Primary diabetes – It is an auto immune disorder. Genetic susceptibility is major determinant & environmental factor acts as a trigger. Primary diabetes is either type 1 or type 2.Type 1 DM implies an insulin dependent diabetes mellitus in which patient runs the risk of developing ketoacidosis.A. Immune mediated - Atleast 90 % of beta cells of islets of langerhans of pancreas are destroyed & alpha cells are spared.Type 2 DM or NIDDM implies that patient can easily be controlled without Insulin, except in a few conditions such as in Type 2 DM with complication . Beta cells are intact but there is peripheral resistance to Glucose.
Hormones produced in the islets of Langerhans are secreted directly into the blood flow by different types of cells.Alpha cells producing glucagon (15–20% of total islet cells) glycogenolysisand gluconeogenesis in liver increases blood glucose levelBeta cells producing insulin and amylin-Intake of glucose, glycogenesis and glycolysis in liver and muscle from blood intake of lipids and synthesis of triglycerides in adipocytes.Delta cells producing somatostatin-Inhibit release of insulin Inhibit release of glucagon. Suppress the exocrine secretory action of pancreas.PP cells producing pancreatic polypeptide-Self regulate the pancreas secretion activities and effect the hepatic glycogen levels.
Cushing's syndrome is a hormone disorder caused by high levels of cortisol in the blood. This can be caused by taking glucocorticoid drugs, or by tumors that produce cortisol or adrenocorticotropic hormone (ACTH) or CRH.Cushing's disease refers to one specific cause of the syndrome: a tumor (adenoma) in the pituitary gland that produces large amounts of ACTH, which in turn elevates cortisol. It is the most common cause of Cushing's syndrome.A pheochromocytoma or phaeochromocytoma (PCC) is a neuroendocrine tumor of the medulla of the adrenal glands (originating in the chromaffin cells), or extra-adrenal chromaffin tissue that failed to involute after birth and secretes excessive amounts of catecholamines, usually noradrenaline (norepinephrine), and adrenaline (epinephrine) to a lesser extent.Catecholamines cause increase in blood level.
Hypoglycaemia – its fall in blood glucose level below 3.1 mmol/l or 55.0 gm%.Severe hypoglycaemia – fall in blood glucose concentration level below 2.2mmol/l or below 40 mg%
Diuresis - Increased secretion of urine.
Microaneurysm - These are small discrete red spots near to retinal blood vessels. They arise from venous end of capillaries.Haemorrhage - Blot haemorrhages which are deeply situated are charecterstics of diabetes retinopathy..DOT AND BLOT APPEARANCE-On retina in Diabetes indicate presence of microaneurysms (dots) and Blots(hemorrhages).Hard and soft exudate - Hard exudates are variable in shape and size and appear as white specks or patches on the retina..They are characterstic of diabetic retinopathy. These are due to leakage of proteins from the capillaries of proteins.Soft exudates are superficial cotton wool exudates that occour near optic disc in diabetes who are hypertensives. They indicate advanced retinopathy.Neovascularisation - Formation of new blood vessels near the optic disc is called cellular Neovascularisation. These vessels appear as a tuft of capilllaries on retina and extend into the vitreous. They are soft and are likely to rupture leading to vitreous hemorrhage or preretinal (subhyaloid) hemorrhage.
1. Presented By-Kamini Singh
2. o Introduction - What Is Diabetes Mellitus ?o Classification of Diabetes Mellitus .o Clinical features of various types of Diabetes Mellitus .o Complications from Diabetes Mellitus .o Diagnosis of Diabetes Mellitus .o Management of Diabetes Mellitus .o Diabetes and its importance in Oral & Dental Surgery.
3. Diabetes Mellitus – Diabetes Mellitus is a clinical syndrome of hyperglycaemia with glycosuria due to lack of insulin or insulin resistance. It is a chronic disorder of carbohydrate, fat and protein metabolism. The condition of Glycosuria or high blood sugar produces the classical symptoms of polyuria(frequent urination), polydipsia(increased thirst) and polyphagia(increased hunger).
4. Primary Diabetes Or Idiopathic Secondary Diabetes Diabetes: I. Type – 1 IDDM (INSULIN Pancreatic diabetes due to DEPENDENT DIABETES MELLITUS) pancreatitis Its Sub-divided into: Diabetes due to endocrinal or hormonal disturbances i.e. A. Immune Mediated (Islet cell Acromegaly , Cushing’s antibodies) syndrome , Phaeochromocytoma B. Non immune (No antibodies Drug Induced Diabetes or Iatrogenic Diabetes - Due to II. Type – 2 NIDDM (NON INSULIN steroids and Thiazides (medium DEPENDENT DIABETES MELLITUS) efficacy diuretics) Diabetes caused by insulin Its sub-divided into: receptor antibodies A. Obese (Insulin resistance with Diabetes caused by Genetic relative insulin deficiency) Syndrome i.e. Lipodystrophies, muscular B. Non- Obese (Insulin secretory dystrophy, Klinefelter’s defect with insulin resistance syndrome,Turner’s C. Maturity Onset Diabetes of the Syndrome, Down’s Young (MODY) Syndrome, and DIDMOAD ( Diabetes Insipidus , Diabetes D. Gestational Onset Diabetes Mellitus , Optic Atrophy and
5. Type 1 diabetes or Insulin Dependent Diabetes Mellitus is also known as childhood-onset diabetes & juvenile diabetes. Type 1 Diabetes Mellitus usually occurs in childhood or early adulthood i.e. usually begins below the age of 30 yrs. And manifests itself in two ways: Classic Triad Of Type 1 Diabetes Mellitus : Polydipsia, Polyuria and Polyphagia. Ketoacidosis: Patient present with Diabetic Ketoacidosis following an acute infection or surgery as an first episode without any apparent cause. In severe cases, patient may develop mental apathy, confusion and may lapse into coma. This accounts for 10 % cases of Diabetes Mellitus.
6. Type 1 diabetes is caused due to failure of Beta cells of islets of langerhans. This occurs due to multifactorial causes such as genetic predisposition, viral and auto-immune attack on the beta cells of islets of langerhans of pancreas. The abrupt onset of symptoms with polyuria, polydipsia and polyphagia and weight loss developing over days or over weeks. Some cases may present as Ketoacidosis. It is followed by a symptom free period during which no treatment is required . Characteristically, the plasma insulin is low or immeasurable . Glucagon intervals are elevated but suppressible with insulin.
7. Type 2 diabetes mellitus or Non insulin dependent diabetes mellitus, usually begins after the age of 40 years and 60 % of the patients are obese. However young patients of type 2DM are also seen nowadays. Type 2 DM occurs with intact beta cells of islets of langerhans, but there is peripheral tissue resistance to insulin. There may be some decrease in insulin production or a hyper insulin state. These patients are not ketosis prone, but may develop it under conditions of stress.
8. The symptoms begin gradually over a period of months to years. Frequently, hyperglycaemia is detected in an asymptomatic person on a routine examination. These patients usually does not develop Ketoacidosis. In the decompensated state, they are susceptible to the syndrome of Hyperosmolar Hypoglycaemic state i.e. Hyperosmolar Non Ketotic Coma due to polyuria and increased osmotic concentration. The plasma insulin levels are normal to high. Glucagon levels are high but resistant to insulin.
9. Gestational type of diabetes occur when diabetes onset is during pregnancy and resolves with pregnancy and resolves with delivery. These patients are at a higher risk of developing Diabetes mellitus at a later stage. Age: The occurence of Type 2 DM after 30 years of age, indicates the age as an important factor. Environmental factor: Physical inactivity and inactivity acts an diabetogenic factor who are genetically susceptible to develop type 2 DM.
10. They include diseases of exocrine pancreas, various endocrinopathies(cushings syndrome(increased level of cortisol), phaeocromocytoma(increased level of catecholamines), drug or chemical induced Diabetes Mellitus (beta blockers, oral contraceptives) or genetic syndromes(lipodystrophies), associated with Diabetes.
12. A. Diabetic Ketoacidosis or Diabetic Coma - It results from a shortage of insulin , in response to which the body starts lipolysis and breakdown of fatty acids, producing Acidic Ketone bodies, namely acetone, Aceto-acetic acid and beta Hydroxy Butryic acid. Presence of these Ketone bodies results in acidosis known as Diabetic Ketoacidosis.B. Features :C. Ketoacidosis ; Kussmaul hyperventilation: deep, rapid breathing ; Confusion or a decreased level of consciousness; Dehydration due to glycosuria and osmotic diuresis ; Acute hunger and/or thirst Fruity smelling breath odor Impairment of cognitive function, along with increased sadness and anxiety.
13. B. Hypoglycemia or Hypoglycemic Coma – It may develop in Type 1 Diabetes patient, due to hypoglycemia caused by excessive administration of insulin, missing a meal or due to stress. Hypogycemic episodes may produce:Permanent brain damage or worsening of diabetic control and rebound hyperglycaemia. This condition is called Somogyi’s effect.
14. C. Non- Ketotic Hyperosmolar Diabetic Coma : Its usually a complication of Type 2 Diabetes Mellitus. Its caused due to severe dehydration resulting from sustained hyperglycaemic diuresis. D. Lactic Acidosis: Lactic acidosis is a physiological condition characterized by low pH in body tissues and blood (acidosis) accompanied by the buildup of lactate especially D- lactate, and is considered a distinct form of metabolic acidosis. The condition typically occurs when cells receive too little oxygen (hypoxia), In this situation, impaired cellular respiration leads to lower pH levels. Simultaneously, cells are forced to metabolize glucose anaerobically, which leads to lactate formation. Therefore, elevated lactate is indicative of tissue hypoxia, hypoperfusion, and possible damage.
16. Microvascular complictions : 1. Diabetic Retinopathy – Diabetic Retinopathy is a leading cause of blindness. Characterstic features are: Microaneurysms . Hard and soft exudates. Retinal Hemorrhage. Neovascularisation. Vitreous Hemorrhage. Fibrosis.
17. Types of Diabetic Retinopathy- Benign –Dilatation of retinal venules and vein Premalignant – Dots , Blots appear, Multiple hard exudates, Retinal hemorrhage, soft exudate , macular oedema and perimacular exudates. Malignant – Retinal hemorrhage, Neovascularisation, Exudates at macula and fibrosis.
18. Diabetic Neuropathy-Its an early and common complication and may affect any part of the nervous system except brain. Its an important cause of morbidity and disabilty. Poor glycemic control and long duration of Diabetes are associated with high incidence of neuropathy.Diabetic Nephropathy-It is a common cause of mortality and morbidity in Type 2 DM. About 40-50% patients develop this complication. Its less common in type 2 DM. 25 % patients in type 1 DM develop end stage renal disease and die of it.
19. MiscellaneousInfections-Diabetics have enhanced susceptibility to various infections such as T.B. , pneumonia, Pyelonephritis, Otitis, carbuncl es and Diabetic ulcers as in Diabetic ulcer.
20. Macrovascular complications of Diabetes Mellitus Atherosclerosis - Atherosclerotic lesions appear earlier than in general population in patients of DM both type 1 and type 2. Causes for atherosclerotic process is not known , but possible contributory factors are Hyperlipidaemia, Reduced LDL levels, Non enzymatic glycosylation, increased platelet adhesiveness, obesity and associated hypertension in diabetes.
21. Other Complications Are- Hypertension, Peripheral vascular disease, foot ulcer.Diabetic foot- Foot is frequent site of complication in diabetics and for this reason, prevention is most important aspect in foot care. Pathogenic components of Diabetic Foot Care are- Neuropathy, peripheral vascular disease producing ischaemia (vasculopathy), secondary infection following ulcer.
22. Symptoms of Diabetic Foot: It may be varying from none to numbness, parasthesia , and pain. Signs- Ulcers, Sepsis, Abcess, Osteomyelitis, Gangrene Chercot ‘s Joint, Loss of toe
23. Diagnosis of Diabetes mellitus is based on symptoms signs and biochemical test. In the presence of suggestive symptoms, the confirmation of diagnosis be mellitus, finding a random blood glucose level of more than 200mg%or 11.5mmol/L. However, many patients , particularly those with type 2 diabetes either have few or no symptoms and diagnosis is made on fasting and postprandial blood glucose level
24. METABOLIC SYNDROME(syndrome x) AND RISK FACTORS ASSOCIATED WITH DIABETES MELLITUS:WHO DIAGNOSTIC CRITERION -1.CONTROL OBESITY BMI>30KG/METRE SQUARE WAIST /HIP RATIO MEN>0.90 WOMEN>0.852. TRIGLYCERIDE >150mg/dl3.HDL CHOLESTEROL Men<35mg/dl Women<39mg/dl
25. 4. Fasting Glucose >110mg/dld.5. Microalbuminurea Urinary albumin excretion rate >/ =20 mu gm/min DIAGNOSIS IS MADE WHEN 3 OR MORE OF THESE RISK FACTORS ARE PRESENT
26. Impaired fasting glucose(IFG) This is a biochemical abnormality detected on oral glucose tolerance test Normal fasting plasma glucose is taken as <=110mg/dl,6.1mmol/l Fasting plasma glucose levels between 110- 126mg/dl(6.1-7 mmol/l)is taken as impaired fasting glucose.. This group of individuals are at increased risk of developing Type 2 DM . It’s a feature of MODY Type 2 DM. It’s a risk factor as well as an alternative diagnostic criterion for DM
27. Impaired glucose tolerance -This is defined as normal fasting plasma with impaired postprandial glucose on G.I.T The two hours levels on OGT between 140mg- 200mg/dl(7.8-11.1mmol/l) indicate IGT This is a transition phase between a normal and diabetic person. hence constitute a risk factor to the development of TYPE 2 DM and increased risk of cardiovascular mortality. Females with IGT are at increased risk of still birth , delivering large and heavy babies and babies with congenital defect
28. 1.Classic symptoms of diabetes and a casual plasma glucose 200mg/dl(11.1mmol/l) Casual is defined as any time of day without regard to time since last meal. The classic symptoms of diabetes include polyuria, polyphagia, polydipsia and unexplained weight loss.OrFasting Plasma Glucose / FPG>=126mg/dl(7.0mmol/l). Fasting is define as no caloric intake for at least 8 hrsOr2 hour Plasma Glucose / 2h PG>=200mg/dl(11.1mmol/dl), during an OGTT.
29. Diabetes Mellitus is confirmed by demonstrating hyperglycaemia with ketonuria and acidosis. Urine test for Detection of Glycosuria Urine test for presence of ketone bodies Oral glucose tolerance test Diagnosis of pre-diabetic state Impaired Fasting Glucose Impaired Glucose Tolerance
30. Condition Venous Plasma Glucose Concentration in mg%(mmol/l) Fasting Postprandial(2hr GTT)Normal <110 (6.1) <140(7.3)Diabetes Mellitus >=126 >200Impaired Fasting >=110 and < 126(6.1-7.0) <140(7.8)GlycaemiaImpaired Glucose <126(7.0) >=140 & 200(7.8-11.1)Tolerance* * 2hrs GTT means following 75gms Glucose load
31. Detection of glycosuria- Urine For Glycosuria is employed for screening the public or individual for presence of diabetes. Glycosuria does not mean Diabetes Mellitus, and require further evaluation by blood sugar or glycosylated haemoglobin. HbA1c is a type of glycosylated Hb. Acc. to WHO criterion for Diabetes control regarding HbA1c The normal value of HbA1c is <6 % and value more than 10% suggests poor control of Diabetes. In between values- Excellent (7%) , Good(7-8%), and Poor control(>8%)
32. Urine test for Ketone Bodies Acetotest or ketostix test papers utilising Nitroprusside reactions are employed to detect ketone bodies in the urine , Ketonuria also occours in prolonged fasting, following high fat diet & after repeated vomiting. Ketonuria is not pathognomic of Diabetes but when it occours along with glycosuria , Diagnosis of Diabetes is almost certain.
33. Oral glucose tolerance test Patient is advised to take unrestricted carbohydrate diet for 3 days prior to that. Before the test ,patient keeps fast overnight. Patient should rest for half an hour before the test. Fasting sample of blood is taken for glucose estimation and then 75.0 g of glucose dissolved in 300 ml(a glass) of water is given by mouth. Sample of blood and urine are collected at half an hour intervals for next two hours for glucose measurement.
34. Impaired Fasting Glucose(IFG) Its diagnosed when fasting glucose level is abnormal(between 110 and 126mg%). It was introduced by American Diabetes Association just to avoid the need for OGT. Impaired Glucose Tolerance-The intermediate values of postprandial blood sugar (140 -200mg%) between normal and diabetics are classified as impaired glucose tolerance.
35. Diet Planning Exercise Drugs Therapy
36. The diet most often recommended is high in dietary fiber, especially soluble fiber, but low in fat (especially saturated fat). This involves allocation of calories in a proper proportion to carbohydrates , fats and proteins. It is as followed: Carbohydrate-50-65% Proteins-10-20% Total Fat-25-30%
37. Isotonic exercises like brisk walking , swimming or cycling are recommended.
38. ORAL HYPOGLYCAEMIC AGENTS (OHA) Oral Hypoglycemic are drugs which upon administration lower the blood glucose level. These drugs are used in patients of Type 2 Diabetes Mellitus (NIDDM), who do not respond to dietary management and who would otherwise require treatment with insulin. In later situation, they are used as adjuvant to insulin in obese patients. These drugs require presence of Insulin secreting Beta cells for their action and that is the reason , why they are not effective in type 1 Diabetes Mellitus.
39. Classification of oral hypoglycaemicdrugs (depending upon the mechanismof actionInsulin Secretagogues – They increase thesecretion of insulin from surviving beta cells ofpancreas .Insulin Sensitizers – They sensitize the action ofinsulin and overcome insulin resistance.
40. Sulphonylureas –These include: 1st generation-like tolbutamide 2nd generation-like glipizide They are effective in treatment of non-obese patient with Type 2 DM who fail to respond to dietary measures alone. Side effects : Hypoglycemia , weight gain.Meglitinide Thisincludes- Drugs like Repaglinide,Naliglinide,Meglitinide Dose : .5-16mg per day
41. Biguanides –Metformin is the only drug used in this group. Its particularly useful in obese patients with Type 2DM, who do not respond to dietary measures and weight reduction.Thiazolidinediones –Drugs used in this group are rosiglitazone and pioglitazone.Side Effect : Weight gain, mild rise in LDL.
42. Insulin is required for treatment of all patients with Type 1 DM and many patients with Type 2 DM. Indications in Type 2 DM In primary or secondary sulphonylureas failure Major trauma Surgery Pregnancy Diabetic ketoacidosis Myocardial infarction Infection Liver failure Renal failure Respiratory failure
43. Surgery whether performed electively or during emergency acts as a stress inducing catabolic hormones such as Cortisol, Catecholamines, Glucagon and Growth hormone in diabetic patients as well as normal persons . These endocrine hormones are anti insulin in their action , hence increase sometimes may lead to Hyperglycaemia and sometimes may lead to acute metabolic decompensation such as diabetic ketoacidosis , in both Type 1 and Type 2 DM with uncontrolled , poorly controlled or untreated Diabetes.
44. Starvation before surgery may exacerbate hyperglycaemia The major risk of surgery in diabetes is increased risk of infections and delayed wound healing due to impaired phagocytic activity of leucocytes , as well as impaired immunity dental or oral surgery , should only be carried out only in the states of uncontrolled diabetes and avoided or postponed in uncontrolled state of diabetes.FOR MINOR DENTAL PROCEDURES- Minor orodental procedures can easily be performed in type 1 and type 2 Diabetes mellitus, if patient is well maintained on either insulin or oral hypoglycaemics. For minor surgery its imp. to control the blood glucose effectively before surgery.
45. Post operatively, 5%Glucose Infusion ,with 10-12 units of insulin may be started with 20mmol of Pottasium. After wound is healed the patient is shifted back to its previous regimen of treatment.