Diabetes Mellitus Exam 2: Metabolism - Lakeland Community College PDF

LAKELAND COMMUNITY COLLEGE URS 1250 NURSING CARE OF ADULTS II EXAM 2 CONCEPT OF METABOLISM DIABETES MELLITUS ROWENA A. BAUTISTA, MSN, RN, CMSRN TOPIC OUTLINE o US Data & Statistics o Overview & Pathophysiology o Clinical Man...

LAKELAND COMMUNITY COLLEGE URS 1250 NURSING CARE OF ADULTS II EXAM 2 CONCEPT OF METABOLISM DIABETES MELLITUS ROWENA A. BAUTISTA, MSN, RN, CMSRN TOPIC OUTLINE o US Data & Statistics o Overview & Pathophysiology o Clinical Manifestations o Contributing Factors o Screening Tests o Pathological Outcomes o Clinical Management US DATA & STATISTICS  Pre- Diabetes Diabetes Yearly 11.2% of the 29% of the Cost US adult US population $413 Billion population (38 million) (98 million) US DIABETES DATA & ANNUAL COSTS US DATA & STATISTICS: CULTURAL CONSIDERATIO NS American Indians/Alaska Natives – 16% Black, non-Hispanic – 12.5% Hispanic – 10.3% Asian, non-Hispanic – 9.2% White, non-Hispanic – 8.5% Risk of early death is 60% higher. Medical costs as twice as high. Higher risk of serious health complications: Heart disease Stroke Kidney failure Blindness Amputation US DATA & STATISTICS: DIABETES RISKS, MORTALITY, COSTS, & COMPLICATIONS US DATA & STATISTICS: DIABETES AND OBESITY 30.7% of US adult population are overweight —34.1% are men —27.5% are women 42.4% have obesity, including severe obesity 16.1% of children and adolescents ages 2 to 19 are overweight — 19.3% have obesity — 6.1% have severe obesity IMPACT OF OBESITY ON CARDIOMETA BOLIC HEALTH FAT CLASSIFICATI ONS BMI, OBESITY, AND DIABETES: A CLEAR CONNECTION ENDOCRINE SYSTEM FUNCTIONS OF ENDOCRINE HORMONES PANCREAS AND SERUM GLUCOSE  GLUCOSE 101 Monosaccharide Functions: —Energy source —Brain fuel —Glycogen storage —Regulator —Overall metabolism GLYCEMIC EFFECTS Sources: —Dietary —Endogenous production When we ingest food —CHO → glucose —Absorbed from intestines into the blood. When blood glucose ↑ —Pancreas is triggered to secrete insulin. SERUM GLUCOSE AND CELL ENERGY  INSULIN Insulin — Hormone made by β cells in the Islets of Langerhans of the pancreas. — The key to open the cell membrane. Prandial – peaks after meal. Basal – continuous release. Bolus – released in response to ↑ in blood glucose.  INSULIN REGULATORY FUNCTIONS Promotes cellular uptake of glucose, amino acids (protein) and fats. Regulate carbohydrates. Metabolize lipid and protein. Promotes cell division and growth. INSULIN MECHANISM OF ACTION ENDOGENOUS INSULIN SECRETION PATTERN DIABETES MELLITUS A chronic, metabolic disorder that affects how the body turns food into energy related to: —Insulin deficiency —Insulin resistance Greek word Diabeinein, meaning “siphon” Latin word Mellitus, meaning “sweetened with honey”  Pallor, moist skin Shakiness Hungry and angry TYPES OF DIABETES IATROGENIC DIABETES Glucocortico Antipsychoti ids cs Antiretrovira Immune l Inhibitors  GESTATIONAL DIABETES Glucose intolerance in pregnancy. ↑ insulin resistance 20 placental hormones. Inadequate insulin secretion for increased insulin needs. Potential progression to diabetes >30% over 15 years.  MATERNAL OBESITY AND GDM GDM increased from 6.0% in 2016 to 8.3% in 2021. – CDC, 2023 Obesity promotes insulin resistance. Complications: —Mother: preeclampsia —Baby: macrosomia MATURITY-ONSET DIABETES OF THE YOUNGS (MODY) Less common. Autosomal dominant. Caused by mutation in a single gene. Typically develops before age 25. TYPE 1 DIABETES MELLITUS Autoimmune —Destruction of the β cells of the Islets of Langerhans. —80%-90% of β cells functions are lost before symptoms. Insulin-dependent DM TYPE 1 DIABETES MELLITUS Additional Factors: —Exposure to virus —Exposure to certain climates —Gestation period and maternal weight  “3 Ps” —Polyuria —Polydipsia —Polyphagia Less common symptoms: —Tiredness —Weight loss —Gastrointestinal symptoms TYPE 1 DM: RECOGNIZE CUES TYPE 2 DIABETES MELLITUS Insulin resistance. β cell dysfunction. Reduced glucose uptake by muscles and fat cells. ↑ glucose release and production by the liver.  CELLULAR FUNCTION IN HEALTHY BODY VS T2DM TYPE 2 DM: RECOGNIZE CUES TYPE I VERSUS TYPE 2  INSULIN REGULATION: NORMAL, T1DM & T2DM CONTRIBUTING FACTORS  Obesity T2D Hypertensi on M MODIFI ABLE Sedentar y RISKS Lifestyle Elevated Choleste rol  Age T2D Family History M NON- MODIFI Race, ABLE Ethnicity RISKS Medical Conditio ns DIABETES MELLITUS: METABOLIC SYNDROME Cluster of risk factors that raises your risk for heart disease and other health problems, such as Diabetes SCREENING TESTS HEMOGLOBIN A1C HBA1C GLYCATED HEMOGLOBIN GLYCOHEMOGLOBI N Amount of glucose attached to Hgb over the life of the RBC for 120 days UNDERSTAN DING HEMOGLOBI N A1C HEMOGLOBI N A1C CONVERSIO N CHART FASTING BLOOD SUGAR (FBS)  ORAL GLUCOSE TOLERANCE TEST (OGTT) NPO x 8 hours prior to the test. BGM prior to the test. Drink glucose solution. BGM after 2 hours. STAGES OF GLUCOSE TOLERANCE C-PEPTIDE TEST (0.5-2.7 NG/ML) Type 2 DM ↑ Insulinoma Cushing’s Syndrome Level Kidney Disease Type 1 DM ↓ Addison’s Disease Level Liver Disease  HYPOGLYCEMIA “Insulin Shock” “The Lows” Usually less than 70 mg/dl. May cause patient to become unresponsive. Consider any unconscious person hypoglycemic. HYPOGLYCEMIA: ETIOLOGY Reactive hypoglycemia —Too much insulin/oral diabetics. Fasting hypoglycemia —Too little food/delayed eating. Kidney disease/failure. Strenuous physical activity. Excessive alcohol consumption.  Pallor, moist skin Shakiness Hungry and angry RECOGNIZE CUES  HYPOGLYCE MIA: ADDITIONAL CUES HYPOGLYCEMIA PROTOCOL Follow the “15/15 rule” —Check blood sugar —Treat depending on severity of symptoms —Wait 15 minutes —Recheck blood sugar —If