Diabetes Mellitus PDF

Diabetes Mellitus  Objectives between the extremes of hyperglycemia and hypoglycemia in Differentiate terms of etiology and pathophysiology. the etiology and pathophysiology of the complications of diabetes mellitus: Diabetic ketoacidosis (DKA), Hyper...

Diabetes Mellitus  Objectives between the extremes of hyperglycemia and hypoglycemia in Differentiate terms of etiology and pathophysiology. the etiology and pathophysiology of the complications of diabetes mellitus: Diabetic ketoacidosis (DKA), Hyperosmolar Describe hyperglycemic syndrome (HHS), Macrovascular disease, and Microvascular disease health assessment, medications, laboratory/diagnostic Identify findings, and interprofessional care associated with the acute and chronic complications of diabetes mellitus.  Endocrine System (5 general functions) 1. Role in productive and central nervous development in the fetus 2. Stimulating growth and development during childhood and adolescence Structures 3. Sexual reproduction and 4. Maintaining homeostasis Functions 5. Responding to emergency demands Glands ◦ Endocrine Glands ◦ Hypothalamus, pituitary, thyroid, parathyroids, adrenals, pancreas, ovaries, testes and pineal glands ◦ Make and release special chemical messengers called hormones (chemical substances that control and regulate the activity of cells and organs) Location of the major endocrine glands  Pancreas Long, tapered, a lobular soft gland located behind the stomach and anterior to the first and second lumbar vertebrae. Islets of Langerhans ◦ Make 2% of the gland ◦ Hormone secreting part of the pancreas: alpha, beta, delta, and F cells. ◦ Alpha cells secrete glucagon ◦ Beta cells secrete insulin and amylin ◦ Delta cells secrete somatostatin ◦ F cells secrete pancreatic polypeptide  Glucagon and Insulin Glucagon Alpha cells release in response to low blood glucose, protein ingestion, and exercise Increases blood glucose by providing fuel for energy by stimulating glycogenolysis (breakdown of glycogen into glucose) Gluconeogenesis (formation of glucose from non carbohydrate molecules) Ketogenesis Insulin Main regulator of metabolism and storage of ingested carbohydrates, fats, and proteins Facilitates glucose uptake into cells Storage hormone that promotes fat production and prevents fat from being down; In the liver, insulin allows glucose to be made into glycogen. Synthesis of amino acids into protein in the peripheral tissue preventing breaking down protein. Diabetes Mellitus (DM) Chronic multisystem disease ◦ Characterized by hyperglycemia from abnormal insulin production, impaired insulin use or both In the U.S ◦ 29.1 million people ◦ 9.3% of the population ◦ 86 million have prediabetes ◦ 8.1 million with diabetes have not been diagnosed or unaware ◦ 7th leading cause of death ◦ Leading cause of adult blindness, ESRD, and lower limb amputation  Etiology and Pathophysiology Causes ◦ Genetic, autoimmune, and environmental factors ◦ Primarily a disorder of glucose metabolism ◦ Regardless of its cause, a disorder of glucose metabolism related to absent or insufficient insulin supply and/or poor use of available insulin 4 Different classes of DM ◦ Type 1 (most common) ◦ Type 2 (most common) ◦ Gestational diabetes ◦ Other specific diabetes with various causes  Normal Glucose Glucose ◦ Sources of energy ◦ Food intake ◦ Carbs- broken down into glucose molecules ◦ Can be used immediately ◦ Excess is stored ◦ Insulin is needed to utilize serum glucose ◦ Protein ◦ Fat- used in place of glucose for energy if insulin is not available ◦ Ketones are released as a byproduct of this process ◦ Storage ◦ Excess glucose is converted into glycogen which is stored in the liver, fat, and muscles ◦ Function ◦ Supplies energy to the brain, heart, muscles, and every other organ Insulin Metabolism Insulin is a hormone made by the beta cells in the islets of Langerhans of the pancreas Insulin travels through the blood to your body's cells. It tells the cells to open and let the glucose in. Once inside, the cells convert glucose into energy or store it to use later. Without insulin, your body can't use or store glucose for energy. Instead, the glucose stays in your blood.  DM Diagnostic Studies Diagnosis is made by using 1 of the following 4 methods: 1. A1C of 6.5% or higher ◦ Measurement of glucose over the previous 2 to 3 months ◦ 4.0-6.0% is normal ◦ A1C of 6.5% or higher indicates DM 2. Fasting plasma glucose (FPG) level of 126 mg/dL (7.0 mmol/L) or greater. Fasting is defined as no caloric intake for at least 8 hours ◦ Pt fasts for 8 hours ◦ 70-99mg/dL ◦ Glucose of 126 mg/dL indicates DM 3. A 2-hour plasma glucose level of 200 mg/dL (11.1 mmol/L) or greater during an OGTT, using a glucose load of 75 g ◦ Pt drinks 75g of glucose ◦ Glucose is drawn at 30, 60 and 120 minutes to see ability to compensate ◦ Glucose of 200 mg/dL or higher at 120 minutes indicates DM 4. In a patient with classic symptoms of hyperglycemia (polyuria, polydipsia, unexplained weight loss) or hyperglycemic crisis, a random plasma glucose level of 200 mg/dL (11.1 mmol/L) or greater ◦ Normal range 70-120mg/dL Diabetes Diagnostic Tests Urine studies CT Scan Glucose May show tumors or No glucose should be lesions on pancreas present in the urine Ketones No ketones should be present in the urine Indicates lack of insulin and DKA Glucose Lowering Agents Exogenous (injected) Insulin ◦ All persons with type 1 diabetes require ◦ Rapid acting ◦ Lispro (Humalog) ◦ Aspart (NovoLog) ◦ Short acting ◦ Regular (Humulin R) ◦ Intermediate acting ◦ NPH (Humulin) ◦ Long acting ◦ Glargine (Lantus) ◦ Detemir (Levemir) Insulin  Allergic Reactions ◦ Local inflammatory reactions at the injection site ◦ True insulin allergy is rare Lipodystrophy and Hypertrophy ◦ Lipodystrophy: loss of subcutaneous fatty tissue ◦ Hypertrophy: thickening of the subcutaneous tissue Somogyi Effect and Dawn Phenomenon ◦ Somogyi effect: hyperglycemia in the morning Problems of ◦ High doses of insulin causes a decline in blood glucose levels during the night. As a result, counterregulatory hormones are released, rebound hyperglycemia Insulin ◦ Checking blood glucose between 2:00 and 4:00am will help determine. Therapy ◦ Dawn phenomenon: hyperglycemia present in the morning Two counterregulatory hormones are released early in the morning hours ◦ Affects many people with diabetes and is most severe in adolescence and young adult (Growth hormone peak) ◦ Careful assessment is needed to diagnose the Somogyi effect or dawn phenomenon because treatment is different. ◦ Somogyi: bedtime snack or reducing insulin or both ◦ Dawn: increase insulin dose or adjustment in administration time  Oral agents Sulfonylureas: stimulates the release of insulin Glipizide(Glucotrol) Glyburide (Micronase) Glimepiride(Amaryl) Meglitinides: stimulates the release of insulin Gepalinide (Prandin) Glucose Biguanides: decrease glucose production by the Lowering liver and increase sensitivity to insulin Metformin (Glucophage) Agents Noninsulin injectable agents Amylin: slows gastric emptying and decreases glucagon secretion from the liver Pramlintide (Symlin) Glucagon-Like Peptide-1 receptor agonists: stimulates the release of insulin and decrease glucagon secretion Dulaglutide (Trulicity)  Pathophysiology Too much insulin in proportion to available glucose in the blood Serum glucose 35 YO, now seen in children, 80-90% of clients are overweight ◦ Greater rates in Blacks, Hispanics, Native Hawaiians, Asian Americans, Pacific Islanders, and American Indians ◦ Native Americans and Alaskan Natives have the highest prevalence, and Pima Indians have the highest in the world ◦ Characterized by inadequate insulin secretion and insulin resistance ◦ Not able to make enough insulin or does not use it effectively or both ◦ Genetic link with first-degree relative, 10 times more likely to develop ◦ Metabolic syndrome ◦ Increased glucose levels, abdominal obesity, high blood pressure, high levels of triglycerides and decreased levels of high-density lipoproteins  Clinical Manifestations Nonspecific May have classic symptoms like Type 1 Polyuria, polydipsia, and polyphagia May have fatigue Recurrent infections Vaginal yeast infections Candida infections Type 2 DM Prolonged wound healing Vision problems Chronic Complications Angiopathy: damage to blood vessels from chronic hyperglycemia that lead to end-organ damage  Hyperosmolar Hyperglycemia Syndrome (HHS) This condition is characterized by hyperglycemia, hyperosmolarity, and dehydration without significant ketoacidosis who make enough insulin to prevent DKA. Less common than DKA, and differs in the magnitude of dehydration, ketosis, and acidosis. HHS usually presents in older patients over 60 y/o age with type 2 DM Carries a higher mortality rate than DKA. Life-threatening syndrome Causes of HHS o UTI, Pneumonia, Sepsis, Newly diagnosed type 2 DM, Acute illness, and Impaired thirst sensation and/or functional ability to replace fluids  Hyperosmolar Hyperglycemia Syndrome (HHS) Develops in days/weeks Fewer symptoms in early stages Blood glucose can be high before the problem is recognized More severe neurological manifestations ◦ Coma, seizures, hemiparesis and aphasia Glucose levels greater than 600 mg/dl and marked increase serum osmolality Ketone bodies are absent or minimal ◦ Has enough circulating insulin so that ketoacidosis does not occur  HHS Interprofessional Care ◦ Management is similar to DKA ◦ IV administration of insulin and IV fluids (0.9 or 0.45%) ◦ Usually requires large volumes of fluid replacement ◦ Once blood glucose drops to about 250mg/dl ◦ IV fluid containing dextrose are given to prevent hypoglycemia ◦ Hypokalemia is not as significant compared to DKA ◦ Often older and may have cardiac or renal compromise ◦ Assess vital signs ◦ Monitor I&O ◦ Cardiac monitoring  Type II Diabetes Complications Large glucose molecules begin to destroy vasculature in the body ◦ Macrovascular complications (medium to large vessels) ◦ Cerebrovascular ◦ Cardiovascular ◦ Peripheral vascular ◦ Microvascular complications (small vessels) ◦ Retinopathy ◦ Nephropathy ◦ Neuropathy  Goals ◦ Reduce symptoms and Promote well being ◦ Nutrition Therapy, Exercise, Self-monitoring of blood glucose, Medications, and ◦ Prevent acute complications related to hyperglycemia and hypoglycemia Interprofessional ◦ Infection Care DM ◦ DKA ◦ HHS ◦ Prevent or delay the onset and progression of long-term complications ◦ Neuropathy ◦ Retinopathy ◦ Nephropathy  DM Macrovascular Screening Blood glucose management:  Self-monitoring of blood glucose  Perform A1C test routinely, depending on glucose control  Lifestyle therapy (exercise, diet, attain ideal weight)  Pharmacologic therapy  A1C goal < 6.5% Blood pressure management:  Prehypertension: lifestyle therapy (diet, exercise)  Hypertension: lifestyle therapy and medications (ACE Inhibitor or ARB, and a thiazide or loop diuretic, if necessary)  Treatment goal: < 130/80  DM Macrovascular Screening Lipid Management  Measure fasting lipid profile at least annually (in those with low risk values, measure every two years)  Lifestyle and statin therapy  If targets are not reached on maximally tolerated doses of statins, combination therapy using statins and other lipid lowering agents may be considered to achieve lipid targets  Treatment goal: LDL < 100 mg/dl Antiplatelet agents  ASA therapy for women older than 50 and men older than 40 and who have at least one other risk factor (family history, smoking, dyslipidemia, HTN, albuminuria)  If allergic to ASA, use clopidogrel Smoking Cessation  Advise all patients not to smoke.  Include smoking cessation counseling and other forms of treatment as a routine component of diabetes care  DM Microvascular Screening Nephropathy ▪Perform an annual test to assess urine albumin excretion in type 1 diabetic patients with diabetes duration of 5 years and in all type 2 diabetic patients, starting at the time of diagnosis. ▪Measure serum creatinine at least annually in all adults with diabetes regardless of the degree of urine albumin excretion. The serum creatinine should be used to estimate GFR and stage the level of chronic kidney disease if present  DM Microvascular Screening Screening for microvascular disease: Retinopathy ▪Adults and children aged 10 years or older with type 1 diabetes should hav an initial dilated and comprehensive eye examination b an appropriate clinician within 5 years after the onset of diabetes. ▪Patients with type 2 diabetes should have an initial dilated and comprehensive eye examination shortly after the diagnosis of diabetes. ▪Subsequent examinations for type 1 and type 2 diabetic patients should be repeated annually. by an ophthalmologist. Less frequent exams (every 2–3 years) may be considered following one or more normal eye exams. ▪Examinations will be required more frequently if retinopathy is progressing. Normal retina vs Diabetic retinopathy Diabetic neuropathy  Diabetic Neuropathy  Education for self-care of feet to prevent ulcers and amputations  Check feet every day for abnormalities (injury)  Wear shoes/socks at all times  Protect from extremes of temperature  Wash feet every day; keep them from drying out  Wear well-fitting shoes, use custom-fit shoes if necessary  When sitting, keep feet elevated  Visit a qualified healthcare provider at least annually  Keep toenails trimmed regularly; may need toenails trimmed by a qualified health care provider on a regular basis  DM Infections More susceptible to infections like yeast infections, skin infections, and communicable infections ◦ Infections must be prompt ◦ Prevent infection by practicing good handwashing and avoid exposure to communicable illness ◦ Annual flu and pneumococcal vaccine Diabetic nephropathy Microvascular complication with damage to small blood vessels that supply the glomeruli of the kidney Leading cause of ESRD Risk factors: HTN, smoking and chronic hyperglycemia If Hemodialysis is required, several times a weeks to decrease toxins in the blood  References Harding, M., Kwong, J., Roberts, D., Hagler, D., & Reinisch, C. (2023). Lewis's medical-surgical nursing: Assessment and management of clinical problems (12th ed). Elsevier, Inc. https://pageburstls.elsevier.com/books/9780323792332