisation.
 Vitreous Hemorrhage.
 Fibrosis.

18.  Types of Diabetic Retinopathy-
 Benign –Dilatation of retinal venules and vein
 Premalignant – Dots , Blots appear, Multiple hard
exudates, Retinal hemorrhage, soft exudate
, macular oedema and perimacular exudates.
 Malignant – Retinal
hemorrhage, Neovascularisation, Exudates at macula
and fibrosis.

19. Diabetic Neuropathy-Its an early and common
complication and may affect any part of the nervous
system except brain.
 Its an important cause of morbidity and disabilty.
 Poor glycemic control and long duration of Diabetes are
associated with high incidence of neuropathy.
Diabetic Nephropathy-It is a common cause of
mortality and morbidity in Type 2 DM. About 40-50%
patients develop this complication. Its less common in
type 2 DM.
 25 % patients in type 1 DM develop end stage renal
disease and die of it.

20.  MiscellaneousInfections-Diabetics have
enhanced susceptibility to various infections
such as T.B.
, pneumonia, Pyelonephritis, Otitis, carbuncl
es and Diabetic ulcers as in Diabetic ulcer.

21. Macrovascular complications of Diabetes Mellitus
 Atherosclerosis - Atherosclerotic lesions appear
earlier than in general population in patients of DM
both type 1 and type 2.
Causes for atherosclerotic process is not known , but
possible contributory factors are
Hyperlipidaemia, Reduced LDL levels, Non enzymatic
glycosylation, increased platelet
adhesiveness, obesity and associated hypertension in
diabetes.

22.  Other Complications Are-
Hypertension, Peripheral vascular disease, foot
ulcer.
Diabetic foot- Foot is frequent site of complication
in diabetics and for this reason, prevention is most
important aspect in foot care.
 Pathogenic components of Diabetic Foot Care are-
 Neuropathy, peripheral vascular disease producing
ischaemia (vasculopathy), secondary infection
following ulcer.

24.  Symptoms of Diabetic Foot: It may be varying from none
to numbness, parasthesia , and pain.
 Signs- Ulcers, Sepsis, Abcess, Osteomyelitis, Gangrene
Chercot ‘s Joint, Loss of toe

25.  Diagnosis of Diabetes mellitus is based on
symptoms signs and biochemical test.
 In the presence of suggestive symptoms, the
confirmation of diagnosis be mellitus, finding
a random blood glucose level of more than
200mg%or 11.5mmol/L.
 However, many patients , particularly those
with type 2 diabetes either have few or no
symptoms and diagnosis is made on fasting
and postprandial blood glucose level

26. METABOLIC SYNDROME(syndrome x) AND RISK FACTORS
ASSOCIATED WITH DIABETES MELLITUS:
WHO DIAGNOSTIC CRITERION -
1.CONTROL OBESITY
BMI>30KG/METRE SQUARE
WAIST /HIP RATIO
MEN>0.90
WOMEN>0.85
2. TRIGLYCERIDE
>150mg/dl
3.HDL CHOLESTEROL
Men<35mg/dl
Women<39mg/dl

27. 4. Fasting Glucose
>110mg/dld.
5. Microalbuminurea
Urinary albumin excretion rate >/ =20 mu gm/min
 DIAGNOSIS IS MADE WHEN 3 OR MORE OF THESE RISK
FACTORS ARE PRESENT

28.  Impaired fasting glucose(IFG)
This is a biochemical abnormality detected on oral glucose
tolerance test
 Normal fasting plasma glucose is taken as
<=110mg/dl,6.1mmol/l
 Fasting plasma glucose levels between 110-
126mg/dl(6.1-7 mmol/l)is taken as impaired fasting
glucose..
 This group of individuals are at increased risk of
developing Type 2 DM .
 It’s a feature of MODY Type 2 DM.
 It’s a risk factor as well as an alternative diagnostic
criterion for DM

29.  Impaired glucose tolerance -This is defined as normal
fasting plasma with impaired postprandial glucose on
G.I.T
 The two hours levels on OGT between 140mg-
200mg/dl(7.8-11.1mmol/l) indicate IGT
 This is a transition phase between a normal and diabetic
person. hence constitute a risk factor to the development
of TYPE 2 DM and increased risk of cardiovascular
mortality.
 Females with IGT are at increased risk of still birth ,
delivering large and heavy babies and babies with
congenital defect

30.  1.Classic symptoms of diabetes and a casual plasma
glucose 200mg/dl(11.1mmol/l)
 Casual is defined as any time of day without regard to
time since last meal.
 The classic symptoms of diabetes include
polyuria, polyphagia, polydipsia and unexplained weight
loss.
Or
Fasting Plasma Glucose / FPG>=126mg/dl(7.0mmol/l).
Fasting is define as no caloric intake for at least 8 hrs
Or
2 hour Plasma Glucose / 2h
PG>=200mg/dl(11.1mmol/dl), during an OGTT.

31. Diabetes Mellitus is confirmed by demonstrating
hyperglycaemia with ketonuria and acidosis.
 Urine test for Detection of Glycosuria
 Urine test for presence of ketone bodies
 Oral glucose tolerance test
 Diagnosis of pre-diabetic state
 Impaired Fasting Glucose
 Impaired Glucose Tolerance

32. Condition Venous Plasma Glucose Concentration in
mg%(mmol/l)
Fasting Postprandial(2hr GTT)
Normal <110 (6.1) <140(7.3)
Diabetes Mellitus >=126 >200
Impaired Fasting >=110 and < 126(6.1-7.0) <140(7.8)
Glycaemia
Impaired Glucose <126(7.0) >=140 & 200(7.8-11.1)
Tolerance
* * 2hrs GTT means following 75gms Glucose load

33.  Detection of glycosuria- Urine For Glycosuria is
employed for screening the public or individual
for presence of diabetes.
 Glycosuria does not mean Diabetes Mellitus, and
require further evaluation by blood sugar or
glycosylated haemoglobin.
 HbA1c is a type of glycosylated Hb.
 Acc. to WHO criterion for Diabetes control
regarding HbA1c
 The normal value of HbA1c is <6 % and value
more than 10% suggests poor control of Diabetes.
 In between values-
 Excellent (7%) , Good(7-8%), and Poor
control(>8%)

34.  Urine test for Ketone Bodies
 Acetotest or ketostix test papers utilising
Nitroprusside reactions are employed to detect
ketone bodies in the urine , Ketonuria also occours in
prolonged fasting, following high fat diet & after
repeated vomiting.
 Ketonuria is not pathognomic of Diabetes but when it
occours along with glycosuria , Diagnosis of Diabetes
is almost certain.

35.  Oral glucose tolerance test
 Patient is advised to take unrestricted carbohydrate diet for 3
days prior to that.
 Before the test ,patient keeps fast overnight.
 Patient should rest for half an hour before the test.
 Fasting sample of blood is taken for glucose estimation and
then 75.0 g of glucose dissolved in 300 ml(a glass) of water is
given by mouth.
 Sample of blood and urine are collected at half an hour
intervals for next two hours for glucose measurement.

36.  Impaired Fasting Glucose(IFG) Its diagnosed
when fasting glucose level is
abnormal(between 110 and 126mg%).
 It was introduced by American Diabetes
Association just to avoid the need for OGT.
 Impaired Glucose Tolerance-The
intermediate values of postprandial blood
sugar (140 -200mg%) between normal and
diabetics are classified as impaired glucose
tolerance.

37.  Diet Planning
 Exercise
 Drugs Therapy

39.  The diet most often recommended is high in dietary
fiber, especially soluble fiber, but low in fat (especially
saturated fat).
 This involves allocation of calories in a proper proportion
to carbohydrates , fats and proteins.
It is as followed:
 Carbohydrate-50-65%
 Proteins-10-20%
 Total Fat-25-30%

40. Isotonic exercises like brisk
walking , swimming or
cycling are recommended.

43. ORAL HYPOGLYCAEMIC AGENTS (OHA)
 Oral Hypoglycemic are drugs which upon administration lower
the blood glucose level.
 These drugs are used in patients of Type 2 Diabetes Mellitus
(NIDDM), who do not respond to dietary management and who
would otherwise require treatment with insulin. In later
situation, they are used as adjuvant to insulin in obese
patients.
 These drugs require presence of Insulin secreting Beta cells for
their action and that is the reason , why they are not effective
in type 1 Diabetes Mellitus.

44. Classification of oral hypoglycaemic
drugs (depending upon the mechanism
of action
Insulin Secretagogues – They increase the
secretion of insulin from surviving beta cells of
pancreas .
Insulin Sensitizers – They sensitize the action of
insulin and overcome insulin resistance.

45. Sulphonylureas –
These include:
 1st generation-like tolbutamide
 2nd generation-like glipizide
 They are effective in treatment of non-obese patient with
Type 2 DM who fail to respond to dietary measures alone.
 Side effects : Hypoglycemia , weight gain.
Meglitinide
 Thisincludes- Drugs like
Repaglinide,Naliglinide,Meglitinide
 Dose : .5-16mg per day

46. Biguanides –
Metformin is the only drug used in this group. Its particularly
useful in obese patients with Type 2DM, who do not respond
to dietary measures and weight reduction.
Thiazolidinediones –
Drugs used in this group are rosiglitazone and pioglitazone.
Side Effect : Weight gain, mild rise in LDL.

48.  Insulin is required for treatment of all patients with Type 1 DM and
many patients with Type 2 DM.
 Indications in Type 2 DM
 In primary or secondary sulphonylureas failure
 Major trauma
 Surgery
 Pregnancy
 Diabetic ketoacidosis
 Myocardial infarction
 Infection
 Liver failure
 Renal failure
 Respiratory failure

50.  Surgery whether performed electively or during
emergency acts as a stress inducing catabolic
hormones such as
Cortisol, Catecholamines, Glucagon and Growth
hormone in diabetic patients as well as normal
persons . These endocrine hormones are anti
insulin in their action , hence increase sometimes
may lead to Hyperglycaemia and sometimes may
lead to acute metabolic decompensation such as
diabetic ketoacidosis , in both Type 1 and Type 2
DM with uncontrolled , poorly controlled or
untreated Diabetes.

51.  Starvation before surgery may exacerbate hyperglycaemia
 The major risk of surgery in diabetes is increased risk of
infections and delayed wound healing due to impaired
phagocytic activity of leucocytes , as well as impaired
immunity dental or oral surgery , should only be carried out
only in the states of uncontrolled diabetes and avoided or
postponed in uncontrolled state of diabetes.
FOR MINOR DENTAL PROCEDURES-
 Minor orodental procedures can easily be performed in type
1 and type 2 Diabetes mellitus, if patient is well maintained
on either insulin or oral hypoglycaemics.
 For minor surgery its imp. to control the blood glucose
effectively before surgery.

52.  Post operatively, 5%Glucose Infusion ,with
10-12 units of insulin may be started with
20mmol of Pottasium.
 After wound is healed the patient is shifted
back to its previous regimen of treatment.