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:
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
, 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
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:
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
, 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
