Exam (elaborations) NR 507 Week 5 TD and Quiz Chamberlain University

Ms. Blake is an older adult with diabetes and has been too ill to get out of bed for 2 days. She has had a severe cough and has been unable to eat or drink during this time. She has a history of Type I diabetes. On admission her laboratory values show: Sodium (Na+) 156 mEq/L H Potassium (K+) 4.0 mEq/L N Chloride (Cl–) 115 mEq/L H Arterial blood gases (ABGs) pH- 7.30; Pco2-40; Po2-70; HCO3-20 METABOLIC ACIDOSIS with respiratory compensation, High anion gap Normal values Sodium (Na+) 136-146 mEq/L Potassium (K+) 3.5-5.1 mEq/L Chloride (Cl–) 98-106 mEq/L Arterial blood gases (ABGs) pH- 7.35-7.45 Pco2- 35-45 mmHg Po2-80-100 mmHg HCO3–22-28 mEq/L  List three (3) reasons on why she may have become bed ridden?  Flu? Pneumonia?  Based on these reasons what tests would you order?  Accu check? CXR? Lactic Acid level, serum and urine ketone levels  Describe the molecular mechanism of the development of ketoacidosis. (p. 744) *Pt’s who develop DKA do so bc bicarbonate buffering does not occur, which begins the development of metabolic acidosis NR 507 Week 5 TD and Quiz Chamberlain University pH 7.30 = acid CO2 40 = Normal O2 70 = Low HCO3 20 = acid Ms. Baker became bed ridden because she suffered from some sort of infection, most likely the flu, bronchitis, or pneumonia, which led to her not eating or drinking for 2 days and not checking/taking her insulin as prescribed. This is especially worrisome for patients with diabetes mellitus (DM), specifically DM type 1, since diabetic ketoacidosis (DKA) is most often seen in these patients (Papadakis & McPhee, 2017). Precipitating factors for DKA include infection, such as pneumonia and urinary tract infections, as well as trauma, stress, delayed insulin treatment or non-compliance, cocaine and other drug use, and socio-economic circumstance (Cooper, Tekiteki, Khanolkar, & Braatvedt, 2016). The patient’s medical history and presentation alone are enough to suspect DKA. The labs provided indicate a high anion gap and the arterial blood gas (ABG) shows metabolic acidosis with respiratory compensation. Assuming these labs also showed an increased serum glucose, I would also order a serum lactic acid, a urinalysis with reflex culture (UA C&S), and a chest x-ray (CXR). I would also check phosphate, blood urea nitrogen (BUN), and creatinine levels because typically these labs will be elevated in DKA patients (Papadakis & McPhee, 2017). Patients in DKA will have elevated lactic acid levels from elevated anaerobic metabolism and from tissue hypoperfusion (Papadakis & McPhee, 2017). Patients in DKA will also accumulate ketones in the blood and urine however, current literature indicates this is not the most reliable indicator for DKA (Papadakis & McPhee, 2017). Never-the-less, a UA C&S will show the amount of glucose that has spilled into the urine. I would order a CXR because Ms. Baker had a severe cough that precipitated this event; visualizing the lung fields plays an important part in her assessment and treatment. DM type 1 is an autoimmune disorder that destroys the beta cells within the pancreas, which hinders the pancreas from creating and producing sufficient insulin, causing an absolute insulin deficiency. Absolute insulin deficiency hinders glucose uptake, increases fatty acid metabolism, and speeds up ketogenesis and gluconeogenesis (McCance, Huether, Brashers, & Rote, 2013). When the cells cannot convert glucose to energy, it accumulates in the blood, essentially starving the cells (Papadakis & McPhee, 2017). This inability to convert glucose to energy signals to the liver that the cells are “hungry”, therefore the liver responds by converting glycogen to glucose, which is also released into the blood (Papadakis & McPhee, 2017). Eventually, the increased glucose overloads the renal system and glucose is excreted into the urine. Since the cells cannot use the glucose, they are basically starving, which causes the cells to metabolize protein, ultimately leading to intracellular potassium and phosphorous loss and an excess of amino acids (Papadakis & McPhee, 2017). The aftermath of this is known as osmotic diuresis, which creates a severe electrolyte imbalance and severe dehydration (Papadakis & McPhee, 2017). In DKA, another process occurs that results in metabolic acidosis called ketogenesis. The brain and the heart use ketones for energy during times of starvation (Papadakis & McPhee, 2017). Normally, the human body can buffer this process however, in DKA such large quantities are produced that the body’s ability to buffer bicarbonate is overcome (McCance et al., 2013). Patients who develop DKA do so because bicarbonate buffering fails, which in turn begins the development of metabolic acidosis (McCance et al., 2013). Cooper, H., Tekiteki, A., Khanolkar, M., & Braatvedt, G. (2016). Risk factors for recurrent admissions with diabetic ketoacidosis: A case-control observation study. Diabetic Medicine: A Journal of the British Diabetic Association, 33(4), 523-528. doi: 10.1111/dme.13004 url= direct=true&db=mdc&AN=&site=eds-live&scope=site McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (2013). Pathophysiology: The biologic basis for disease in adults and children (7th ed.). St. Louis, MO: Mosby