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Summary wk6 PathO case study.docx NUR2063 Module 6 Assignment: Endocrine Pathophysiology Rasmussen College NUR2063: Essentials of Pathophysiology Module 6 Assignment: Endocrine Pathophysiology of Diabetic Ketoacidosis This paper is a case study of a 21-year€7,31
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Summary wk6 PathO case study.docx NUR2063 Module 6 Assignment: Endocrine Pathophysiology Rasmussen College NUR2063: Essentials of Pathophysiology Module 6 Assignment: Endocrine Pathophysiology of Diabetic Ketoacidosis This paper is a case study of a 21-year
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wk6 PathO case NUR2063 Module 6 Assignment: Endocrine Pathophysiology Rasmussen College NUR2063: Essentials of Pathophysiology Module 6 Assignment: Endocrine Pathophysiology of Diabetic Ketoacidosis This paper is a case study of a 21-year -old female (A.M) who presents to the urgent care wi...
Module 6 Assignment: Endocrine Pathophysiology of Diabetic Ketoacidosis
This paper is a case study of a 21-year -old female (A.M) who presents to the urgent care
with symptoms of nausea, vomiting, diarrhea, and a fever for the past 3 days. She states that she
has Type I diabetes and has not been managing her blood sugars since she’s been ill and unable
to keep any food down. She has only tolerated sips of water and juices. Since she has also been
unable to eat, she hasn’t taken any insulin as directed. While helping A.M. from the lobby to the
exam room it is noted that her balance is unsteady, her skin in warm and flushed and that she is
not very coherent and seems drowsy. It’s also noted that she’s breathing rapidly and smells of a
slightly sweet/fruity odor. A.M. has challenges answering questions, but it is noted that she
continues to keep asking for water to drink. Additional information retrieved from A.M., some
readings on her glucometer were reading ‘high,” she reports she has been vomitting almost every
time she takes in fluid, and has not voided for a day, but voided a great deal the day before, and
she has been sleeping long hours.
Pathogenesis of Diabetic Ketoacidosis
One of the possible conditions A.M could be experiancing could be diabetic ketoacidosis
and nonketotic hyperglycemic hyperosmolar syndrome (NHHS). NHHS occurs mostly in older
adults with type 2 diabetes (Banaski, 2019). With this information in mind, I believe A.M is more
likely to be experiencing diabetic ketoacidosis. According to Pathophysiology, fatty acids are
transformed into ketoacids which can be used in certain tissue by energy metabolism (2019). If
there becomes too much ketoacids, the pH in the body lowers and ketones are lost via urine
, which can result in increased fluid loss. Potassium may also be lost in the urine. Loss of fluid and
dehydration leads to many other complications and abnormal lab values. A.M also has increased
respiratory rate, which is the body’s way of trying to compensate for the metabolic acidosis. The
body is constantly trying to stay in homeostasis.
Etiology and Clinical Manifestations of Diabetic Ketoacidosis
Diabetic ketoacidosis (DKA) is a potentially life threatening complication of diabetes. If
a present with ketonemia, hyperglycemia an/or acidosis resulting from insulin ineffectvity or
insufficiency. DKA is the most common cause of death in people with type 1 diabetes under the
age of 40 years (Mills & Garrett, 2016). During DKA there is a deficiency of effective, acting,
circulating insulin, therefore cells are not able to obtain glucose, causing the body go into a
‘starvation’ state resulting in the liver to break down fat at a very high speed. The body cannot
keep up with the breakdown process and the liver converts the broken down fat into ketones and
this causes metabolic acidosis. DKA occurs when signal from the insulin in the body are too low
to be detected. This can often be the first diagnosis of diabetes for a patient. DKA is usually
experienced by patients with Type I diabetes, but can happen to those with Type II with the
disease being less severe. Two precipitating factors can be ineffective insulin therapy and
infection. DKA is often diagnosed among patients who are poorly compliant to insulin
administration during an acute illness. DKA is commonly precipitated by an acute stressful
event such as the development of infection leading to sepsis, organ infarction, burns, pregnancy
or intake of drugs that affect carbohydrate metabolism such as corticosteroids, anti-
hypertensives, loop diuretics, alcohol, cocaine, and ecstasy (Pathophysiology of Diabetic
Ketoacidosis, 2018). These stressful events cause the body to release counter-regulatory
hormones. These hormones initiate the mobilization of fat stores in the body, and this ultimately
results in the production of glucose. Insulin deficiency is the main cause of DKA. Diabetics
already have ineffective insulin in their circulation. With the addition of the stressful event
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