Dentistry endocrine disease

Endocrine Diseases

Disorder of Glucose Metabolism

Diabetes Mellitus

Endocrinology

Study of DUCTLESS GLANDS that produce HORMONES which are released directly into the bloodstream permitting

effects at distant sites called TARGET GLANDS

Endocrine GlandsEndocrine Glands

Pure Endocrine Glands:

1. Pituitary1. Pituitary

2. Pineal2. Pineal

3. Thyroid3. Thyroid

4. Parathyroid4. Parathyroid

5. Adrenals5. Adrenals

Dual Function Endocrine Glands

1. Pancreas1. Pancreas

2. Kidneys2. Kidneys

3. Ovaries3. Ovaries

4. Testes4. Testes

:A fish shaped organ that lies behind the stomach: retroperitoneal organ: the head and neck are located in the curve of the

duodenum and its body extends horizontally across posterior abdominal wall

: it is usually 6 – 9 inches long and 1-1.5 cm wide

:Exocrine function: production of digestive enzymes

:Endocrine function: release of hormones (INSULIN and GLUCAGON)

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DIABETES MELLITUS

Definition:

a syndrome characterized by chronic hyperglycemia

and a disturbance of carbohydrate , fat and protein metabolism

associated with absolute or relative deficiency in insulin secretion

and/ or insulin action

Pathophysiology:

1. Abnormal/ inadequate insulin secretion and gradual deterioration in islet cell function

2. Resistance to insulin action in target tissues

3. Insulin stimulated fat synthesis in liver with fat transport (VLDL) leading to fat storage in muscle.Increased fat oxidation impairs glucose uptake and glycogen synthesis

4. Alpha cells > Beta cells therefore excess glucagon And other counterregulatory hormones (epinephrine, cortisol,growth hormone)

5. Inadequte insulin action

increased hepatic glucose production( increased glycogenolysis and increased gluconeogenesis)

Peripheral Glucose Utilization falls

Hyperglycemia

5 COMMON FORMS OF GLUCOSE INTOLERANCE5 COMMON FORMS OF GLUCOSE INTOLERANCE

1.1. Diabetes mellitus type 2Diabetes mellitus type 2::most common type of diabetes:affects mostly adults (>40 yrs of age):Also called Non insulin dependent diabetes mellitus or NIDDM:Maturity onset:may range from predominantly insulin resistance with insulin

deficiency to a predominantly secretory defect with insulin resistancePathogenesis:

A. Genetic Factor: unclear=powerful genetic influence=risk to offspring and siblings higher than in Type1

(concordance rate in identical twins—90-100%)B. Obesity

80 % of patients are more than 20 % above their ideal body weight

2. Diabetes mellitus Type 12. Diabetes mellitus Type 1:seen usually in the young (juvenile onset):associated with total dependence on exogenous insulin : total beta cell destruction leading to absolute insulin

deficiency:they can go into diabetic ketoacidosis and die if deprived

of insulin: also called Insulin dependent diabetes mellitus or IDDM

Pathogenesis:genetic susceptibility (HLA DR3; DR4) environmental event

(virus?/Food?) Insulitis (infiltration of activated T lymphos) Activation

Of autoimmunity (self to non-self transition) Immune attack on beta cells

(islet cell antibodies, cell mediated immunity) DIABETES MELLITUS

(90 % beta cell destruction)

3. Impaired Glucose Tolerance3. Impaired Glucose ToleranceBlood sugars are not normal but not high enough to be Blood sugars are not normal but not high enough to be

LabelledLabelled as Diabetes as DiabetesFasting glucose: > 100 mg/dl - <126 mg/dlFasting glucose: > 100 mg/dl - <126 mg/dl

4. Gestational Diabetes mellitus4. Gestational Diabetes mellitus:seen in pregnant women, not previously diabetic, who :seen in pregnant women, not previously diabetic, who

develop the diabetes during 24-28 weeks age of gestationdevelop the diabetes during 24-28 weeks age of gestation: diabetes disappears right after the delivery of the fetus: diabetes disappears right after the delivery of the fetus

5. Diabetes mellitus 2ndary to pancreatic tumors/ inflammation/ drugs5. Diabetes mellitus 2ndary to pancreatic tumors/ inflammation/ drugs::genetic defects in beta cellsgenetic defects in beta cells: genetic defects in insulin action: genetic defects in insulin action: disease of the exocrine pancreas: disease of the exocrine pancreas:Genetic syndromes associated with Diabetes:Genetic syndromes associated with Diabetes

Diagnostic Criteria:Diagnostic Criteria:

A.A. (+) classical symptoms (eg. Thirst, polyuria, unexplained(+) classical symptoms (eg. Thirst, polyuria, unexplainedweight loss, drowsiness, coma)weight loss, drowsiness, coma)

Marked glucosuria (sugar in the urine)Marked glucosuria (sugar in the urine)Random blood sugar : > 200 mg/dl or 11.1 mmol/l orRandom blood sugar : > 200 mg/dl or 11.1 mmol/l orFBS : >126 mg/dl or 7.0 mol/l or FBS : >126 mg/dl or 7.0 mol/l or 2 hour post prandial values : > 200 mg/dl2 hour post prandial values : > 200 mg/dl

B. (-) or minimal symptomsB. (-) or minimal symptomsFBS : equivocal FBS : equivocal perform an Oral Glucose perform an Oral Glucose

Tolerance TestTolerance TestOral Glucose Tolerance Test: test to confirm or excludeOral Glucose Tolerance Test: test to confirm or exclude

the diagnosis of diabetes or to establish the presence the diagnosis of diabetes or to establish the presence of impaired glucose tolerance of impaired glucose tolerance

DIAGNOSTIC CRITERIADIAGNOSTIC CRITERIA

Normal Value IGT DM

Fasting Blood 70-100 101-125 >126Glucose (mg/dl)

2 hr Post < 140 >140 - <200 >200Glucose Load

Clinical Features and other Diagnostic PromptsClinical Features and other Diagnostic Prompts::

1. Polyuriaincreased urine volume because of glucose

induced osmotic diuresis

2. Polydipsiaincreased fluid intake is a response to

the resulting dehydration and thirst

3. Polyphagiaexcessive ingestion of food

4. Weight lossresults from loss of glucose in the urine and the

catabolic effects of the decrease in insulin action despite the increase in food intake

5. General itching6. Impairment of Visual Acuity

changes in refractile qualities of lens secondary to

hyperglycemiainduced osmotic alterationsdue to diabetic retinopathy or to

cataract

7. Repeated skin sepsis

8. Unaccountable pains and paresthesia in the limbs

9. Presentation with chronic foot ulceration or incipient gangrene

10. Chance finding of glycosuria, discovery in routine employment or insurance examination

11. Positive diabetic close family member12. Presence of overweight and obesity (centrally situated fat)13. Achieving maturity14. History of previous pregnancy giving birth to an unusually

large baby15. History of pregnancy ending in miscarriages and stillbirth

1.1. DietDiettotal caloric requirement in 24 hrs computedtotal caloric requirement in 24 hrs computed

against ideal body weight and lifestyleagainst ideal body weight and lifestyle

2. Exercise2. Exerciseexhibit fall in glucose concentrationsexhibit fall in glucose concentrationsmaximum benefit achieved when glucose levelsmaximum benefit achieved when glucose levels

are below 200 mg/dl are below 200 mg/dl -discourage in the presence of retinopathy-discourage in the presence of retinopathy

3. Oral Hypoglycemics3. Oral Hypoglycemics

a. Sulfonylurea : ex. Glibenclamide, a. Sulfonylurea : ex. Glibenclamide, gliclazidegliclazide

b. Biguanides: ex. Metforminb. Biguanides: ex. Metformin

c. Alpha glucosidase inhibitors: ex. Acarbosec. Alpha glucosidase inhibitors: ex. Acarbose

d. Thiazolinediones: Rosiglitazone, d. Thiazolinediones: Rosiglitazone, PioglitazonesPioglitazones

e. Incretins : Sitagliptine. Incretins : Sitagliptin

4. Insulin4. Insulinpolypeptide (digested in the GUT, hence inactive polypeptide (digested in the GUT, hence inactive

by mouthby mouthslowly diffuse out into the subcutaneous tissue after slowly diffuse out into the subcutaneous tissue after

InjectionInjection5. Monitor control of blood sugar5. Monitor control of blood sugar

Hemoglobin A1CHemoglobin A1C

COMPLICATIONS:COMPLICATIONS:I.I. AcuteAcuteII.II. ChronicChronic

I. Acute Complications:I. Acute Complications:1.1. HypoglycemiaHypoglycemia statistical deviation from the normal blood glucose rangestatistical deviation from the normal blood glucose range plasma glucose values of 3.3 mmol/l (60 mg/dl )plasma glucose values of 3.3 mmol/l (60 mg/dl )due to:due to: 1.1 excess insulin dose (insulin shock)1.1 excess insulin dose (insulin shock) 1.2 delay in meal ingestion1.2 delay in meal ingestion 1.3 excess in physical activity1.3 excess in physical activity

2.2. Diabetic KetoacidosisDiabetic Ketoacidosiscirculating insulin is not enough to allow glucose utilizationcirculating insulin is not enough to allow glucose utilization

by peripheral tissues and to inhibit glucose productionby peripheral tissues and to inhibit glucose productionand tissue catabolismand tissue catabolism

: seen in Type 1 DM: seen in Type 1 DM3. Hyperosmolar Nonketotic Coma3. Hyperosmolar Nonketotic Coma

enough insulin is present to inhibit hepatic ketogenesisenough insulin is present to inhibit hepatic ketogenesis: (-) ketoacidosis: (-) ketoacidosis

II. Chronic ComplicationsII. Chronic Complications

A.A. Microvascular DiseasesMicrovascular Diseasessmall blood vessels (eyes, kidneyssmall blood vessels (eyes, kidneys

B. Macrovascular DiseasesB. Macrovascular Diseases““Atherosclerosis” in medium to large blood vessels Atherosclerosis” in medium to large blood vessels

(cerebral arteries, coronary arteries, arteries of the(cerebral arteries, coronary arteries, arteries of thelower limbs)lower limbs)

C. Autonomic neuropathyC. Autonomic neuropathy

Microvascular Complications:Microvascular Complications:

1.1. Diabetic RetinopathyDiabetic Retinopathyretinal capillary vasoproliferationretinal capillary vasoproliferation

: “microaneurysm”: first reliable sign of the onset of : “microaneurysm”: first reliable sign of the onset of this complicationthis complication

:cause of blindness in adults:cause of blindness in adults

2. Diabetic Nephropathy2. Diabetic Nephropathypresence of persistent proteinuria presence of persistent proteinuria (more than 0.5 g/24 hrs) in a diabetic patient (more than 0.5 g/24 hrs) in a diabetic patient with concomitant retinopathy andelevated bloodwith concomitant retinopathy andelevated blood pressure, but without urinary tract infection, pressure, but without urinary tract infection, other renal disease or heart failureother renal disease or heart failure

3. Diabetic Neuropathy3. Diabetic NeuropathyA. Peripheral neuropathyA. Peripheral neuropathy

Distal bilateral sensory changesDistal bilateral sensory changes* paresthesia* paresthesia* lancinating pain* lancinating pain* loss of vibration/ pain sensation* loss of vibration/ pain sensation

Neuropathic FootNeuropathic Foot* neuropathic ulcer* neuropathic ulcer*neuropathic joint ( Charcot’s joint)*neuropathic joint ( Charcot’s joint)* neuropathic edema* neuropathic edema

Ischemic Foot/ Diabetic FootIschemic Foot/ Diabetic Foot* mainly due to athrosclerosis of the large blood vessels* mainly due to athrosclerosis of the large blood vessels

of the legof the leg*minor trauma inducing tissue necrosis, often*minor trauma inducing tissue necrosis, often

complicated by infection complicated by infection GANGRENE GANGRENE

4. Clotting Disorders in Diabetes4. Clotting Disorders in Diabetes Hypercoagulable state due to increased fibrinogen levelsHypercoagulable state due to increased fibrinogen levels : predicts the cardiovascular problems and microvascular: predicts the cardiovascular problems and microvascular diseasedisease

5. Autonomic Neuropathy 5. Autonomic Neuropathy Less common than peripheral neuropathy Less common than peripheral neuropathy

a. Postural Hypotension: chief manifestationa. Postural Hypotension: chief manifestation b. Sexual impotenceb. Sexual impotence c. Urinary incontinencec. Urinary incontinence d. Delayed gastric emptying time (diabetic diarrhea)d. Delayed gastric emptying time (diabetic diarrhea)

Treatment Summary:Treatment Summary:Control blood sugar through:

1. Medication2.2. Appropriate nutritional intakeAppropriate nutritional intake3.3. Preventing oral infection Preventing oral infection

::underestimated significance

HOW?1. Promote preventive strategies against oral infection2. Early diagnosis of oral problems3. Utilization of dental services among diabetic patients

Address patient’s misgivings and fears regardingDental treatment

fear of uncontrolled bleeding and delayed healing

Address the dentist’s misgivings and fears in treating diabetic patients

- probable consequences of hyperglycemiaeg. Diabetic ketoacidosis

Hyperosmolar nonketotic coma-possibility of hypoglycemia