Diabetes and application in OMFS

1. DIABETES MELLITUS
DR. SAVITA SAHU
IIND YR POSTGRADUATE
SRI SIDDHARTHA DENTAL COLLEGE

2. CONTENTS
ANATOMY
PHYSIOLOGY OF PANCREASE
CARBOHYDRATE
DIGESTION AND ABOSORPTION OF CARBOHYDRATE
DIABETES
INVESTIGATIONS
COMPLICATIONS
SURGICAL MANAGEMENT OF DIABETIC PATIENTS

3. ANATOMY OF PANCREASE
Pancreas is a soft, lobulated, and
greyish-pink gland, 12-15 cm long.
It has 3 parts-1) head
2)neck
3)body
4)tail
It has a endocrine as well as excocrine function

5. EXOCRINE PART-
of pancreas consist of acinar
glands made up of acinar cells.
These cells are pyramidal in
shape. They are arranger in
flask or tubular shape.

8. ENDOCRINE PART- this consist of the pancreatic islets or insulae of
Langerhans, consist of spheroidal or ellipsoidal shaped cells. There
are millions of islets of Langerhans most numerous in the tail of
pancreas.
There are four different types of cells present in the islets
1)A cells- alpha cells(glucagon)
2)B cells- beta cells(insulin)
3) C & 4) D cells .
There are Peptide secreting cells with smaller granules than those of
A, B and the cells, scattered over the endocrinal part of pancreas.
They are
PP and pancreatic D1 cells.

10. DAILY PRODUCTION OF INSULIN-33U.
MEAL TIME REQIREMENT-3-5 U.
BASAL REQUIREMENT- 1U/Hr.
Ketosis prone diabetic patient produces 10% of daily insulin.
In TYPE II patient produce average of 15U/24

11. NERVE SUPPLY-parasympathetic- vagus ( control pancreatic
secretion)
sympathetic- splanchnic nerve(vasomotor).
Secretions are also controlled by cholecystokinin.
VENOUS DRAINAGE- veins drain into splenic, superior mesenteric
and portal vein.
LYMPHATIC DRAINAGE-pancreatosplenic, coelic,superior
mesemtric group of lymoh node

12. PHYSIOLOGY OF PANCREAS
Pancreas is a dual organ having endocrine as well as exocrine
function.
Volume of juice secreted- 500 to 800ml/day.
Ph- 8to 8.5

13. Excorine part is made up of acini or alveol.
Acinar cells contain zymogen granules.

14. COMPOSITION OF PANCREATIC JUICE
WATER(99.5) SOLIDS(0.5)
ORGANIC SUBSTANCES INORGANIC SUBTANCES
Enzymes Na
Other oragnic substances calcium
potassium
magnesium
HCO3
etc.

15. CARBOHYDRATE
Is defined as polyhydroxyaldehydes or ketone or compounds which
produce them on hydrolysis.

16. CLASSIFICATION
MONOSACHHARID OLIGOASCCHARIDES POLYSACCHARIDES
Aldose ketone homo hetero
Diasaccharide Trisaccharides Tetrasaccharide Pentasaccharide
Sucrose raffinose stachyose verbascos
Maltose
Lactose

17. DIGESTION OF CARBOHYDRATES
IN THE MOUTH-
Salivary amylase aids in digestion of starch, breaks the 1:4alpha linkage and produces
diasaccharides like- dextrin and maltose.
IN THE STOMACH
Gastric jucies contain week amylase, therefore play minor role in carbohydrate digestion
IN THE DUODENUM
Starch and maltose
Dextrin (completely)
IN THE SMALL INTESTINE-contains enzyme for splitting disacchardases into monosaccharadases
Sucrose glucose and fructose
Maltose 2 glucose
Lactose glucose and galactose
Alpha glucose
limiting dextrin

18. ABSORPTION OF CARBOHYDRATES
Includes the monosaccharide movement across the cell into blood capillaries by
1) SIMPLE DIFFUSION- occurs when concentration of sugar in the gut exceeds that in
the blood, that is along the concentration gradient.
2) ACTIVE TRANSPORT- this causes absorption of sugar against the concentration
gradient.

19. MECHANISM OF TRANSPORT
STEP1glucose combines with a carrier(SGLT1-sodium gluose linked
transporter or GLUT) , which moves along the lipid barrier of cell
membrane and releases glucose inside the cell.
STEP2to concentrate the glucose within the cell , the carrier is coupled
with source of energy which is provided indirectly by active transport of
NA+ out of the cell. Sodium affects the supply of energy from ATP by
activating ATPase in the cell membrane.
Absorption of monosaccharaides is more in jejunum and proximal part of
ileum

20. ENTERY OF GLUCOSE INTO CELLS
INSULIN DEPENDENT TRANSPORT SYSTEM includes-
1) glycolysis
2)citric acid cycle
3)gluconeogenesis
4)glycogen metabolism
5)uronic acid pathway

21. GLYCOLYSIS GLUCOSE
ATPADP hexokinase or glucokinase
GLUCOSE 6-PHOPPHATE
Pohosphohexokinase
isomerase
FRUCTOSE 6-PHOSPHATE
ATPADP phosphofructokinase
FRUCTOSE 1.6-BISPHOSPHATE
aldolase

22. phosphoisomerase
DIHYDROXYACETONE GLYCERALDEHYDE
PHOSPHATE 3PHOSPHATE
NAD+iP, NADH+H+
1,3BISPHOSPHOGLYCERATE
ADPATP Phosphoglycerate kinase
3-PHOSPHOGLYCERATE
2-PHOSPHOGLYCERATE

23. Mg, H2O  enolase
PHOPHOENOLPYRUVATE
ADPATP
PYRUVATE(enol)
PYRUVATE (keto)
NADH+H+NAD
L-LACTATE

24. FATE OF PYRUVATE
IN AEROBIC CONDITION - pyruvate is converted to acteyl CoA .
This Acetyl CoA which is now produced undergoes citric acid cycle.
This TCA cycle occurs in the mitochondria in close proximity to the
electron transport chain(ETC).
C6H12O6 +602+ 38ADP + 38iP6CO2 + 6H2O +38ATP
IN ANAEROBIC CONDITION-pyruvate is converted to lactate and is
the end product.
C6H12O6 + 2ADP +iP2lactate + 2ATP

25. GLUCONEOGENESIS
Non-carbohydrate compound  glucose.
Gluconeogenesis mostly takes place in the liver, the cytosol of the cell.
Its is the reverse cycle of glycolysis, expect the three irreversible steps
that are carried out different enzymes.
Because of the enzyme glucose 6 phosphatase absence the brain,
muscle, and adipose tissue these cannot produce glucose from
glucose6phospahte (1st step in glycolysis). Only liver and kidney contain
glucose 6phosphatase enzyme.
GLUCONOGENESIS FROM AMINO ACID-
Results in formation of pyruvate or intermediate of TCA cycle, which
results in synthesis of glucose.

26. GLUCONEOGENISIS FROM LACTATE.
GLUCOSE FROM ALANINE CYCLE-
There is continuous transport of amino acid from muscle to liver during
starvation. These aminoacids are transported to liver for
gluconeogenesis.

27. REGULATION OF GLUCONEOGENESIS
1) INFLUENCE OF GLUCAGON- secreted by alpha cells of pancreatic
islets. Glucagon stimulates gluconeogenesis.
2) SUBSTRATE AVAILABILITY-glucogenic aminoacid produced from
muscles have stimulating influence on gluconeogensis.
3) ALCHOL- oxidation of alcohol in liver uses NAD+ and produces
NADH+, this excessive NADH+ interferes which gluconeogenesis
and increases the risk of hypoglycaemia especially in patient
taking insulin.

28. GLYCOGEN METABOLISM
Includes
GLYCOGENESIS- the synthesis of glycogen from glucose is
glycogenesis. It takes place in cytosol and requires ATP, and UTP
apart from glucose
(glucose)n + glucose +2ATP (glucose)n+1 +2ADP +Pi
GLYCOGENOLYSIS- the degradation of stored glycogen in liver and
muscle constitues glyogenolysis

29. INTRODUCTION
Diabetes is a clinical syndrome characterised by an increase in
plasma blood glucose.
TYPES OF DIABETES
TYPE I- Insulin dependant
TYPE II- non insulin dependent
OTHER SPECIFIC TYPE-
GESTATIONAL DIABETES-

30. OTHER TYPES OF DIABETES
a)Genetic defect of beta cell function
b)Genetic defect of insulin function(lipodystrophies)
c)Pancreatic disease
d)Excess endogenous production of antagonist hormones to
insulin.
e)Drug induced (steroid, thaizide, phenytoin)
f)Uncommon forms of immune mediated diabetes
g)Associated with genetic syndrome
GESTATION DIABETES.

31. FUNCTIONAL ANATOMY &PHYSIOLOGY
Brain has a little capacity to store energy in form of triglyceride or glycogen. So,
brain largely depends on liver for constant supply of glucose for oxidation and
hence generation of ATP.
After the food has been ingested the blood glucose is maintained by
1)Supression of heptatic glucose production.
2)Stimulation of hepatic glucose uptake.
3)Stimulation of glucose uptakeb by peripheral tissue.
GLUCOSE HEMOSTASIS
Uptake of
glucose by
peripheral
tissues
Entery of glocose in
blood from liver
Supplement of
glucose by intestine

32. In fasting condition- insulin and glucose level decreases, the glucagon
increases this leads to increased hepatic glucose output via
gluconeogenesis and glycogen breakdown.
In well feed state there is rise in glucose and insulin along with
decrease in glucagon concentration.
High insulin level after meals promotes triglycerides accumulation.
In contrast, in the fasting state low insulin level permits lipolysis and
release of FFA in to the circulation.
The partial oxidation of FFA in the mitochondria of liver produces
ketone bodies (acetoacetate).
When the rate of production exceeds the rate of excretion ketonaemia
may result, this normally occurs in case of fasting when the insulin
level is low and catecholamine levels are high.

33. AETIOLOGY & PATHOGENESIS OF
DIABETES TYPE I
TYPE ONE DIABETES- is a T cell mediated autoimmune disease
involving destruction of the insulin secreting beta cells in pancreatic
islets.
The symptoms usually occurs when 80-90% of the functional
capacity of the beta cells has been lost.
They are usually associated with other auto immune disease like-
thyroid disease, coeliac disease, adissons disease, pernicious
anaemia, vitiligo.

34. GENETIC PREDISPOSITION OF TYPE I DIABETES-
Account for 1/3rd of the susceptibility of the population.
It is polygenic, 200 different human genome shows linkage to type I
diabetes.
Most focused is the human leucocytes antigen region within the MHC on
the short arm of chromosome no 6; this locus is designated as IDDM 1
ENVIRONMENTAL PREDISPOSITION OF TYPE I DIABETES-
The nature of these factors are uncertain. They may cause diabetes either
by direct toxicity to beta cells or by stimulating autoimmune reaction
against the beta cells.
Eg. Viruses-(mumps, coxsackieB4, retrovirus, rubella, etc)
Dietary nitrosamines(coffee, bovine serum milk)
Also specific drugs or chemicals.

36. AETIOLOGY OF TYPE II DIABETS
INSULIN RESISTANCE- it is thought to be an cluster of condition caused
by insulin resistance. These include hypertension, non alcoholic fatty
liver dyslipidaemia.
PANCREATIC BETA CELLS- in type II is 50% destroyed at the time of
diagnosis.
GENETIC PREDISPOSITION-65 genes or gene regions are associated with
type II diabetes.
ENVIRONMENTAL AND OTHER RISK FACTOR-
DIET, OBESITY AND AGE- associated with over eating,obesity. It is usually
present in middle aged and elderly patients

37. PATHOGENESIS OF DIABETES TYPE II

38. METABOLIC DISTURBANCES –
Patient are often asymptomatic, or give a long history
Long h/f fatigue with or without- osmotic symptoms.
In case of infection, increase the production of stress hormones
which opposes insulin action , such as cortisol, GH, and
catecholamine's. This can precipate acute exacerbation of insulin
deficiency, and results in more severe hyperglycemia and
dehydration.

39. INVESTIGATIONS
URINE ANALYSIS-
GLUCOSE- dipstick test is common for screening.
KETONES- it can be identified by nitroprusside reaction.
PROTEIN-dipstick detect only albumin >300mg/l.

40. BLOOD TESTING-
GLUCOSE-relies upon an enzymatic reaction(glucose oxidase). Blood
glucose also depends on weather the patient has eaten anything or
not.
Glucose conc. In venous is less than in arteries or capillary. Whole
blood glucose concentration is less than plasma glucose. Venous
plasma is therefore the reliable one
KETONE- it is difficult to perform. Whole blood ketone monitoring
detects beta-hydroxybutyrate.
<0.6mmol/L-noraml, no action needed
0.6-1.5mmol/L-metabolic control deteriotating, monitor.
1.5-3.0-high risk of DKA (BG>10 mmol/L).
>3.0- SEVERE KETOSIS. Seek urgent medical help.

41. GLYCATED HAEMOGLOBIN- there is a slow non-enzymatic covalent
attachment of glucose to Hb. These fractions can be separated by
chromatography. HbA concentration reflects the integrated blood
glucose control over 120 days

43. DIAGNOSIS OF DIABETES
Glycaemia can be classified into three categories depending on
BSL-
SYMPTOMATIC PATIENTS- diagnosis is either confirmed by fasting
or random glucose test.
ASYMPTOMATIC PATIENTS-should under go 2 confirmatory test.
PREDIABETIC –can be diagnosed based on Impaired fasting
glucose- based on fasting glucose.
And, impaired glucose tolerance-2 hours after food.

44. PRE DIABETES CLASSIFIED AS
IMPAIRED FASTING GLUCOSE FPG>6.0(108mg/dl) and <7.0 mmol/L(126mg/dl)
IMPAIRED GLUCOSE TOLERANCE FPG<7.0mmol(126mg/dl)
And 2hrs after 75 mg of glucose drink
7.8-11.1mmo/Ll (140-200mg/dl)
DIABETES CONFIRMED BY
RBS 2hrs after 75 mg of
glucose load > 11.1(200mg/dl)
OR Fasting plasma glucose
> 7.0 mmol/L(126 mg/dl)

45. HOW TO PERFORM OGTT
Test is to be done in patient with plasma glucose 6.1-7.0 (110-
126mg/dl). Or when uncertain about the disease.
PREPARATION BEFORE TEST-
Unrestricted diet of carbohydrate for 3 days.
Overnight or 8hrs fasting.
Rest for 30 mins.
Remain seated during test, no smoking

46. SAMPLING-
Measure plasma glucose before and 2hrs after 75mg oral glucose
drink.
INTERPRETATION
FASTING 2HRS AFTER GLUCOSE
IMPAIRED FASTING
GLUCOSE
6.1-6.9mmol/L
110-125mg/dl
<7.8mmol/L
<140 mg/dl
IMPAIRED GLUCOSE
TOLERANCE
7.0mmol/L
<126mg/dl
7.8-11.0mmol/L
140-199mg/dl
DIABETES ≥7.0mmol/L
>126mg/dl
≥11.1 mmol/L
>200mg/dl

47. COMPLICATIONS
ACUTE COMPLICATIONS-diabetic ketoacidosi
-hyperglycaemic hyperosmolar state
-hypoglycemia
CHRONIC COMPLICATIONS-
MACRO VASCULAR MICROVASCULAR
Coronary circulation(MI)
Cerebral circulation(stroke,)
Peripheral circulation(cludication)

48. MICROVASCULAR COMPLICATION-
1) Retinopathy
2) Nephropathy
3) Peripheral neuropathy
4) Autonomic neuropathy
5) Foot disease

49. DIABETIC KETOACIDOSIS
When the rate of production exceeds the rate of excretion,
ketonaemia may result, this normally occurs in case of fasting when
the insulin level is low and catecholamine levels are high.
It occurs most commonly in TYPE I diabetes
KETONE>3mmol/L
Blood sugar >200mg/dl
Venous bicarbonate<7.3

50. SYMPTOMS SIGN
polyuria dehydration
Weightloss hypotension
Weakness cold extremities
Nausea tachycardia
Vomiting air hunger
Leg cramps smell of acetone
Blurred vision hypothermia
Abdominal pain drowsiness, coma

51. MANAGEMENT TIME (0-60 mins)
1)commence 0.9% sodium chloride. 1L over 60 mins
2)commence insulin treatment-50 U human soluble insulin in 50 ml 0.9%
sodium chloride infused iv at 0.1 U/kg body weight/hr
3)perform further investigation-hourly blood glucose and ketone testing.
TIME(60mins-12hrs) -IV infusion of 0.9%sodium chloride with potassium
chloride with as indicated below
1L over 2hr
1L over 2hrs
1Lover 4 hrs
1L over 4 hrs
1L over 6 hrs
Add 10 % glucose 125ml/hr iv when glucose <14 mmol/L

52. TIME 12-24 hrs
Ketonameia and acidosis must have been resolved.
If patient is not eating and drinking-
Continue IV insulin infusion at slower rate of 2-3 U/hr
Continue iv fluid replacement
Reinitiate SC insulin . Donot disconitue IV infusion until 30 mins
after SC-short acting insulin injection

53. HYPOGLYCEMIA
It is the 2nd and much more common acute complication of diabetes
mellitus.
It develops very quickly as compared to hyperglycaemia.
Episodes of hypoglycaemia usually develops when the patient has
not eaten for several hours.

54. SYMPTOMS-
AUTONOMIC-sweating NON-SPECIFIC-
trembling Nausea
pounding of heart tiredness
hunger headache
anxiety
NEUROLOGICAL-Confusion
drowsiness
speech difficulty
inability to concentrate
incoordination
irritability, anger

55. MANAGEMENT
CONSCIOUS AND RESPONSIVE PATIENT
Oral fast acting carbohydrate(10-15 g)is taken.
Follow by snacking (complex carbohydrate)
HYPOGLYCEMIC UNRESOPNSIVE PATIENT
Iv 75ml 20% dextrose
4)Im or iv injection of 1mg glucagon
5)0.5mg of 1:1000 epinephrine im

56. DIABETIC RETINOPATHY
Almost all individual of type I diabetes will suffer.
PATHOGENESIS-
Hyperglycaemia inc. retinal blood flow (disrupts the metabolism of
retinal blood cells)increased production of vasoactive substances
and endothelial proliferationleading to capillary hypoperfusion and
closure chronic retinal ischaemia

57. DIABETIC NEPHROPATHY
It develops in 30% of patient having type I diabetes.
1st there will be microalbuminuria  thickening of glomeular
basement membrane  accumulation of matrix material in
mesangium.
Nodular deposits characteristic of diabetic glomerulosclerosis
worsens as heavy proteinuria develops

58. DIABETIC NEUROPATHY
It affects 50-90% of patient having diabetes
PATHOLOGICAL FEATURE–
1)Axonal degeneration occurs in myelinated
and unmyelinated nerve fibers.
2)thickening of basal lamina of schwann cells.
3)Patchy segmental demyelination and
abnormal intraneural capillary formation

59. THE
DIABETIC
FOOT

60. Tissue hyperglycemia effects immune system including neutrophil and
lymphocyte function, chemotaxis, and phagocytosis.
Uncontrolled blood glucose hinders RBC permeability and
impairs blood flow through the critical small vessels at the
wound surface.
The hemoglobin release of oxygen is impaired, resulting in oxygen and
nutrient deficiency in the healing wound. Wound ischemia and impaired
recruitment of cells resulting from the small vessel occlusive disease
render the wound vulnerable to bacterial and fungal infections.
Therefore, diabetic patients are more prone to infections.

61. STRESS AND DIABETES
During stress there is an increase of-
Cortisol
Catecholamine
And glucagon.
These hormones have affect opposite to that of INSULIN, producing
stress induced glucose tolerance.
This is the reason to increase the dose of insulin during the surgical
procedure

62. SURGERY AND DIABETES
When a surgery is planned and the pt. is supposed to be nil by mouth the night
before surgery. Then , half morning dose of insulin is given and i.v glucose is
administered i.v.
If, sign of hypoglycaemia develops intraoperatively then, some caloric source of
food should be given intraorally within 3 hrs of surgery.
If more major surgery is and long duration of GA is required it can be best
managed where continuous monitoring of sugar is done and insulin can be
administered as an when needed.
When pateint is unlikely to maintain enterally insulin monitoring is done every 6
hrly to maintain blood glucose level of 150-250 mg/dl

63. ANTIDIABETIC DRUGS
TYPES OF INSULIN
1)RAPID ACTING- insulin lispro
insulin aspart
insulin glulisine
2)SHORT ACTING- regular soluble insulin
3)INTERMEDIATE ACTING- lente
NPH(isophane insulin)
4)LONG ACTING- insulin glargine
insulin detemir

64. INSULIN
Insulin was discovered by
Banting and Best.
2 chains chain A (21 A.A.)
chain B (30 A.A.)
---------------------
Total 51 amino acid.
Initially human insulin was used.
Later more purified form of insulin made by recombinant DNA
technology in E.coli proinsulin recombinant bacterial and in yeast-
enztmetic modification of procine insulin began to come in use

65. INSULIN PUMP
INSULIN INHALER

66. ORAL HYPOGLYCAEMIC DRUGS
A)ENHANCES INSULIN SECRETION-
1)SULFONYLUREAS- 1st gen-Tolbutamide
2nd gen Glibenclamide,glipizide,
,gliclazide, glimipiride.
2)MEGLITINIDE- repaglinide, nateglinide
3)GLUCAGON-LIKE PEPTIDE-
4)DIPEPTIDYL PEPTIDASE-4 INHIBITOR- sitagliptin,
linagliptin.

67. B) OVERCOME INSULIN RESISTANCE-
1)BIGUANIDE- metformin
2)THIAZOLIDINEDIONES-pioglitazone
C) MISCELLANEOUS ANTIDIABETIC DRUGS-
1)αGLUCOSIDASE INHIBITOR- acrobose, miglitol
2) AMYLIN ANALOGUE- pramlinitide
3)DOPAMINE D-2 RECEPTOR AGONIST- bromocriptin
4)SODIUM GLUCOSE CO-TRANSPORT INHIBITOR- dapagliflozin

68. SULFONYLUREAS
2st generation are commonly used.
MOA- it stimulates the release of insulin
Sensitizes the target tissue to insulin.
PHARMACOKINETICS- well absorbed orally. Metabolites excreted in
urine. Should be used cautiously in liver or kidney dysfunction.

69. INTERACTION
1)DRUGS THAT ENHANCES SU ACTION
A) Displaces from protein binding- phenylbutazone, sulfinpyrazone,
salicylates, sulfonamides,
B) Inhibit metabolism/excretion-cimetidine, ketoconazole, sulfonamide,
warfarin, chloramphenicol, alcohol.
C)Synergise with or prolong pharmacodynamic action- salicylates,
propranolol, lithium, alcohol.
2)DRUGS THAT DECREASE SU ACTION
A)Induces metabolism- phenobarbitone, phenytoin, rifampicin, alcohol
B)OPPOSITE ACTION-corticosteroids, thiazides, furosemide, oral
contraceptive

70. ADVERSE EFFECTS
1) HYPOGLYCAEMIA
2) NONSPECIFIC SIDE EFFECTS
3) HYPERSENSITIVITY
4) WEIGHT GAIN

71. METFORMINS
It’s a biguanide-
MOA- inhibits release of sugar from liver.
Reduces absorption of sugar from intestine.
Increases the sensitivity of insulin receptor.
Promote peripheral glucose utilization.
USES- non hypoglycemia.
weight loss promotion.
prevents micro and macrovasular complications
No acceleration of beta cell failure
C/I- hypotensive, heart failure, hepatic and renal disease, alcohlic

72. MEGLITINIDE
Binds to SUR closure of potassium channel depolarisation
insulin release.
Administered before meal. Should be ommited if meal is missed.
Rapid onset of action, short lasting insulin release.
Its is given in case of pronounced post prandil hyperglycemia

73. GLP AGONIST & DPP INHIBITOR

74. KEY TO MANAGE MEDICALLY
COMPROMISED PTS. ARE
Risk assessment- components are :
(1)the nature, severity, and stability of the patient’s medical
Condition
(2) the functional capacity of the patient;
(3)the emotional status of the patient; and
(4) the type and magnitude of the planned procedure

75. DENTAL MANAGEMENT
The cornerstone of patient evaluation and risk assessment is the
1) medical history,
2) physical examination,
3) laboratory tests,
4) medical consultation.

76. MEDICAL EXAMINATION
The two basic techniques used to obtain a medical history consist of
the interview (medical model), and a printed questionnaire that the
patient fills out.
Patient on insulin should be asked about-
Dose
Frequency
Self monitoring
Method frequency
Recent values
Insulin reaction and the time it happened.

77. MEDICAL CONSIDERATION
Undiagnosed patients with cardinal symptoms should be referred to
doctor.
Patients with clinical findings should be also be referred.
In a study it was concluded that 28.9% of the diabetic patients coming
for dental treatment had poor glycaemic control.

78. WHAT OTHER PATIENTS TO
REFER ??
1) I AM 45yrs OLD 2)can I get
diabetes?
3)Patients who gave birth of babies of > 10 pounds.
4)Women who had multiple spontaneous absorption / still birth.

79. VITALS- patient with abnormal pulse rate and rhythm or increase
blood pressure should be approached with cautions.
FUNCTIONAL CAPACITY-patient with FC<4 should be approached
with cautions.
Patient with TYPE II with good control don’t need any consultation
can be treated like a normal patient.
Patient with renal and cardiovascular complication need special
consideration.
Patient with poor glycaemic control, frequent insulin shock and
brittle diabetes should be treated cautiously.

80. INSULIN SHOCK
Patient who forgets to take food after insulin injection or who take
excessive insulin or hypoglycaemic agents. May experience a
hypoglycaemic. Reaction caused can be described In 3 well defined
stages.
Occurs in TPE I diabetes only

81. MANAGEMENT OF INSULIN SHOCK
PRE-OPERATIVE-
Patient should take usual insulin dosage.
Eat normal meal before appointment.
Appointment is scheduled in morning.
Source of sugar should be kept ready.
Patient should be informed to tell during the procedure , if he/she
feels any insulin shock symptoms.

82. POST-OPERATIVE-
Patient should be instructed to eat properly postoperatively so as to
maintain normal glucose level.
Patient should consult physician about dietary recommendation of
food.
Patient can alter the insulin dose postoperatively with consultation ,
if he is not able to eat .
Patient can use blender to prepare their usual food or special food
supplement can be give.

83. BRITTLE DIABETES
Patient having period of hyper or hypo glycaemia even after best of
medical management.
Patient have increased risk of postoperative infection so , proper
systemic antibiotic should be given.
i.v. sedation involves fasting before t/t and so, ½ insulin dose should
be given prior and i.v. glucose during the procedure.

84. MANAGEMENT OF PATIENT WITH DIABETES AND
ACUTE ORAL INFECTION
1)Non insulin controlled diabetes may require insulin-consultation
should be done.
2)Insulin controlled require more insulin- consultation needed.
3)BRITTLE DIABETES- sample should be taken from infected area
for antibiotic sensitivity testing-
Culture should be sent
Antibiotic-penicillin therapy should be initiated.
In case of poor clinical response to 1st antibiotic, more effective
antibiotic is selected acc. To the test.

85. 4) Infection should be treated with use of standard methods-
a) warm intraoral rinses
b) Incision and drainage
c) Extraction, pulpectomy, pulpotomy etc.
d) Antibiotic
5) Patients electrolyte and fluid management should also be done
properly.

86. LOCAL ANESTHETICS EPINEPHRINE-diabetic pt.- local anesthetic
with 1:100,000 epinephrine should be tolerated well. However, epinephrine
has a pharmacologic effect that is opposite that of insulin, so blood
glucose could rise with the use of epinephrine.
In diabetic patients with hypertension, post myocardial infarction, cardiac
arrhythmia caution may be indicated with epinephrine.
Adrenaline, which is one of the most commonly used vasoconstrictors,
causes glycogenolysis, thus interacting with insulin. Noradrenaline has
less of a glycogenolytic effect compared to adrenaline, and so is preferred
in diabetics.
Generally, though, the amount of vasoconstrictor in an ampoule is very
small (the greatest concentration being 1:50,000) and so the risk is
considered minor.

88. REFERENCES
1) B.D CHAURAS. human ANATOMY volume 2 , 7th edition
2) K. sembhulingam, essential of medical physiology, 6th edition
3) U.Styanaryan, essential of biochemistry
4) Churchill livingstone, davidsons principles and practise of
medicine, 22nd edition.
5) Petersons principle of oral and maxillofacial surgery, 2nd edition,
volume 1
6) K.D. tripathi, essential of medical pharmacology