Dentistry endocrine disease
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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)
5
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