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Analyze pathophysiologic mechanisms associated with selected disease states. No unread replies. No replies. Week 5 Summary Hello Class, Congratulations on completing Week 5! The course outcomes for this week were: Course Outcomes Program Outcomes 1 Analyze pathophysiologic mechanisms associated with selected disease states. (PO 1) 2 Differentiate the epidemiology, etiology, developmental characteristics, pathogenesis and clinical and laboratory manifestations of specific disease processes. (PO 1) 3 Examine the way in which homeostatic, adaptive, and compensatory physiological mechanisms can be supported and/or altered through specific therapeutic interventions. (PO 1,7) 4 Distinguish risk factors associated with selected disease states. (PO 1) 5 Describe outcomes of disruptive or alterations in specific physiologic processes. (PO 1) 6 Distinguish risk factors associated with selected disease states. (PO 1) 7 Explore age-specific and developmental alterations in physiologic and disease states. (PO 1, 4) Case Study Summary Discussion Part 1 (graded) 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 Potassium (K+) 4.0 mEq/L Chloride (Cl–) 115 mEq/L Arterial blood gases (ABGs) pH- 7.30; Pco2-40; Po2-70; HCO3-20 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 five (3) reasons on why she may have become bed ridden? Based on these reasons what tests would you order? Describe the molecular mechanism of the development of ketoacidosis. What is the general differential? 1. Diabetic Ketoacidosis 2. Hyperglycemic hyperosmolarity 3. Dehydration 4. Sepsis 5. Acute kidney damage Assuming that DKA is likely, what could have caused her sudden decline? 1. Respiratory infection 2. Dehydration 3. Medication non-compliance 4. Stroke 5. Sepsis What tests are appropriate? Blood glucose every 1-2hrs until stable, every 4-6 after that. Electrolytes q1-2hr, q4-6 once stable. Calculate anion gap (likely very high in a DKA patient). Repeat ABG Initial BUN to assess renal function and possible acute kidney injury. What symptoms would you expect to find in Ms. Blake? Those of ketoacidosis: tachypnea, confusion, lethargy, decreased level of consciousness, cardiac arrhythmias, and fruity acetone breathe (a break down ketone product acetone from either acetoacetate or alpha hydroxybutyrate). What would be the treatment? Insulin (short and long acting), ringers lactate or 0.45 saline, oxygen, and monitor K and Na. Be sure to anticipate the drop in K that will come when you correct the acidosis with fluids and insulin and begin preemptively replacing K. Molecular mechanism of ketoacidosis: In uncontrolled diabetes hepatic gluconeogenesis and serum glycogenolysis increase and exacerbate hyperglycemia. Lipolysis leads to metabolism of free fatty acids which produces ketones and ketoacids. Ketone bodies are produced when oxaloacetate enters the glugoneogenesis process rather than the citric acid cycle when insulin deficiency produces high levels of acetyl co-A. Ketones, such as beta-hydroxybutyrate, acetone, and acetoacetate then build up in the blood. Discussion Part Two 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 Differential diagnoses: 1. Pyloric stenosis which “is an obstruction of the pyloric sphincter caused by hypertrophy of the sphincter muscle.” (McCance, et al, 2013, p. 1488). 2. Gastrointestinal Reflex Disease (GERD) 3. Lactose Intolerance Is there any genetic component to the top of your differentials? The incidence of pyloric stenosis among males is approximately 5 in 1000, whereas among females it is only 1 in 1000. Whites are affected more often than blacks or Asians, and full-term infants are affected more often than premature infants. There is an increased incidence of pyloric stenosis in those children who have a family member with pyloric stenosis, suggesting a genetic predisposition. What tests would you order? A firm, small, movable mass, approximately the size of an olive, can be palpated over the right upper quadrant in 70% to 90% of infants with pyloric stenosis. McCance, et al, (2013) stated ”a visible gastric peristaltic wave after eating is observed in some infants. Ultrasound shows the hypertrophied pyloric muscles and narrowed pyloric channel” (p. 1489). Discussion Part Three · Write a one (1) paragraph case study of your own for a patient with Ulcerative Colitis As you write your case study, consider the following signs and symptoms of ulcerative colitis: 1) Diarrhea, often with blood or pus 2) Abdominal pain and cramping 3) Rectal pain 4) Rectal bleeding — passing small amount of blood with stool 5) Urgency to defecate 6) Inability to defecate despite urgency 7) Weight loss 8) Fatigue 9) Fever 10) In children, failure to grow The exact cause of ulcerative colitis remains unknown. Previously, diet and stress were suspected, but now doctors know that these factors may aggravate but don’t cause ulcerative colitis”. An immune system malfunction can be attributed to this disease where ones “immune system tries to fight off an invading virus or bacterium, an abnormal immune response causes the immune system to attack the cells in the digestive tract, too” (The Mayo Clinic Staff, 2014). There seems to have a heredity component that may take a part in ulcerative colitis and is more common in people who have family members with the disease “even though most people with ulcerative colitis don’t have this family history” (The Mayo Clinic Staff, 2014).
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