diabetes mellitus- dr sanjana ravindra
TRANSCRIPT
Diabetesmellitus
Seminar -5
Dr.Sanjana.RavindraRajarajeswari Dental collegeBangalore
Contents
Introduction History Epidemiology Anatomy of Pancreas Synthesis & Secretion of
Insulin Action of Insulin Homoeostasis of
Metabolic Fuels Pathophysiology of
Diabetic mellitus Risk factors Classification
Clinical features Oral Manifestations Acute complications Chronic
complications Laboratory Findings Management Dental Management
Of Diabetic Patients Prevention of Diabetic
mellitus Conclusion References
Introduction
Introduction
Diabetes mellitus (DM) is a clinically and genetically heterogeneous metabolic disease characterized by:
Abnormally elevated blood glucose levels (hyperglycemia) and
Dysregulation of carbohydrate, protein, and lipid metabolism.
Lynch MA. Diabetes Mellitus. In: Lynch MA, Brightman VJ, Greenberg MS eds. Burket's Oral Medicine: Diagnosis and Treatment. 8th ed. USA: JB Lippincott Company; 1984. 842-848.
Glucose cannot enter cells and, without energy, weakness results
Hyperglycaemia
Glucosuria, polyuria, polydipsia Fat and protein stores are metabolized with weight loss, peripheral
muscle wasting, production of ketone bodies (acetoacetate, β-hydroxybutyrate and acetone)
Ketonaemia, ketonuria Metabolic ketoacidosis Hyperventilation
Introduction
Lynch MA. Diabetes Mellitus. In: Lynch MA, Brightman VJ, Greenberg MS eds. Burket's Oral Medicine: Diagnosis and Treatment. 8th ed. USA: JB Lippincott Company; 1984. 842-848.
Chronic hyperglyc
emia
Defect in insulin
secretion from
pancreas
Resistance of body’s cells to insulin
action
Both
Introduction
Lynch MA. Diabetes Mellitus. In: Lynch MA, Brightman VJ, Greenberg MS eds. Burket's Oral Medicine: Diagnosis and Treatment. 8th ed. USA: JB Lippincott Company; 1984. 842-848.
Scarcity in plenty
History
History
The earliest known record of diabetes was written on 3rd Dynasty Egyptian papyrus by physician Hesy-Ra.
He stated recurring
urination as a sign of this
illness
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
The Indian physician Sushruta in the 6th century B.C. noticed the sweet nature of
urine in such patients and termed the
condition Madhumeha.
History
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
Aretaeus of Cappadocia, a Greek physician who lived during 120-200 AD
Mentioned a condition associated with unquenchable thirst, excessive drinking of water and excessive passing of urine.
The word "Diabetes" signifies a greek word meaning a siphon, appropriately describing how fluid cannot be retained in the body.
Arateus described Diabetes as "the melting down of flesh and limbs" into
urine.
History
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
Greek physicians and ancient Hindu physicians, used to taste the patient's urine to detect abnormal constituents.
This unpleasant practice perhaps enabled them to detect diabetic patients.
History
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
Thomas Willis, in 1764, observed that the urine
of a diabetic patient was sweet and he concluded that it
contained either sugar or honey.
History
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
Diabetes mellitus
Greek word "diabainein"
meaning "to siphon or pass through"
Latin word "mellitus" meaning
"sweetened with honey"
"to pass through sweetened with honey"
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
Definition
Definition
Gaw et al(1955)-defined as syndrome
characterized by hyperglycemia due to an absolute or relative
risk of insulin or insulin resistance.
Maline(1968)- defined as chronic disorder of
carbohydrate metabolism
characterized by hyperglycemia and
glycosuria.
National diabetes data group(1979) defined diabetes mellitus as a
genetically and clinically heterogenousgroup of disorders that
shared glucose intolerance in common.
Olokoba AB, Obateru OA, Olokoba LB. Type 2 Diabetes Mellitus: A Review of Current Trends. Oman Med J 2012; 27(4): 269-273
Bennet (1994)- defined as a syndrome characterized by hyperglycemia and disturbances of carbohydrate, fat and protein metabolism associated with absolute or relative
deficiencies in insulin action and secretion.
Definition
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
Epidemiology
Globally382 million people had diabetes in 2013
By 2035, this number will rise to 592 million
In India65.1 million people had diabetes in 2013
By 2035, this number will increase by 70.6%
Epidemiology
Guariguata L, Whiting DR, Hambleton I, Beagley J, Linnenkamp U, Shaw JE. Global estimates of diabetes prevalence for 2013 and projections for 2035. Diabetes Res Clin Prac 2014; 103: 137-149
Courtesy: 2015 International Diabetes Federation
Epidemiology
Epidemiology
Courtesy: IDF Diabetes atlas, 6th Edition
Epidemiology
Almost half of all people with diabetes live in just three
countries
• China• India• USA
Epidemiology
Wang C, Li J, Xue H, Li Y, Huang J, Mai J, et al. Type 2 Diabetes Mellitus incidence in Chinese: contributions of overweight and obesity. Diabetes Res Clin Prac 2014.
Prevalance (%) of people with diabetes by age and sex, 2015
IDF Diabetes Atlas. 6th ed. 2015
Wang C, Li J, Xue H, Li Y, Huang J, Mai J, et al. Type 2 Diabetes Mellitus incidence in Chinese: contributions of overweight and obesity. Diabetes Res Clin Prac 2014.
Anatomy of pancreas
EXOCRINE secretion
pancreatic juice enzymes promote the digestion of carbohydrates, proteins and fats
ENDOCRINE secretion
Insulin and glucagon- enter portal vein – transported directly to the liver – regulate metabolism of carbohydrates, proteins and fats
Normal adult: 50-75 gm (1 gm – islet tissue)
0.5- 1.5 million Islets of Langerhans[ 75 – 175 micrometer]
Pancreas
B D Chaurasia.Human Anatomy Regional and Applied Dissection and Clinical Vol.3 CBS Publishers & Distributers;2004.
Pancreas
15-20%, α cells synthesize and secrete GLUCAGON
70- 80% β cells synthesize and secrete INSULIN
1-8% δ cells synthesize and secrete
STOMATOSTATIN and GASTRIN
1-2% F- cells secrete PANCREATIC POLYPEPTIDE which decreases the
absorption of food from the GIT
B D Chaurasia.Human Anatomy Regional and Applied Dissection and Clinical Vol.3 CBS Publishers & Distributers;2004.
Glucagon
Mobilizer of glucose
Normal fasting glucagon levels: 100-150 pg/ml
Blood glucose level plasma
concentration of glucagon
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
Insulin
Polypeptide hormone
produced by β-
cells of islets of
Langerhans of pancreas
ANABOLIC HORMONE
STRUCTURE OF INSULIN
Insulin, Glucose homeostasis, and diabetes mellitus. In Satyanarayan U, Chakrapani U eds. Essentials of Biochemistry. 2nd ed. Uppala Author- publisher, Vijayavada 2008.
Gluconeogenesis : The synthesis of glucose from non-carbohydrate precursors( e.g. amino acids, glycerol)
Glycogenesis: The formation of glycogen from glucose.
Glycogenolysis : The breakdown of glycogen to glucose
Insulin, Glucose homeostasis, and diabetes mellitus. In Satyanarayan U, Chakrapani U eds. Essentials of Biochemistry. 2nd ed. Uppala Author- publisher, Vijayavada 2008.
Synthesis & secretion of
insulin
The synthesis of insulin involves two precursors, namely preproinsulin with 108
amino acids (mol . wt . 11,500)and proinsulin with 86 amino acids (mol. wt.
9,000).
They are sequentially degraded to form the active hormone insulin and a connecting
peptide (C-peptide).
Insulin and C-peptide are produced in equimolar concentration. C-peptide has no biological activity, however its estimation in the plasma serves as a useful index for the
endogenous production of insulin.
Synthesis & secretion of insulin
Insulin, Glucose homeostasis, and diabetes mellitus. In Satyanarayan U, Chakrapani U eds. Essentials of Biochemistry. 2nd ed. Uppala Author- publisher, Vijayavada 2008.
Synthesis & secretion of insulin
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
Factors regulating islet-cell secretion
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
Regulation of insulin secretion
Factors stimulating insulin secretion : Glucose amino acids gastrointestinal hormones
Factors inhibiting insulin secretion Epinephrine
Insulin, Glucose homeostasis, and diabetes mellitus. In Satyanarayan U, Chakrapani U eds. Essentials of Biochemistry. 2nd ed. Uppala Author- publisher, Vijayavada 2008.
Glucose is the most important stimulus for insulin release. The effect is more predominant when glucose is administered orally (either direct or through a carbohydrate-rich meal). Arise in blood glucose level is a signal for insulin secretion.
Amino acids induce the secretion of insulin. This is particularly observed after the ingestion of protein-rich meal that causes transient rise in plasma amino acid concentration Among the amino acids, arginine and leucine are potent stimulator of insulin release.
Gastrointestinal hormones (secretin, gastrin, pancreozymin) enhance the secretion of insulin. The GIT hormones are released after the ingestion of food.
Factors stimulating insulin secretion
Regulation of insulin secretion
Insulin, Glucose homeostasis, and diabetes mellitus. In Satyanarayan U, Chakrapani U eds. Essentials of Biochemistry. 2nd ed. Uppala Author- publisher, Vijayavada 2008.
• Epinephrine is the most potent inhibitor of insulin release.
• In emergency situations like stress, extreme exercise and trauma, the nervous system stimulates adrenal medulla to release epinephrine.
• Epinephrine suppresses insulin release and promotes energy metabolism by Mobilizing energy-yielding compounds-glucose from liver and fatty acids from adipose tissue
Factors inhibiting insulin secretion
Regulation of insulin secretion
Insulin, Glucose homeostasis, and diabetes mellitus. In Satyanarayan U, Chakrapani U eds. Essentials of Biochemistry. 2nd ed. Uppala Author- publisher, Vijayavada 2008.
Actions of insulin
Actions of insulin
Stimulation of the activity of glycolytic enzymes
Reduces the activity of the enzymes of gluconeogenesis
Increased synthesis of glycogen
Increased uptake of of glucose by resting skeletal muscles
Reduction of blood glucose level
Reduction of lipolysis and stimulation of lipid synthesis
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
Maitra A, Abbas AK. The Endocrine System. In Kumar Abbas Fustao eds. Robbins and Cotran Pathologic Basis of Disease. 7th ed. Elsevier Saunders, China 2005.
Homoeostasis of metabolic
fuels
Glucose homeostasis
Maitra A, Abbas AK. The Endocrine System. In Kumar Abbas Fustao eds. Robbins and Cotran Pathologic Basis of Disease. 7th ed. Elsevier Saunders, China 2005.
Colledge NR, Walker BR, Ralston SH. Davidson’s Principles and Practice of Medicine. 21st ed. China: Elsevier; 2010.
Homoeostasis of metabolic fuels
Pathophysiology of diabetes
mellitus
Hormonal regulation of blood glucoseHormone Main site of hormone
productionEffect on blood glucose
levels
Insulin
Glucagon
Growth hormone
Thyroid hormone
Catecholamines(Epinephrine)
Glucocorticoids
Pancreas (beta cells)
Pancreas (alpha cells)
Pituitary gland
Thyroid gland
Adrenal gland (medulla)
Adrenal gland (cortex)
Decrease
Increase
Increase
Increase
Increase
Increase
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
Insulin, Glucose homeostasis, and diabetes mellitus. In Satyanarayan U, Chakrapani U eds. Essentials of Biochemistry. 2nd ed. Uppala Author- publisher, Vijayavada 2008.
Classification
Classification
Hereditary, primary or idiopathic diabetes
Prediabetes• Subclinical, latent or stress diabetes• Chemical diabetes• Overt, or clinical diabetes• Juvenile, or early-onset diabetes• Maturity, adult or late-onset diabetes
Nonhereditary, secondary diabetes• Damage to or removal of pancreatic islet tissue• Disorders of other endocrine glands• Drugs or chemicals
Malamed SF. Medical Emergencies in the Dental Office. 5th ed. Noida: Mosby; 2000. p. 251-274.
Prior classification of diabetes by the American
Diabetes Association,
1975
Classification
Endocrinology. In: scully C. Medical problems in dentistry. 6th ed. China: elsevier; 2010. P. 138-145.
Classification
Maitra A, Abbas AK. The Endocrine System. In Kumar Abbas Fustao eds. Robbins and Cotran Pathologic Basis of Disease. 7th ed. Elsevier Saunders, China 2005.
Classification
Endocrinology. In: scully C. Medical problems in dentistry. 6th ed. China: elsevier; 2010. P. 138-145.
Type Ketosis Islet cell antibodies
Human lymphocyte antigen association
Treatment
Insulin Dependent-type I
Present Present at onset
Positive Insulin (mixtures of rapid acting and intermediate acting insulin at least twice daily) and diet
Non-insulin dependent- type IINon-obese
Absent Absent Negative Eucaloric diet aloneOrDiet plus insulin or sulfonylureas
Obese Absent Absent Negative Weight reduction and Hypocaloric diet plus sulfonylureas or insulin for symptomatic control only
Malamed SF. Medical Emergencies in the Dental Office. 5th ed. Noida: Mosby; 2000. p. 251-274.
Classification
The American Diabetes Association provided the most recent classification
of diabetes mellitus (1997).
Classification
Cumming CG. Diabetes. In: Lynch MA, Brightman VJ, Greenberg MS eds. Burket's Oral Medicine: Diagnosis and Treatment. 9th ed. USA: JB Lippincott Company; 1994. 607-614
1. Type 1 DM
It is due to insulin deficiency and was formerly known as:
Type I
Insulin Dependent DM (IDDM)
Juvenile onset DM
2. Type 2 DMIt is a combined insulin resistance and relative deficiency in insulin secretion and is frequently known as:
Type II
Noninsulin Dependent DM (NIDDM)Adult onset DM
Classification
What goes wrong in diabetes?
Multitude of mechanisms
Insulin
Regulation
Secretion
Uptake
Beta cells
Damage Type 1 DM
Type 2 DM
Cumming CG. Diabetes. In: Lynch MA, Brightman VJ, Greenberg MS eds. Burket's Oral Medicine: Diagnosis and Treatment. 9th ed. USA: JB Lippincott Company; 1994. 607-614
Risk factors
Risk factorsFamily history: risk of
developing diabetes rises if a close relative such as a parent or sibling has the
disease
Overweight individuals
Inactivity
Age: the risk of developing type 2 diabetes increases with age especially after
45 years
Race: Type 1 diabetes is more common in Caucasians and in
European countries, such as Finland and Sweden. Type 2 diabetes is especially common in people of
African heritage, Asians.
Genetics: The HLA haplotypes DR3 and/or DR4 are associated with
increased susceptibility to type 1 diabetes in
Caucasians.Cumming CG. Diabetes. In: Lynch MA, Brightman VJ, Greenberg MS eds. Burket's Oral Medicine: Diagnosis and Treatment. 9th ed. USA: JB Lippincott
Company; 1994. 607-614
Type 1 diabetes mellitus
Type 1 DM
Autoimmune destruction of
pancreatic beta cells.
Individual has an absolute
insulin deficiency and
no longer produces insulin.
Such patients are absolutely dependent on exogenously administered
insulin for survival.
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848..
It comprises 5 to 10% of all DM cases.
Sudden onset
Develops over a period of a few days to weeks.
Type 1 DM occurs before the age of 25 years in 95% of affected persons but may occur at any age.
Affects both sexes equally
More prevalent in Caucasians.
Most type 1 diabetic individuals are of normal weight or are thin in stature.
Type 1 DM
Cumming CG. Diabetes. In: Lynch MA, Brightman VJ, Greenberg MS eds. Burket's Oral Medicine: Diagnosis and Treatment. 9th ed. USA: JB Lippincott Company; 1994. 607-614
T cell-mediated autoimmune disease destruction of the insulin-secreting β cells; 70–90% of β cells
Islet cell antibodies variable predictive value as a marker
Glutamic acid decarboxylase (GAD) antibodies latent autoimmune diabetes in adults (LADA)
Associated with other autoimmune disorders thyroid disease, coeliac disease, Addison’s disease, pernicious anemia and
vitiligo
Type 1 DM
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848..
Genetic factors one-third of the susceptibility to type 1 diabetes
20 different regions of the human genome; human leucocyte antigen (HLA) region, major histocompatibility complex on the short arm of chromosome 6 IDDM 1
HLA haplotypes DR3 and/or DR4 Caucasians
Other genes implicated CD25, PTPN22, IL2RA
Type 1 DM
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848..
Hygiene hypothesis Viral infection-
mumps, Coxsackie B4, retroviruses, rubella (in
utero), cytomegalovirus, Epstein–Barr
virus
StressDietary factors
nitrosamines
Bovine serum albumin
Type 1 DM
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848..
Pathogenesis of type 1 diabetes mellitus
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848..
Type 1 DM
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848..
Fats
Lipolysis
Glycerol Free fatty acids
Glucose Ketones
Cumming CG. Diabetes. In: Lynch MA, Brightman VJ, Greenberg MS eds. Burket's Oral Medicine: Diagnosis and Treatment. 9th ed. USA: JB Lippincott Company; 1994. 607-614
Type 2 diabetes mellitus
NORMALLY In THE BODY
DIABETES TYPE 2
Type 2 DM
Most common type
Comprises 90 to 95% of DM cases
Multifactorial etiology genetic predilection, advancing age, obesity and lack of exercise.
• The genetic influence in type 2 DM is greater than that seen in type 1 DM.
• More prevalent in African Americans, Native Americans, Hispanics, and Pacific Islanders than in Caucasians.
Cumming CG. Diabetes. In: Lynch MA, Brightman VJ, Greenberg MS eds. Burket's Oral Medicine: Diagnosis and Treatment. 9th ed. USA: JB Lippincott Company; 1994. 607-614
Most type 2 DM patients
are overweight, and most are diagnosed as
adults.
Slow onset
Approximately half of the patients are unaware of their disease
The insidious nature of the disease allows prolonged
periods of hyperglycemia to begin exerting negative effects on major organ
systems
By the time many type 2 diabetic
patients are diagnosed,
diabetic complications have already
begun.
Type 2 DM
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
Peripheral resistance to insulin, especially in muscle cells
Increased production of glucose by the liver
Insulin secretory defect of the beta cells
• Obesity contributes greatly to insulin resistance• Insulin resistance generally decreases with weight loss
Type 2 DM
The underlying pathophysiologic defect in type 2 DM is characterized by the following three
disorders:
Maitra A, Abbas AK. The Endocrine System. In Kumar Abbas Fustao eds. Robbins and Cotran Pathologic Basis of Disease. 7th ed. Elsevier Saunders, China 2005.
The high blood glucose levels often stimulate an increase in insulin production by the pancreas
Excessive insulin production Hyper insulinemia
Type 2 DM
Cumming CG. Diabetes. In: Lynch MA, Brightman VJ, Greenberg MS eds. Burket's Oral Medicine: Diagnosis and Treatment. 9th ed. USA: JB Lippincott Company; 1994. 607-614
Maitra A, Abbas AK. The Endocrine System. In Kumar Abbas Fustao eds. Robbins and Cotran Pathologic Basis of Disease. 7th ed. Elsevier Saunders, China 2005.
Complex condition resistance to the actions of insulin in liver and muscle + impaired pancreatic β-cell function ‘relative’ insulin deficiency
Colledge NR, Walker BR, Ralston SH. Davidson’s Principles and Practice of Medicine. 21st ed. China: Elsevier; 2010.
Type 2 DM
Type II Diabetes Mellitus-Insulin resistance
Intra-abdominal adipose tissue Free Fatty acids
Compete with glucose for oxidation +
Releases a number of hormones
(adipokines- IL-6, TNF α, leptin, adiponectin )
Adipose tissue drains into the portal veinpotent influence on insulin sensitivity in the liver
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848..
Type II Diabetes Mellitus-Insulin resistance
Physical inactivity downregulation of insulin-sensitive kinases Promote accumulation of FFAs within skeletal muscle Sedentary people > active people Physical activity non-insulin-dependent glucose uptake into
muscle Deposition of fat in the liver non-alcoholic fatty liver disease
Non-alcoholic steatohepatitis and cirrhosis
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848..
Insulin resistance syndrome / Reaven’ssyndrome /Syndrome X
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
Type II DmGenetic predisposition
Marked differences in susceptibility in different ethnic groups Genome-wide Association studies 20 genes or gene regions;
TCF7L2 Altered regulation of β-cell mass primary predisposing factor
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848..
William Boyd A Textbook of Pathology- Structure and Function in Disease; 8th edition
Type II DmEnvironmental and other risk factors
Diet and Obesity: Overeating Obesity + underactivity BMI > 30 kg/m2
risk increases tenfold Obesity diabetogenic factor; genetically predisposed both to
insulin resistance and to β-cell failure Constituents of the diet and the style of eating Sweet foods rich
in refined carbohydrate consumed frequently may increase the demand for insulin secretion, while high-fat foods may increase FFAs and exacerbate insulin resistance
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848..
Type II DmEnvironmental and other risk factors
Age: Prevalence increases with age; ~10% over 65 years Renal threshold for glucose rises with age GlycosuriaPregnancy: Insulin sensitivity is reduced through the action of placental
hormones Insulin-secreting cells of the pancreatic islets unable to meet
this increased demand “Gestational diabetes” 80% of women develop permanent
diabetes
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848..
Metabolic disturbances in type II diabetes
Slow onset of ‘relative’ insulin deficiency Lipolysis and proteolysis are not unrestrained and weight loss and
ketoacidosis Polyuria and polydipsia degree of glycosuria Rise in renal threshold for glucose Large number of cases remain undetected
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848..
Obesity & insulin resistance
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.
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848..
Gestational DM
Development of type 1 DM or discovery of undiagnosed
asymptomatic type 2 DM during pregnancy
Occurs in 2 to 5% of pregnant women
However, about 30 to 50% of women will develop type 2 DM
within 10 years.
Seen during the third trimester, which significantly increases
perinatal morbidity and mortality
Pathophysiology: Associated with increased insulin resistance
Risk factors: Older women, overweight women and women
of minority ethnic groups
Most patients return to a normoglycemic state after
parturition
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848..
Other specific types of DM
Comprises 1 to 2% of DM cases
Caused by various specific genetic defects of beta cell
function and insulin action, diseases of the
exocrine pancreas, endocrinopathies,
pancreatic dysfunction induced by drugs,
chemicals, or infections.
Genetic syndromes sometimes associated with
DM include Turner’s syndrome, Down
syndrome, Wolfram syndrome, Klinefelter’s syndrome, Friedreich’s ataxia, Huntington’s
chorea, Laurence-Moon-Biedl syndrome, myotonic dystrophy, porphyria, and Prader-Willi syndrome.
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848..
William Boyd A Textbook of Pathology- Structure and Function in Disease; 8th edition
Type II Diabetes Mellitus-Pancreatic β-cell failure
β-cell dysfunction in type2 diabetes manifests as both in qualitative& quantitative.
Qualitative beta cell dysfunction is initially seen as loss of normal pulsatile, oscillating pattern of insulin secretion.
Followed by rapid phase of insulin secretion which is triggered by an elevation in plasma glucose.
Quantitative beta cell dysfunction is reflected by an beta cell mass, islet degeneration, & deposition of amyloid.
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
Type II Diabetes Mellitus-Pancreatic β-cell failure
Impaired Glucose Tolerance & Impaired Fasting Glucose
Represent metabolic states lying between diabetes and
normoglycemia
Risk factors for future diabetes
30 to 40% of individuals with IGT or IFG will develop type 2 diabetes within 10 years after
onset
Pathophysiology increased
insulin resistance whereas
endogenous insulin secretion
is normal
People with IFG have increased fasting blood
glucose levels but usually have normal levels following food consumption
Those with IGT are normoglycemic most of the time but can become hyperglycemic
after large glucose loads
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848..
Warnakulasuriya S, Tilakaratne WM. Oral Medicine and Pathology A Guide to Diagnosis and Management. New Delhi: Jaypee Brothers Medical Publishers (P) Ltd; 2014.
Insulin, Glucose homeostasis, and diabetes mellitus. In Satyanarayan U, Chakrapani U eds. Essentials of Biochemistry. 2nd ed. Uppala Author- publisher, Vijayavada 2008.
References 1. IDF diabetes atlas. 6th ed. 20152. B D chaurasia. Human anatomy regional and applied dissection and clinical vol.3 CBS
publishers & distributers;2004.3. Malamed sf. Medical emergencies in the dental office. 5th ed. Noida: mosby; 2000. 4. Warnakulasuriya s, tilakaratne wm. Oral medicine and pathology A guide to diagnosis and
management. New delhi: jaypee brothers medical publishers (P) ltd; 2014.5. Frier BM, fisher M. Diabetes mellitus. In: boon NA, Colledge NR, Walker BR eds. Davidson’s
principles and practice of medicine. 20th ed. India: elsevier; 2006. P. 805-848..6. Endocrinology. In: scully C. Medical problems in dentistry. 6th ed. China: elsevier; 2010. P. 138-
145.7. Lynch MA. Diabetes mellitus. In: lynch MA, brightman VJ, greenberg MS eds. Burket's oral
medicine: diagnosis and treatment. 8th ed. USA: JB lippincott company; 1984. 842-848.8. Cumming CG. Diabetes. In: lynch MA, brightman VJ, greenberg MS eds. Burket's oral medicine:
diagnosis and treatment. 9th ed. USA: JB lippincott company; 1994. 607-614.9. Mandal AK, Chaudhury S. Textbook of pathology for dental students. 2010.
10. Mealey B. Diabetes Mellitus. Greenberg MS, Glick M eds. Burket's Oral Medicine. 10th ed. Spain: BC Decker Inc; 2003. 563-577.
11. Joshi SK, Shrestha S. Diabetes mellitus: A review of its associations with different environmental factors. Kathmandu University Med J 2010; 8(1): 109-115.
12. Wang C, Li J, Xue H, Li Y, Huang J, Mai J, et al. Type 2 Diabetes Mellitus incidence in Chinese: contributions of overweight and obesity. Diabetes Res Clin Prac 2014. In Press.
13. Guariguata L, Whiting DR, Hambleton I, Beagley J, Linnenkamp U, Shaw JE. Global estimates of diabetes prevalence for 2013 and projections for 2035. Diabetes Res Clin Prac 2015; 103: 137-149.
14. Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
15. Olokoba AB, Obateru OA, Olokoba LB. Type 2 Diabetes Mellitus: A Review of Current Trends. Oman Med J 2012; 27(4): 269-273.
16. Maitra A, Abbas AK. The Endocrine System. In Kumar Abbas Fustao eds. Robbins and CotranPathologic Basis of Disease. 7th ed. Elsevier Saunders, China 2005.
17. William Boyd A Textbook of Pathology- Structure and Function in Disease; 8th edition.18. Insulin, Glucose homeostasis, and diabetes mellitus. In Satyanarayan U, Chakrapani U eds.
Essentials of Biochemistry. 2nd ed. Uppala Author- publisher, Vijayavada 2008.
References
Diabetesmellitus
Seminar -5
Contents
Introduction History Epidemiology Anatomy of Pancreas Synthesis & Secretion of
Insulin Action of Insulin Homoeostasis of
Metabolic Fuels Pathophysiology of
Diabetic mellitus Risk factors Classification
Clinical features Oral Manifestations Acute complications Chronic
complications Laboratory Findings Management Dental Management
Of Diabetic Patients Prevention of Diabetic
mellitus Conclusion References
Glucose cannot enter cells and, without energy, weakness results
Hyperglycaemia
Glucosuria, polyuria, polydipsia Fat and protein stores are metabolized with weight loss, peripheral
muscle wasting, production of ketone bodies (acetoacetate, β-hydroxybutyrate and acetone)
Ketonaemia, ketonuria Metabolic ketoacidosis Hyperventilation
Lynch MA. Diabetes Mellitus. In: Lynch MA, Brightman VJ, Greenberg MS eds. Burket's Oral Medicine: Diagnosis and Treatment. 8th ed. USA: JB Lippincott Company; 1984. 842-848.
Insulin, Glucose homeostasis, and diabetes mellitus. In Satyanarayan U, Chakrapani U eds. Essentials of Biochemistry. 2nd
ed. Uppala Author- publisher, Vijayavada 2008.
Clinical features
Clinical featuresThe onset of type 1 diabetes is usually abrupt whereas type 2
diabetes is often present for years without overt signs or symptoms
When complications of poor glucose control develop, patients complain of:• Visual impairment• Neurologic symptoms: numbness,
dizziness• Chest pain • Gastrointestinal symptoms • Genitourinary symptoms, especially
urinary incontinence
Lynch MA. Diabetes Mellitus. In: Lynch MA, Brightman VJ, Greenberg MS eds. Burket's Oral Medicine: Diagnosis and Treatment. 8th ed. USA: JB Lippincott Company; 1984. 842-848.
Clinical features
Endocrinology. In: Scully C. Medical problems in dentistry. 6th ed. China: Elsevier; 2010. P. 138-145.
Oral manifestations
Oral manifestations
Related to poor glycemic control
1. Burning mouth syndrome2. Altered wound healing3. Increased incidence of infection4. Candidal infection Median Rhomboid
glossitis, Angular cheilitis, Acute pseudomembranous candidiasis of tongue, buccal mucosa and gingiva
Lynch MA. Diabetes Mellitus. In: Lynch MA, Brightman VJ, Greenberg MS eds. Burket's Oral Medicine: Diagnosis and Treatment. 8th ed. USA: JB Lippincott Company; 1984. 842-848.
Bilateral generalized salivary gland enlargement Xerostomia Gingivitis Periodontitis, periodontal abscesses Dental caries
Oral manifestations
Lynch MA. Diabetes Mellitus. In: Lynch MA, Brightman VJ, Greenberg MS eds. Burket's Oral Medicine: Diagnosis and Treatment. 8th ed. USA: JB Lippincott Company; 1984. 842-848.
Related to medications
Salivary hypofunction
Xerostomia
Dry mucosal surfaces
Gets easily irritated
Causing minor mucosal ulcerations, oral burning sensation, increased susceptibility of fungal infections
Drug induced lichenoid reactions (Metformin)
Oral manifestations
Lynch MA. Diabetes Mellitus. In: Lynch MA, Brightman VJ, Greenberg MS eds. Burket's Oral Medicine: Diagnosis and Treatment. 8th ed. USA: JB Lippincott Company; 1984. 842-848.
ORAL CANDIDIASIS
Oral manifestations
POOR ORAL HYGEINe WITH EXCESS CALCULUS
FORMATION
TENDENCY FOR PROGRESSIVE
CARIES
Lynch MA. Diabetes Mellitus. In: Lynch MA, Brightman VJ, Greenberg MS eds. Burket's Oral Medicine: Diagnosis and Treatment. 8th ed. USA: JB Lippincott Company; 1984. 842-848.
Oral manifestations
CHRONIC PERIODONTITIS- multiple abscess, SUPPURATIOn, MOBILITY
Palmer R, Soory M. Modifying factors. In: Lindhe J, Lang NP, Karring T. Clinical Periodontology and Implant Dentistry. 5th ed. Singapore: Blackwell Munksgaard; 2008. p. 307-311.
In the diabetic patient, the abnormal host defence
mechanism in addition to hyperglycemia state can lead to the growth of particular
fastidious organism.
The most frequently isolated microrganism are prevotella
intermedia followed by camphylobacter rectus.
The association of aac & capnocytophaga is similar to
periodontitis in healthy patient & periodontitis in diabetic
patient.
Effect on periodontal flora:
Palmer R, Soory M. Modifying factors. In: Lindhe J, Lang NP, Karring T. Clinical Periodontology and Implant Dentistry. 5th ed. Singapore: Blackwell Munksgaard; 2008. p. 307-311.
Klokkevold PR, Mealy BL. Influence of systemic disorders and stress on the periodontium. In: Newman MG, Takei HH, Klokkevold PR. Carranza’s Clinical Periodontology. 10th ed. China: Elsevier; 2011. p. 285-288.
Effect on periodontal flora:
Palmer R, Soory M. Modifying factors. In: Lindhe J, Lang NP, Karring T. Clinical Periodontology and Implant Dentistry. 5th ed. Singapore: Blackwell Munksgaard; 2008. p. 307-311.
PERIODONTAL VASCULATURE
Increased thickening of gingival capillary endothelial basement membrane & the walls of small blood vessels seen in diabetes.
This thickening may impair oxygen diffusion& nutrient provision across the basement membrane.
Increased thickness of small vessel wall results in narrowing of the lumen, altering normal periodontal tissue homeostasis.
Palmer R, Soory M. Modifying factors. In: Lindhe J, Lang NP, Karring T. Clinical Periodontology and Implant Dentistry. 5th ed. Singapore: Blackwell Munksgaard; 2008. p. 307-311.
Klokkevold PR, Mealy BL. Influence of systemic disorders and stress on the periodontium. In: Newman MG, Takei HH, Klokkevold PR. Carranza’s Clinical Periodontology. 10th ed. China: Elsevier; 2011. p. 285-288.
Radiographic Features
Preshaw PM. Periodontal diseases. In: Warnakulasuriya S, Tilakaratne WM. Oral Medicine and Pathology A Guide to Diagnosis and Management. New Delhi: Jaypee Brothers Medical Publishers (P) Ltd; 2014.p. 72.
Diagnosis
Clinical Diagnosis
Polyuria, Polydipsia, polyphagia with periodontal problems
Radiological problems
Not specific
Plasma Glucose concentration
Unequivocal elevation of plasma glucose concentration greater than 140 mg/dl
Diagnosis
Family history Personal history
Mealey B. Diabetes Mellitus. Greenberg MS, Glick M eds. Burket's Oral Medicine. 10th ed. Spain: BC Decker Inc; 2003. 563-577.
Laboratory diagnosis
Urine analysis
Blood chemistry
Immunological Assays
• Glucose • Ketone• Microalbuminuria
• Blood glucose estimation• Glucose tolerance test• Glycated hemoglobin
measurement• Lipid profile
Diagnosis
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
Laboratory test for diagnosis
Laboratory test for diagnosis
Estimation of blood glucose.
Oral glucose tolerance test.
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
DiagnosisThe diagnosis of diabetes is based on the presence of clinical signs and symptoms,
along with specific laboratory findings
Diagnosis
Lynch MA. Diabetes Mellitus. In: Lynch MA, Brightman VJ, Greenberg MS eds. Burket's Oral Medicine: Diagnosis and Treatment. 8th ed. USA: JB Lippincott Company; 1984. 842-848.
Diagnosis
Estimation of blood glucose
Depending on time of collection
Measurement of blood glucose is indicative of current state of carbohydrate metabolism.
Fasting blood glucose- after an overnight fast.Post meal or postprandial blood glucose-2 hrs after the subject has taken a normal meal.Random blood glucose – Any time of the day.
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
Total glucose in 100 ml of plasma is about 15% greater than in 100 ml of whole blood.
Plasma is prefered as whole blood is affected by concentration of proteins (especially haemoglobin).
In capillary blood the value of blood glucose at rest is about 5 % higher than venous blood.
diagnosis
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848..
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848..
Urine analysis
GLUCOSE:• Dipsticks- common screening procedure• Urine passed 1-2 hours after a meal• Disadvantage individual variation in renal threshold for glucose
KETONE BODIES:• Nitroprusside reaction acetoacetate, using either tablets or dipsticks• Ketonuria normal people who have been fasting, exercising strenuously for
long periods, vomiting repeatedly, diet high in fat and low in carbohydrate
Diagnosis
Normally less than 500mg/24 hrs or less than 15 mg/dl of glucose is present in urine.
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848..
Urine analysis Protein: Dipstick > 300mg/L Microalbuminuria
specific albumin dipsticks/ laboratory measurement
Diagnosis
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848..
Qualitative test.
Benedicts. Clintest tablet test. Reagent strip test
Quantitative test.
Benedicts.
Diagnosis
Insulin, Glucose homeostasis, and diabetes mellitus. In Satyanarayan U, Chakrapani U eds. Essentials of Biochemistry. 2nd ed. Uppala Author- publisher, Vijayavada 2008.
Procedure
Add 8 drops of urine
Boil for 2 to 3 min
CoolTake 5.0ml of Benedict’s
reagent
Observe
Benedict reagent : sodium citrate 173 gm, sodium carbonate 100 gm, cupric sulphate17.3 gm and distill water 900 ml.
Benedicts test Diagnosis
Insulin, Glucose homeostasis, and diabetes mellitus. In Satyanarayan U, Chakrapani U eds. Essentials of Biochemistry. 2nd ed. Uppala Author- publisher, Vijayavada 2008.
Observations Color Sugar
Blue Absent
Green without
precipitate
Present, trace
Green with precipitate 1+ (0.5 g/dl)
Brown precipitate 2+ (1.0 g/dl)
Yellow - Orange
precipitate
3+ (1.5 g/dl)
Brick red precipitate 4+ (≥ 2.0 g/dl)
Benedicts test
Diagnosis
Insulin, Glucose homeostasis, and diabetes mellitus. In Satyanarayan U, Chakrapani U eds. Essentials of Biochemistry. 2nd ed. Uppala Author- publisher, Vijayavada 2008.
Triglycerides (mg/dl)
Category
<150 Low risk150-199 Intermediate risk≥ 200 High riskLDL cholesterol<100 Low risk100-129 Intermediate risk≥130 High riskHDL cholesterol<35 High risk35-45 Intermediate risk>45 Low risk
Diagnosis
Blood analysisGlucose
Enzymatic reaction (glucose oxidase) random/ fasting
Colorimetric or other testing sticks capillary (fingerprick) testing to monitor diabetes treatmentDiagnosis of diabetes accurate laboratory method
Glucose venous < arterial/capillary blood
Whole blood glucose concentrations < plasma concentrations
Venous plasma valuesmost reliable for diagnostic purposes
Diagnosis
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848..
Blood analysisDiagnosisGlycated haemoglobin:
Accurate and objective measure of glycaemic control over a period of weeks to months
Assessment of glycaemic control by repeated measurements every few months
Slow non-enzymatic covalent attachment of glucose to haemoglobin (glycation) increases the amount in the HbA1 (HbA1c) fraction relative to nonglycated adult haemoglobin (HbA0); chromatography
Total glycated haemoglobin (GHb), HbA1 or HbA1c
Rate of formation of HbA1c α ambient blood glucose concentration
1% HbA1c 2 mmol/L (36 mg/dL) blood glucose
Indications
In all diabetics to monitor long term blood glucose level control, index of diabetic control:-
7% hba₁с – good 10% hba₁с- fair13-20% hba₁с- poor.
To monitor patient compliance.
To predict development & progression of microvascular complication.
For determining the therapeutic option whether to use oral agents, insulin ,or βcell transplantation.
Also increasingly used for primary diagnosis of dm.Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians,
Mumbai; 1097-1136.
At what interval should HbA₁с be determined?
Treatment by time of diabetes Recommended frequency
Type-1 DM( minimal /conventional therapy)
4 times a year
Type – 1 DM (intensified therapy) Every (1) -2 months.
Type-2 DM Twice a year in stable patients.
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
Another assay that can be used to determine long-term
glucose control
Not used as widely as the glycated hemoglobin assay
but is often helpful in managing women with
gestational diabetes
The fructosamine assay assesses glycemic control 2 to
4 weeks preceding the test.
The normal range for fructosamine is 2.0 to 2.8
mmol/L
This test may become more widely used in the future,
since at-home testing is now available.
Diagnosis
FRUCTOSAMINE TEST
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
Colledge NR, Walker BR, Ralston SH. Davidson’s Principles and Practice of Medicine. 21st ed. China: Elsevier; 2010.
In asymptomatic persons with sustained or transient glycosuria.
In persons with symptoms of diabetes but no glycosuria or hyperglycemia.
Persons with family history but no symptoms or positive blood findings.
In persons with or without symptoms of diabetes mellitus showing one abnormal
blood findings.
In patients with neuropathies or retinopathies of unknown origin.
Diagnosis
Indications of Glucose tolerance test
Confirmed diabetics mellitus.
GTT has no role in follow-up of diabetics.
The test should not be done in ill patients
Contraindications of glucose tolerance test
Types of glucose tolerance test
Standard Oral glucose tolerance test
I/V Glucose tolerance test
Mini Glucose tolerance test
Patient should on carbohydrate rich unrestricted diet for 3 days.
Patient should be ambulatory with normal physical activity.
Medications should be discontinued on the day of testing.
Exercise, smoking and tea or coffee are not allowed during test period.
OGTT carried out in the morning after patient has fasted overnight for 8-14 hours.
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
Test
A fasting venous blood sample is collected in the morning.
Patients ingest 75 g of anhydrous glucose in 250-300 ml of water over 5 minutes. ( for children, the dose is
1.75 g of glucose per kg).
• In the classical procedures, the blood and urine samples are collected at half hourly interval of the next three hours.
• A curve is plotted with the blood glucose levels on the vertical axis against the time of collection on the horizontal axis.
• The curve so obtained is called glucose tolerance curve.
Standard ogtt
Intravenous Gtt
•This test is undertaken for patients with malabsorption (Celiac disease or enteropathies).
•Under these conditions oral glucose load is not well absorbed and the results of oral glucose tolerance test become inconclusive.
•Carried out by giving 25 g of glucose dissolved in 100 ml distilled water as intravenous injection within 5 minutes. •Completion of infusion is taken as time zero.•Blood samples are taken at 10 minutes interval for the next hour. •The peak value is reached within a few minutes.
INTERPRETATION•Normally, blood glucose level returns to normal range within 60 minutes.•In diabetes mellitus, this decline is slow.
Zero Hour After 2 Hours
Normal Person < 110 mg/dL < 140 mg/dL
Increase Glucose Tolerance 110 – 126 mg/dL 140 – 199 mg/dL
Gestational diabetes is diagnosed if the woman is at or exceeds any two of the following four plasma glucose levels during 100 gm test
Fasting – 95 mg/dl1 hr – 180 mg/dl2 hr – 155 mg/dl3 hr – 140 mg/dl
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
Laboratory test for screening
Laboratory test for screening
Recommended screening test is fasting plasma glucose.
American Diabetes Association recommends screening for Type 2 DM in all asymptomatic individuals >= 45 yrs of age using fasting plasma glucose.
If fasting test is normal, screening test should be repeated every three years.
If fasting blood glucose level is normal but there is strong clinical suspicion then OGTT.
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
Selective screening
High risk individuals ---Obese Family h/o DMHypertension DyslipidemiaImpaired glucose tolerance
Screening test is performed at earlier age ( 30 yrs )and repeated more frequently
Laboratory test to assess
glycemiccontrol
Laboratory test to assess glycemic control
Periodic measurement of glycated
haemoglobin.
Daily self assessment of blood glucose.
Others
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
Insulin assay
Measurement of insulin level by radioimmunoassay & ELISA.
Crucial for type I DM.
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
Self–blood glucose monitoring (SBGM)Diagnosis
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
COMPLICATIONS OF DIABETES
Affected body part
or condition
Complications
Vascular system Atherosclerosis
Large vessel disease
Microangiopathy
Kidneys Diabetic glomerulosclerosis
Arteriolar nephrosclerosis
Pyelonephritis
Nervous system Motor, sensory, and autonomic neuropathy
Eyes Retinopathy
Cataract formation
Glaucoma
Extraocular muscle palsies
Skin Diabetic xanthoma
Necrobiosis lipoidica diabeticorum
Pruritis
Furunculosis
Mycosis
Mouth Gingivitis, Increased incidence of dental caries and
and periodontal disease, Alveolar bone loss
Pregnancy Increased incidence of large babies, still births,
miscarriages, newborn deaths, and congenital defects
COMPLICATIONS OF DIABETES
COMPLICATIONS OF DIABETES
Acute complications:HypoglycemiaDiabetic ketoacidosisNon ketotic hyperosmolar diabetic coma
Late complications :Retinopathy - blindnessNephropathy – renal failureNeuropathy – sensory , autonomicMacro vascular disease - atherosclerosis, strokeAltered wound healingDiabetic foot and ulcers
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848.
Pathogenesis of complications of diabetes
Formation of advanced glycation
end products .
Intracellular hyperglycemia with
disturbances in polyol pathways.
Metabolic pathways appear to
be involved in pathogenesis of
long term diabetic complication
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
Protein glycationleading to AGE is one of the major cause of
diabetic complication.
The carbohydrate-containing proteins which accumulate in
patients with sustained hyperglycemia are known as
advanced glycosylation endproducts (AGEs).
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.
Acute complications
Hypoglycemia Imbalance between food intake and usage, and insulin therapy Rapid onset Fainting Blood glucose < 3.5 mmol/L (63 mg/dL) Non diabetics ‘Spontaneous’ hypoglycemia Brittle diabetes – adolescent girls
Colledge NR, Walker BR, Ralston SH. Davidson’s Principles and Practice of Medicine. 21st ed. China: Elsevier; 2010.
Acute complications
Acute complications
Endocrinology. In: scully C. Medical problems in dentistry. 6th ed. China: elsevier; 2010. P. 138-145.
Colledge NR, Walker BR, Ralston SH. Davidson’s Principles and Practice of Medicine. 21st ed. China: Elsevier; 2010.
Hypoglycemia
• Serious morbidity• Mortality of upto 4% in
insulin treated patients• Healthy young patients
(type 1 diabetes) ‘dead-in-bed syndrome’
Acute complications
Hypoglycemia
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848.
Slow onset over many hours, with deepening drowsiness
Signs of dehydration (dry skin, weak pulse, hypotension), acidosis (deep breathing) and ketosis (acetone smell on breath and vomiting) Type 1 diabetes
An unconscious diabetic should always be assumed to be
hypoglycemic
Acute complications
Hypoglycemia
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848.
Terminate dental procedure
P- position patient supine with legs elevated slightly
A-B-C- Assess and perform BLS (check airway, check breathing, check the pulse)
D- initiate definitive care Emergency medical assistance
Establish IV infusionAdminister oxygen
Transportation to hospital for further management
Colledge NR, Walker BR, Ralston SH. Davidson’s Principles and Practice of Medicine. 21st ed. China: Elsevier; 2010. Malamed SF. Medical Emergencies in the Dental Office.
5th ed. Noida: Mosby; 2000.
Acute complications
Hypoglycemia
HYPOGLYCEMIA UNAWARENESS
more common in diabetic patients with good glycemic control Inability to perceive the warning symptoms of hypoglycemia Signs and symptoms most common when blood glucose levels fall <60 mg/dLGlucose levels can fall to 40mg/dL or lower before an individual feels hypoglycemic
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848.
Hyperglycaemic coma usually has a slow onset over many hours with: Drowsiness Signs of dehydration (Dry
skin, weak pulse, hypotension)
Florid appearance of face (Bright Red)
Acidosis (Deep breathing) Ketosis (Acetone smell in
breath)
Acute complications
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848.
Diabetic ketoacidosi
s (DKA)
Accumulation of ketones in body fluids
Decreased pH
Electrolyte loss & dehydration from excessive
urination
Alterations in the
bicarbonate buffer system
Untreated DKA can result in coma or death
Diabetic ketoacidosis
Acute complications
• Serious cause of morbidity type 1 diabetes
• Established diabetesintercurrent infection lose appetite stop/reduce dose of insulin
Olokoba AB, Obateru OA, Olokoba LB. Type 2 Diabetes Mellitus: A Review of Current Trends. Oman Med J 2012; 27(4): 269-273.
Diabetic Ketoacidosis
Acute complications
Diabetic ketoacidosis Hyperglycemia osmotic diuresis
Dehydration & electrolyte loss (Na+ , K+) Potassium loss is exacerbated by secondary
hyperaldosteronism as a result of reduced renal perfusion
Ketosis insulin deficiency; elevated catecholaminesand other stress hormones, resulting in unrestrained lipolysis and supply of FFAs for hepatic ketogenesis
Accumulate in blood metabolic acidosis
Acute complications
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848.
Courtesy: Colledge NR, Walker BR, Ralston SH. Davidson’s Principles and Practice of Medicine. 21st ed. China: Elsevier; 2010.
Acute complications
Diabetic ketoacidosis
Investigations
Venous blood
Arterial blood gases severity of acidosis (<12mmol/L)
Urine analysis for ketones
ECG
Full blood count, blood and urine culture, C-reactive protein
Acute complicationsDiabetic ketoacidosis
Olokoba AB, Obateru OA, Olokoba LB. Type 2 Diabetes Mellitus: A Review of Current Trends. Oman Med J 2012; 27(4): 269-273.
Methods to detect ketone bodies
1. Rothera’s test
2. Reagent strip
3. Gerhardt ferric chloride test
Rothera test
ProcedureTake 5.00 ml urine and saturate it with
ammonium sulphate. Add a crystal of sodium nitroprusside.
Slowly pour concentrated ammonium hydroxide (1-2ml) by the side of test tube.
Pink-purple ring
Based on nitroprusside reaction
Diabetic ketoacidosis
Insulin, Glucose homeostasis, and diabetes mellitus. In Satyanarayan U, Chakrapani U eds. Essentials of Biochemistry. 2nd ed. Uppala Author- publisher, Vijayavada 2008.
Acute complications
Diabetic ketoacidosis
Colledge NR, Walker BR, Ralston SH. Davidson’s Principles and Practice of Medicine. 21st ed. China: Elsevier; 2010.
Chronic complications
Chronic Complications
Lynch MA. Diabetes mellitus. In: lynch MA, brightman VJ, greenberg MS eds. Burket's oral medicine: diagnosis and treatment. 8th ed. USA: JB lippincott company; 1984. 842-848.
VASCULAR COMPLICATIONS
Occurs due to microangiopat
hy and atherosclerosis
Changes seen in blood
vessels:
Endothelial proliferation
Thickening of
basement membrane
Thickening of walls of
blood vessels
Increase lipid
metabolism
Atheroma formation
Chronic Complications
Lynch MA. Diabetes mellitus. In: lynch MA, brightman VJ, greenberg MS eds. Burket's oral medicine: diagnosis and treatment. 8th ed. USA: JB lippincott company; 1984. 842-848.
DIABETIC RETINOPATHY
Increases with increase in duration of
diabetes and more common in type I
Dilation
OcclusionIncrease
permeability of blood vessels
Chronic Complications
Lynch MA. Diabetes mellitus. In: lynch MA, brightman VJ, greenberg MS eds. Burket's oral medicine: diagnosis and treatment. 8th ed. USA: JB lippincott company; 1984. 842-848.
RENAL FAILURE
35-45% occur in type I and 20% in type II Mechanism: Mesangium expands, membrane supporting capillary loops
in renal glomeruli expands due to increased production of mesangial matrix products
Surface area for capillary glomerular filtration decreases and gfr declines
Chronic Complications
Lynch MA. Diabetes mellitus. In: lynch MA, brightman VJ, greenberg MS eds. Burket's oral medicine: diagnosis and treatment. 8th ed. USA: JB lippincott company; 1984. 842-848.
Basement membrane in glomerular thickens and decrease GFR.
Earliest sign is microalbuminuria.
Increase renal blood pressure
Expanding mesangium, thickening of basement membrane and renal hypertension and declining of gfrleads to end stage renal disease.
Chronic Complications
Olokoba AB, Obateru OA, Olokoba LB. Type 2 Diabetes Mellitus: A Review of Current Trends. Oman Med J 2012; 27(4): 269-273.
DIABETIC NEUROPATHY
50% diabetic individuals
Affect sensory,moto
r and autonomic
Peripheral sensorimotor
is most common
manifesting with muscle weakness,nu
mbness
As neuropathy worsens
paresthesia disappears and
replaced by hypoesthesia, this
reduction in sensory ability makes affected
area highly prone to imjury as there
is absence to perceive stimuli
Chronic Complications
Olokoba AB, Obateru OA, Olokoba LB. Type 2 Diabetes Mellitus: A Review of Current Trends. Oman Med J 2012; 27(4): 269-273.
Most common cause of death in TYPE II is MYOCARDIAL INFARCION
Increase intimal thickness and atheroma formation are hyperglycemic induced tissue
alterations
Increase thickness of walls leads to partial obstruction and educed blood flow.
Increase thrombus formation along vessel wall and increase platelet aggregation lead to
intravascular thrombi leading to intermittent hypercoagulation
Chronic Complications
Baliga V, Sapsford R. Review article: Diabetes mellitus and heart failure -- an overview of epidemiology and management. Diabetes Vascular Dis Res 2009; 6: 164.
Management
MEDICAL MANAGEMENT OF DIABETES
1. Educate the patient 2. Diet
a.Obese pt – weight reducing diet, restrict calorie content
b.Ideal body weight – maintenance diet Carbohydrates - 55 – 65%Proteins - 10 – 15%Fat - 20 – 30%
Abdullah A, Peeters A, Courten M, Stoelwinder J. The magnitude of association between overweight and obesity and the risk of diabetes: A meta-analysis of prospective cohort studies. Diabetes Res Clin Prac 2010; 89: 309-319.
3. Exercise -Aerobic exercise - Walking, swimming, cycling- Brisk walking – 30mins for 5 days / week- Evaluate CVS status before advising exercise
4. Therapy Type 1 (IDDM) - Insulin - Combination of long acting and short acting insulin - Twice daily
MEDICAL MANAGEMENT OF DIABETES
Abdullah A, Peeters A, Courten M, Stoelwinder J. The magnitude of association between overweight and obesity and the risk of diabetes: A meta-analysis of prospective cohort studies. Diabetes Res Clin Prac 2010; 89: 309-319.
ManagementPRIMARY TREATMENT GOALS
Achieving blood glucose levels that are as close to normal Prevention of diabetic complications. Normal growth and development Normal body weight Avoidance of sustained hyperglycemia or symptomatic
hypoglycaemia Prevention of diabetic ketoacidosis and nonketotic acidosis Immediate detection and treatment of long-term diabetic
complications
Bastaki S. Diabetes mellitus and its treatment. Int J Diabetes & Metabolism 2005; 13:111-134.
Diet, exercise, weight control and medications are the mainstays of diabetic care
The primary medication used in type 1 diabetes management is insulin, on which the type 1 diabetic patients are dependent for survival.
Type 2 diabetic individuals frequently take oral medications although many also use insulin to improve glycemiccontrol.
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848.
• The first-generation sulfonylureas have been replaced with second-generation agents that are more potent, have fewer drug interactions, and produce less significant side effects.
• Sulfonylureas stimulate pancreatic insulin secretion.
• Relatively long duration of action of 12 to 24 hours
• Taken once or twice per day. • Hypoglycemia is a major side effect.• Food intake must be adequate to prevent
glucose levels from falling too low.
Lynch MA. Diabetes mellitus. In: lynch MA, brightman VJ, greenberg MS eds. Burket's oral medicine: diagnosis and treatment. 8th ed. USA: JB lippincott company; 1984. 842-848.
MEDICAL MANAGEMENT OF DIABETES
• Repaglinide stimulates pancreatic insulin secretion
• Rapidly absorbed, reaches peak plasma levels in 30 to 60 minutes, and is then rapidly metabolized.
• The drug is taken with meals and lowers the peaks of postprandial plasma glucose in type 2 diabetes
Lynch MA. Diabetes mellitus. In: lynch MA, brightman VJ, greenberg MS eds. Burket's oral medicine: diagnosis and treatment. 8th ed. USA: JB lippincott company; 1984. 842-848.
• Metformin is a biguanide agent that lowers plasma glucose mainly by preventing glycogenolysis in the liver.
• Metformin also improves insulin use, counteracting the insulin resistance seen with type 2 diabetes.
• Because metformin does not stimulate increased insulin secretion, hypoglycemia is much less common with this drug.
Lynch MA. Diabetes mellitus. In: lynch MA, brightman VJ, greenberg MS eds. Burket's oral medicine: diagnosis and treatment. 8th ed. USA: JB lippincott company; 1984. 842-848.
//www.google.co.in/search?q=met +of+diabetes+mellitus&biw
• The thiazolidinedione agents act to increase tissue sensitivity to insulin, thus increasing glucose utilization and decreasing blood glucose levels.
• These drugs also decrease hepatic gluconeogenesis.
• Like metformin, the thiazolidinediones generally do not cause hypoglycemia.
Lynch MA. Diabetes mellitus. In: lynch MA, brightman VJ, greenberg MS eds. Burket's oral medicine: diagnosis and treatment. 8th ed. USA: JB lippincott company; 1984. 842-848.
• Acarbose is taken with meals, and it slows the digestion and uptake of carbohydrates from the gut.
• This serves to lower postprandial plasma glucose peaks.
Lynch MA. Diabetes mellitus. In: lynch MA, brightman VJ, greenberg MS eds. Burket's oral medicine: diagnosis and treatment. 8th ed. USA: JB lippincott company; 1984. 842-848.
Site of actions of drugs in the treatment of type 2 DM
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848.
Insulin
All type 1 diabetic 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.
Bastaki S. Diabetes mellitus and its treatment. Int J Diabetes & Metabolism 2005; 13:111-134.
Side effects of insulin therapy1. Hypoglycaemia2. Weight gain3. Peripheral oedema (insulin treatment
causes salt and water retention in the short term)
4. Insulin antibodies (animal insulins)5. Local allergy (rare)6. Lipodystrophy at injection sites
Lynch MA. Diabetes mellitus. In: lynch MA, brightman VJ, greenberg MS eds. Burket's oral medicine: diagnosis and treatment. 8th ed. USA: JB lippincott company; 1984. 842-848.
//www.google.co.in/search?q=drugs+of+diabetes+mellitus&biw
Lynch MA. Diabetes mellitus. In: lynch MA, brightman VJ, greenberg MS eds. Burket's oral medicine: diagnosis and treatment. 8th ed. USA: JB lippincott company; 1984. 842-848.
//www.google.co.in/search?q=prevention+of+diabetes+mellitus&biw
Cure to Diabetes Using Stem Cells
Dental management of diabetic
patients
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 levelsFrequency of hypoglycemic episodesMedication, dosage and times.Consultation
Dental management considerations
Malamed SF. Medical emergencies in the dental office. 5th ed. Noida: Mosby; 2000.
Dental management considerations
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
Prophylactic antibiotics • Established infection • Pre-operation contamination wound • Major surgery
Malamed SF. Medical emergencies in the dental office. 5th ed. Noida: Mosby; 2000.
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.
Dental management considerations
Malamed SF. Medical emergencies in the dental office. 5th ed. Noida: Mosby; 2000.
Stress reduction
Changes in medication regimens
Management of emergencies
Dental management considerations
Malamed SF. Medical emergencies in the dental office. 5th ed. Noida: Mosby; 2000.
Dental management of diabetic patients
General management
Assess patient’s level of glycemic control prior to initiating treatment
Maintain a close working relationship with patient’s physician
Refer patients with signs & symptoms suggestive of undiagnosed or
uncontrolled diabetes to physician
Antibiotic prophylaxis
Dentists should have in-office glucometer and glucose source in
dental office
• If patient’s HbA1c level is >11-12%• If there are signs of recurrent
intraoral bacterial infections
Malamed SF. Medical emergencies in the dental office. 5th ed. Noida: Mosby; 2000.
Specific management Use of epinephrine Oral candidiasis Management of Recurrent herpes simplex virus Management of burning mouth syndrome Surgical considerations Periodontal disease management Oral disease management with corticosteroids
Dental management of diabetic patients
Malamed SF. Medical emergencies in the dental office. 5th ed. Noida: Mosby; 2000.
Use of epinephrine in LA is not contraindicated Promotes better anaesthesia Lowers amount of endogenous epinephrine released in response to
pain and stress Endogenous epinephrine elevate blood glucose levels
Dental management of diabetic patients
Specific management
Malamed SF. Medical emergencies in the dental office. 5th ed. Noida: Mosby; 2000.
Oral fungal infections
• Signifies uncontrolled DM• Treatment is similar to that of standard
regimen except topical antifungals should be sugar free
• Oral fungal infections uncontrolled diabetes mellitus
• Recurrent orofacial herpes simplex infection
Dental management of diabetic patients
Specific management
Malamed SF. Medical emergencies in the dental office. 5th ed. Noida: Mosby; 2000.
Management of Recurrent herpes
simplex virus
• Treatment of recurrent cases should be initiated early in the prodromal stage• If patient has insufficiency or renal failure, nephrotoxic antiviral drugs require dose
modification
Management of BMS
• In uncontrolled DM, xerostomia and candidiasis can contribute to BMS• Treatment of xerostomia and candidiasis• Improve glycemic control• Counselling and reassurance in mild cases• Amitryptyline, Doxepin, Clonazepam given for analgesic effect
Dental management of diabetic patients
Specific management
Malamed SF. Medical emergencies in the dental office. 5th ed. Noida: Mosby; 2000.
Surgical consideration
• Prior to surgical procedure, review previous h/o surgical complications and assess glycemic control
• Maintain normal diet after surgical procedure• Antibiotic administration in poorly controlled DM patients
Periodontal disease management
• 6th complication of DM• Primary treatment: Nonsurgical debridement + Systemic Antibiotics• Tetracycline + Scaling & root planning• Supportive periodontal therapy at intervals of 2-3months
Dental management of diabetic patients
Specific management
Malamed SF. Medical emergencies in the dental office. 5th ed. Noida: Mosby; 2000.
Dental management of diabetic patients
Specific management
Lynch MA. Diabetes mellitus. In: lynch MA, brightman VJ, greenberg MS eds. Burket's oral medicine: diagnosis and treatment. 8th ed. USA: JB lippincott company; 1984. 842-848.
Every dental office should have readily available source of carbohydrate glucose powder, fruit juice, hard candy
When patient experiences signs and symptoms of hypoglycemia, dentist should check blood glucose level with a glucometer
If glucometer is unavailable, by default treat it like hypoglycaemia
Following treatment, signs and symptoms should revert back in 10-15min
Dental management of diabetic patients
Lynch MA. Diabetes mellitus. In: lynch MA, brightman VJ, greenberg MS eds. Burket's oral medicine: diagnosis and treatment. 8th ed. USA: JB lippincott company; 1984. 842-848.
Treatment of Hyperglycaemia Terminate dental procedure Position patient supine with legs elevated slightly Follow the A-B-Cs Open airway Administer oxygen Maintain and monitor circulation and vital signs Transportation to hospital for further management
Malamed SF. Medical emergencies in the dental office. 5th ed. Noida: Mosby; 2000.
Malamed SF. Medical emergencies in the dental office. 5th ed. Noida: Mosby; 2000.
Dental management of diabetic patients
Bastaki S. Diabetes mellitus and its treatment. Int J Diabetes & Metabolism 2005; 13:111-134.
Prevention
Conclusion
Conclusion
Diabetes mellitus is a metabolic condition affecting multiple organ systems.
The oral cavity undergoes changes that are related to the diabetic condition, and oral infections may adversely affect metabolic control of the diabetic state.
Hence, Oral healthcare professional is a crucial part of the health care team in screening and monitoring patients with Diabetes Mellitus.
References1. IDF Diabetes Atlas. 6th ed. 2014.2. Malamed SF. Medical Emergencies in the Dental Office. 5th ed. Noida: Mosby; 2000. 3. Davidson’s Principles and Practice of Medicine. 21st ed. China: Elsevier; 2010. 4. Warnakulasuriya S, Tilakaratne WM. Oral Medicine and Pathology A Guide to Diagnosis and
Management. New Delhi: Jaypee Brothers Medical Publishers (P) Ltd; 2014.5. Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s
Principles and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848.6. Frier BM, Fisher M. Diabetes mellitus. Colledge NR, Walker BR, Ralston SH. Davidson’s Principles
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11. Cumming CG. Diabetes. In: Lynch MA, Brightman VJ, Greenberg MS eds. Burket's Oral Medicine: Diagnosis and Treatment. 9th ed. USA: JB Lippincott Company; 1994. 607-614.
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Essentials of Biochemistry. 2nd ed. Uppala Author- publisher, Vijayavada 2008. 18. Olokoba AB, Obateru OA, Olokoba LB. Type 2 Diabetes Mellitus: A Review of Current
Trends. Oman Med J 2012; 27(4): 269-273
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