Using the video from on Ms. Fernandez, answer of the following prompts: Prompt 1: Explain in detail the pathogenesis of Diabetes Mellitus Type 1 & 2 and Diabetic ketoacidosis(DKA). Please be specific and thorough. Prompt 2: Explain how Ms. Fernandez’s past medical history correlates to her current condition. Prompt 3:Describe treatments that would be used for Diabetes Mellits and DKA. Please correlate your responses to Ms. Fernandez’s case. Content in this case scenario incorporates topics from Chapters 36 and 41.

Prompt 1: Pathogenesis of Diabetes Mellitus Type 1 & 2 and Diabetic Ketoacidosis (DKA)

Diabetes Mellitus (DM) is a chronic metabolic disorder characterized by elevated blood glucose levels resulting from deficiencies in insulin secretion, insulin action, or both. There are two main types of DM: Type 1 and Type 2 diabetes.

Type 1 diabetes is an autoimmune disease in which the body’s immune system mistakenly attacks and destroys the insulin-producing beta cells of the pancreas. This destruction leads to an absolute deficiency of insulin in the body. The exact cause of this autoimmunity is not fully understood, but genetic and environmental factors are thought to play a role. It usually presents in childhood or early adulthood.

Without sufficient insulin, glucose cannot enter the cells for energy production, leading to hyperglycemia. The body tries to compensate for the lack of insulin by breaking down fats and proteins, resulting in the production of ketones. However, ketone production can lead to a dangerous condition known as diabetic ketoacidosis (DKA).

Type 2 diabetes, on the other hand, is characterized by insulin resistance, where the body’s cells become less responsive to the effects of insulin. Initially, the pancreas compensates for this resistance by producing more insulin. However, over time, the pancreas may fail to keep up with the increased demand, leading to relative insulin insufficiency. Unlike Type 1 diabetes, Type 2 diabetes does not usually result in autoimmunity or destruction of beta cells.

Insulin resistance is influenced by genetic factors, obesity, sedentary lifestyle, and poor diet. Insulin resistance and impaired insulin secretion contribute to hyperglycemia in Type 2 diabetes.

Diabetic ketoacidosis (DKA) is a potentially life-threatening complication that can occur in both Type 1 and Type 2 diabetes, but it is more commonly associated with Type 1 diabetes. DKA is characterized by severe hyperglycemia, dehydration, electrolyte imbalances, and the accumulation of ketones in the blood. It usually occurs when there is a lack of insulin in the body, such as during illness, infection, or a missed dose of insulin.

In the absence of insulin, the body cannot effectively use glucose for energy. As a result, the body breaks down fats as an alternative energy source, leading to the production of ketones. The accumulation of ketones causes the blood to become acidic, leading to metabolic acidosis. This can result in symptoms such as increased thirst, frequent urination, abdominal pain, nausea, vomiting, and altered mental status.

Prompt 2: Correlation of Ms. Fernandez’s past medical history to her current condition

In the case of Ms. Fernandez, her past medical history of obesity, sedentary lifestyle, and poor diet is highly correlated with her current condition of Type 2 diabetes and DKA. These risk factors contribute to the development of insulin resistance and impaired insulin secretion, leading to hyperglycemia and the onset of diabetes.

Obesity is a significant risk factor for Type 2 diabetes as excess adipose tissue releases inflammatory substances that disrupt insulin action and promote insulin resistance. Sedentary lifestyle and poor diet, particularly high in refined carbohydrates and saturated fats, further exacerbate insulin resistance and contribute to weight gain.

Additionally, Ms. Fernandez’s infection and subsequent pneumonia likely triggered her DKA. During illness, the body requires more insulin to maintain glucose homeostasis. However, if there is insufficient insulin, as in Ms. Fernandez’s case due to Type 2 diabetes, the body resorts to breaking down fats, leading to ketone production and DKA. Infection can also cause stress and hormonal changes that further worsen insulin resistance.

Overall, Ms. Fernandez’s past medical history and her current condition are closely linked. Her lifestyle and dietary choices, along with the development of obesity and sedentary habits, have contributed to the development of Type 2 diabetes. The infection and subsequent pneumonia added further stress to her already compromised insulin regulation, resulting in the onset of DKA.

Prompt 3: Treatments for Diabetes Mellitus and DKA, and their correlation to Ms. Fernandez’s case

The treatment approach for diabetes mellitus and DKA includes both pharmacological and non-pharmacological interventions. The overall goal is to achieve glycemic control, prevent complications, and restore metabolic balance. The treatment approach may vary based on the type of diabetes and the severity of DKA.

For Type 2 diabetes, lifestyle modifications are crucial. This involves weight loss through a combination of dietary changes and increased physical activity. A balanced diet, focusing on whole grains, fruits, vegetables, lean proteins, and healthy fats, is recommended. Regular exercise helps improve insulin sensitivity and glucose uptake by the muscles.

In some cases, oral antidiabetic medications (such as metformin) are prescribed to improve insulin sensitivity, reduce glucose production by the liver, and enhance glucose uptake by the muscles. In more advanced cases, when oral medications are not sufficient, insulin therapy may be initiated to provide exogenous insulin support.

For DKA treatment, the primary focus is on correcting the metabolic imbalances. Intravenous fluids are administered to restore dehydration and correct electrolyte disturbances. Regular monitoring of blood glucose levels is critical, and insulin therapy is initiated to lower blood glucose levels and stop ketone production. Additionally, monitoring and correction of electrolyte imbalances, particularly potassium, is crucial.

In Ms. Fernandez’s case, her treatment would involve a comprehensive approach. Lifestyle modifications, including dietary changes and increased physical activity, would be recommended to improve her insulin resistance and overall glycemic control. Depending on the severity of her Type 2 diabetes, oral medications or insulin therapy may be initiated.

During her hospitalization for DKA, intravenous fluids and insulin therapy would be administered to correct her hydration status, normalize blood glucose levels, and stop ketone production. Close monitoring of electrolyte levels and appropriate supplementation would also be necessary.

In conclusion, the pathogenesis of Type 1 and Type 2 diabetes involves different mechanisms, with Type 1 diabetes being an autoimmune condition and Type 2 diabetes being characterized by insulin resistance. DKA is a severe complication of diabetes caused by a lack of insulin that leads to hyperglycemia and ketone production. Ms. Fernandez’s past medical history of obesity, sedentary lifestyle, and poor diet correlates with her current condition of Type 2 diabetes and DKA. The treatment for diabetes involves lifestyle modifications, medications, and insulin therapy if needed. DKA treatment involves correcting metabolic imbalances through intravenous fluids and insulin therapy. These treatments would be applicable to Ms. Fernandez’s case, focusing on lifestyle modifications and the management of DKA during her hospitalization.