Free Diabetes Ketoacidosis Pathophysiology Essay Sample

Diabetes ketoacidosis (DKA) is a serious hyperglycemic abnormality that commonly results from considerable type 1 diabetes mellitus (T1DM) progression. Stress, infections, long-lasting diuretic or corticosteroid therapy, alcohol intake, drug abuse, an insulin catheter blockage, or insulin infusion pump dysfunction can ultimately induce the stated condition. Individuals of any gender, age, race, and ethnicity can acquire DKA, particularly diabetic patients with T1DM, although the conducted surveillance showed that the reviewed condition is predominant in women compared to men and whites compared to other races. The incidence of the studied disease is variable considering improved therapeutic and diagnostic strategies that allow managing patients with DKA appropriately. The present paper can be beneficial for understanding the pathophysiology of DKA and its diagnostics for improving medical and nursing care in perspective.

Pathophysiology of DKA and Why It occurs in Patients with Type 1 Diabetes

DKA is an acute, multifactorial, life-threatening, metabolic disorder characterized by dehydration, hyperglycemia, ketonuria, ketonemia, and ketoacidosis. The stated condition primarily results from significant hormonal disturbance and relative or absolute insulin deficiency, which is a reason why patients with type 1 diabetes are at a greater risk of acquiring the reviewed complication. Deficient insulin release or its absence facilitate to the development of a certain range of pathological processes inherent in DKA. The aforementioned aberrations entail the development of gluconeogenesis, lipolysis, and glycogenolysis, which are impairments that ultimately underlie DKA pathogenesis. Furthermore, lipolysis is responsible for an increased release and concentration of free fatty acids, which eventually results in hepatic agglomeration of ketone bodies and ketoacids. Moreover, hepatic gluconeogenesis and glycogenolysis both initiate the development of hyperglycemia that is one of the hallmarks of the reviewed condition. In addition, hepatic gluconeogenesis is associated with increased production of ketoacids that cannot be involved in energy production due to insulin deficiency. The latter prevents from involving excessive ketoacids into energy production, which, in its turn, contributes to their accumulation in the serum and urine, and leads to DKA. Importantly, increased protein breakdown and reduced protein formation, “decreased glucose uptake by peripheral tissues and increased counter regulatory hormones” are additional aberrations that underlie the pathophysiology of the reviewed disorder, which exacerbate the process of gluconeogenesis and hyperglycemia. Next, ketogenesis typical of DKA develops due to excessive fatty acids beta-oxidation and excessive acetyl coenzyme A, whereas ketonemia appears due to significantly increased level of acidic substances in the serum. Finally, impaired body ability of extracting excessive ketones entail ketonuria progression, whiles DKA-related metabolic acidosis results from considerable accumulation of acids in the blood. In addition, nausea, vomiting, fatigue, and low appetite are symptoms indicative of the described disorder, which are presented in the provided clinical case. However, DKA can be accompanied with dehydration, abdominal pain, hypotension, tachycardia, and hyperventilation. The highlighted aberrations appear due to excessive release of ketones and ketoacids in the blood and urine, electrolyte loss, and fluid deficit, which entail the progression of the studied condition. Hence, DKA is a severe hyperglycemic disorder that primarily results from insulin deficiency, which interrupt normal metabolic processes.

Assessment Findings Relevant to DKA

Various diagnostic procedures such as complete blood count (CBC), blood glucose test, urinalysis, plasma glucose test, test for measuring arterial blood gases, bicarbonates, ketones, and blood acidity rate are useful for asserting DKA diagnosis. Patients with the stated diagnosis can have hyperglycemia that is “over 250 mg/dL, a bicarbonate level less than 18 mEq/L, and a pH less than 7.30, with ketonemia and ketonuria,” which can be correlated to the discussed disorder. Ketone test can show excessive concentration of ketone bodies in the blood, which can gradually be detected in the urine. Furthermore, arterial blood gases test assists in revealing abnormal pH, Po2, and HCO3 levels, which can be indicative of low pH level, acidosis, and deficient bicarbonate rate. Bicarbonate test is used for evaluating intensity of metabolic acidosis, whereas amylase test allows measuring amylase level which is commonly high at DKA diagnosis. Ultimately, the reviewed metabolic abnormality is diagnosed in case of increased anion gap that varies in the range of 10 mEq/L to 12 mEq/L, and elevated plasma osmolality. The aforementioned laboratory findings can be indicative of metabolic and electrolyte impairments that allow confirming the diagnosis of the studied disease and initiating adequate therapy.

Conclusion

DKA is a serious hyperglycemic emergency that requires competent therapeutic intervention for preventing life-threatening consequences. The discussed disorder occurs due to insulin deficiency, hormonal and electrolyte instability, although other environmental factors can contribute to its progression. Primarily deficient insulin release or its absence, which is typical of T1DM, explains the predisposition of diabetic patients with T1DM to having this abnormality. DKA is associated with gluconeogenesis, lipolysis, and glycogenolysis, which induce the development of hyperglycemia, metabolic acidosis, and ketonuria. Ultimately, excessive concentration of ketones in the blood and urine underlies the reviewed condition. Lastly, increased glycose level, high amylase rate, high ketone concentration, increased anion gap, and impairments in arterial blood gases test as well as other findings indicative of metabolic acidosis allow the nurse to correlate these aberrations to DKA.

 

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