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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 $7.49   Add to cart

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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...

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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

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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