Diabetes mellitus/endodontic courses

INDIAN DENTAL ACADEMYLeader in continuing Dental Education

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CONTENTS

• Introduction• Classification• Epidemiology & prevalence• Etiology & pathogenesis• Pathophysiology• Clinical features• Diagnosis & Management• Metabolic control & assessment• Complications & management• Special problems and management• Prevention & future prospects


Definition

Group of metabolic disorders having a common phenotypic expression of hyperglycemia. Complex interaction of genetics, environmental factors & lifestyle influences the course & outcome.The metabolic dysregulation associated with DM causes multitude of secondary pathophysiologic changes in multiple organs leading to macro & micro vascular complications.


PREVALENCE-Growing menace in India

• 300 million diabetics in world by 2025• India-World’s largest diabetic population.• Every 4th diabetic in the world is an

Indian• 30-33 million diabetics in India will go up

to 40 million by 2010 & 72 million by 2025.


Why increased prevalence in India?

• Ethnic susceptibility• Central obesity• Sedentary lifestyle• Hypertension• Atypical tubercular presentation• GDM-baby weighing more than 4.5 kg• Stress hyperglycemia• Premature atherosclerosisMore in urban high income group

populations.


NORMAL PHYSIOLOGY


NORMAL GLUCOSE METABOLISM & HOMEOSTASIS


REGULATION OF INSULIN SECRETION


INSULIN ACTIONSstimulus for insulin release hypoglycemia ketone bodies B2 stimulation

Stimulus to inhibit release A1 stimulation glucocarticoids glucagon Thyroid harmone


Insulin is a potent anabolic hormone,known with multiple synthetic & growth promoting effects

Its principle metabolic function is increase in rate of glucose uptake by tissues (skeletal muscle,adipose tissue)

• muscle-glucose stored as glycogen-ATP• adipose tissue-promotes lipogenesis• Stimulates protein synthesis


Etiology & pathogenesis

Type 1 diabetesa. Immune mediated-cellular

mediated autoimmune destruction of B- cells of pancreas

b. Idiopathic-no etiology,suffer from episodic ketoacidosis,lack immunological evidence of B-cell autoimmunity & is not HLA associated.


Genetics -1/3rd susceptibility-HLA DR3/DR4 are more

susceptible. -40% prevalence in monozygotic twins

Environmental factors -Viruses-mumps,rubella,retro virus, CMV,EBR -Diet-bovine serum albumin implicated in

triggering disease. -Stress-progress the development of disease

by secretion of counter regulatory hormones.


Type 1 diabetes -Cell mediated autoimmune disease.

• HLA linked genetic predisposition• Association with other autoimmune diseases• Circulating islet cell antibodies in new cases• Mononuclear cell infiltration of pancreatic

islets• Recurrence of insulitis & selective destruction

of B-cells in pancreatic grafts• Induction of remission by immunosuppressive

drugs such as cyclosporin


Type-2 diabetes

The two metabolic pathways that characterize type 2 diabetes are

• Insulin resistance -Decrease ability of peripheral tissues to respond to insulin

• B-cell dysfunction-manifested as inadequate insulin secretion in face of insulin resistance

THUS RESULTING IN HYPERGLYCEMIA


Insulin resistance• Defined as resistance to effects of insulin

on glucose uptake, metabolism & storage.• Three causes:a. an abnormal insulin moleculeb. excessive amounts of circulatory antagonistsc. target tissue defects.(common)• Resistance in diabetics is due to Genetic susceptibility,sedentary life style,

obesity, TNF alpha, glucotoxicity, drugs like glucocarticoids, B-blockers & adrenergic agonists.


Obesity• Insulin resistance is present in simple

obesity unaccompanied by hyperglycemia• In diabetes the resistance is further

increased.• The mechanisms are1. Role of free fatty acids-inverse

correlations exist b/w FFA & insulin sensitivity.Further intercellular triglcerides is increased in liver & muscles in obese persons(more FFA).This results in potent inhibition of insulin signalling

Acquired insulin resistance.


2. Role of adipokines• Adipokines are proteins released by

adipocytes in systemic circulation• Dysregulation of adipokine

secretion(increase or decrease) is one of mechanism insulin resistance is tied to obesity.

decrease in leptin, & increase in resistin.

• Thus obesity is central factor in insulin resistance-diabetogenic.


Tumour necrosis factor alpha cytokine produced by adipocytes & if in

excess, it exerts inhibitory effects on insulin signaling mechanisms,exacerbating insulin resistance.

furthermore acute infections increase secretion of TNF, thus worsening insulin resistance.

Glucotoxicity severe hyperglycemia aids in production of

glucosamine which directly influences glucose transport functions-thus insulin resistance.


B-cell dysfunction1.Qualitative-initially secretion is

subtle,followed by loss of normal oscillating pattern of secretion,finally affecting all phases of secretion.

2. Quantitative-decrease in B-cell mass,islet cell degeneration & deposition of amyloid.

it is uncertain if amyloid is involved in or as a consequence of reduction in B-cell mass.


PATHOPHYSIOLOGYType 1 diabetes


TYPE 2 DIABETESwww.indiandentalacademy.com

Clinical features-type 1


CLINICAL FEATURESwww.indiandentalacademy.com

SECONDARY DIABETESMaturity onset diabetes of young(MODY)

• Primary defect in B-cell function, that occurs without B-cell loss affecting either B-cell mass or insulin production.

• Is the outcome of heterogenous group of genetic defects characterised by

-autosomal dominant inheritance -early onset usually before 25 years -absence of obesity. -lack of islet cell antibody & insulin resistance syndrome


DIAGNOSIS

OGTT not recommended for routine clinical use as it is poorly reproducible,difficult to use & rarely performed in practice.(though more sensitive & modestly specific than FPG).But required in evaluation of IFG or when diabetes is stilL suspected despite normal FPG O


TESTING FOR TYPE 2 DIABETES IN CHILDREN

CRITERIAWeight (BMI>85th percentile for that age & sex or

>120% of ideal for weight)

ANY TWO OF FOLLOWING RISK FACTORS• Family history in first or second degree relative• Race-native American,African American.• Signs or conditions associated with insulin resistance

(acanthosis nigricans, hypertension, dyslipidemia, polycystic ovary syndrome.

• Puberty occurs at young ageTEST PREFERRED-FPG


VALUE OF SCREENINGRECOMMENDATIONS

• Evaluation should be performed within the health care setting,for particularly those with BMI>25kg/m2.They should be screened at 3 yr interval beginning at age 45.Testing considered early & frequently if additional risk factors are present.

• FPG is recommended screening test.• Diagnostic screening performed in any clinical

situation that warrants testing • Community screening-not beneficial


DIABETES CONTROL & ASSESMENTTESTS OF GLYCEMIA

TESTS USED TO MONITER THE GLYCEMIC STATUS OF DIABETICS ARE

• Urine sugar -urine glucose & ketones• Blood glucose testing- SMBG• Glycated proteins -Glycated hemoglobin & -Glycated serum proteins


URINE SUGARS-GLUCOSE TESTING

THE TEST IS NOT RECOMMENDED BECAUSE• There is wide individual variation in renal

threshold esp in long standing adult diabetics (underestimation) ,pregnant women & children (overestimation)

• Fluid intake & urine concentration affects results• It reflects an average level of blood glucose since

the last voiding & not the level at time of test. • Negative results does not distinguish

hypoglycemia, euglycemia or even mild hyperglycemia-hence limited in preventing complications


• Errors in interpreting the results • Some drugs interfere with urine glucose

determinations• Alimentary glycosuria after gastric surgery

and in pts with hyperthyroidism,peptic ulcer & hepatic disease.

Hence presently it is recommended that all diabetics esp those who are on insulin should monitor blood & not urine glucose levels. Urine testing should be considered only if pts are unable or unwilling to perform Self monitoring of blood glucose(SMBG).


KETONE TESTSKetone testing is very important,esp in type I diabetics.

• Frequent urine ketone tests are important in the first few days after diagnosis to determine if enough insulin is being given to turn off ketone production. Turning off ketone production is the first goal in the treatment of newly diagnosed diabetes managed in the outpatient setting. This usually takes one or two days after starting insulin.

• It is important to test for urine or blood ketones because they can build up in the body. This can result in one of the two emergencies of diabetes-ketoacidosis


• Recommended that all pts test for ketones during acute illness,stress (blood glucose constantly>300),pregnancy & anytime the person feels sick or nauseated (especially if he/she vomits, even once). If the person is sick, ketones can be present even when the sugar is not high.

• False positive values-in normal individuals during fasting,in pts with captopril, & 30%of pregnant women.

• False negative values-when strips are exposed to air & in acidic urine specimens.


The Precision Xtra™ meter is now available to do a home fingerstick test for blood ketones


SELF MONITORING BLOOD GLUCOSE TESTING

• Allows patient to evaluate their individual response to therapy & assess if glycemic targets are being achieved.

• Results can be used to prevent hypoglycemia,to adjust medications & physical activity.

• Daily SMBG for pts on insulin is recommended. For type 1 diabetics & pregnant women,it recommended 3-4 times daily.

• Technically sensitive & interpretation of data is difficult.• ? Stable diet treated patients.


GLYCATED PROTEIN TESTINGGLYCATED HEMOGLOBINThis test helps to provide the pts average

glycemia over past 2-3 months & thus to assess treatment efficacy.


Varied results in

Conditions reducing RBC LIFE SPAN, Vit C & Vit E lowers test values.Iron deficiency anemia increases test values.Hyperbilirubenemia,anemia,chronic alcoholism,ingestion of salicylates, & hypertriglyceridemia interfere with assay.


ADA RECOMMENDATIONS

• Test to be performed at initial patient visit, & atleast twice a year in pts who meet the treatment goals & quarterly in pts whose therapy has changed or who is not meeting glycemic controls.

• Develop the management plan to achieve AIC values to 7%.More stringent (6%) in high risk groups.

• Lowering AIC lowers the risk of micro & macrovascular complications

• Less stringent goals for pts with h/o severe hypoglycemia,limited life expectancy, very young children & older adults.


Fructosamine (or Glycosylated Albumin) Test

• This test measures the amount of sugar attached to the main serum protein, albumin. It reflects the blood sugars every second of the day for the past 2-3 weeks (whereas the HbA1c reflects the past two or three months).

• It is often helpful to know how someone is doing more recently (in contrast to the past three months).

• The test is also helpful for someone who is changing treatment (more shots, an insulin pump, etc.).


• A commercial meter, the In Charge™, is available and measures either blood sugar or fructosamine in the home setting.

• This home meter may be particularly helpful to families who are unable to have an HbA1c determined every three months when attending a diabetes clinic.


MANAGEMENT

1.Diet alone 2.Diet+OAD3.Diet+OAD+insulin


DIETARY MANAGEMENT

Medical nutrition therapy describes optimal coordination of calorie intake with other aspects of diabetes(insulin, exercise,weight loss & drugs)

Nutritional recommendations(ADA-1998 & 02)

• Protein-15-20%• Saturated fat<10%• 60-70% of calories divided b/w

carbohydrates & unsaturated fats.www.indiandentalacademy.com

• Use of caloric sweetners ,including sucrose is acceptable.much emphasis on risk factors like hypertension & dyslipidemia.(increased dietary fibre, & decreased fat)

• Fibre-20-35g/d & sodium< 3000mg/d are recommended

• Cholesterol-</= 300mg/d.

For alcohol users• Alcohol to be taken with food as it increases

the risk of hypoglycemia• Tendency for lactic acidosis with biguanides• Similarity b/w its effects & hypoglycemia.


IMPORTANCE OF EXERCISE


ORAL HYPOGLYCEMIC AGENTSClassification-According to mechanism of action.1.Drugs that stimulate insulin secretion - Sulfonylureas & Meglitide

analogs.2.Drugs that alter insulin action.(decrease

gluconeogenesis & increase insulin sensitivity.

- Biguanides & Thiazolidines3.Drugs that affect absorption of glucose. - Acarbose & Miglitol.


INSULIN

• Exogenous insulin is the most physiologic , most rapid & most effective treatment available for enabling pts to reach normoglycemia.(Rosentock & Riddle)

• Anabolic hormone that helps in utilization of glucose, in lipogenesis & storage of proteins.

• No fixed upper dose of insulin.(Nathan- 2002)

• No insulin failure described, always works, though higher doses are required in those with insulin resistance (obesity)

• Longest established safety.


Advantages of Insulin Aspart over Actrapid. •Superior postprandial control in diabetics due to twice as fast onset & a high peak.•Lower risk of noctural hypoglycemia (duration remains for 4 hrs.

•Freedom from meal time constrints•Can be given just before or after meals.•Less need to snack b/w meals to avoid hypoglycemia.


Advantages of Actrapid (regular) over Aspart / Lispro (ultrashort)

• Intravenous infusions are particularly helpful in treatment of ketoacidosis & during perioperative management.

• In case of pump failure, users of ultrashort acting insulins will have more rapid onset of hyperglycemia & ketosis when compared to regular insulin users.

• Also indicated when subcutaneous insulin requirements change rapidly.(post surgery & during acute infections).


MIXTURES OF INSULIN

1. Intermediate+ Regular/Lispro• Given preprandially,as require several

hours to reach therapeutic levels.• NPH is preferred to Lente as zinc binds to

soluble insulin's & partially blunts its action.• Premixed preparations of Lispro/Aspart &

NPH are unstable because of exchange of human insulin with Protamine complex,hence Neutral Protamine Lispro was developed.

2.Long acting +Regular/lispro


Different Insulin Regimens1.Basal Bolus2.Split Mix or Self Mix Regimen3.Premixed Insulins.

ADVANTAGES OF PREMIXED INSULINS (Novomox 30(30%insulin Aspart + 70%

Protamined insulin Aspart.)• Simple convenient meal time regimen• Better 24 hr physiological basal control• Controls FPG, PPG, & HbAic.• High safety-low risk of hypoglycemia• Once a day regimen


• Different methods of insulin administration are Insulin syringes & needles,Insulin pen injection devices, Insulin pumps, & inhaled Insulins.

• Most important complication of Insulin administration is Hypoglycemia.Human Insulins have less immunogenic reactions.

• Should not be given with Carticosteroids & B-blockers.

• Pancreas transplantation & Asprin therapy are other treatment modalities to treat diabetes


NEW THERAPEUTIC STRATEGIES IN TYPE 2 DIABETICS1.Three thresholds for AIC Monotherapy- If AIC remains b/w 6-6.5,its

necessary to introduce an OAD after 6 months without any hypoglycemia-metformin

Bitherapy-AIC exceeds 6.5 with max dose of metformin, then bitherapy not delayed.

metformin+Glitazones/insulin secretor.

Tritherapy- AIC>7%.then choose tritherapy b/w metformin+ glitazones+ insulin secretor or insulin therapy.


2.Target Goal for Blood pressure 130/80 with as many hypertensives as

necessary.

3.Target goals for lipidsLDL Cholesterol < 1g/L in pts with increased

CVS risk for primary & secondary prevention

LDL Cholesterol b/w 1.3-1.6g/L for other type 2 diabetics.


HYPOGLYCEMIA

Lab diagnosis-plasma glucose<2.5-2.8nmol/L or <45-50 mg/dl(individual variation)Whipple triad symptoms consistent with hypoglycemia a low plasma glucose concentration relief of symptoms after plasma glucose conc is

raised.

Causes -a. Fasting-underproduction or over utilization of glucose

b. Post Prandial /reactive-post gastric surgery & rare enzymatic defects.


clinical featuresAutonomic-sweating,tremors, pounding heart,

hunger & anxiety.Neuroglycopenia-confusion,drowsiness,speech

difficulty & disorientationNon specific-nausea, tiredness & headache.

ManagementAcute therapy-oral glucose or 25g of 50% soln of

dextrose(I.V) with constant infusion of 5-10% dextrose.

Glucagon-1mg IM-effective in pts who do not respond to IV glucose.

Dose of insulin is reduced by 20% unless cause is known.


DIABETIC KETOACIDOSIS

DKA is the acute complication of diabetes mellitus associated with relative or absolute deficiency of insulin.

Causes: inadequate insulin administration,

infection, surgery, drugs and pregnancy.Signs: dehydration, hypotension, tachycardia,

air hunger, hypothermia, confusion, drowsiness and coma.

Symptoms: polyurea, weight loss, weakness, nausea, vomiting, blurred vision and abdominal pain.


LATE COMPLICATIONS

The morbidity associated with long standing diabetics result from number of serious complications involving both large & medium sized muscular arteries (macrovascular disease) as well as capillary dysfunction in target organs (microvascular disease).


GESTATIONAL DIABETES MELLITUSGDM is defined as any degree of glucose

tolerance with first onset of pregnancy.This definition applies regardless of whether insulin or dietary modification is used for treatment & whether condition persists after treatment.

It is a prodromal form of type 2 diabetes ,being unmasked by pregnancy.

Pregnancy is associated with increased insulin resistance thus necessitating increased production.


Foetal complications• Congenital malformations are atypical since

glucose tolerance occurs late in pregnancy.• Macrosomia-20% (gestational age.maternal

weight)• Neonatal hypoglycemiaOther complications includerespiratory distress syndrome,polycythemia,

hypocalcimia, hyperbilirubenemia.

Maternal surveillance should include B.P & urine protein monitoring.


Management• All women with GDM should receive

nutritional counseling which includes provision of adequate calories & nutrients to meet demands of pregnancy.(200kc/day)

• For obese –calories is reduced• If target values not achieved with diet,

human insulin should be initiated.OHA not approved.

• GDM is not in itself an indication for cesarean delivery.(before 38 weeks) but prolongation beyond time will increase the risk of macrosomia without decreasing cesarean rates.


Management during pregnancy

• Maintain good glycemic control –AIC within range of 6.5-8% by use of 3-4 injections daily.

• Do not strive for normoglycemia at the expense of hypoglycemia.

• Check overnight sample of urine for ketones regularly.increase intake of glucose & dose of insulin to abolish ketonuria.

• Insulin stopped during delivery & resumed 12 hours after pregnancy.


SURGERY AND DIABETES

WHY IS GOOD DIABETIC CONTROL

NECESSARY IN SURGERY???


PRE OPERATIVE ASSESSMENT Assess CVS and renal function. Check signs of neuropathy Assess diabetic control Review treatment of diabetes - replace long acting insulin with

intermediate insulins - stop OADs and replace with insulins


CONCLUSION

DIABETES CAN ONLY BE PREVENTED AND NEVER CURED.


Diabetes mellitus/endodontic courses

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