NR 507
Week 5 – Part 1, 2 & 3
Case Study Discussions and Quiz
, NR 507 Week 5 TD and Quiz
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:
3.5-5.1
• 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
, 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
Week 5 – Part 1, 2 & 3
Case Study Discussions and Quiz
, NR 507 Week 5 TD and Quiz
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:
3.5-5.1
• 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
, 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
