NR 507 Week 5 TD and Quiz Chamberlain University (NR507)

Exam (elaborations) NR 507 Week 5 TD and Quiz Chamberlain University (NR507) PART 1: 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. Papadakis, M. & McPhee, S. (Eds.). (2017). Current medical diagnosis and treatment. New York, NY: McGraw Hill. PART 2: A three-month-old baby boy comes into your clinic with the main complaint that he frequently vomits after eating. He often has a swollen upper belly after feeding and acts fussy all the time. The vomiting has become more frequent this past week and he is beginning to lose weight.  Write three (3) differential diagnoses at this time?  Is there any genetic component to the top of your differentials?  What tests would you order? Pyloric Stenosis – Pyloric stenosis (PS), also referred to as infantile hypertrophic pyloric stenosis (IHPS) is depicted by obstruction of gastric emptying related to atypical thickening in the antropyloric section of the stomach (Dogar, Mehdi, Gautam, Abbas, Fareeda, & Rageh, 2015). PS is most common in early infancy, such as weeks 1 and 2 or at months 3 and 4 and it occurs more often in males than females (McCance, Huether, Brashers, & Rote, 2013). Vomiting, usually forceful and projectile, happens right after eating and babies usually want to eat again after vomiting. Food retention is characteristic and can been seen 4 hours after eating unless the baby has vomited (McCance et al., 2013). These babies are usually constipated, which can attribute to some of their fussiness. In advanced cases, severe fluid and electrolyte imbalances can occur as well as weight loss and irritability related to hunger and esophagitis (McCance et al., 2013). Distention around the antrum can occur, which decreases after vomiting (Olivé & Endom, 2017). It has been noted that there is an increased prevalence of PS in infants born into families with a history of PS, leading medical professionals to propose a possible genetic predisposition (McCance et al., 2013). Palpating the abdomen can reveal the hypertrophied pylorus in some infants however, the infant must be relaxed and the area over the antrum must not be distended, making this a difficult task most of the time (Olivé & Endom, 2017). If the hypertrophied pylorus can be palpated, it will feel like an olive and can be felt at the lateral portion of the abdominal muscle located in the right upper quadrant (Olivé & Endom, 2017). Laboratory testing can be ordered to check for abnormal electrolytes, such as low serum chloride and potassium, elevated bicarbonate, and/or hyper or hyponatremia (Olivé & Endom, 2017). Per one study, 88 percent of patients with a pH greater than 7.45, chloride less than 98, and a base excess greater than 3 were positive predictors in diagnosing PS (Olivé & Endom, 2017). Imaging is a good diagnostic tool, specifically ultrasound, barium studies, and endoscopy (Olivé & Endom, 2017). Ultrasound is the diagnostic imaging of choice when PS is suspected (Dogar et al., 2015). The treatment for PS is a pyloromyotomy (McCance et al., 2013). This is the most likely diagnosis however, an ultrasound would need to be completed to confirm the diagnosis and rule out other disorders that present with similar symptoms, such as intestinal malrotation. Intestinal Malrotation – Intestinal malrotation (IM) is a congenital disorder where the colon does not rotate out of the right upper quadrant (McCance et al., 2013). If this happens, the abnormal membrane can cause an obstruction (McCance et al., 2013). One of the most significant findings associated with malrotation is a periduodenal band, which is a band that obstructs the duodenum (McCance et al., 2013). In malrotation, the small intestines do not fixate posteriorly, as they should. Instead, there is limited attachment near the beginning of the mesenteric artery. This can cause the intestines to twist on themselves, also called volvulus, from the duodenojejunal junction to the mid transverse colon (McCance et al., 2013). When intestinal twisting occurs at the beginning of the mesentery, it obstructs the intestinal lumen, which, in turn partially or fully occludes the superior mesenteric artery, causing an intestinal infarct and necrosis of the whole midgut (McCance et al., 2013). Clinical manifestations for IM include abdominal distension, vomiting after feeding, pain, scanty stools, diarrhea, bloody stools, fever, and severe dehydration can occur after IM progresses. Per McCance et al. (2013), diagnosis is dependent upon accurate reporting of clinical manifestations and imaging studies. A chest x-ray should be performed to exclude perforation however, it is not the best diagnostic tool for malrotation (Brandt, 2017). Ultrasound is the preferred imaging study for malrotation screening (Brandt, 2017). Treatment for IM is laparoscopic or open abdomen surgery to either reduce the volvulus or resect the bowel (Brandt, 2017). While I believe the problem is pyloric stenosis, intestinal malrotation is a very plausible diagnosis as well. Imaging studies must be ordered to confirm diagnosis. Gastroesophageal Reflux – Gastroesophageal reflux (GER) occurs when the contents of the stomach return up to the esophagus related to the lower esophageal sphincter being relaxed or incompetent (McCance et al., 2013). GER is typical in newborns, especially in premature infants, and usually subsides between 6 to 12 months (McCance et al., 2013). Reflux will remain if any pressure-maintaining factors continue to be altered (McCance et al., 2013). GER becomes gastroesophageal reflux disease (GERD) when the bodies protective mechanisms become or remain inadequate, resulting in complications like erosion of the mucosa, dysphagia, failure to thrive, and bleeding (McCance et al., 2013). Infants with GER typically experience excessive vomiting during their first week and by 6 weeks experience additional symptoms such as refusing to eat or difficulty with feedings and failure to thrive (McCance et al., 2013). The infants vomiting may be forceful and therefore the practitioner must make the distinction between GER and PS (McCance et al., 2013). The excessive vomiting will cause insufficient nutrient absorption, which will affect the infant’s growth and ability to gain weight (McCance et al., 2013). Methods used to diagnose GERD include esophageal pH monitoring and endoscopy with biopsy (McCance et al., 2013). Patients with mild GER tend to resolve with specific techniques which help decrease reflux, including longer feeding times with a slower flow rate, small but frequent feedings, and frequent burping (McCance et al., 2013). Medications are not advised for infants and small children, therefore surgical procedures are typically performed. I do not believe this is the diagnosis however, the clinical manifestations can present similarly to PS and all other disease processes should be ruled out. Brandt, M. (2017). Intestinal malrotation in children. UpToDate. Retrieved from source=search_result&search=intestinal malrotation&selectedTitle=1~41 Dogar, I.H., Mehdi, A., Gautam, M., Abbas, F., Fareeda, & Rageh, A. (2015). Diagnostic accuracy of gray scale and colour Doppler ultrasound in the diagnosis of infantile hypertrophic pyloric stenosis. Annals of King Edward Medical University, 21(3), 155-158. url= direct=true&db=a9h&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. Olivé, A. & Endom, E. (2017). Infantile hypertrophic pyloric stenosis. UpToDate. Retrieved from stenosis?source=search_result&search=pyloric stenosis children&selectedTitle=1~76 - H PART 3: Write a one (1) paragraph case study of your own for a patient with Ulcerative Colitis? Elizabeth is a 33 year old Caucasian female who presents to the office with complaints of watery, bloody, diarrhea, cramping, urgency, and fever. She states that she has experienced the diarrhea, cramping and urgency before however, these symptoms have been worse and consistent over the past 3 days. Elizabeth stated that she assumed it was just “a bug” that was going around or that she ate something bad. However, she has not been able to eat or drink for 3 days because of the pain she experiences after eating. She has progressively become weaker, when she realized she had a fever she decided to come to the office. Upon examination, Elizabeth is found to have a temperature of 100.4, she is tachycardic at 112 beats per minute, and her abdomen is tender upon palpation. Elizabeth denies having any allergies and denies a history of smoking. For Elizabeth, a stool sample should be obtained to rule out infectious colitis and to confirm if blood, pus, and/or mucus is present (Papadakis & McPhee, 2017). Lab work such as hematocrit (low), white blood cells (low), serum albumin (low), potassium (low), magnesium (low), and sedimentation rates (elevated) will be abnormal (Papadakis & McPhee, 2017). An x-ray with contrast can be ordered however, it is only helpful in moderate to severe disease processes. In moderate to severe disease, the normal haustral folds will be lacking and the x-ray will show a lead pipe like appearance instead. Ulcerative colitis (UC) typically starts in the rectum and can extend into the colon as the disease continues to advance (Casey, 2017). Therefore, a sigmoidoscopy and colonoscopy should be ordered to evaluate the extent of involvement and a biopsy should be obtained during the endoscopic procedure to confirm the disease (Papadakis & McPhee, 2017). Treatment of UC depends on the severity of the disease and can include diet modifications, topical mesalamine, topical corticosteroids, oral aminosalicylates (if patient is unable to use or tolerate topical medications), anti-TNF agents (adalimumab, infliximab, and golimumab), vedolizumab, probiotics, cyclosporine, and surgery (Papadakis & McPhee, 2017). Casey, G. (2017). Inflammatory bowel disease. Kai Tiaki Nursing New Zealand, 23(2), 20-26. url= direct=true&db=rzh&AN=&site=eds-live&scope=site Papadakis, M. & McPhee, S. (Eds.). (2017). Current medical diagnosis and treatment. New York, NY: McGraw Hill. PEER: Hi Christina, Great job on your post! Diabetic ketoacidosis (DKA) is a life-threatening