NUR 239 FINAL EXAM 2025

NUR 239 FINAL EXAM 2025 What is the pathophysiology of type 1 diabetes? -Beta cell destruction usually leading to absolute insulin deficiency. -Type IA: immune system destroys beta cells -Type IB: genetic cause What are the signs and symptoms of type 1 diabetes? -Polyuria: increased urination -Polydipsia: increased thirst -Polyphagia: increase hunger -Weight loss -Fatigue -Increased frequency of infections -Rapid onset -Insulin dependent -Familial tendency -Peak incidence from 10-15 years What is the pathophysiology of type 2 diabetes? -May range from predominantly insulin resistance with relative insulin deficiency to a predominantly secretory defect with insulin resistance. -Result of beta-cell exhaustion due to long-standing insulin resistance. -Genetics and family history put you at an increased risk 1. Stomach converts food to glucose 2. Glucose enters bloodstream 3. Pancreas produces sufficient insulin but it is resistant to effective use 4. Glucose unable to enter body effectively 5. Glucose levels increase What are risks factors for type 2 diabetes? -Sedentary lifestyle -Familial tendency -Average age 50 years -Hx of increased BP -Fatigue and decreased energy -Obese -Recurrent infections -Polyuria -Polydipsia -FBS 126 mg/dl What are the metabolic abnormalities? -Insulin resistance -failure of target cells to respond to insulin. Often predated by compensatory beta cell hyperfunction and hyperinsulinemia -Increased glucose production in liver - overproduction of glucose despite fasting hyperinsulinemia -Impaired secretion of insulin by pancreatic beta cells - may be result of decrease in Phlebotomy Phlebotomy beta cell mass, increased apoptosis, decrease regeneration of beta cells, beta cell exhaustion due to long standing insulin resistance What are the characteristics of hyperglycemia hyperosmolar state? -BG 600 mg/dL -High plasma osmolarity (pulls fluid out of cells and into extracellular fluid) -Severe dehydration, thirst -Absence of ketoacidosis (suppressed by insulin available) -Many neurological symptoms -Insidious onset -More common is Type 2 DM -May also occur with MI, acute pancreatitis, severe infections, oral or parenteral nutrition solutions -Treatment similar to DKA, but with larger amounts of IV fluid replacement What are the characteristics of diabetic ketoacidosis and what do they need to treat it? -Hyperglycemia: BG250mg/dL -Begins with polyuria, polydipsia, N, V, fatigue, stupor -Onset: over 4-10 hours -Causes: lack of insulin, GI upset, febrile illness -Symptoms: ^Breath smells like juicy fruit gum ^Kussmaul respirations ^Thirsty, dehydration, dry mouth ^Stomach pain ^Sleepiness ^Increased pulse ^Vomiting ^Flushed face ^Tachycardia ^Hypotension ^Acidosis ^High Blood Sugar (240mg/dl) ^Hyperkalemia ^Polyuria -Patient will need hydration, insulin, and electrolyte replacement. ^Regular Insulin IV push and infusion ^K+ replacement ^IV fluids (NS at first, then add Dextrose as BG lowers) ^Frequent BS checks, labs What diabetes patients are critical care? 140-180mg/dL What are the characteristics of hypoglycemia and what do they need? -BG 70 -Low blood sugar symptoms -Symptoms: ^Headache ^Shaking Phlebotomy Phlebotomy ^Hunger ^Weakness ^Feeling tired ^Sweating ^Tachycardia ^Irritability ^Restless ^Excessive hunger ^Diaphoresis ^Depression ^Anxious ^Confusion ^Blurred/Double vision ^Cool, clammy skin -Onset: Rapid. 1-3 hours. -Causes: Insufficient food, excess exercise, excess insulin -Patients need their blood sugar increased with glucose, glucagon, or dextrose (IV) What is the somogyi effect? -Rebound hyperglycemia -Cycle of insulin induced post-hypoglycemic episodes -Insulin induced hypoglycemia produces compensatory increase in blood levels of catecholamines, glucagon, cortisol, growth hormone -Causes blood glucose to become elevated -Produces some degree of insulin resistance -Hypoglycemic episode may occur at night -Requires change in diet and dose or time of insulin What is the blood sugar mnemonic? -Hot and dry: sugar high -Cold and clammy: need some candy What are the chronic complications of diabetes? -Angiopathy -Peripheral vascular disease -Retinopathy -Nephropathy -Neuropathy -Infections -Lesions What are the chronic diabetic lesions caused by? -Intracellular hyperglycemia -Excess sorbitol production alters cell function -Glycoproteins damage vessels -Elevated DAG and PKC damages vessels -Macrovascular ^Atherosclerosis, CAD, cerebrovascular disease, peripheral vascular disease, foot ulcers ^Risk factors- obesity, HTN, hyperglycemia, hyperinsulinemia, hyperlipidemia, altered Phlebotomy Phlebotomy platelet function, endothelial dysfunction, systemic inflammation, elevated fibrinogen -Microvascular ^Neuropathy, retinopathy, nephropathy What are the 4 main types of insulin and their onset, peak, and duration? How do you describe the NPH/regular combination BID? -Most common insulin regimen, but not as tight of blood glucose control as other regimens -Two daily doses of NPH + regular or insulin analog (Humalog) First dose given before breakfast - covers breakfast and lunch, peaks in afternoon -Second dose before dinner - covers dinner and through night -Instruct- ^Not to change insulin or dosages ^Notify provider if unable to take insulin What are the short acting insulins, the usage of them, route, onset, peak, and duration? -Names: Humulin R, Novolin R (regular insulin) -Use: only insulin given IV, used for DKA/HHS and acute/emergency situations -Route: IV, SubQ -Onset: 30-60 minutes -Peak: 2-3 hours -Duration: 5-7 hours What are the intermediate insulins, the usage of them, route, onset, peak, and duration? -Names: NPH, Humulin N, Novolin N -Use: long-term administration usually given in conjunction with short-acting insulin for more consistent blood glucose regulation -Route: SubQ -Onset: 1-1.5 hr -Peak: 8-12 hr -Duration: 18-24 hr What are the long acting insulins, the usage of them, route, onset, peak, and duration? -Names: glargine, detemir -Use: provides basal amount of insulin, cannot be diluted or mixed with other types of insulin, usually given at bedtime -Route: SubQ -Onset: 1 hr -Peak: No peak -Duration: 6-23 hrs A patient with diabetes mellitus asks how insulin injections help to control this disease. The nurse's best response is that insulin acts to lower blood glucose by ___? -Transporting glucose into the cell -Glycogenolysis -Gluconeogenesis -Releasing glucose from the liver What are the main classes of oral hyperglycemic agents? -Biguanides -Amylin Analogs -Sulfonylureas Phlebotomy Phlebotomy -Alpha-glucosidase Inhibitor -Dipeptidyl Peptidase-4 (DPP-4) Inhibitor -Thiazolidinediones What are the general nursing implications of oral antidiabetic meds? -Check last BG level -Monitor labs: liver and renal function tests -Note: look alike names -Make sure you have correct med -Patient teaching- see text boxes, also to avoid alcohol -Assess for improvement in BG levels, HbA1C -Assess for S&S AE -Newer meds are expensive -Some meds have Black Box Warnings What are the characteristics of metformin? -Biguanide -Anti-hyperglycemic (does not cause hypoglycemia even with large doses) -First-line drug to use -Action: Reduces production of glucose by liver and decreases intestinal absorption of glucose which increases insulin sensitivity -Use: may be use alone or in additional to other medications as needed to control blood glucose levels (layering medications) -AE: Lactic Acidosis, GI distress -Contraindications: Severe infections, trauma, major surgery, severe liver or kidney impairment (decreases glomerular filtration rate), cardiac or respiratory insufficiency -*May need to hold med prior to diagnostic tests using iodine contrast media (48 hours before and after) -Benefits: weight loss, lowers triglycerides, LDL; increases HDL -Take with meal What are the characteristics of pramlintide? -Amylin Analog -Newer drug; subcut injection -Used as an adjunct treatment with mealtime insulin to regulate glucose control during postprandial periods. -Action: slows gastric emptying -Take injection immediately before meals, mimics body's natural processes -Not mixed with insulin or near insulin injection site -Oral diabetic meds must be 1 hour before or 2 hours after injection -AE: nausea - decreases with time, severe insulin-induced hypoglycemia with type 1 DM -Contraindications - hypersensitivity, gastroparesis What are the characteristics of acarbose? -Alpha-glucosidase inhibitor -Improves HbA1C -Works best when given with sulfonylurea to control blood glucose levels -Action: inhibits alpha-glucosidase enzymes in GI tract -Delays digestion of carbohydrates and regulates blood glucose after meals Phlebotomy Phlebotomy -Slows glucose absorption -May be used in combination with insulin or oral meds such as sulfonylureas -AE: bloating, diarrhea, leukopenia, thrombocytopenia, anemia -Contraindications: DKA, hepatic disease, GI disorders (IBD, malabsorption disorder), severe renal impairment -Note can decrease digoxin levels -Take with first bite of each meal What are the characteristics of sitagliptin? -Dipeptidyl peptidase-4 inhibitor -Action: Incretin hormones stimulate insulin release in response to meals, which normalizes glucose levels -Sitagliptin minimizes (slows) rate of inactivation of incretin hormones and prolongs activity -Increases and lengthens release of insulin and decreases hepatic glucose production, promoting glycemic control -Use: Type 2 Diabetic take in addition to following diet and exercise -May also take in combination with metformin and/or TZD -AE: Upper respiratory tract infections, stuffy or runny nose, sore throat, headache -Contraindications: Type 1 Diabetes, insulin use, ketones in urine, end-stage renal disease What are the characteristics of rosiglitazone maleate? -Thiazolidinediones -"Glitazones", insulin sensitizers -Rosiglitazone maleate (Avandia) -Actions: ^stimulates receptors on muscle, fat, liver- increased uptake of glucose by peripheral tissues ^increases or restores effectiveness of insulin ^decreases insulin resistance -AE: hepatotoxicity -May take up to 12 weeks for maximum effect -Black box warning- Heart failure risk -Take with meals How do stresses damage cells? By direct damage to proteins, membranes, and DNA. What does reversible cell injury do? -Impairs function. -Doesn't cause cell death. What can aging to do a cell? Cause necrosis. What is atrophy and what are 3 examples? -Decrease in size of a tissue or organ due to decrease in cell size of individual cells or decrease in number of cells. -Ex: Disuse atrophy, denervation atrophy, and aging. What is hypertrophy? Phlebotomy Phlebotomy -Increase in size of cell and then organ and amount of functioning tissue mass. -Results from increased workload imposed on an organ. -Commonly seen in cardiac and skeletal muscle tissue, which cannot adapt to increase in workload by forming more muscle cells. What are the types of hypertrophy? -Physiologic -Pathologic -Compensatory What is and example of physiologic hypertrophy? Increased muscle mass due to exercise. What is an example of pathologic hypertrophy? Cardiomyopathy (due to HTN). What is an example of compensatory hypertrophy? -Enlargement of remaining organ after portion has been surgically removed. -Ex: kidney enlarges when one is removed. What is hyperplasia? -Increase in number of cells in response to increased demands. -Occurs in tissues with cells capable of mitotic division. (ex: epidermis, intestinal epithelium, and glandular tissue). -Ex: pregnant women and breast tissue increasing in number of cells to accommodate for breast feeding. What is an example of physiologic hyperplasia? Hormone stimulation of breast tissue during pregnancy. What is an example of pathologic hyperplasia? Skin warts (hyperplasia caused by growth factors produced by human papillomavirus). What is an example of compensatory hyperplasia? Regeneration of liver after partial removal. What is metaplasia and what is an example? -Reversible replacement of one mature cell type by another cell type. -Usually occurs in response to chronic irritation and inflammation (substitutes "hardier" cell for more fragile one). -Substitutions are within the same cell. *-Ex: Laryngeal respiratory epithelium in a smoker. What is dysplasia?* -Abnormal changes in size, shape, and organization of mature cells. -Results in cells that vary in size, shape, and appearance. -Not truly adaptive; no purpose served. -Can revert to their former structure and function OR become precancerous. What are the cardinal signs of local inflammation? -Redness -Heat -Swelling -Pain -Loss of function What is acute inflammation? Phlebotomy Phlebotomy -Rapid onset -Short duration- few minutes to several days. -Can occur with chronic inflammation -If a chronic inflammatory disease such as chronic lung disease gets worse, it becomes an acute flare-up or exacerbation. What is chronic inflammation? -At least 3 months. -May result in fibrosis and scarring. -Self perpetuating. -Develops from acute inflammation or as insidious low-grade, asymptomatic inflammatory process. -Evidence recurrent -Persistent inflammation induces/promotes/influences susceptibility to cancer. -Main WBCs are Macrophages/Monocytes and Lymphocytes. -Fibroblasts lead to higher risk for scarring. -Granuloma may form around area- walls it off. -Ex: arthritis, chronic lung disease. What are the causes of chronic inflammation? -Causes are typically low-grade, persistent infections or irritants that are unable to penetrate deeply or spread rapidly. -Foreign agents such as talc, asbestos, surgical suture material -Viruses, bacteria, fungi, Diseases that cause excessive or inappropriate activation of immune system. -Autoimmune Diseases -Obesity is newly suspected cause of chronic inflammation. What is primary intention? -Wound edges approximated and held together. -Granulation tissue grows across and epithelialization. -Clean wound that can be closed- sutured closed incision, small cut. -Usually incisions, cuts, and puncture wounds. What is secondary intention? -Wound left open. -Fills with granulation tissue from sides and bottom - slower. Infected wounds -Wounds with edges that cannot be pulled together -Ex-pressure injury. -Loss of a lot of tissue. What is pharmacotherapy/drug therapy? How are drugs classified? -Use of drugs to prev