NR 507 Week 5: Discussion Part One

Chamberlain University NR 507 Week 5: Discussion Part One– Step-By-Step Guide

This guide will demonstrate how to complete the Chamberlain University NR 507 Week 5: Discussion Part One   assignment based on general principles of academic writing. Here, we will show you the A, B, Cs of completing an academic paper, irrespective of the instructions. After guiding you through what to do, the guide will leave one or two sample essays at the end to highlight the various sections discussed below.

How to Research and Prepare for NR 507 Week 5: Discussion Part One              

Whether one passes or fails an academic assignment such as the Chamberlain University NR 507 Week 5: Discussion Part One  depends on the preparation done beforehand. The first thing to do once you receive an assignment is to quickly skim through the requirements. Once that is done, start going through the instructions one by one to clearly understand what the instructor wants. The most important thing here is to understand the required format—whether it is APA, MLA, Chicago, etc.

After understanding the requirements of the paper, the next phase is to gather relevant materials. The first place to start the research process is the weekly resources. Go through the resources provided in the instructions to determine which ones fit the assignment. After reviewing the provided resources, use the university library to search for additional resources. After gathering sufficient and necessary resources, you are now ready to start drafting your paper.

How to Write the Introduction for NR 507 Week 5: Discussion Part One              

The introduction for the Chamberlain University NR 507 Week 5: Discussion Part One  is where you tell the instructor what your paper will encompass. In three to four statements, highlight the important points that will form the basis of your paper. Here, you can include statistics to show the importance of the topic you will be discussing. At the end of the introduction, write a clear purpose statement outlining what exactly will be contained in the paper. This statement will start with “The purpose of this paper…” and then proceed to outline the various sections of the instructions.

How to Write the Body for NR 507 Week 5: Discussion Part One              

After the introduction, move into the main part of the NR 507 Week 5: Discussion Part One assignment, which is the body. Given that the paper you will be writing is not experimental, the way you organize the headings and subheadings of your paper is critically important. In some cases, you might have to use more subheadings to properly organize the assignment. The organization will depend on the rubric provided. Carefully examine the rubric, as it will contain all the detailed requirements of the assignment. Sometimes, the rubric will have information that the normal instructions lack.

Another important factor to consider at this point is how to do citations. In-text citations are fundamental as they support the arguments and points you make in the paper. At this point, the resources gathered at the beginning will come in handy. Integrating the ideas of the authors with your own will ensure that you produce a comprehensive paper. Also, follow the given citation format. In most cases, APA 7 is the preferred format for nursing assignments.

How to Write the Conclusion for NR 507 Week 5: Discussion Part One              

After completing the main sections, write the conclusion of your paper. The conclusion is a summary of the main points you made in your paper. However, you need to rewrite the points and not simply copy and paste them. By restating the points from each subheading, you will provide a nuanced overview of the assignment to the reader.

How to Format the References List for NR 507 Week 5: Discussion Part One              

The very last part of your paper involves listing the sources used in your paper. These sources should be listed in alphabetical order and double-spaced. Additionally, use a hanging indent for each source that appears in this list. Lastly, only the sources cited within the body of the paper should appear here.

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Sample Answer for NR 507 Week 5: Discussion Part One

What is the etiology of Diabetic Ketoacidosis?

Diabetic ketoacidosis is a severe complication of diabetes that occurs when your body produces high levels of blood acids called ketones. “Diabetic ketoacidosis (DKA) develops when there is an absolute or relative deficiency of insulin and an increase in the levels of counterregulatory insulin hormones” (McCance, 2013). This disease commonly found in patients with type 1 diabetes. However, it can also occur in type 2 diabetes. The most common triggering aspect for DKA is other illness, such as infection, trauma, surgery, or myocardial infarction. Interruption of insulin administration also may result in DKA. (McCance, 2013).

The condition develops when your body can’t produce enough insulin. Insulin usually plays a crucial role in helping sugar (glucose) — a significant source of energy for your muscles and other tissues — enter your cells. Without enough insulin, your body begins to break down fat as fuel. This process produces a buildup of acids in the bloodstream called ketones, eventually leading to diabetic ketoacidosis if untreated. (Mayo clinic staff, 2018).

Describe the pathophysiological process of Diabetic Ketoacidosis.

Diabetic ketoacidosis characterized by a serum glucose level greater than 250 mg per dL, a pH less than 7.3, a serum bicarbonate level less than 18 mEq per L, an elevated serum ketone level, and dehydration. Insulin deficiency is the main precipitating factor. Diabetic ketoacidosis can occur in persons of all ages, with 14 percent of cases arising in persons older than 70 years, 23 percent in persons 51 to 70 years of age, 27 percent in persons 30 to 50 years of age, and 36 percent in persons younger than 30 years. The case fatality rate is 1 to 5 percent. About one-third of all cases are in persons without a history of diabetes mellitus. (Westerberg, 2013). According to, McCance, 2013. In a state of relative insulin deficiency, there is an increase in the concentrations of insulin counterregulatory hormones including catecholamines, cortisol, glucagon, and GH. “These counterregulatory hormones antagonize insulin by increasing glucose production and decreasing tissue use of glucose. Profound insulin deficiency results in decreased glucose uptake increased fat mobilization with the release of fatty acids and accelerated gluconeogenesis and ketogenesis. “(McCance, 2013).

Identify the hallmark symptoms of Diabetic Ketoacidosis.

Hallmark symptoms include polyuria with polydipsia (98 percent), dehydration, weight loss (81 percent), fatigue (62 percent), dyspnea (57 percent), vomiting (46 percent), preceding febrile illness (40 percent), abdominal pain (32 percent), and polyphagia (23 percent). Other symptoms of diabetic ketoacidosis include Kussmaul respirations (hyperventilation to compensate for the acidosis), postural dizziness, central nervous system depression, ketonuria, anorexia, nausea. 

Identify any abnormal lab results provided in the case and explain why these would be abnormal given the patient’s condition.

Sodium (Na+) 156 mEq/L elevated normal range 136-146 mEq/L. The American Diabetes Association criteria for the diagnosis of DKA are: (1) a serum glucose level >250 mg/dl, (2) a serum bicarbonate level <18 mg/dl, (3) a serum pH <7.30, (4) the presence of an anion gap, and (5) the presence of urine and serum ketones. Arterial blood gases (ABGs) Pco2-40; Po2-70; HCO3-20. Metabolic acidosis confirmed by arterial blood gas (ABG) analysis is one of the diagnostic criteria for diabetic ketoacidosis (DKA). Given the direct relationship between end-tidal carbon dioxide (ETCO2), arterial carbon dioxide (PaCO2), and metabolic acidosis, measuring ETCO2 may serve as a surrogate for ABG in the assessment of possible DKA. (Soeimanpour et al., 2013). These labs are abnormal because the body is compensating for the high level of glucose in the renal system and the loss of glucose in the urine. Ms. Blake has not been eating and probably has been taken her insulin as she was before she got sick. When you have diabetes and don’t get enough insulin and get dehydrated, your body burns fat instead of carbs as fuel, and that makes Ketones. Lots of ketones in your blood turn it acidic. People who drink much alcohol for a long time and don’t eat also enough build up ketones. It can happen when you aren’t eating at all, too. This condition can all lead to or be a predictor of existing Ketoacidosis.

What teaching would you provide this patient to avoid Diabetic Ketoacidosis symptoms?

First, I would emphasize the importance of managing her insulin regimen, instruct her that DKA is a life-threatening condition. I would teach Ms. Blake to Monitor her blood sugar levels closely, especially if you have an infection, are stressed, or experience trauma. Check your blood sugar levels often. You may need to check at least three times each day. If your blood sugar level is too high, give yourself insulin as directed by your healthcare provider. Manage your sick days. When you are sick, you may not eat as much as you usually would. You may need to change the amount of insulin you give yourself. You may need to check your blood sugar level more frequently than typical. Strategize with your healthcare provider about how to manage your diabetes when you are sick.

References

Mayo clinic staff (2018). Diabetic ketoacidosis/ Symptoms & causes. Retrieved from https://www.mayoclinic.org/diseases-conditions/diabetic-ketoacidosis/symptoms-causes/syc-20371551

McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (2013). Pathophysiology: The biologic basis for disease in adults and children (7th ed.). St. Louis, MO: Mosby.

Soleimanpour,H., Taghizadieh, A., Niafar, M., Rahmani, F., Golzari, S.E.J., Estanjani, R.M. (2013). Predictive Value of Capnography for Suspected Diabetic Ketoacidosis in the Emergency Department. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3876300/

Westerberg, D.P. (2018). Diabetic Ketoacidosis: Evaluation and Treatment. Retrieved fromhttps://www.aafp.org/afp/2013/0301/p337.html

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Sample Answer 2 for NR 507 Week 5: Discussion Part One

Great post and thank you for sharing you made some very informative points. Timely management of diabetic ketoacidosis (DKA) is essential to avoid lengthy hospitalizations and poor clinical outcomes (Joyner-Blair, Hamilton & Spurlock, 2018). There is often an absence of ownership for glycemic management in hospitalized patients, most notably in those with a diagnosis other than diabetes. This lack of ownership supports the use of evidence-based DKA protocols. Joyner-Blair, Hamilton & Spurlock (2018) conducted a project to determine whether utilization of an evidence-based order set versus an individualized provider approach for the treatment and management of DKA decreases resolution time and occurrences of hypoglycemia and improves clinical outcomes.

    They retrospectively reviewed electronic medical record of 150 non-pregnant adult patients diagnosed with DKA, pre and post-interventions, for retrieval of relevant outcome data. They concluded that implementation of the institutionally approved evidence-based order set affirmed anticipated outcomes (Joyner-Blair, Hamilton & Spurlock, 2018). Results showed improvements (Joyner-Blair, Hamilton & Spurlock, 2018) in the (a) total length of stay, (b) arrival to intravenous fluid time, (c) intravenous insulin initiation to discontinuation (resolution) time, (d) arrival to subcutaneous insulin administration time, (e) time from initial to sequential laboratory testing, (f) use of a basal, prandial, and correction insulin approach (physiological mimic), and (g) the incidence of hypoglycemia. Outcomes substantiate the importance and need for maintaining an evidence-based and systems approach for the management of DKA.    Although hyperosmolar hyperglycemic state can be confused with DKA, ketone levels are low or absent in persons with hyperosmolar hyperglycemic state. Other causes of high anion gap metabolic acidosis, such as alcoholic ketoacidosis and lactic acidosis, must be ruled out.

Reference

Joyner Blair, A. M., Hamilton, B. K., & Spurlock, A. (2018). Evaluating an Order Set for Improvement of

Quality Outcomes in Diabetic Ketoacidosis. Advanced Emergency Nursing Journal, 40(1), 59-72. doi:10.1097/TME.0000000000000178

Sample Answer 3 for NR 507 Week 5: Discussion Part One

Diabetic Ketoacidosis seems to be a very common occurrence in the healthcare setting I currently work in. While many of the individuals recognize the symptoms but do not have common occurrences some patients seem to experience this complication frequently. I feel that education is essential when a patient is first diagnosed with diabetes to ensure the signs and symptoms are known and prevention methods are implemented. In some cases, it can be seen that the patients are not aware of the seriousness of DKA or the long-term effects it can cause. According to Smith and Schub (2018, p. 3), “Complications of DKA include electrolyte imbalances, cerebral edema, thrombotic events (e.g., pulmonary embolism, stroke, DVT), and acute kidney injury”. Complications such as these can be very serious and result in long term effects that could cause further debilitation. In order for the best outcome in the present and future quick treatment is essential and correct treatment of elevated glucose levels independently of the patient to prevent future episodes is essential. You included great information in the discussion allowing for a clear understanding of DKA.

Paige Schnittker

Reference

Smith, N. C., & Schub, T. B. (2018). Diabetic Ketoacidosis in Adults. CINAHL Nursing Guide.

Sample Answer 4 for NR 507 Week 5: Discussion Part One

What is the etiology of Diabetic Ketoacidosis?

Diabetic Ketoacidosis (DKA) is a possible fatal metabolic emergency that arises as a complication of unregulated diabetes (MacArthur & Phillips, 2015).  Low serum insulin amounts in DKA inhibit glucose from moving into the cells to accomplish normal metabolic activity, initiating the cells to feedback just as if in starvation phase (MacArthur & Phillips, 2015). The generation of contra-regulative hormones (e.g., catecholamines, cortisol, glucagon, growth hormone) with regard to the decreased insulin levels induces the identified state of deprivation (MacArthur & Phillips, 2015). To remunerate, the liver starts to disintegrate saved glycogen and fat to generate glucose, this creates ketone acid derivatives that result in metabolic acidosis and hyperlipidemia (MacArthur & Phillips, 2015).  DKA arises primarily in individuals with diabetes mellitus, type 1 (DM1), but it may affect individuals with diabetes mellitus, type 2(DM2) or, infrequently, individuals with gestitational diabetes (MacArthur & Phillips, 2015). Irregardless of whether affected by diabetes mellitus 1(DM1) or diabetes mellitus 2 (DM2), the individual may have damaged beta-cell such as the pancreatic cells that generate insulin operation (MacArthur & Phillips, 2015).  Pregnant women have a decreased buffering capability, which puts them at risk of acidosis; they may not be able to generate adequate amounts of insulin to keep up with fetal needs in spite of normal beta-cell activity (MacArthur & Phillips, 2015).  The most frequent triggering factors include medications like cortical steroids, thiazides, aspirins, atypical antipsychotics, recreational drug utilization, alcohol misuse, serious illness, malnourishment, surgery, pregnancy and emotional stress (MacArthur & Phillips, 2015). The seriousness of DKA does not correlate to the plasma glucose levels (MacArthur & Phillips, 2015). Many individuals with DKA evaluated in the emergency department need admission to the intensive care unit for close observation and management (Benoit, Zhang, Geiss, Gregg, & Albright, 2018).  The disclosed occurrence of DKA in DM1 is 0-56 per 1,000 individuals annually (Benoit et al., 2018).  DKA is the most prevalent reason of fatality in individuals with DM1 who are below the age forty (Benoit, Zhang, Geiss, Gregg, & Albright, 2018). The disclosed incident of DKA is as high as 10 percent (Benoit, et al., 2018).

 Two primary risk factors for DKA includes insulin reliance and age less than twenty five years. Other important risk determinants include belonging black race, long-term alcohol misuse, and recreational drug utilization, all of which are a lead to not being compliant with drug treatment and drug actuated hyperglycemia (MacArthur & Phillips, 2015). More specific health risk determinants include new onset of diabetes (DM), illness, disruption of insulin regimen, heart attack, gastroparesis, pancreatitis, stroke, and trauma, but any serious infection can cause DKA (MacArthur & Phillips, 2015).  

Describe the pathophysiological process of Diabetic Ketoacidosis.

In a condition of relative insulin insufficiency, there is a build up in the concentrations of insulin counter-regulative hormones in addition to catecholamines, cortisol, glucagon, and growth hormone (McCance, Huether, Brashers, & Rote, 2013). These converse-regulative hormones oppose insulin by rising glucose generation and reducing tissue utilization of glucose (McCance, Huether, Brashers, & Rote, 2013).  This absence of insulin causes malfunction for glucose acceptance, enhanced fat metabolism with discharge of phospholipids, and increased gluconeogenesis and ketogenesis. Somewhat, elevated glucagon quantities also influence stimulation of glucogenic (glucose-forming) and ketogenic (ketone forming) passageways in the liver (McCance, Huether, Brashers, & Rote, 2013).   Because of the insulin insufficiency, liver excess production of betahydroybutyrate and acetoacetic acids result in rise in ketone accumulations (McCance, Huether, Brashers, & Rote, 2013). Normally, ketones are utilized by tissue as energy supply to reproduce bicarbonate. This stabilized deficit of bicarbonate happens when ketone is made. Hyperketomia which implies elevated plasma levels of ketone can be a consequence malfunction in the utilization of ketones by peripheral tissue, which allows robust organic acids to disseminate voluntarily (McCance, Huether, Brashers, & Rote, 2013).  Bicarbonate buffering the does not happen, and the individual expounds metabolic acidosis (McCance, Huether, Brashers, & Rote, 2013).

Identify the hallmark symptoms of Diabetic Ketoacidosis.

The clinical characteristics of DKA are not specific. Prevalent clinical manifestations of DKA involve polyuria and dehydration arises from osmotic dieresis linked with hyperglycemia. In this state the blood glucose amount is greater than the person’s kidney threshold, permitting large quantities of glucose to be lost in the urine (McCance, Huether, Brashers, & Rote, 2013).  Deficiency of sodium, magnesium and phosphorous is common. The most vital electrolyte disruption, however, is a notable deficiency in the amount of absolute body potassium (McCance, Huether, Brashers, & Rote, 2013). Even though, the serum potassium concentrations can seem normal or increased because of volume concentrations and a movement of potassium out of the cell and into the plasma maybe a consequence of metabolic acidosis (McCance, Huether, Brashers, & Rote, 2013).  The entire body defalcation of potassium can be up to 3 or 5 mEq/kg. Manifestations of diabetic Ketoacidosis include kussmaul respirations, postural virtigo, central nervous system depression, malnutrition, ketonuria, nausea, stomach pain (McCance, Huether, Brashers, & Rote, 2013).

Identify any abnormal lab results provided in the case and explain why these would be abnormal given the patient’s condition

Sodium 156mEq/L- Upsurge in the blood glucose concentration may result in changes of plasma sodium concentration by way of numerous methods (MacArthur & Phillips, 2015). Rise in glucose concentration raise plasma tone, making an osmotic impelling cause that supports the transport of water from inside the cell to the extra cellular space, there for diluting the additional concentration of sodium (MacArthur & Phillips, 2015). The blood plasma sodium concentration is normally low due to the osmotic reflux of water (MacArthur & Phillips, 2015).  Elevated or usual plasma sodium concentration in the existence of hyperglycemia demonstrates a clinically major insufficiency in complete water body weight (MacArthur & Phillips, 2015).  

Chloride (Cl-) – Hyperchloremia is a result of the reabsorption of sodium chloride by the kidneys in an attempt to conserve extracellular volume (MacArthur & Phillips, 2015).  Furthermore, the loss of sodium salt of beta-hydroxybutyrate and acetoeacetate, collectively with water, sets aside a fixed amount of chloride to be distributed in lesser volume, thus, expanding its concentration.  Additionally, diarrhea including hyporeninemic hyposldosteronism is seen in a few patients could be caused by the materialization of hyperchloremia acidosis (MacArthur & Phillips, 2015).  

Acid –Base Imbalance:

pH-7.30- In diabetes, a decreased pH is normally  related to a decrease in bicarbonate of at least 15 mmol/L or below, even though a milder type of DKA can present with a bicarbonate level between 15 and 18 mmol/L. Less serious DKA is usually followed by mild to enormous amounts of ketones in the blood and urine.

Po2-70-Oversupply of hydrogen ions causes quantum tissue oxygen deficiency which consecutively reduces the partial pressure of oxygen and decreasing Po2 (MacArthur & Phillips, 2015).  

  HCO3-20mEq/L- The buildup of ketoacids in the extra cellular fluid space result in loss of bicarbonate anions and acquire ketoacids anions result in the ontogenesis of anion gap acidosis (MacArthur & Phillips, 2015). Determining the seriousness of metabolic academia is normally based upon the degree of decrease in the blood plasma bicarbonate concentration (MacArthur & Phillips, 2015). The anion gap may be computed utilizing the equation: Na+- (C1-+ HCO3) (MacArthur & Phillips, 2015).  Based on this equation the normal anion gap is 12mmol/L.  In DKA, bicarbonate is exchanged by beta-hydroxybutyric acid and acetoacetic acid, in that the sum of bicarbonate and chloride concentrations is decreased and the anion gap is therefore increased (MacArthur & Phillips, 2015). In spite of considerable losses of ketoacids in the urea, the reduction in serum bicarbonate concentration and upsurge in the anion gap seen in DKA are almost equal (MacArthur & Phillips, 2015).  

Diagnosis of Ketoacidosis is recommended when persons have manifestations of emesis, stomach pain, dehydration, an acetone smell of breath, and change in sensorium pain (McCance, Huether, Brashers, & Rote, 2013). Therapy of DKA includes administering of insulin to reduce glucose amounts (McCance, Huether, Brashers, & Rote, 2013). Fluids are given to replenish depleted fluid volume. Electrolyte deficiency become obvious as fluid volume is replenished and intravenous sodium, potassium and phosphorous are administered if needed (McCance, Huether, Brashers, & Rote, 2013).

What teaching would you provide this patient to avoid Diabetic Ketoacidosis symptoms?

Ketone is an acid produced when the body utilizes fat for energy. Normally, glucose is the primary source of energy for the body and fat is utilized as a reserve. If there is not adequate insulin, the body cannot utilize the glucose in the blood. Rather, the body utilizes fat as the primary supply of fuel. The excess utilization of fat results in a accumulation of ketones in the body termed Ketoacidosis (MacArthur & Phillips, 2015).  Ketoacidosis may bring about severe sickness. Knowing what causes the Ketoacidosis and taking necessary steps will assist prevent future events. Continue to monitoring your blood glucose levels and ketones, drink a lot of sugar-free and caffeine free fluids to assist in flushing out ketones (MacArthur & Phillips, 2015). Avoid drinking alcohol. Do not skip meals. If you are having difficulty eating because of sickness, make befitting adjustments to your insulin doses. Do not work out if you have elevated glucose levels and if your urine test shows elevated levels of ketones. Exercise increases the utilization of fat for energy and will make the Ketoacidosis worse (MacArthur & Phillips, 2015).  Talk to a physician about your insulin adjustments if you are sick, have elevated blood glucose levels, or have difficulty eating, you might need to modify some of your insulin doses (MacArthur & Phillips, 2015).  Take your medications as directed, do not change the amount or schedule. Call your doctor have drowsiness, vomiting and nausea, severe stomach pain, shortness of breath, fruity breath odor and rapid heart rate (MacArthur & Phillips, 2015).

References

Benoit, S.R., Zhang, Y., Geiss, L. S., Gregg, E.W., & Albright, A. (2018). Trends in diabetic Ketoacidosis hospitalizations and in-hospital mortality-United States, 2000-2014. MMWR. Morbidity And Mortality Weekly Report, 67(12), 362-365.doi:10.15585/mmwr.mm6712a3

MacArthur, C., & Phillips, A. (2015). Ketoacidosis in diabetes. Recognition and avoidance. Practice Nursing, 26(8), 393-399. McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (2013). Pathophysiology: The biologic basis for disease in adults and children (7th ed.). St. Louis, MO: Mosby

Sample Answer 5 for NR 507 Week 5: Discussion Part One

Etiology of Diabetic Ketoacidosis

The causation or origination of Diabetic Ketoacidosis is a reduction in the production of the insulin hormone and an abnormal spike in the production of counter-regulatory hormones glucagon, catecholamines, epinephrine, cortisol, and growth hormone (ADA, 2017). Insulin and counter-regulatory hormones regulate and affect the blood-sugar levels in the body. In healthy people, insulin helps maintain blood sugar levels from getting too high (hyperglycemia) and too low (hypoglycemia); counterregulatory hormones are the primary defense against hypoglycemia, as levels are expected to rise as the glucose falls—just not at such a rapid rate (ADA, 2017).

Extreme changes in the body’s hormone secreting system lead to metabolic derangement (disturbance of normal bodily functions) that can occur in diabetes. The most common causes of DK are insufficient insulin therapy, infection/illness, underlying medical conditions such as myocardial infarction or stroke, drugs that affect carbohydrate metabolism, second-generation antipsychotic agents used to treat psychiatric conditions (ADA, 2017). The use of sodium-glucose cotransporter 2 inhibitors has also been implicated as a trigger of DKA in type 1 and type 2 diabetes patients (ADA, 2017). To summarize the etiology of DKA, three general reasons for the body to over-produce ketones is the body does not get enough insulin (maybe the diabetic did not inject enough insulin, or the body is not producing enough due to illness); the diabetic is not eating enough of the right foods (maybe the person is sick and does not feel like eating, or the diabetic has missed a meal); the body is having a negative insulin reaction.

That was excellent!

Describe the pathophysiological process of Diabetic Ketoacidosis

The pathophysiology of DKA results as reduced insulin action, increased production of insulin counter-regulatory hormones, and volume depletion of hormones and electrolyte imbalance occurs. The hormonal changes that occur in DKA lead to increased gluconeogenesis (generation of glucose from non-carbohydrate carbon substrates such as lactate, glycerol, and glucogenic amino acids), hepatic (liver) and renal (kidney) glucose production, and impaired glucose utilization in peripheral tissues (ADA, 2017).  The pathophysiology of DKA results in hyperosmolarity (the body tries to rid itself of the excess blood sugar by passing it into your urine) and hyperglycemia (ADA, 2017).

Insulin deficiency leads to the release of free fatty acids from adipose tissue (lipolysis), hepatic fatty acid oxidation, and formation of beta-hydroxybutyrate and acetoacetate  (compounds produced during the metabolism of fats), resulting in ketonemia and acidosis (Gosmanov, Gosmanova, & Dillard-Cannon, 2014). Also associated with DKA is the increase of proinflammatory cytokines and inflammatory biomarkers, markers of oxidative stress, lipid peroxidation, and cardiovascular risk factors with hyperglycemic crises (Gosmanov, Gosmanova, & Dillard-Cannon, 2014). The body starts to return to a normal state when insulin and hydration therapies are administered within 24 hours of a hyperglycemic crises (Gosmanov, Gosmanova, & Dillard-Cannon, 2014). The proinflammatory and procoagulant states that occur during a hyperglycemic crisis are adaptive responses to acute stress on the body’s systems. DK syndromes vary in patients and is based on autoantibody status (a type of protein produced by the immune system), human leukocyte antigen (HLA) genotype (cell-surface proteins responsible for the regulation of the immune system in humans), and pancreatic beta-cell functional reserves (Gosmanov, Gosmanova, & Dillard-Cannon, 2014).  

Complications associated with DKA include sepsis and multiple diffuse ischemic processes (biochemical changes within the body) (Hamdy, 2018). Other complications include myocardial infarction (MI), acute gastric dilatation, erosive gastritis, late hypoglycemia, urinary tract infection (UTI), cerebral venous thrombosis (CVT), deep vein thrombosis (DVT), hypophosphatemia (an electrolyte imbalance that creates abnormally low levels of phosphate in the blood), mucormycosis (fungal infection), cerebrovascular accident (stroke), and/or respiratory distress (Hamdy, 2018). Furthermore, high levels of ketones in the bloodstream are toxic to the body, so a person can die or fall into a diabetic coma when the blood becomes too acidic.

Outstanding job with this section!

Hallmark symptoms of Diabetic Ketoacidosis

DKA can develop slowly or rapidly, but a hallmark sign is vomiting. When this occurs, DKA has become life-threatening (Misra & Oliver, 2015).  Early symptoms include feeling dehydrated or dry mouth, frequent urination, abnormally high blood sugar levels, high levels of ketones in the urine. If the patient does not address these physical changes, other symptoms begin to appear that include fatigue, parched skin, nausea, abdominal pain, difficulty breathing, fruity smelling breath, flushed face, headache. The patient must head to a hospital if vomiting occurs for more than 2 hours, severe disorientation, respiratory distress, muscle paralysis, intense or throbbing abdominal pain. Since DK can develop rapidly, patients should check their blood sugar and ketone levels at the first signs of physical abnormality. Blood sugar readings should be lower than 230 milligrams per deciliter (mg/dL), ketone level should be under 0.6 millimoles per liter (mmol/liter). A ketone level reading between 1.6 and 3.0 mmol/L means the person is at risk for DK, anything higher is a medical emergency.  

Nice work!

Identify any abnormal lab results provided in the case and explain why these would be abnormal given the patient’s condition

The sodium level is abnormal. A normal blood sodium level should read between 135 and 145 milliequivalents per liter (mEq/L); hyponatremia occurs when the sodium in your blood falls below 135 mEq/L. (Misra & Oliver, 2015).

The potassium level is normal. Potassium levels above 5.1 mEq/L are considered to be mild hyperkalemia (Misra & Oliver, 2015).

The chloride level in the blood is too high. The normal level for chloride is 97-107 mEq/L; any level higher places the patient at risk for hyperchloremia, an electrolyte imbalance (Misra & Oliver, 2015).

Arterial blood gases:

The pH is too low and indicates the blood is more acidic and has higher carbon dioxide levels (Misra & Oliver, 2015). The Pco2 level is fine; however, if it were too low acidemia and respiratory alkalosis occur–and too high will result in pH respiratory acidosis (Misra & Oliver, 2015). The Po2 (partial pressure of oxygen) level is too low. Po2 measures the amount of oxygen gas dissolved in the blood and the effectiveness of the lungs. The low reading means the lungs are not pulling in enough oxygen to the blood (Misra & Oliver, 2015). If the Po2 level is too high, polycythemia occurs; this is a form of excess RBC production in which the marrow makes too many red blood cells, causing the blood to thicken and form blood clots that can cause a stroke or heart attack (Misra & Oliver, 2015). The HCO3 (bicarbonate) level is too low and means the blood has become acidic. An HCO3 greater than 26 means a metabolic alkalosis issue may occur (Misra & Oliver, 2015).

Very nice work here.

What teaching would you provide this patient to avoid Diabetic Ketoacidosis symptoms?

I would advise the patient to keep fresh blood glucose and ketone urine test strips, as well as a functioning blood glucose meter. I would also recommend she take diabetes medications as prescribed and directed because skipping or doubling doses can lead to DKA. I would also encourage the patient to check blood sugar and ketone levels before and after meals and at minimum four times a day when she catches a cold, the flu, or has a UTI. The patient must also be instructed to check her ketone level whenever her blood sugar rises above 250 mg/dl. The patient must throw out all ketone or blood glucose strips that have expired, as well as any expired insulin. She should also contact her primary provider if she has a bad reaction to an insulin batch. I would also instruct the patient to watch for DKA warning signs, such as too high or low blood sugar readings, persistent headaches, extreme fatigue and weakness.

How scholarly inquiry informed or changed professional or academic decisions

I have learned that diabetic patients suspected of having DKA or associated symptoms should be tested before treatment begins. A urine dipstick test is best to use as it shows highly positive for glucose and ketones. Just giving someone insulin can do more harm than good. Since treatment includes replacing electrolytes (sodium, potassium, chloride, bicarbonate) and insulin, I must know the patient’s exact laboratory values. For example, if the patient receives too much insulin, he or she becomes hypoglycemic. If I focus on insulin replacement and allow the electrolytes to become too low, I can induce vomiting or cause a fever to develop. For instance, low potassium affects heart, muscle, and nerve function. The goal is to keep the patient stable until help or treatment is available, so flushing the body is important—even if the patient is urinating frequently. DKA urination is caused by excess ketones, so drinking water promotes urination and helps flush excess ketones from the body.

References:

American Diabetes Association (ADA). (2017). Standards of medical care in diabetes. BMJ: Diabetes Care, 40(1), S1-S135. Retrieved from https://doi.org/10.2337/dc17-S001

Gosmanov, A. R., Gosmanova, E. O., & Dillard-Cannon, E. (2014). Management of adult diabetic      ketoacidosis. Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy, 7, 255–264.             http://doi.org/10.2147/DMSO.S50516

Hamdy, O. (2018). Diabetic ketoacidosis clinical presentation. Medscape. Retrieved from                   https://emedicine.medscape.com/article/118361-clinical#b5

Misra, S., & Oliver, N. S. (2015). Diabetic ketoacidosis in adults. The BMJ, 351(5866). Retrieved from https://doi.org/10.1136/bmj.h5660 (Links to an external site.)

NR 507 Week 6 Case Study 

Pathophysiology and Clinical Findings of the Disease 

The symptoms the 48-year-old male patient reports relates to type 2 diabetes. The diagnosis has been derived from the patient’s description of his symptoms and past medical history. Besides, the condition entails the lack of adequate insulin being produced in the pancreas, leading to deficiency. The muscle and fat cells’ malfunction can prevent them from responding appropriately to insulin, causing them to absorb less sugar.  

The pathophysiology of diabetes mellitus type 2 entails the failure of the B-cells to function correctly. B-cells produce insulin that helps maintain normal blood sugar levels (Galicia-Garcia et al., 2020; Mann et al., 2020). The insulin is synthesized as pre-proinsulin. Upon maturation, the pre-proinsulin undergoes modification with the help of specific proteins in the endoplasmic reticulum to become proinsulin (Galicia-Garcia et al., 2020). The proinsulin gets transported to the Golgi bodies from the endoplasmic reticulum and undergoes further modification to become insulin and C-peptide. Besides, the insulin is stored until it is ready to be released. Response to high glucose concentrations triggers the release of insulin (Galicia-Garcia et al., 2020). The B-cells take in the glucose and release it to the plasma membrane following a series of electrolyte actions in the B-cells. However, the B-cells could be impaired and fail to function as required. This patient’s case could be due to extreme nutritional conditions, including obesity and hyperlipidemia. These conditions lead to insulin resistance and chronic inflammation. Hence, the B-cells experience significant pressure, leading to their death.  

The diagnosis of type 2 diabetes in this patient results from subjective and objective findings. The subjective findings from this client include fatigue, extreme thirst, frequent urination at night, increased appetite, and unintended weight loss (Trikkalinou et al., 2017). The patient reports that these symptoms began around three weeks ago. He had been living normally until this period. Conversely, the objective findings leading to this diagnosis include a high fasting glucose level of 132 mg/dL, a high blood pressure of 136/80, and a BMI of 36.5 (Malone & Hansen, 2019). The objective and subjective patient information confirms that this patient has type 2 diabetes. The patient’s medical history, including obesity, hyperlipidemia, and hypertension, further support the diagnosis. Besides, the patient’s brother has the condition, indicating that genetics could have played a role in the patient developing diabetes.   

Management of the Disease 

Management of type 2 diabetes entails ensuring that the glucose level in the blood remains within the normal range. Medications and non-pharmacological treatments apply in this scenario. The two common medication classes for this condition are biguanides and sodium-glucose transporter (SGLT) 2 inhibitors. According to Grytsai et al. (2020), biguanides function by decreasing the amount of glucose produced by the liver. The medications also regulate the glucose absorbed in the intestines, causing the body to be more sensitive to insulin. Metformin is a common drug in this class. It is always the first drug patients are prescribed to manage the condition. The physician may combine the medication with others depending on the severity of the patient’s symptoms. The patient should take 500 mg to 2250 mg daily, depending on the physician’s observation of his symptoms. The patient can take the medication alongside or after meals.  

The physician starts the dosage at low levels and increases it gradually. The patient can take the drug once to three times a day, depending on the form. The drug is suitable for this patient because it controls blood glucose levels throughout the day. By increasing the body’s sensitivity to insulin, the medication helps in weight management. However, the physician must evaluate the patient’s kidney function before administering the medication since people with advanced kidney disease may develop complications when they take this drug. Other side effects of the drug include nausea, stomach upsets, and diarrhea. The patient should also share with the physician whether he takes other drugs to avoid adverse drug interaction issues.  

The other drug class for treating type 2 diabetes is sodium-glucose transporter (SGLT) 2 inhibitors. Joshi et al. (2021) indicate that the medications prevent the kidneys from holding onto glucose. Instead of maintaining glucose, the liver eliminates it through urine (Xu et al., 2022). Hence, these drugs are suitable for this patient’s condition because of his other underlying issues like obesity. The drugs also reduce the chances of cardiovascular problems, chronic kidney disease, and heart failure, possibly due to the patient’s underlying conditions. A typical drug under this medication category is dapagliflozin. The patient can take this drug with others, like metformin, based on the physician’s instructions. For instance, a physician may prescribe a dosage of 5 mg daily, which could increase to 10 mg based on the physician’s observation of the patient. The physician must monitor the patient’s kidney function before and during treatment to determine the drug’s effect on the organ.  

Apart from the medications used to address type 2 diabetes mellitus, the patient can also undergo non-pharmacological treatment. The patient should strictly observe a healthy diet (Magkos et al., 2020). For example, this entails eating the healthiest foods in moderate amounts and having regular meal times. The diet should be rich in nutrients and low in calories and fats. Healthy food allows the client to control the glucose levels in the body. Foods with too much fat and calories often increase blood glucose levels. Failure to keep this level in check could lead to adverse outcomes like hyperglycemia and kidney and heart problems. Since this patient is already obese, he needs to see a dietician who would help him develop a healthy diet plan.  

Another non-pharmacological treatment for type 2 diabetes entails regular physical activity. Physical activities help manage a person’s weight (Magkos et al., 2020). They help burn calories that would otherwise accumulate and increase blood sugar levels, increasing the risk of adverse effects. Being physically active improves the body’s sensitivity to insulin, helping to manage the client’s condition. Two common exercise categories suitable for this client are aerobic and resistance exercises. Aerobic exercise allows the patient to manage his blood pressure and triglyceride levels, lowering the chances of cardiovascular problems. Conversely, resistance exercise enables the client to build muscle strength and mass. Often, exercise allows the patient to manage his weight, considering that excess calories get burned up, preventing the chances of uncontrolled weight gain. Therefore, the patient must work with an exercise expert to develop a regular exercise plan.  

Conclusion 

The patient has type 2 diabetes mellitus. The diagnosis results from the patient’s symptoms, including fatigue, extreme thirst, frequent urination, weight loss, and increased appetite. The patient’s medical history also confirms that he is at risk of this condition, considering he has obesity and hyperlipidemia. Besides, the patient’s brother has type 2 diabetes. The most appropriate treatment for this client entails a combination of medication and non-pharmacotherapy. He can take metformin alongside dapagliflozin. He should also create a healthy diet plan and a regular exercise schedule with the assistance of relevant experts.  

References 

Galicia-Garcia, U., Benito-Vicente, A., Jebari, S., Larrea-Sebal, A., Siddiqi, H., Uribe, K. B., … & Martín, C. (2020). Pathophysiology of type 2 diabetes mellitus. International Journal of Molecular Sciences, 21(17), 6275. 

Grytsai, O., Myrgorodska, I., Rocchi, S., Ronco, C., & Benhida, R. (2021). Biguanides drugs: Past success stories and promising future for drug discovery. European Journal of Medicinal Chemistry, 224, 113726. 

Joshi, S. S., Singh, T., Newby, D. E., & Singh, J. (2021). Sodium-glucose co-transporter 2 inhibitor therapy: Mechanisms of action in heart failure. Heart, 107(13), 1032–1038. 

Magkos, F., Hjorth, M. F., & Astrup, A. (2020). Diet and exercise in the prevention and treatment of type 2 diabetes mellitus. Nature Reviews Endocrinology, 16(10), 545-555. 

Malone, J. I., & Hansen, B. C. (2019). Does obesity cause type 2 diabetes mellitus (T2DM)? Or is it the opposite? Pediatric diabetes, 20(1), 5–9. 

Mann, E., Sunni, M., & Bellin, M. D. (2020). Secretion of insulin in response to diet and hormones. Pancreapedia: The Exocrine Pancreas Knowledge Base. 

Trikkalinou, A., Papazafiropoulou, A. K., & Melidonis, A. (2017). Type 2 diabetes and quality of life. World Journal of Diabetes, 8(4), 120. 

Xu, B., Li, S., Kang, B., & Zhou, J. (2022). The current role of sodium-glucose cotransporter 2 inhibitors in type 2 diabetes mellitus management. Cardiovascular Diabetology, 21(1), 83.