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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
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
5. Acute kidney damage
Assuming that DKA is likely, what could have caused her sudden decline?
1. Respiratory infection
3. Medication non-compliance
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