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Suffering because of Diabetic KetoAcidosis - Case Study Example

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Summary
This case study highlights that the patient suffers from is Diabetic KetoAcidosis (DKA), with a secondary diagnosis as hypertension. At 49 years with a history of cigarette smoking and alcohol consumption, these are crucial clinical history findings that are important precipitating factors of this condition. …
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Suffering because of Diabetic KetoAcidosis
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 It is certain that the patient suffers from is Diabetic KetoAcidosis (DKA), with a secondary diagnosis as hypertension. At 49 years with a history of cigarette smoking and alcohol consumption, these are crucial clinical history findings that are important precipitating factors of this condition. DKA is an acute metabolic disorder characterized by elevated ketone levels in the blood, metabolic acidosis and hyperglycemia. Coupled with hypertension, it explains why the patient appears disoriented with impaired renal clearance. In essence, DKA is a complication seen among patients with Type 1 Diabetes Mellitus (DM). Task 1: Pathophysiology of DKA Insulin deficiency as seen in type 1 DM compels the body to breakdown amino acids and triglycerides as opposed to glucose for energy production. Due to high breakdown of glyceride and amino acids, the levels of serum free fatty acids and glycerol goes abnormally leading to high level of uncontrolled lipolysis. The Free Fatty Acids (FFA) rises substantially in the blood ; meanwhile, muscle's lysis goes up (Koda-Kimble & Alldredge 2013). Due to production of acetoacetic acids and hydroxybutyric acids, both of which are strong organic acids increases leading to metabolic acidosis. Metabolic acidosis is one of the classical symptoms of DKA during the initial stage. Because of increased metabolic acidosis, the patients' physiologic compensation takes over. In order to restore normal pH, there is Kausmal respiration that attempt to increase the expiration. Many patients will present with acetone-breathe. Hyperglycemia arises due to insulin insufficiency leading to high sugar levels in the blood and osmotic diuresis that leads to loss of urinary function. This is a striking similarity with the case study presented. In addition, the urinary excretion of ketones causes increased loss of sodium, potassium and water is lost at large amounts leading to reduced urinary excretion as seen in the patient. As a result of increased loss of electrolytes, potassium often migrates into extracellular component leading to increased potassium levels, often driven back to intracellular by insulin therapy. Task 2: Diagnosis In order to diagnose DKA, first the patient history and physical assessment helps in identifying which laboratories test to be done. Clinical diagnosis depends on three key laboratory findings; the arterial blood pH normally less than 7.30 with an anion gap of more than 12. Secondly, serum ketones levels are an important diagnostic measurement. The presence of serum ketones and urine ketones indicate definitive diagnosis. In physiologically stable patient, ketones should not be found in serum or blood. Moreover, the adults should have an ECG to rule out any MI as a differential diagnosis because of high levels of potassium. Other laboratories findings that are indicative include high levels of sodium, elevated creatinine, high plasma osmolality; this is measured through taking Blood Urea Nitrogen (BUN) measurements (Koda-Kimble & Alldredge 2013). Intervention should focus on correcting the core clinical disease; that is diabetes. Another management should be conservative and aimed at minimizing symptoms. Notably, in order to improve patient's response to drug therapy, there should be two important clinical interventions. Restoration of normal sugar levels and restoring hydration status that would also correct urine excretion. There should be a clear clinical priority in intervention that would see the patient conditions restored back to physiological parameters. Management of hypertension should be the incorporation of drug therapy, fluid balance with stringent monitoring of vital signs. Task 3: Drug Table Drug Doze Route Mode of Action (MOA) Adverse Effects Amiodarone 200mg per 12 hours Oral It is an antiarrytthmic drug whose action is to prolong phase 3 of cardiac cycle. Induces hypothyroidism and may cause interstistsal lung disease. Neurotoxicity and hepatoxicity Amlodipine 5mg once per day Oral Treats High Blood pressure due to its Calcium channel-blocking ability thus causes reduced heart rate. Peripheral edema Dizziness, Hepatotoxicity, insomnia, Steven-Johnson syndrome. Carvedilol 25mg every 12 hours Oral It is a Beta blocker drug that is used to treat hypertension because it is both beta and alpha blockers. It reduces heart rate and pumping force. Dizziness Fatigue Hypotension Bradycardia Weight gain Diarrhea Cefazolin 2 grams after every 8 hours Intravenous It is an antibiotic given as prophylaxis. It is a broad spectrum antibiotic that kills many microorganisms. Less adverse effects, diarrhea, stomach pain, rash and vomiting Clonidine 0.1 mg every 8 hours Oral It is an alpha 2 adrenergic agonist that reduces levels of circulating epinephrine. Treat Hypertension, narcotics and alcohol withdrawal and may act as sedative. Dizziness Shortness of breath, headache and diarrhea. Lovenox 40 mg once daily Subcutaneous route Binds to facilitate activity of antithrombin 3. Treat unstable angina and myocardial Infarction (MI) Hyperkalemia, headache, bleeding and abdominal pain are some of the adverse effects of this drug. Hydromorphone 2 mg every 3 hours Intravenous It is a central acting analgesic component of morphine family. It treats pain. Respiration depression, dizziness, sedation, constipation, itching and light-headedness Linagliptin 5 mg once per day Oral It is DPP-4 inhibitor, an enzyme that is important in metabolism of Glucose-like Peptides. It also increase insulin biosynthesis May cause hypoglycemia, dizziness and hepatotoxicity. Metformin 500mg two times a day Oral Reduces hyperglycemia by suppressing glucose production by hepatocytes and increases insulin sensitivity of the cells Gastrointestinal irritation, cramps, nausea, vomiting, diarrhea and increased flatulence. Oxycodone 30 mg every 12 hours Oral The drug bids to the opioid receptor, which inhibit release of neurotransmitters by reducing amount of cAMP thus closes calcium channels. Constipation, dizziness, urine detention, anxiety, fatigue, nausea and vomiting. Tamsulosin 0.4mg once per day Oral It is a selective alpha one antagonist used in treatment of urination problem. Cataract, severe hypotension and iris syndrome Task 4: Analysis Questions from the case study are myriad; firstly, what could be the priority intervention in the DKA clinical management. Certainly, management of this patient should focus on four important areas. Firstly, the sciatic pain management is treated using hydromorphone analgesic, while stabilizing the patient, pain management should be a number one priority. Secondly, restoring hydration status of the patients important because it allows uptake of medication. Koda-Kimble & Alldredge (2013) states that stabilizing sugar levels is an integral component in treating DKA. It is a central part in the management of this patient. However, administration of metformin alone without fluid replacement therapy in the management leaves a lot to be desired. Based on my clinical opinion, the initial management should focus on restoring lost fluid, pain management and sugar levels stabilization. Although the sugar levels will not fall immediately, it is important to put it as a priority step. Moreover, there should have been insulin administration to offer immediate intervention to reverse devastating effects of the DKA. It should be noted that DKA is a complication of uncontrolled sugars. Based on the proposed drug regimen, it poses questions about what priority intervention should have been considered. In order to reverse all these progressive urinary and metabolic complications, the management should focus on controlling sugars and all these other defects would shift towards physiological normalcy (Koda-Kimble & Alldredge 2013). While administering metformin as a central drug in the management, there should be caution to the patient because of compromised kidney functions. This drug usually increases risks of lactic acidosis in the patient with creatinine levels of over 150 miliMoles per liter (Koda-Kimble & Alldredge 2013). The focus in the management of this patient should be fluid balance with a view of balancing blood osmolality. References Koda-Kimble, M., & Alldredge, B. (2013). Applied Therapeutics: The Clinical Use of Drugs. Baltimore: Wolters Kluwer Health/Lippincott Williams & Wilkins. Read More
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