3. It is a metabolic disorder of
multiple aetiology
characterized by chronic
HYPERGLYCAEMIA with
disturbance of carbohydrate,
fat & protein metabolism
resulting from defect in
insulin secretion, insulin
action, or both.
4. 250 BC- Apollonius of Memphis coined the name "diabetes”
meaning “siphon- to pass through”
Thomas Willis in 1675 added "mellitus" to the word "diabetes”
1869- Paul Langerhans, a German medical student, discovered
islet cells in the pancreas
1910- Sharpey-Shafer of Edinburgh suggested a single chemical
was missing from the pancreas. He proposed calling this chemical
"insulin.”
1922, Leonard Thompson became the first human to be
successfully treated for diabetes using insulin
5. 1921- Frederick G. Banting and Charles H. Best
successfully purified insulin from a dog's pancreas
1923- 1st
Nobel prize for insulin
6. 14th November of every
year: to mark the birthday
of Frederick Banting
7. Around 7% of Indian Adults
Most of the world’s Diabetics dwell in India
PREVALENCE OF
DIABETES-2010
Country Prevalence
India 7.1%
China 4.5%
USA 12.3%
Source: International
Diabetes Federation
8. 1. Type 1 DM: -cell destructionβ
a. Immune-mediated
b. Idiopathic
2. Type 2 DM
3. Other specific types of diabetes:
a. Genetic defects of cell function: MODYβ
b. Genetic defects in insulin action
c. Diseases of the exocrine pancreas
d. Endocrinopathies
e. Drug- or chemical-induced
f. Infections
4. Gestational diabetes mellitus (GDM)
9. How does this happen?
Glucose enters the bloodstream, from
food we eat. This is later used for fuel
in the body. Our pancreas located near
the stomach makes insulin, which plays
a role in moving glucose to muscles,
liver cells, and fat.
The pancreas then fails to make enough
insulin or the muscle or…
Fat or liver cells fail to respond to the
insulin properly
As a result, our body’s cells are
starving for energy and over time, high
blood glucose levels change our overall
health damaging the kidney, heart,
eyes, and nerves
11. Pancreas secretes 40-50
units of insulin daily in two
steps:
Secreted at low levels during
fasting ( basal insulin
secretion)
Increased levels after eating
(prandial)
An early burst of insulin
occurs within 10 minutes of
eating
Then proceeds with increasing
release as long as
hyperglycemia is present
12. Insulin allows glucose to move
into cells to make energy
Inhibits glucagon activity
13. Type 1 diabetes is a chronic (lifelong) disease that
occurs when the pancreas does not produce
enough insulin to properly control blood sugar
levels.
What Causes Type 1 Diabetes
The body's own immune system attacks and
destroys beta cells in the pancreas that are
responsible for creating the hormone insulin.
14. 1.Type I
formerly known as Insulin – Dependent Diabetes
Mellitus (IDDM) / juvenile onset
Autoimmune (Islet cell antibodies)
•Early introduction of cow’s milk and cereals
•Intake of medicine during pregnancy
•Indoor smoking of family members
destruction of beta cells of the pancreas little or
no insulin production
requires daily insulin admin.
may occur at any age, usually appears below age 15
15.
16.
17. Type 2 diabetes formerly called non-insulin-
dependent diabetes is a disorder that is
characterized by high blood glucose in the context
of insulin resistance and relative insulin deficiency.
What Causes Type 2 Diabetes
Type 2 diabetes occurs when the pancreas doesn't
make enough insulin or the cells of the body
become resistant to insulin.
18. 2. Type II
formerly known as Non Insulin–Dependent
Diabetes Mellitus (NIDDM) / maturity onset
probably caused by:
disturbance in insulin reception in the cells
number of insulin receptors
loss of beta cell responsiveness to glucose
leading to slow or insulin release by the
pancreas
occurs over age 40 but can occur in children
common in overweight or obese
19.
20.
21.
22. The diabetes during pregnancy is called gestational
diabetes.
It’s a temporary type of diabetes.
The blood glusose level above 90mg% is considered
as a gestational diabetes.
It may occur in 1st
Trimester, 2nd
Trimester or
3rd
Trimester.
35. HbA1c is a test that measures the
amount of glycated hemoglobin in your
blood. Glycated hemoglobin is a
substance in red blood cells that is
formed when blood sugar (glucose)
attaches to hemoglobin.
40. Risk of diabetes typically increases in
following conditions:
Older age (45 years or older)
Less active (sedentary life)
Overweight or obese
Family history of diabetes
41. To minimize the risk of an intraoperative emergency,
clinicians need to consider some issues before initiating
dental treatment.
Medical history: Take history and assess glycemic
control at initial appointment.
Glucose levels
Frequency of hypoglycemic episodes
Medication, dosage and times.
Consultation
42. Scheduling of visits
Morning appointment
Do not coincide with peak activity.
Diet
Ensure that the patient has eaten normally and taken medications as
usual.
Blood glucose monitoring
Measured before beginning. (<70 mg/dL)
Prophylactic antibiotics
Established infection
Pre-operation contamination wound
Major surgery
43. During treatment
The most complication of DM occur is hypoglycemia episode.
Hyperglycemia
After treatment
Infection control
Dietary intake
Medications : salicylates increase insulin secretion and
sensitivity avoid aspirin.
44. Hypoglycemia, also called low blood
glucose or low blood sugar, occurs when
blood glucose drops below normal levels.
It can lead to life-threatening consequences
It occurs when the concentration of blood
glucose drops below 60 mg/dL
45.
46. •Hypo glycaemia: administering oral glucose just before the
extraction.
•Blood glucose level is tested before surgical procedure.
•Drugs should be sugar-free.
•Amoxicillin is the drug of choice
•Drugs which can disturb diabetes control should be avoided
like steroids,ciprofloxacin,tetracycline.
•Acetoaminophen is the drug of choice.
•NSAIDs should be used with caution.
47. Numerous studies have demonstrated that the higher incidence of
wound infection associated with diabetes is because of
hyperglycaemia.
Tissue hypoglycaemia effects every aspect of wound healing by
adversely affecting the immune system including neutrophil and
lymphocyte function, chemotaxis and phagocytosis.
Diabetes have a negative impact on the vascular system. Vessels
of all sizes are affected , from the aorta down to the smallest
arterioles and capillaries.
Myocardial infarction caused by atherosclerosis of the coronary
arteries is the most common cause of death in diabetic patients.
48.
49. “Golden Rule” is that manage the patients as if they
are hypoglycemic.
Placing the patient in the head-low-feet-up position
50. If patient is conscious and able to take food by
mouth, give 15g of oral carbohydrate in one of the
following forms;
4-6 ounce fruit juice or soda,
3-4 teaspoon sugar,
a hard candy.
Small amount of honey/sweet syrup can also be placed in
the buccal fold
51. In unconscious patients, give 50ml of dextrose in
50% concentration or 1mg glucagon
intaravenously, or give 1ml glucagon
intramuscularly at almost any body site.
Following treatment, the signs and symptoms of
hypoglycemia should resolve in 10 to 15 minutes
The patient should be observed for 30 to 60
minutes after recovery. Normal blood glucose level
is confirmed by a glucometer before the patient is
allowed to leave.
52. Hyperglycemia, or high blood sugar is a
condition in which an excessive amount of
glucose circulates in the blood plasma.
53.
54. If your sugar is above 240 you should do the
followings:
Drink lots of sugar-free fluids like water or diet drinks
Eat the right food and the right amounts
Check your blood sugars more often
Check keytones if over 240
Call doctor or nurse if you have a positive keytones
55. Severe hyperglycemia
A prolonged onset
Ketoacidosis may develop with nausea, vomiting,
abdominal pain and acetone odor.
Difficult to differentiate hypoglycemia or
hyperglycemia
Hyperglycemia needs medical intervention and
insulin administration.
While emergency, give glucose first !
Small amount is unlikely to cause significant
harm.
.
56.
57. Patients, receiving good medical management
without serious complications such as renal disease,
hypertension, or coronary atherosclerotic heart
disease, can receive any indicated dental treatment
Local anesthesia is preferred, but such patients can
even be safely treated in general anesthesia
Patients with complications require different
treatment plan
58. Preoperative Stop biguanides
If
chlorpropamide,switch
to tolbutamide 1 wk
Stabilize on atleast b.d.
insulin for 2-3 days 1
day pre op short acting
insulin.
perioperative Omit oral
hypoglycaemic
Estimate blood glucose
level
Omit OHGs
Set up intravenous
infusion of 10%glucose
500 ml containing
actrapid 10 units plus kcl
1g at 8 am.
Estimate blood glucose
2hrly.
Postoperative Estimate blood glucose
4h
Continue infusion 4 h
Estimate blood glucose 4
hrly
On resuming normal
diet
Start sulphonylureas
Start usual regimen
Stop infusion ,start
normal insulin.
Minor operations Major operations
59.
60. Be physical active….
Eat a healthy diet
Abcs(know and control) a1c, blood
pressure, cholesterol, and smoking
Take your medication
Notes de l'éditeur
Too much emptying of the urine
Thomas Willis who in 1675 added &quot;mellitus&quot; to the word &quot;diabetes&quot; as a designation for the disease, when he noticed the urine of a diabetic had a sweet taste (glycosuria)
Paul Langerhans, noted that the pancreas contains two distinct groups of cells—the acinar cells, which secrete digestive enzymes, and cells that are clustered in islands, or islets, which he suggested served a second function.
Banting announced that he would share his prize with Best; Macleod did the same with Collip
Frederick Sanger established the amino acid sequence Nobel Prize in 1958. Dorothy Hodgkin elucidated insulin&apos;s three-dimensional structure.
Insulin was the hormone for which Yalow and Berson first developed the radioimmunoassay, which was recognized with the Nobel Prize in 1977
India-7.1%
China-4.5%
USA-12.3 %
3.Other specific Types of DM:
a. Genetic defects of beta cell function : MODY
b. Genetic defects in insulin action:
1. Type A insulin resistance
2. Leprechaunism
3. Rabson-Mendenhall syndrome
4. Lipodystrophy syndromes
c. Diseases of the exocrine pancreas—pancreatitis, pancreatectomy, neoplasia, cystic fibrosis, hemochromatosis, fibrocalculous pancreatopathy, mutations in carboxyl ester lipase
d. Endocrinopathies-—acromegaly, Cushing&apos;s syndrome, glucagonoma, pheochromocytoma, hyperthyroidism, somatostatinoma, aldosteronoma
e. Drug or Chemical induced-—Vacor, pentamidine, nicotinic acid, glucocorticoids, thyroid hormone, diazoxide, β-adrenergic agonists, thiazides, phenytoin, α -interferon, protease inhibitors, clozapine
F. Infections—congenital rubella, cytomegalovirus, coxsackie
the terms insulin-dependent diabetes mellitus (IDDM) and noninsulin-dependent diabetes mellitus (NIDDM) are obsolete. Since many individuals with type 2 DM eventually require insulin treatment for control of glycemia, the use of the term NIDDM generated considerable confusion. A second difference is that age is not a criterion in the classification system. Although type 1 DM most commonly develops before the age of 30, an autoimmune beta cell destructive process can develop at any age. It is estimated that between 5 and 10% of individuals who develop DM after age 30 have type 1 DM. Likewise, type 2 DM more typically develops with increasing age but is now being diagnosed more frequently in children and young adults, particularly in obese adolescents.