Diabetes Mellitus Presentation PDF

DIABETES MELLITUS DR. SIBI PETER, PHD,RN,CCRN  DEFINITION A CHRONIC MULTISYSTEM DISEASE RELATED TO ABNORMAL INSULIN PRODUCTION IMPAIRED INSULIN UTILIZATION OR BOTH LEADING CAUSE OF END-STAGE RENAL DISEASE ADULT BLINDNESS NONTRAUMATIC LOWER LIMB AM...

DIABETES MELLITUS DR. SIBI PETER, PHD,RN,CCRN  DEFINITION A CHRONIC MULTISYSTEM DISEASE RELATED TO ABNORMAL INSULIN PRODUCTION IMPAIRED INSULIN UTILIZATION OR BOTH LEADING CAUSE OF END-STAGE RENAL DISEASE ADULT BLINDNESS NONTRAUMATIC LOWER LIMB AMPUTATIONS MAJOR CONTRIBUTING FACTOR HEART DISEASE STROKE 2  TYPES TWO MOST COMMON TYPES TYPE 1 TYPE 2 OTHER TYPES GESTATIONAL PREDIABETES SECONDARY DIABETES 3  ETIOLOGY AND PATHOPHYSIOLOGY THEORIES LINK CAUSE TO SINGLE/ COMBINATION OF THESE FACTORS GENETIC AUTOIMMUNE VIRAL ENVIRONMENTAL NORMAL INSULIN METABOLISM PRODUCED BY THE  CELLS ISLETS OF LANGERHANS RELEASED CONTINUOUSLY INTO BLOODSTREAM IN SMALL INCREMENTS WITH LARGER AMOUNTS RELEASED AFTER FOOD STABILIZES GLUCOSE RANGE TO 70 TO 120 MG/DL 4  ETIOLOGY AND PATHOPHYSIOLOGY INSULIN PROMOTES GLUCOSE TRANSPORT FROM BLOODSTREAM ACROSS CELL MEMBRANE TO CYTOPLASM OF CELL DECREASES GLUCOSE IN THE BLOODSTREAM STIMULATES STORAGE OF GLUCOSE AS GLYCOGEN IN LIVER AND MUSCLE INHIBITS GLUCONEOGENESIS ENHANCES FAT DEPOSITION ↑ PROTEIN SYNTHESIS 5  COUNTERREGULATORY HORMONES OPPOSE EFFECTS OF INSULIN INCREASE BLOOD GLUCOSE LEVELS PROVIDE REGULATED RELEASE OF GLUCOSE FOR ENERGY HELP MAINTAIN NORMAL BLOOD GLUCOSE LEVELS EXAMPLES GLUCAGON, EPINEPHRINE, GROWTH HORMONE, CORTISOL 6  TYPE 1 DIABETES MELLITUS FORMERLY KNOWN AS “JUVENILE-ONSET” OR “INSULIN-DEPENDENT” DIABETES MOST OFTEN OCCURS IN PEOPLE YOUNGER THAN 40 YEARS OF AGE OCCURS MORE FREQUENTLY IN YOUNGER CHILDREN PROGRESSIVE DESTRUCTION OF PANCREATIC  CELLS BY BODY’S OWN T CELLS AUTOANTIBODIES CAUSE A REDUCTION OF 80% TO 90% IN NORMAL -CELL FUNCTION BEFORE MANIFESTATIONS OCCUR. 7  TYPE 1 DIABETES MELLITUS ONSET OF DISEASE LONG PRECLINICAL PERIOD ANTIBODIES PRESENT FOR MONTHS TO YEARS BEFORE SYMPTOMS OCCUR MANIFESTATIONS DEVELOP WHEN PANCREAS CAN NO LONGER PRODUCE INSULIN. RAPID ONSET OF SYMPTOMS PRESENT AT ED WITH KETOACIDOSIS WILL REQUIRE EXOGENOUS INSULIN TO SUSTAIN LIFE DIABETIC KETOACIDOSIS (DKA) OCCURS IN ABSENCE OF EXOGENOUS INSULIN LIFE-THREATENING CONDITION RESULTS IN METABOLIC ACIDOSIS 8  CLINICAL MANIFESTATIONS TYPE 1 DIABETES MELLITUS CLASSIC SYMPTOMS POLYURIA (FREQUENT URINATION) POLYDIPSIA (EXCESSIVE THIRST) POLYPHAGIA (EXCESSIVE HUNGER) WEIGHT LOSS WEAKNESS FATIGUE 9  PREDIABETES INDIVIDUALS ALREADY AT RISK FOR DIABETES BLOOD GLUCOSE HIGH BUT NOT HIGH ENOUGH TO BE DIAGNOSED AS HAVING DIABETES IFG: FASTING GLUCOSE LEVELS ARE 100 TO 125 MG/DL IGT: 2-HOUR PLASMA GLUCOSE LEVELS ARE BETWEEN 140 AND 199 MG/DL AIC IS IN RANGE OF 5.7% TO 6.4%. 10  PREDIABETES LONG-TERM DAMAGE ALREADY OCCURRING HEART, BLOOD VESSELS USUALLY PRESENT WITH NO SYMPTOMS MUST WATCH FOR DIABETES SYMPTOMS POLYURIA POLYPHAGIA POLYDIPSIA 11  TYPE 2 DIABETES MELLITUS MOST PREVALENT TYPE OF DIABETES MORE THAN 90% OF PATIENTS WITH DIABETES USUALLY OCCURS IN PEOPLE OVER 35 YEARS OF AGE 80% TO 90% OF PATIENTS ARE OVERWEIGHT. PREVALENCE INCREASES WITH AGE. GENETIC BASIS GREATER IN SOME ETHNIC POPULATIONS 12  TYPE 2 DIABETES MELLITUS ETIOLOGY AND PATHOPHYSIOLOGY PANCREAS CONTINUES TO PRODUCE SOME ENDOGENOUS INSULIN. INSULIN PRODUCED IS INSUFFICIENT OR IS POORLY UTILIZED BY TISSUES. OBESITY (ABDOMINAL/VISCERAL) MOST POWERFUL RISK FACTOR GENETIC MUTATIONS LEAD TO INSULIN RESISTANCE 13  TYPE 2 DIABETES MELLITUS - ETIOLOGY AND PATHOPHYSIOLOGY FOUR MAJOR METABOLIC ABNORMALITIES 1. INSULIN RESISTANCE BODY TISSUES DO NOT RESPOND TO INSULIN. INSULIN RECEPTORS ARE EITHER UNRESPONSIVE OR INSUFFICIENT IN NUMBER. 2. PANCREAS ↓ ABILITY TO PRODUCE INSULIN Β CELLS FATIGUED FROM COMPENSATING Β-CELL MASS LOST 3. INAPPROPRIATE GLUCOSE PRODUCTION FROM LIVER LIVER’S RESPONSE OF REGULATING RELEASE OF GLUCOSE IS HAPHAZARD. 4. ALTERATION IN PRODUCTION OF HORMONES AND ADIPOKINES PLAY A ROLE IN GLUCOSE AND FAT METABOLISM TWO MAIN ADIPOKINES ADIPONECTIN AND LEPTIN 14  CLINICAL MANIFESTATIONS TYPE 2 DIABETES MELLITUS NONSPECIFIC SYMPTOMS MAY HAVE CLASSIC SYMPTOMS OF TYPE 1 GRADUAL ONSET PERSON MAY GO MANY YEARS WITH UNDETECTED HYPERGLYCEMIA. OSMOTIC FLUID/ELECTROLYTE LOSS FROM HYPERGLYCEMIA MAY BECOME SEVERE. HYPEROSMOLAR COMA FATIGUE RECURRENT INFECTION RECURRENT VAGINAL YEAST OR MONILIA INFECTION PROLONGED WOUND HEALING VISUAL CHANGES 15  DIABETES MELLITUS DIAGNOSTIC STUDIES FOUR METHODS OF DIAGNOSIS 1. AIC ≥ 6.5% 2. FASTING PLASMA GLUCOSE LEVEL >126 MG/DL 3. RANDOM OR CASUAL PLASMA GLUCOSE MEASUREMENT ≥200 MG/DL PLUS SYMPTOMS 4. TWO-HOUR OGTT LEVEL ≥200 MG/DL WHEN A GLUCOSE LOAD OF 75 G IS USED 16  DIABETES MELLITUS DIAGNOSTIC STUDIES HEMOGLOBIN A1C TEST USEFUL IN DETERMINING GLYCEMIC LEVELS OVER TIME SHOWS THE AMOUNT OF GLUCOSE ATTACHED TO HEMOGLOBIN MOLECULES OVER RBC LIFE SPAN APPROXIMATELY 120 DAYS IDEAL GOAL ADA ≤7.0% AMERICAN COLLEGE OF ENDOCRINOLOGY 400 MG/DL INCREASE IN SERUM OSMOLALITY ABSENT/MINIMAL KETONE BODIES MEDICAL EMERGENCY HIGH MORTALITY RATE THERAPY SIMILAR TO DKA EXCEPT HHS REQUIRES GREATER FLUID REPLACEMENT 42  HYPOGLYCEMIA LOW BLOOD GLUCOSE OCCURS WHEN TOO MUCH INSULIN IN PROPORTION TO GLUCOSE IN THE BLOOD BLOOD GLUCOSE LEVEL LESS THAN 70 MG/DL COMMON MANIFESTATIONS CONFUSION IRRITABILITY DIAPHORESIS TREMORS HUNGER WEAKNESS VISUAL DISTURBANCES UNTREATED CAN PROGRESS TO LOSS OF CONSCIOUSNESS, SEIZURES, COMA, AND DEATH 43  HYPOGLYCEMIA- MANAGEMENT AT THE FIRST SIGN CHECK BLOOD GLUCOSE IF 70 MG/DL, INVESTIGATE FURTHER FOR CAUSE OF SIGNS/SYMPTOMS IF MONITORING EQUIPMENT NOT AVAILABLE, TREATMENT SHOULD BE INITIATED TREATMENT IF ALERT ENOUGH TO SWALLOW 15 TO 20 G OF A SIMPLE CARBOHYDRATE 4 TO 6 OZ FRUIT JUICE REGULAR SOFT DRINK AVOID FOODS WITH FAT DECREASE ABSORPTION OF SUGAR 44 HYPOGLYCEMIA-MANAGEMENT IF ALERT ENOUGH TO SWALLOW RECHECK BLOOD SUGAR 15 MINUTES AFTER TREATMENT. REPEAT UNTIL BLOOD SUGAR >70 MG/DL. PATIENT SHOULD EAT REGULARLY SCHEDULED MEAL/SNACK TO PREVENT REBOUND HYPOGLYCEMIA. CHECK BLOOD SUGAR AGAIN 45 MINUTES AFTER TREATMENT. PATIENT NOT ALERT ENOUGH TO SWALLOW ADMINISTER 1 MG OF GLUCAGON IM OR SUBCUTANEOUSLY. SIDE EFFECT: REBOUND HYPOGLYCEMIA HAVE PATIENT INGEST A COMPLEX CARBOHYDRATE AFTER RECOVERY. IN ACUTE CARE SETTINGS 20 TO 50 ML OF 50% DEXTROSE IV PUSH 45  MEDICAL ALERT. Medical alerts. A patient with diabetes should carry a card and wear a bracelet or necklace that indicates diabetes. If the patient with diabetes is unconscious, these measures will ensure prompt and appropriate attention. 46  CHRONIC COMPLICATIONS ANGIOPATHY MACROVASCULAR DISEASES OF LARGE AND MEDIUM-SIZED BLOOD VESSELS TIGHT GLUCOSE CONTROL MAY DELAY ATHEROSCLEROTIC PROCESS. RISK FACTORS OBESITY SMOKING HYPERTENSION HIGH FAT INTAKE SEDENTARY LIFESTYLE 47  CHRONIC COMPLICATIONS ANGIOPATHY MICROVASCULAR RESULT FROM THICKENING OF VESSEL MEMBRANES IN CAPILLARIES AND ARTERIOLES IN RESPONSE TO CHRONIC HYPERGLYCEMIA IS SPECIFIC TO DIABETES, UNLIKE MACROVASCULAR AREAS MOST NOTICEABLY AFFECTED EYES (RETINOPATHY) KIDNEYS (NEPHROPATHY) SKIN (DERMOPATHY) CLINICAL MANIFESTATIONS USUALLY APPEAR AFTER 10 TO 20 YEARS OF DIABETES. 48  CHRONIC COMPLICATIONS DIABETIC RETINOPATHY MICRO VASCULAR DAMAGE TO RETINA RESULT OF CHRONIC HYPERGLYCEMIA MOST COMMON CAUSE OF NEW CASES OF BLINDNESS IN PEOPLE 20 TO 74 YEARS EARLIEST AND MOST TREATABLE STAGES OFTEN PRODUCES NO CHANGES IN VISION MUST HAVE ANNUAL DILATED EYE EXAMINATIONS FOR TYPE 1 DIABETES 49  CHRONIC COMPLICATIONS DIABETIC NEPHROPATHY ASSOCIATED WITH DAMAGE TO SMALL BLOOD VESSELS THAT SUPPLY THE GLOMERULI OF THE KIDNEY LEADING CAUSE OF END-STAGE RENAL DISEASE CRITICAL FACTORS FOR PREVENTION/DELAY TIGHT GLUCOSE CONTROL BLOOD PRESSURE MANAGEMENT ANGIOTENSIN-CONVERTING ENZYME (ACE) INHIBITORS USED EVEN WHEN NOT HYPERTENSIVE ANGIOTENSIN II RECEPTOR ANTAGONISTS YEARLY SCREENING MICROALBUMINURIA IN URINE SERUM CREATININE 50  CHRONIC COMPLICATIONS DIABETIC NEUROPATHY 60% TO 70% OF PATIENTS WITH DIABETES HAVE SOME DEGREE OF NEUROPATHY NERVE DAMAGE DUE TO METABOLIC DERANGEMENTS OF DIABETES SENSORY VERSUS AUTONOMIC NEUROPATHY SENSORY NEUROPATHY DISTAL SYMMETRIC MOST COMMON FORM AFFECTS HANDS AND/OR FEET BILATERALLY CHARACTERISTICS INCLUDE LOSS OF SENSATION, ABNORMAL SENSATIONS, PAIN, AND PARESTHESIA FOOT INJURY AND ULCERATIONS CAN OCCUR WITHOUT THE PATIENT HAVING PAIN. 51  SENSORY NEUROPATHY TREATMENT TIGHT BLOOD GLUCOSE CONTROL DRUG THERAPY TOPICAL CREAMS TRICYCLIC ANTIDEPRESSANTS SELECTIVE SEROTONIN AND NOREPINEPHRINE REUPTAKE INHIBITORS ANTISEIZURE MEDICATIONS 52  AUTONOMIC NEUROPATHY DIABETIC NEUROPATHY CAN AFFECT NEARLY ALL BODY SYSTEMS COMPLICATIONS GASTROPARESIS DELAYED GASTRIC EMPTYING CARDIOVASCULAR ABNORMALITIES SEXUAL DYSFUNCTION NEUROGENIC BLADDER 53  COMPLICATIONS OF FOOT AND LOWER EXTREMITY FOOT COMPLICATIONS MOST COMMON CAUSE OF HOSPITALIZATION IN DIABETES RESULT FROM COMBINATION OF MICROVASCULAR AND MACROVASCULAR DISEASES RISK FACTORS SENSORY NEUROPATHY PERIPHERAL ARTERIAL DISEASE OTHER CONTRIBUTORS SMOKING CLOTTING ABNORMALITIES. IMPAIRED IMMUNE FUNCTION AUTONOMIC NEUROPATHY 54  NECROTIC TOE BEFORE AND AFTER AMPUTATION The necrotic toe developed as a complication of diabetes. A, Before amputation. B, After amputation. 55  Student Response Question IDEALLY, THE GOAL OF PATIENT DIABETES EDUCATION IS TO: 1. MAKE ALL PATIENTS RESPONSIBLE FOR THE MANAGEMENT OF THEIR DISEASE. 2. INVOLVE THE PATIENT’S FAMILY AND SIGNIFICANT OTHERS IN THE CARE OF THE PATIENT. 3. ENABLE THE PATIENT TO BECOME THE MOST ACTIVE PARTICIPANT IN THE MANAGEMENT OF THE DIABETES. 4. PROVIDE THE PATIENT WITH AS MUCH INFORMATION AS SOON AS POSSIBLE TO PREVENT COMPLICATIONS OF DIABETES. 56  Student Response Question A PATIENT SCREENED FOR DIABETES AT A CLINIC HAS A FASTING PLASMA GLUCOSE OF 125 MG/DL. THE NURSE EXPLAINS TO THE PATIENT THAT THIS VALUE: 1. IS DIAGNOSTIC FOR DIABETES. 2. IS NORMAL, AND DIABETES IS NOT A PROBLEM. 3. REFLECTS IMPAIRED GLUCOSE TOLERANCE, WHICH IS A PREDIABETIC STATE. 4. INDICATES AN INTERMEDIATE STAGE BETWEEN NORMAL GLUCOSE USE AND DIABETES. 57  Student Response Question A PATIENT WITH TYPE 1 DIABETES CALLS THE CLINIC WITH COMPLAINTS OF NAUSEA, VOMITING, AND DIARRHEA. IT IS MOST IMPORTANT THAT THE NURSE ADVISE THE PATIENT TO: 1. HOLD THE REGULAR DOSE OF INSULIN. 2. DRINK COOL FLUIDS WITH HIGH GLUCOSE CONTENT. 3. CHECK THE BLOOD GLUCOSE LEVEL EVERY 2 TO 4 HOURS. 4. USE A LESS STRENUOUS FORM OF EXERCISE THAN USUAL UNTIL THE ILLNESS RESOLVES. 58  Student Response Question CARDIAC MONITORING IS INITIATED FOR A PATIENT IN DIABETIC KETOACIDOSIS. THE NURSE RECOGNIZES THAT THIS MEASURE IS IMPORTANT TO IDENTIFY: 1. DYSRHYTHMIAS RESULTING FROM HYPOKALEMIA. 2. FLUID OVERLOAD RESULTING FROM AGGRESSIVE FLUID REPLACEMENT. 3. THE PRESENCE OF HYPOVOLEMIC SHOCK RELATED TO OSMOTIC DIURESIS. 4. CARDIOVASCULAR COLLAPSE RESULTING FROM THE EFFECTS OF EXCESS GLUCOSE ON CARDIAC CELLS. 59