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DIABETES MELLITUS
Diabetes is the most common endocrine disease .It is a group of disease marked by high levels of blood glucose resulting from defects in insulin production.
DEFINITION
CLASSIFICATION
1.TYPE 1- Insulin dependent or juvenile onset. Immune mediated Idiopathic 2. TYPE 2-Non Insulin dependent or adult onset. Genetic defects of beta cell function Genetic defects of insulin action Disease of exocrine pancrease Drug chemical induce Infections 3.GESTATIONAL DIBETES MELLITUS 4.IMPAIRED GLUCOSE TOLERENCE 5.IMPAIRED FASTING GLUCOSE
TYPE 1 DM
It can occur at any age but is more common among children and young adults. The peak age onset is 10 to 14 yrs. It is characterized by insulin deficiency. In DM circulating insulin is essentially absent. TYPE 2 DM Non-ketotic form of diabetes that is not linked to humans lymphocyte antigen markers on the 6th chromosomes. High incidence of obesity. GESTATIONAL DM It is characterized by abnormal result on the oral glucose tolerance test taken during pregnancy. Risk of prenatal illness and death in all levels of disease severity. IMPAIRED GLUCOSE TOLERANCE/IMPAIRED FASTING GLUCOSE TOLERANCE: Persons with IGT have plasma glucose level between 140 199 mg/dl after a 2 hr oral glucose tolerance test. IFGT The fasting blood sugar level is 100 125mg/dl.
DM RISK FACTORS
Age above 45 yrs BMI Habitual physical activity High risk ethinicity H/O child weight greater than 9 pounds at birth H/O gestational diabetes Hypertension Triglycerides 250 mg/dl Cholestrol 35 mg/dl H/O vascular disease
COMPLICATIONS
ACUTE COMPLICATIONS Hypoglycemia Diabetic ketoacidosis Hyperglycemia CHRONIC COMPLICATIONS Microvasculature Cardiovascular system- Artherosclerosis,Large vessel disease,Microangiopathy. Eyes Retinopathy,Catract , Glaucoma. Kidney- Diabetic glomerulonephritis. Nerves- Motor ,sensory , autonomic neuropathy. Mouth- Gingivitis, Increased dental caries and Periodontal disease. Skin- Pruritis, Mycosis, Diabetic xanthoma.
HYPERGLYCEMIA
ETIOLOGY
High blood sugar Weight gain Cessation of exercise Pregnancy Hyperthyroidism Corticosteroid theraphy Fever Acute infection Hyperglycemia Acidosis with blood PH- 7.3 Dry warm skin Fruity, sweet breath odour Normal to low BP Rapid weak pulse Altered level of consciousness
SIGNS
SYMPTOMS
TYPE 1 DM Repeated skin infection Marked irritability Headache Drowsiness Malaise Dry mouth TYPE 2 DM Decresed vision Parasthesia Loss of sensation Postural hypotension
CLINICAL MANIFESTATION
TYPE 1
POLYURIA POLYDIPSIA POLYPHAGIA WITH WT LOSS RECURRENT BLURRED VISION VULVOVAGINITIS OR PRURITIS LOSS OF STRENGTH NOCTURNAL ENURESIS ABSENCE OS AYMPTOMS
TYPE 2
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MANGEMENT
RECOGNIZE PROBLEM ( Lack of response to sensory stimulation)
HYPOGLYCEMIA
ETIOLOGY
Weight loss Increased physical exercise Termination of pregnancy Termination of other drug therapies Recovery from infection and fever Inadequate food( Carbohydrate intake) Excessive insulin dose Sulfonyl urea theraphy Ethanol intake
SIGNS
Weakness, Dizziness Pale moist skin Normal or depressed respiration Headache Altered level of consciousness
CLINICAL MANIFESTATION
EARLY STAGE Mild reaction
Diminished cerebral function Changes in mood Decreased spontaneity Hunger Nausea
MANGEMENT
RECOGNIZE THE PROBLEM
( Altered consciousness)
DISCONTINUE DENTAL TREATMENT ACTIVE OFFICE EMERGENCY TEAM P- POSITION PATIENT COMFORTABLY A-B-C ASSESS AND PERFORM BASIC LIFE SUPPORT AS NEDDED
DIABETIC KETOACIDOSIS:
Diabetic ketoacidosis (DKA) is a potentially life-threatening complication in patients with diabetes mellitus. It happens predominantly in those with type 1 diabetes, but it can occur in those with type 2 diabetes under certain circumstances. DKA results from a shortage of insulin; in response the body switches to burning fatty acids and producing acidic ketone bodies that cause most of the symptoms and complications. Signs and symptoms Predominant symptoms are nausea and vomiting, pronounced thirst, excessive urine production and abdominal pain that may be severe. Coffee ground vomiting (vomiting of altered blood) occurs in a minority of patients; this tends to originate from erosion of the esophagus.[3] In severe DKA, there may be confusion, lethargy, stupor or even coma (a marked decrease in the level of consciousness). MANAGEMENT: 1 Fluid replacement
2 Insulin
3 Potassium 4 Bicarbonate 5 Cerebral edema
MANAGEMENT BY DRUGS
Metfromin Rosiglitazone Glipizide Acarbose Repaglinide
EPILEPSY
DEFINITION
RECURRENT PAROXYSMAL DISORDER OF CEREBRAL FUNCTION MARKED BY SUDDEN , BRIEF ATTACKS OF ALTERED CONSCIOUSNESS MOTOR ACTIVITY OR SENSORY PHENOMENA. CAUSES Congenital abnormalities Perinatal injuries Metabolic and toxic disorders Head trauma Tumors and other space occupying lesions Vascular disease Infectious disease
MANAGEMENT
RECOGNIZE PROBLEM ( Lack of response to sensory stimulation) DISCONTINUE THE DENTAL TREATMENT ACTIVE OFFICE EMERGENCY TEAM AS NEDDED POSITION THE PT IN SUPINE POSITION WITH FEET ELEVATED
Seizure continues( 75 mins), active emergency medical services A-B-C Perform basic life support
PREMODAL PHASE RECOGNIZE AURA DISCONTINUE DENTAL TREATMENT ICTAL PHASE ACTIVATE OFFICE EMERGENCY TEAM P-POSITION PATIENT IN SUPINE POSTION WITH FEET ELEVATED CONSIDER ACTIVATION OF EMERGENCY MEDICAL SERVICES A-B-C ASSESS & PERFORM BASIC LIFE SUPPORT AS NEEDED
PREMODAL PHASE RECOGNIZE AURA DISCONTINUE DENTAL TREATMENT ICTAL PHASE ACTIVATE OFFICE EMERGENCY TEAM P-POSITION PATIENT IN SUPINE POSTION WITH FEET ELEVATED CONSIDER ACTIVATION OF EMERGENCY MEDICAL SERVICES A-B-C ASSESS & PERFORM BASIC LIFE SUPPORT AS NEEDED
NEW DRUGS
Oxcarbazepine Felbamate Tiagabine