Hybridoma Technology ( Production , Purification , and Application )
DIABETES MELLITUS.ppt
1.
2.
3. DIABETES MELLITUS
Diabetes mellitus is not a single disease entity, but rather a group of
metabolic disorders primarily of carbohydrate metabolism sharing
the common underlying feature of hyperglycemia.
Alteration in lipid and protein metabolism
Secondary damage in multiple organ system
4.
5. 1. Type 1 diabetes ( cell destruction, leads to absolute insulin deficiency)
· Immune mediated
· Idiopathic
2. Type 2 diabetes (insulin resistance with relative insulin deficiency).
DIABETES MELLITUS
3. Genetic defects of cell function.
- Maturity onset diabetes of the young (MODY), caused by mutations in ;
- Hepatocyte nuclear factor 4 (HNF – 4) (MODY3).
- Glucokinase (MODY2).
- Hepatocyte nuclear factor 1 (HNF - 1) (MODY5).
- Insulin promoter factor 1 (HNF - 1) (MODY5).
- Hepatocyte nuclear factor 1 (HNF- 1) (MODY5)
- Neurogenic differentiation factor 1 (Neuro D1) (MODY6).
- Mitochondrial DNA mutations.
10. Has reached epidemic population worldwide
150 million cases in 2000
221 million expected in 2010
90% are type 2 & it parallels the increase in the incidence
of obesity
Prevalence is similar but slightly greater in men of >60
yrs
DIABETES MELLITUS
11. Blood glucose values are normally maintained in a very narrow
range, usually 70 to 120 mg / dl. The diagnosis of diabetes is
established by noting elevation of blood glucose by any one of three
criteria.
1.A random glucose > 200 mg / dl, with classical signs and symptoms .
2.A fasting glucose > 126 mg / dl on more than one occasion.
3. An abnormal oral glucose tolerance test (OGTT) in which the glucose
is > 200 mg /dl 2 hours after a standard carbohydrate load.
DIABETES MELLITUS
12. Individuals with fasting glucoses less than 110 mg / dl or less than 140 mg /
dl following an OGTT are considered to be euglycemic.
However those with fasting glucose greater than 110 but less than 126 or
OGTT values greater than 140 but less than 200 are considered to have
impaired glucose tolerance (IGT). Individuals with IGT have a significant
risk of progressing to overt diabetes over time. In addition those with IGT
are at risk for cardiovascular disease due to the abnormal carbohydrate
metabolism as well as the coexistence of other risk factors such as low
HDL, hypertriglyceridemia and increased plasminogen activator( PAI – 1).
Revised criteria for diagnosis emphasize FBS as a r eliable & convenient test
Random 200 mg/dl with classic symptoms( polyuria,polydipsia&wt loss) is
sufficient for diagnosis.
ADA all individuals >45 yr every 3 yrs & with risk factors at an earlier age
DIABETES MELLITUS
13. NORMAL ENDOCRINE PANCREAS
The endocrine pancreas consists of about
1million microscopic clusters of cells, the islets of
Langerhans.
The first evidence of islet formation in the
human fetus is seen at 9 to 11 weeks.
In aggregate, the islets in the adult human
weigh only 1 to 1.5 gm, individually, most islets
measure 100 to 200 m and consists of four
major and two minor cell types.
DIABETES MELLITUS
14.
15. The four major types are , , and PP (pancreatic polypeptide)
cells and the two minor types are D1 and enterochromaffin cells.
The major types make up about 68%, 20%, 10% and 2%
respectively, of the adult islet cell population. They can be
differentiated morphologically by their staining properties, by the
ultra structural characteristics of their granules, and by their
hormone content.
The cell produces insulin, as will be detailed in the discussion of
diabetes. The insulin – containing intracellular granules contain a
crystalline matrix with a rectangular profile, surrounded by a halo.
The cell produces Glucagon and the granules are found with
closely applied membranes and dense center
16. cells contain Somatostatin, which suppresses both insulin and
glucagon release ; they have large, pale granules with closely
applied membranes.
PP cells contain a unique pancreatic polypeptide that exerts a
number of gastrointestinal effects, such as stimulation of secretion
of gastric and intestinal enzymes and inhibition of intestinal
motility. These cells have small, dark granules and not only are
present in islets, but also are scattered in the exocrine pancreas.
The minor cell type D1 cell elaborate vasoactive intestinal
polypeptide (VIP), a hormone that induces glycogenolysis and
hyperglycemia ; it also stimulates gastrointestinal fluid secretion
and causes secretory diarrhoea and Enterochromaffin cells
synthesize serotonin and are the source of pancreatic tumors that
causes the carcinoid syndrome.
21. FATE OF SECRETED INSULIN
Insulin & insulin like activity in blood
non suppressibleinsulin like activity (NSILA)
IGFI & IGFII
Metabolism
T ½ 5min
destroyed by proteases
22. RAPID [ SEC ]
INCREASED TRANSPORT OF GLUCOSE , AMINOACIDS & K+
INTERMEDIATE [ MIN]
STIMULATION OF PROTEIN SYNTHESIS
INHIBITION OF PROTEIN DEGRADATION
ACTIVATION OF GLYCOLYTIC ENZYMES & GLYCOGEN
SYNTHASE.
INHIBITION OF PHOSPHORYLASE & GLUCONEOGENIC
ENZYMES.
DELAYED [ HRS]
INCREASE IN mRNAs FOR LIPOGENIC & OTHER ENZYMES.
29. IMM T CELL MED ß
CELL DEST
SEVERE LACK
OF INS
DM
GENETIC, ENVIR FACTORS
30. MECHANISM OF ß CELL
DESTRUCTION
Tlymph CD4 & CD8
Cytokines
Express Cl II MHC
molecules
ß cell enzyme(glutamic
acid decarboxylase) &
insulin acts as
autoantigens.
31. GENETIC SUSCEPTIBILITY
Complex pattern of genetic associations
Susceptibility genes ve been mapped to atleast 20 loci
Particuar genes involved are not known
More commonly associated is Cl II MHC
(HLA) locus
They make up half of the genetic susceptibility.
MHC LOCUSMHC located 6p21(HLA-D)
95% with type I DM have HLA DR3,DR4
or both in contrast to 40% of normal subjects.
ENVIRONMENTAL FACTORS
Infections trigger autoimmunity in type I DM
eg., mumps,measles,cytomegalovirus rubella ,infectious
mononucleaosis
32.
33. INSULIN RESISTANCE
decreased ability of peripheral tissues
to respond to insulin.
BETA CELL DYSFUNCTION
decreased insulin secretion in the face
of insulin resistance and
hyperglycemia.
34. INSULIN RESISTANCE
Insulin resistance is defined as resistance to the effects of insulin
on glucose uptake, metabolism, or storage.
Insulin resistance is a characteristic feature of most patients with
type 2 diabetes and is an almost universal finding in diabetic
individuals who are obese.
The role of insulin resistance in the pathogenesis of type 2 diabetes
can be gauged from the finding that
(1) insulin resistance is often detected 10 to 20 years before the onset
of diabetes in predisposed individuals (e.g., offspring of type 2
diabetics) and
(2) in prospective studies, insulin resistance is the best predictor for
subsequent progression to diabetes. Insulin resistance leads to
decreased uptake of glucose in muscle an adipose tissues and an
inability of the hormone to suppress hepatic gluconeogenesis.
35. OBESITY AND INSULIN RESISTANCE
The association of obesity with type 2 diabetes has been recognized
for decades, visceral obesity being a common phenomenon in the
majority of type 2 diabetics.
The link between obesity and diabetes is mediated via effects on
insulin resistance.
Insulin resistance is present even in simple obesity unaccompanied
by hyperglycemia, indicating a fundamental abnormality of insulin
signaling in states of fatty excess.
36. The risk for diabetes increases as the body mass index (a
measure of body fat content) increases. It is not only the
absolute amount but also the distribution of body fat
that has an effect on insulin sensitivity .
Central obesity (abdominal fat) is more likely to be linked
with insulin resistance than are peripheral (gluteal /
subcutaneous) fat depots.
37. MECHANISM
1. circulating FFA
2. peptides & proteins secreted by fat cells
3. white fat harmones
SYNDROME X
Hyperinsulinemia
Dyslipedemia
Accelerated development of atherosclerosis
AGENT EFFECT ON
INSULIN
RESISTANCE
Leptin Decreases
TNF alpha Increases
Adiponectin Decreases
Resistin Increases
38. BETA CELL DYSFUNCTION
- Cell dysfunction in type 2 diabetes reflects the inability of these
cells to adapt themselves to the long – term demands of peripheral
insulin resistance and increased insulin secretion.
In states of insulin resistance, insulin secretion is initially higher
for each level of glucose than in controls.
This hyperinsulinemic state is a compensation for peripheral
resistance and can often maintain normal plasma glucose for years.
Eventually, however, - cell compensation becomes inadequate,
and there is progression to overt diabetes.
The underlying basis for failure of - cell adaptation is not
known, although it is postulated that several mechanisms,
including adverse effects of high circulating free fatty acids
(“lipotoxicity”) or chronic hyperglycemia (“glucotoxicity”), may play
a role. - Cell dysfunction in type 2 diabetes manifests itself as
both qualitative and quantitative defects.
39. PATHOGENESIS OF THE COMPLICATIONS OF
DIABETES
FORMATION OF ADVANCED GLYCATION END PRODUCTS
NON ENZYMATIC RELATIONS
intracellular glucose derived dicarbonyl
precursors (glyoxal,methylglyoxal)
+
Amino group of both intracellular &
extracellular protein
AGEs
Extracellular matrix
components
40. TYPE IV COLLAGEN IN BASEMENT MEMBRANE
AGE TRAPS PROTEIN LIKE LDL
BIOLOGIC EFFECTS OF AGE
1. Release of cytokines
2. Endothelial permeability
3. Precoagulant activity on cells
Endothelial adhesion Fluid filtration
Cholesterol deposition atherogenesis
41. ACTIVATION OF PROTEIN KINASE C
Ca
intracellular protein kinase
DAC
diacyl glycerol
Production of the proangiogenic molecule vascular endothelial growth factor
(VEGF), implicated in the neovascularization characterizing diabetic
retinopathy.
Increased activity of he vasoconstrictor endothelin – 1 and decreased activity of
the vasodilator endothelial nitric oxide synthase (eNOS) .
HYPERGLYCEMIA
42. INTRACELLULAR HYPERGLYCEMIA WITH
DISTURBANCES IN POLYOL PATHWAYS
Production of profibrogenic molecules like transforming
growth factor (TGF), leading to increased deposition of
extracellular matrix and basement membrane material.
Production of the procoagulant molecule plasminogen
activator inhibitor – 1 (PAI – 1) leading to reduced
fibriolysis and possible vascular occlusive episodes.
Production of pro–inflammatory cytokines by the
vascular endothelium.
46. CLINICAL FEATURES DM
TYPE I
Lesser then 20 yrs
Normal weight
Markedly reduced blood insulin
EFFECTS OF HYPERGLYCEMIA
• Catabolic state
• Counter regulatory harmone
Glucose catabolism is
normally a major source of
energy for cellular processes
and in diabetes energy
requirements can be
met only by drawing on protein
& fat
47. CHANGES IN PROTEIN METABOLISM
1) Rate at which aminoacids are catabolized to co2 & H2O is
increased .
2) More aminoacids are catabolized.
• The measure of the rate of gluconeogenesis is obtained by
measuring D/N ratio .
D/N ratio of 3 in DM indicates the conversion to glucose of about
33% of the carbon of the protein metabolized. in diabedes the net
effect of accelerated protein conversion in absence of insulin to co
,ho & glucose ,plus diminished protein synthesis resulting in
a) negative nitrogen balance
b) protein depletion (poor resistance to infection)
c) wasting
48. FAT METABOLISM IN DM
GLUCOSE -----50%burned co2 &h2o
5% converted to glycogen
30%--40% converted to fat
But in DM <than 5% is converted to fat
PRINCIPAL ABNORMALITIES
Acceleration of lipid metabolism
Formation of ketone bodies
Synthesis of fatty acids &triglycerides
Increased glucagon----mobilization of FFA
Thus the FFA level parallels the plasma glucose level in DM and in
some ways is a better indicator of the severity of the diabetic state .
In liver ,FA acetyl COA ketone bodies
49. KETOSIS
acetoacetyl CoA
Excess acetyl – CoA
acetone
acetoacetate
beta hydroxy
butyrate
In fasting ketone bodies are source of energy .but in diabetes it piles up
in the blood stream due to much production.
50. ACIDOSIS
Acetoacetate ,betahydroxybutyrate are anions of the fairly strong
acetoacetic acid &beta hydroxybutyric acid.
ACIDOSIS KUSSMAUL BREATHING
Na & K are lost in urine to compensate
Excessive loss
Dehydration
Hypovolemia
Hypotension
Diabetic coma
52. TYPE II DIABETES MELLITUS
May also present with polyuria ,poludipsia but unlike typeI patients are often
older&frequently obese.
Distinctive features
absence of ketoacidosis
develops hyperosmolar non ketotic coma
PATHOPHYSIOLOGY OF HYPERGLYCEMIC &
HYPEROSMOLAR STATE
relative inadequate fluid hyperglyceamia
Insulin deficiency + intake
intravascular osmotic diuresis
volume
depletion
Differentiating features
1. absence of ketosis
2. Relative insulin defeciency
3. Level of counterregulatory harmones
4. FFA
53. CHRONIC COMPLICATIONS
It affects multiple organ system responsible for the majority of morbitidity and
mortality.
In chronic hyperglycemia prevent or delay microvascular
disease
STUDIES
1. THE DIABETES CONTROL & COMPLICATIONS TRIAL
1400 individuals with type I
conclusion-if all complications of DM were combined individuals in the
intensive diabetes management group would experience 15.3 more yrs of life
without significant microvascular and neurologic complications of DM .
2 UNITED KINGDOM PROSPECTIVE DIABETES STUDY
>5000 individuals with type II
conclusion-there was a continuous relationship b/w glycemic control &
development of complications.
54. Improved diabetic control did not conclusively reduce
cardiovascular martality but was associated with
lipoprotein risk profiles
Major finding strict BP control significantly reduced
both macro & micro vascular complications
moderate goals 144/82 mm Hg reduced
death,stroke,microvascular diseases& heart failure.
These land mark studies prove the value of matabolic
control& emphasize the importance of
1. Intensive glycemic control in all forms of DM.
2. Early diagnosis & strict BP control in type II DM.
55. DIABETIC RETINOPATHY
Intra retinal microvascular abnormalities
Microaneurysms & haemorrhages
Neovascularization
BLINDNESS
RENAL COMPLICATIONS
Individual with diabetic nephropathy almost always
have diabetic retinopathy
Glomerular hyperfiltration
Increased glomerular capillary pressure
BM thickening
Proteinuria in individuals with DM is associated with
markedly reduced survival & increased risk for
cardiovascular disease
56. DIABETIC NEUROPATHY
Both myelinated and unmyelinated nerve fibers are lost
Distal sensory loss
.SYMPTOMS
Numbness,tingling,sharpness and burning that begins in the feet and
spreads proximally
Worsens at night
As diabetic neuropathy progresses the pain subsides & eventually
disappears but a sensory dediciency in the lower extremities persists
Physical examination reveals sensory loss of reflex & abnormal
position sense
57. CARDIOVASCULAR MORBIDITY &
MORTALITY
peripheral arterial disease
Congestive heart failure
MI
Coronary arterial disease
Sudden death
American heart association recently declared DM as a
risk factor (type II)
The absence of chest pain (silent ishcemia) is common in
individuals with diabetes
58. GASTROINTESTINAL
delayed gastric emptying(gastro paresis)
altered small & large bowel motility(constipation or diarrhoea)
nocturnal diarrhoea alternating with constipation isa common feature of common
feature of dm related gi diabetic auto neuropathy
GENITOURINARY
diabetic autoneuropathy symptoms=inability to sense th e full bladder and failure
to void completely
as bladder contractility worsens bladder capacity and post void residual increases
leading to symptoms of urinary hesitancy
decreased voiding frequency
incontinence
recurrent urinary tract infection
59. LOWER EXTREMITY COMPLICATIONS
Neuropathy
Abnormal foot biomechanics
Peripheral arterial disease
Poor wound healing
Risk factor for foot ulcer
Male sex
Diabetic > 10 yrs
Peripheral vascular disease
Poor glycemic control
60. INFECTION
Pneumonia,UTI, skin & soft tissue infection are all common
Reasons
Incompletely defined abnormalities CMI,phagocyte function
Diminished vascularization
Hyperglycemia aids colonization & growth of various organisms
They have greater risk of post operative wound infection
61. alterations in salivary flow and constituents, increased incidence of
infection, burning mouth, altered wound healing, and increased
prevalence and severity of periodontal disease.. These complications
may be related to the degree of glycemic control.
Dry mucosal surfaces are easily irritated and often provide a
favorable substrate for the growth of fungal organisms. The
incidence of candidiasis may be increased in patients with diabetes.
Dental caries rates may also be altered in diabetes. An
increased caries rate may be associated with decreased salivation or
with increased glucose concentrations in the saliva and gingival
crevicular fluid (GCF).
62. 1. Diabetes is a risk factor for periodontal disease
2. Increased gingival inflammation may be seen in diabetic subjects
even though plaque levels are similar to non diabetic controls
3. The prevalence of periodontitis in diabetic adolescents young adults
and adults is significantly greater t5hen similar aged non diabetic
individuals
4. In large population studies type II diabetes has been shown to be a
significant risf factor for periodontitis – PAPANOU
5. By TAYLOR , diabetes may influence not only the prevelance and
severity of periodontitis but also the prognosis of the disease.
63. MECHANISM OF DIABETIC INFLUENCE ON
PERIODONTITIS
Changes in subgingival microbiota?
GCF glucose level = decreased chemotaxis of PDL fibers to PDGF
so decreased wound healing
Peripheral vasculature = increased thickness of gingival capillaries
which impairs oxygen diffusion.
Formation of ADVANCED GLYCATION END PRODUCTS
Altered host immune response is important in pathogenesis (defects
in PMN adherence ,chemotaxis,phagocytosis)
64. Periodontal treatment are designed to decrease the bacterial challenge & reduce
inflammetion might restore insulin sensitivity over time,resulting in improved
metabolic control
There is little evidence regarding the success/failure of dental implant therapy in
diabetic individuals
Diabetic is often considered a reletive contraindications to implant placement but
in well controlled diabetes there is no reason to avoid implant therapy.
Patients with poorly controlled diabetes may not repond well to any surgical
treatment including implant placement due to impaired wound healing
In animals there is decreased implant bone contact & bone density
Long term implant stability is also not known.
65. APPROACH TO PATIENT
History :
Physical examination :
Classification of DM in an individual patient :
Individuals with type IDM tend to have the following characteristics
Onset of disease prior to age 30
Lean body habitus
Requirement of insulin as the initial therapy
Propensity to develop ketoacidosis
An increased risk of other autoimmune disorders.
In contrast, individuals with type 2 DM exhibit
Develop diabetes after the age of 30
Usually obese
May not require insulin therapy initially
May have associated conditions such as insulin resistance, hypertension,
dyslipidemia.
Laboratory assessment :
66. LONG – TERM TREATMENT
Overall principles :
The goals of therapy for type 1 or type 2 DM.
– Eliminate symptoms related to hyperglycemia
– Reduce or eliminate long term microvascular and
macrovascular complications of DM and
– Allow the patient to achieve as normal a life style as
possible.
Diabetes Education :
Nutrition :
Exercise :
67.
68. Medical Management :
Oral Agents :
A number of different oral agents are available for treating
diabetes most of these are taken by those with type 2 diabetes the
first generation sulfonylureas once the only drug available for
treating type 2 diabetes are not much used today. They have been
replaced with the second generation agents that are more potent,
have fewer drugs interaction, and produce less significant side
effects. Sulfonylureas stimulate pancreatic insulin secretion. The
increased quantity of secreted insulin helps counteract the
qualitative decrease in tissue sensitivity to insulin, allowing greater
glucose entry into target cells and thereby lowering blood glucose
levels. Sulfonylureas generally have a relatively long duration of
action of 12 – 24 hours, depending on the drug and are taken once
or twice per day Hypoglycemia is major side effect of sulfonylureas.
In patients taking these agents food intake must be adequate to
prevent glucose levels falling too low.
69.
70.
71.
72. Like the sulfonylureas, repaglimidine stimulates pancreatic insulin
secretion however its pharmacodynamic properties and mechanism
of action are different from those of the sulfonylureas.
Repaglimidine is rapidly absorbed, reaches peak plasma level in 30
– 60 minutes, and is then rapidly metabolised. The drug is taken
with meals and lowers the peaks of post- prandial plasma
glucose common with type 2 diabetes to a much greater degree than
the sulfonylureas are able to do.
Metaformin is biguanide agent that lowers plasma glucose
mainly by preventing glycogenolysis in the liver. Metaformin also
improves insulin use, counteracting the insulin resistance seen with
type 2 diabetes. Because metaformin does not stimulate increase
insulin secretion, hypoglycemia is much less common with this drug.
73. The thiazolidinedione agents troglitayone, rosiglitayone and
pioglitayone act to increase tissue sensitivity to insulin, thus
increasing glucose utilization and decreasing blood glucose levels.
These drugs also decrease hepatic gluconeogenesis like metaformin
.The thiozolidinediones generally donot cause hypoglycemia.
Acarbose has mechanism of action that is unlike that of
the other agents used in diabetes management. Acarbose is taken
with meals, and it slows the digestion and uptake of carbohydrate
from the gut. This serve to lower post prandial plasma glucose
peaks .Acarbose does not cause hypoglycemia, but if the delayed
carbohydrate absorption occurs in a patient whose plasma insulin
levels are increasing due to injection of insulin or the use of a
sulfonylunreas, the level of glucose in the blood stream will be
sufficient to prevent hypoglycemia.
74. Insulin:
All type 1diabetes patients use exogenous insulin, as do many with type 2
diabetes. Insulin is taken via subcutaneous injection most often with a syringe.
Insulin infusion pumps deliver insulin through a subcutaneous catheter. There
are variety of insulin preparation available they vary in their onset, peak, and
duration of activity and are classified as long intermediate, short or rapid acting.
Although beef and pork insulin species are still available, most individuals use
human insulin preparation today. Ideally, the use of exogenous insulin provides
an insulin profile similar to that seen in a nondiabetic individual, with a
continuous basal level of insulin availability augmented by increased availability
following each meal. There is no single insulin preparation that can achieve this
goal with one or two injections per day.Combination of different insulin
preparation taken three or more times daily or use of subcutaneous infusion pump
more closely approximate the ideal profile, but even with such regimen blood
glucose level are often instable.
75. Ultralente insulin is the longest – acting insulin commonly called “peakness”
insulin. Ultralente has a very slow onset of action, minimal peak activity and a
long duration of action.It is usually taken to mimic the BMR of insulin secreted
from normally functioning pancreas. The intermediate long acting insulin (lente
and neutral protamine Hagedron (NPH)) taken several hours after injection to
begin having an effect. Peak activity varies among individuals and site of
injection but generally occurs between 4 – 10 hours after injection. Thus a
patient who injects intermediate acting insulin in early morning will reach peak
plasma insulin level at about lunch time. Regular insulin is short acting, with an
onset of activity at about 30 minutes to 1 hour after injection and peak activity
at 2 – 3 hours.The rapid acting insulin called lispro insulin is rapidly absorbed,
becomes active about 15 minutes after injection and is at peak activity at 30 – 90
minutes. Rapid and short acting insulin are usually taken just prior to or during
meals.Thus regular insulin taken prior to breakfast will peak at about
midmorning; when taken prior to lunch it will peak during midafternoon .The
most common complication of insulin therapy is hypoglycemia a potentially life
threatening emergency. While hypoglycemia may occur in patients who are taking
oral agents such as sulfonylenureas, it is much more common in those who are
using insulin.
76. DENTAL MANAGEMENT OF DIABETIC PATIENT :
Well controlled diabetic patient with periodontitis have positive response to
nonsurgical therapy, periodontal surgery and maintenance that are similar to
those of people without diabetes
The clinician should detetermine the patients recent glycated hemoglobin values
since this test provides a measure of glycemic control over the preceding 2 – 3
months HbA 1c values of less than 8% indicate relatively good glycemic control,
values greater than 10% indicate poor control.
Other key dental treatment consideration for diabetic patients include stress
reduction, treatment setting, the use of antibiotics diet modifications,
appointment timing, changes in medication regimens and the management of
emergencies.
Some clinicians prefer to prescribe prophylatic antibiotic coverage prior to surgical
therapy if the diabetic patient’s glycemic control is poor. This usually applies to
emergency situations since elective procedures are generally deferred until
glycemic control improves. In patients with severe peridontitis, adjunctive use of
tetracycline antibodies in conjunction with the mechanical periodontal therapy
may have beneficial effects on glycemic control as well as on periodontal status.
77. Before dental treatment begun, the patient may check his or her blood
glucose. If the level is near the lower end of the normal range, a small
amount of pre treatment carbohydrate may prevent hypoglycemia
during the appointment. Having the glucometer available also allows
rapid determination of blood glucose, levels when the patient
experience signs and symptoms of hypoglycemia.
Because diet is a major component of diabetes management, diet
alterations that are made because of dental treatment may have a
major impact on the patient.
78. Appointment timing for the diabetic patient in often
determined by the individual’s medication regimen
Peak action of insulin abnormalities to decide about
appointment
Insulin – greatest risk of hypoglycemia will occur
about 30 – 90 min after injection
Lispro insulin – 2 to 3 hrs
Lente insulin – 4 to 10 hrs
Metformin & thiazolidinedione – rarely cause
hypoglycemia
The greatest risk would occur in a patient who has
taken the usual amount of insulin or oral agent but
has reduced or eliminated a meal prior to dental
treatment .
HYPOGLYCEMIA?HYPERGLYCEMIA?
BECAUSE HYPERGLYCEMIC EMERGENCIES
DEVELOP MORE SLOWLY THAN DOES
HYPOGLYCEMIA THEY ARE LESS LIKELY TO
79. MANAGEMENT OF DIABETIC
EMERGENCIES :
The most common medical emergency in diabetic patients
is hypoglycemia. Frequent causes of hypoglycemia are
(1) injection of excess insulin ;
(2) delaying or skipping meals or snacks while taking the
usual dose of insulin or oral sulfonylurea ;
(3) increasing exercise without adjusting food intake or
the dose of insulin or sulfonylurea ;
(4) consuming alcohol and confusing signs of
hypoglycemia with those of alcohol intoxication ; and
(5) stress.
80. CONCLUSION:
Diabetes mellitus is a common medical disorder that will be encountered by every
practicing dentist. Knowledge by the dentist of the general and oral signs and
symptoms of undiagnosed or poorly controlled diabetes mellitus are essential, and
patients displaying these signs or symptoms should receive medical referral
In the event the degree of control of a known diabetic is unknown or the patient
is poorly controlled, antibiotic therapy should be administrated in conjunction
with any necessary surgical procedure or in the presence of oral infection.
The practitioner must be prepared to manage diabetic emergencies if they occur in
the dental office, and hypoglycemic incidents are most likely.
. New evidence suggests that advanced periodontal disease may interfere with
diabetes mellitus control and the physician should be made aware of the patient’s
periodontal status. Under most circumstances, the well-controlled diabetes
mellitus patient can receive safe and effective periodontal therapy with some
modification of office protocol.
