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Diabetes Mellitus Type 2: Pathophysiology and Treatment Research Paper

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Updated: Aug 6th, 2020

Abstract

Type 2 diabetes mellitus (T2DM) is a serious metabolic disease that manifests with chronic conditions such as hypertension, nephropathy, and adverse cardiovascular events. This case report analyzes a patient presenting with T2DM at the ED with the major symptoms being abdominal pain, polydipsia, polyurea, and lightheadedness. The significant vital signs were tachycardia, elevated blood pressure, hyperglycemia (550mmol/dL), subnormal bicarbonate and BUN levels, high creatinine level, and anion gap, consistent with the diagnosis of microvascular and macrovascular complications related to T2DM. The primary etiologies linked to the patient’s T2DM condition include morbid obesity (350lbs) and family history. The treatments considered, including insulin drips, further pharmacological interventions, and diet/weight management plan for the patient are discussed.

Introduction

Diabetes mellitus (DM) is a group of metabolic disorders that manifests clinically as long-term hyperglycemia (PG ≥ 8.0mmol/l) due to impaired insulin production or resistance in the liver and skeletal muscles (Wu, Ping, Tanaka, & Zhang, 2014). Its two major variants include type 1 DM (insulin-dependent) and type 2 DM (non-insulin-dependent). Type 2 DM or T2DM is a major global health problem that affects 90-95% of diabetics worldwide, causing significant implications for health spending (Wu et al., 2014). The primary effect of inadequate insulin or repressed insulin sensitivity is impaired glucose uptake and metabolism, resulting in hyperglycemia.

T2DM is a complex disease whose etiology is linked to a host of genetic and environmental factors and their interactions. The genetic factors implicated in T2DM pathogenesis relate to a family history of the disease. Genetic polymorphisms involving insulin receptor genes expressed in the pancreatic β cells, e.g., PPRAG and IRS receptors, have been associated with T2DM pathogenesis (Zhang et al., 2016). The mutations cause pancreatic β cell dysfunction, resulting in impaired insulin secretion or resistance. Mutations in other genes involved in the insulin transduction pathway, i.e., glucokinase and mitochondrial genes, also lead to the pathophysiological T2DM progression (Wu et al., 2014). Due to repressed postprandial insulin secretion reduced insulin sensitivity the pancreatic β cells are overworked, resulting in their apoptosis.

The apoptotic progression reduces the pancreatic β cell mass, resulting to lower basal insulin release. With regard to environmental/lifestyle risk factors, obesity (BMI>25) due to physical inactivity and high fat intake is associated with a fivefold risk of developing T2DM (Pulgaron & Delamater, 2015). Other risk factors include aging, alcohol abuse, and smoking. Because it manifests with chronic hyperglycemia and related complications, T2DM is associated with low quality of life for diabetics (Kahn, Cooper, & Prato, 2014).

Further, T2DM-related comorbities, including cardiovascular disease (hypertension) and stroke, account for the high morbidity and mortality among diabetics. Studies show that up to 80% of T2DM patients develop hypertension or succumb to poor glycemic control (Handelsman, 2013). T2DM patients also suffer from symptoms like weight loss, nephrosis, and impaired vision that affect their quality of life. This paper will utilize a case study approach to discuss T2DM etiology and pathogenesis, clinical manifestations, psychosocial implications, and diagnosis, among others.

Case Study

Background Information

The patient is a 22-year-old male with morbid obesity (350lbs) with no past medical history who presents to the ED with abdominal pain and vomiting. The pain is located in right upper quadrant, sharp, non-radiating, worse when pressed, and continuous. The pain scale is 8/10. The patient states that he has been vomiting for 3 days without bleeding. He further complains of polydipsia (frequent thirst), poly urea (frequent urination), excessive sweating, and lightheadedness.

Etiology of T2DM

T2DM is a multifactorial disorder linked to genetic and environmental causes. The etiology of T2DM has a heritable genetic correlation with a family history of the disease (Sanghera & Blackett, 2012). Family history is one etiological factor specific to the patient. The patient’s type 2 diabetes new onset could be related to a paternal history of diabetes, as his father has DM type 2. T2DM involves a significant genetic component that accounts for its higher incidence rate first-degree relatives compared to the general population. First-degree relatives with a positive family history have up to 40% T2DM risk compared to those with no first-degree relative with the disease (Cullmann, Hilding, & Ostenson, 2012).

Another etiological factor relevant to the case is obesity. Morbid obesity (BMI>25) is associated with visceral fat mass gains; hence, a significant risk factor for T2DM (Pulgaron & Delamater, 2015). Further, the adiposity gains increases the risk of low insulin sensitivity in key target organs – liver and muscles. The patient has a positive diagnosis of morbid obesity (350lbs), implying that his T2DM has a positive lifestyle factor correlation. He presents with elevated blood pressure (200/94) and metabolic syndrome (glucose level = 550mg/dL), which are the usual co-morbidities related to obesity (Pulgaron & Delamater, 2015).

Obesity is related to lifestyle factors, such as lack of exercise, alcohol use, and smoking. The patient’s obesity could be related to alcohol use, diet, and genetics. Epidemiological studies demonstrate that obesity increases the T2DM risk due to its impact on insulin sensitivity (Cullmann et al., 2012). Further, low-fiber diet and intake of fatty acids also reduce insulin sensitivity contributing to T2DM progression.

The patient’s racial background could also be an etiological factor in T2DM new onset. Individuals of particular racial/ethnic backgrounds, e.g., African-American, have a higher T2DM risk than European or Caucasian descent populations (Sanghera & Blackett, 2012). Further, diabetes-sensitive genes have been identified in Japanese populations that reduce the postprandial insulin production capacity (Sanghera & Blackett, 2012). Thus, the patient’s ethnic/racial background coupled with lifestyle factors significantly increases the T2DM risk.

Pathogenesis

The primary pathophysiological features of T2DM include inadequate insulin secretion and low insulin sensitivity or resistance. In the case of the patient, his morbid obesity is the likely cause of insulin resistance that predisposed him to the insidious onset of T2DM. The patient’s T2DM is at its early stage. The development of insulin resistance in this patient was progressive, leading to T2DM onset at age 22.

Resistance arises when the insulin secreted by the pancreatic β cells does not produce the desired effects on the target organs, i.e., the liver and muscles (Cullmann et al., 2012). As a result, the cells secrete more insulin to compensate for the reduced sensitivity, leading to pancreatic β cell dysfunction. This process causes a decline in the secretory response of the beta cells, even when the blood glucose level is beyond the normal range, which is 7.8 mmol/l two hours postprandial (Wu et al., 2014). Therefore, reduced insulin sensitivity of receptors in the liver and skeletal muscles affects insulin metabolism, leading to hyperglycemic spikes.

Low insulin sensitivity can occur in individuals with morbid obesity; however, T2DM develops when the pancreatic β cells cannot overcome the resistance through more insulin secretion (Pulgaron & Delamater, 2015). Peripheral insulin resistance may occur in obese individuals due to free fatty acids. Elevated fatty acid levels in the blood induce the gluconeogenesis process in the liver that leads to glucose synthesis from non-carbohydrate sources, resulting in hyperglycemia (Pulgaron & Delamater, 2015).

Impaired insulin secretion could also account for the patient’s new onset T2DM. A reduction in glucose-responsive secretion leads to high postprandial blood glucose level (Kahn et al., 2014). In individuals with obesity, a reduction in early-phase secretion occurs when blood glucose levels are high (glucose toxicity).

This process is a pathophysiological feature accounting for the onset of T2DM in overweight individuals. Impaired secretory response occurs in a progressive manner and leads to pancreatic β cell dysfunction (Kahn et al., 2014). While in prediabetes (onset T2DM) is characterized by elevated postprandial glucose due to reduced insulin sensitivity and secretory response, hyperglycemia is due to the pancreatic β cell dysfunction resulting from these processes.

Clinical Manifestations

Patients with either T1DM or T2DM show three major symptoms – polyuria, polydipsia, and polyphagia (Wu et al., 2014). The patient’s complaints of polydipsia and polyurea are symptomatic of early stage acute T2DM. Polyuria manifests as frequent urination due to the elevated blood glucose levels that cause the drawing of water from the cells, resulting in the excretion of large volumes of pale dilute urine by the kidneys (Wu et al., 2014). Polydipsia (frequent thirst) results from polyuria. The cellular dehydration resulting from hyperglycemia triggers the hypothalamus, which monitors blood solute levels and pressure that causes the feeling of thirst (Wu et al., 2014). Thus, the patient’s polydipsia is connected to the polyuria condition that causes body dehydration due to hyperglycemia.

The other symptom of T2DM shown by the patient is abnormal blood urea nitrogen (BUN) level of 6 (the normal level is 7-22). The BUN test indicates the plasma levels of urea nitrogen. Urea is the product of protein metabolism that is excreted through the kidneys (Kahn et al., 2014).

Therefore, the lower than normal BUN levels in the patient indicate reduced liver function due to diabetic neuropathy. However, low protein diet, over-dehydration, and high carbohydrate intake have been associated with low BUN levels. The elevated creatinine level of 1.28mg/dL (normal = 0.6-1.2mg/dL) is another symptom of diabetic nephropathy. The building up of plasma creatinine levels is an indication of impaired renal function due to hyperglycemia.

The patient also presents with excessive sweating, lightheadedness, tachycardia (HR = 127 beats/min), and elevated blood pressure (200/94). Hypertension is a common co-morbid condition in diabetic patients related to impaired insulin metabolic action/resistance. Insulin stimulates glucose metabolism in the muscles and represses the lipoprotein synthesis in the liver cells (Kahn et al., 2014). Insulin resistance causes dyslipidemia whose effects include arterial stiffness and reduced vasodilation.

These effects contribute to elevated blood pressure in patients with T2DM. Other possible symptoms include polyphagia (elevated appetite) and glycosuria. The patient also presents with GI complications, i.e., abdominal pain and vomiting. According to Wu et al. (2014), chronic abdominal pain in diabetic patients is due to T2DM-related complications such as “neuritis and autonomic dysfunction” (p. 1189). Another T2DM-related symptom seen in the patient is ischemia.

Tissues, Organs, and Organ Systems Affected

The pathogenesis of T2DM implicates multiple tissues, organs, and systems involved in glucose homeostasis in the patient presented in this case. They include tissues – skeletal muscle and adipose tissue, organs like the liver, pancreas, kidneys, and brain, and systems such as the digestive system, circulatory system, and the endocrine system. The liver is the main regulatory organ that controls the blood glucose in circulation (Kahn et al., 2014).

It contains glycogen reserves that are converted to glucose for a rapid glycemic control. The liver also synthesizes glucose from non-carbohydrate substrates, e.g., amino acids. It compensates for low plasma glucose through glucagon-mediated glycogen-glucose conversion. The patient’s diabetic ketoacidosis is linked to liver malfunction due to insulin resistance that results in the inhibited glucose release by the liver cells (Kahn et al., 2014). As a result, the body utilizes other substrates, resulting in the buildup of ketones.

The skeletal muscle tissue contributes to hyperglycemia through insulin resistance. In this tissue, the insulin-mediated glucose uptake declines depending on the level of adiposity (Wu et al., 2014). Further, adipocyte-derived factors called adipokines and free fatty acids have been shown to step-up the resistance (Wu et al., 2014). Given the patient’s visceral obesity, insulin resistance in the liver and muscle tissue is the likely cause of his acute hyperglycemia. Visceral fat build-up in insulin-sensitive tissues, including the adipose tissue, liver, and muscle cells is a significant factor in insulin resistance. Increased breakdown of the adipose tissue in T2DM patients to provide cell substrates increases free fatty acids in circulation that cause insulin resistance.

The pancreas is another organ affected by T2DM in the patient presented. Pancreatic β cells (islets of the Langerhans) secrete insulin, while α cells release glucagon (Wu et al., 2014). Glucagon is involved in the conversion of glycogen reserves in the liver/muscle cells into glucose during fasting or hypoglycemia. The two hormones are part of the endocrine system. The pancreas also secretes Amylin that controls the postprandial glucose levels in the blood (Wu et al., 2014).

The patient’s kidneys may also be affected. His lab results include normal sodium level of 139mmol/L, low potassium level of 3.3mmol/L, low bicarbonate/BUN level, and elevated creatinine level (1.28mg/Dl). The anion gap level was also high at 27. From these values, the organ affected includes the kidneys due to electrolyte imbalance that results in low levels of bicarbonate/BUN and potassium.

Lesion Distribution

Hyperglycemia (550mmol/dL) in the patient is a systemic condition that affects multiple body organs. The patient’s vitals and complaints are manifestations of a metabolic disorder involving multiple organs. T2DM patients are at risk of various complications, including macro-vascular disorders (hypertension, CAD, and stroke) and micro-vascular conditions (nephropathy). Hypertension is the leading co-morbid condition associated with T2DM.

The patient presented symptoms of tachycardia (127 beats/min and elevated blood pressure (200/94) may be linked to cardiovascular disease. Studies show common environmental factors cause hypertension and T2DM in most populations (Wu et al., 2014). Reduced insulin sensitivity, oxidative stress, and hyperlipidemia due to obesity have been implicated in the development of T2DM and hypertension.

Some of the patient’s symptoms are a manifestation of diabetic nephropathy. The lab results show elevated creatinine level (1.28mg/dL) and lower BUN levels, consistent with diabetic neuropathy diagnosis. This indicates that T2DM has a systemic effect on renal functioning. The renal disorder correlates with insulin resistance in the patient. Further, the large anion gap (27) indicates a positive diabetic ketoacidosis (DKA) diagnosis (Puttanna & Padinjakara, 2014).

The buildup of the harmful ketones results from insulin resistance by the liver cells. As a result, the liver cannot metabolize glucose, contributing to hyperglycemia. A review by Puttanna and Padinjakara (2014) found insulinopenia (insulin deficiency) and elevated free fatty acids as the primary causes of DKA in prediabetes. The mechanism involves a lack of adequate insulin to control ketosis.

Factors that may have Contributed to T2DM Development

Certain aspects of the patient’s life could have contributed to the development of the disease. His social history shows that he does not use illicit drugs or smokes, but drinks occasionally when out with friends. The consumption of beer and spirits has been associated with increased risk of abnormal glycemic profiles associated with pre-diabetes and T2DM (Cullmann et al., 2012). This study also found that low alcohol use reduced the T2DM risk in females. In this study, the risk of developing T2DM was higher in samples that consumed spirits than those with a moderate wine intake. Therefore, the patient’s occasional alcohol use could have predisposed him to T2DM.

Another risk factor relevant to this case is genetics. The patient’s father has a history of T2DM, an important factor in the pathogenesis of the disease. Family history accounts for the high T2DM incidence of up to 40% in first-degree relatives compared to non-first-degree relatives (Sanghera & Blackett, 2012). The heritable genetic component relates to genes involved in glucose metabolism or homeostasis. Heritable mutations in the insulin receptor genes, such as the KCNQ1 gene, have been associated with impaired insulin secretion and resistance (Sanghera & Blackett, 2012). The patient may have inherited genetic abnormalities that affected insulin function or secretion from his father, predisposing him to T2DM.

The patient’s morbid obesity (350lbs) is another identifiable risk factor for hyperglycemia. Obesity (BMI>25) results from high intake of fat and simple sugars in junk/processed food and physical inactivity. The patient’s obese status may childhood overweight that persisted into adulthood. It indicates that the patient does not engage in healthy dietary practices and physical exercise to achieve normal BMI. Studies show that an overweight condition accounts for up to a fivefold improvement in the risk of developing T2DM (Zhang et al., 2016). Further, morbid obesity is associated with visceral fat accumulation that causes insulin resistance. The father has a medical history of high cholesterol; therefore, the patient has a genetic predisposition to obesity, which is a T2DM risk factor.

Sequelae of T2DM

T2DM is associated with chronic complications such as hypertension and renal disorders. At the time the patient presented to the ED, he manifested symptoms associated with macrovascular disorders. His vitals were tachycardia (HR=127 beats/min), elevated bp = 200/94, normal body temperature (98.6oF), and RR = 20. Tachycardia and elevated blood pressure are signs of hypertension as a comorbid condition.

According to Wu et al. (2014), a positive hypertension diagnosis often precedes T2DM onset, which indicates that the two conditions have a common metabolic cause. Hypertensive individuals have a threefold risk of developing T2DM within a 5-year period, compared to normotensive individuals (Wu et al., 2014). Therefore, in the present case, hypertension is the major sequelae related to the patient’s T2DM. Other sequelae that may occur include cardiovascular disease and strokes.

The patient also presented with symptoms characteristic of microvascular complications. He had a large anion gap, elevated creatinine levels (1.28mg/dL), and electrolyte imbalance (low BUN, K+, and bicarbonate), which are highly suggestive of diabetic nephropathy. The condition develops when the intraglomerular pressure builds up, causing hypertension in the glomeruli (Cullmann et al., 2012).

The patient’s severe abdominal pain (sharp, non-radiating, and continuous) indicates GI abnormalities due to the diabetic neuropathy. The pathogenesis of this condition relates to the hyperglycemic damage of vessels nourishing the nerve fibers in the abdominal area. The condition may also be due to microvascular circulation impairment, which affects the autonomic system and causes pain (Cullmann et al., 2012). Another sequelae that is likely to occur includes diabetic retinopathy that is characterized by blurred vision due to retinal vessel destruction (Cullmann et al., 2012). The patient’s elevated sinus tachycardia (127bpm) could lead to the rupturing of capillaries supplying the retina and occasion blindness.

Further, the signs of ischemia in leads II and III are highly suggestive of possible inferior myocardial infarction (MI). The MI risk factors present in the case include hypertension and T2DM. Hyperglycemic profiles increase the risk of atherosclerotic plaques in T2DM patients that cause high blood pressure and unstable angina. Another possible complication the patient may develop in his old age is diabetic foot ulcers. Peripheral neuropathy related to T2DM causes suppressed pain sensation in the lower extremities of T2DM patients (Cullmann et al., 2012). As a result, non-healing foot ulcers develop due to impaired blood flow.

Patient Prognosis

T2DM is a major risk for adverse cardiovascular prognosis in our patient due insulin therapy. Effective glycemic control through agents like insulin is linked to improved cardiovascular event prognosis in T2DM patients (O’Keefe, Abuannadi, Levie, & Bell, 2012). However, the agents increase the risk of hypoglycemia that causes adverse cardiovascular events. T2DM patients receiving intensive insulin/sulfonylurea therapy may develop mild hypoglycemia. This condition stimulates the sympathetic nervous system that may induce the development of cardiovascular problems, including myocardial infarction, arrhythmias, and cardiopulmonary arrest (O’Keefe et al., 2012). Further, hypoglycemia may cause lengthened QT interval and ventricular tachyarrhythmias that increase the risk of cardiovascular problems.

Aggressive glycemic control may also cause cardiovascular toxicity in the patient given his predisposition to heart disease. He has morbid obesity and a paternal history of elevated cholesterol that could predispose him to adverse cardiovascular events. According to Handelsman (2013), individuals with atherosclerosis and ventricular hypertrophy are at a higher risk of developing cardiovascular complications during an aggressive glycemic control with insulin therapy. Therefore, long-term insulin therapy for T2DM may lead to cardiovascular disease prognosis due to hypoglycemia in the patient.

Glucose-lowering therapies may fail to give a better cardiovascular prognosis due to postprandial hyperglycemia (Handelsman, 2013). The treatments aim to achieve better glycemic profiles during fasting and pre-prandial cycles, as opposed to controlling postprandial spikes. Postprandial hyperglycemia is linked to a high risk of cardiovascular disease due to elevated triglyceride levels (Handelsman, 2013). Another prognosis relevant to the present case is atherosclerosis. The sinus tachycardia is highly suggestive of fatty deposits (atheromas) in arterial walls, causing endothelial dysfunction (arterial narrowing).

Therapies Used/Considered

After presenting at the ED, the patient was started on an insulin drip and hourly glucose check to lower the acute hyperglycemia. Insulin therapy is an effective strategy for achieving normal glycemic profiles in T2DM patients. The underlying mechanism involves the repression of glucose release by the liver and promotion of postprandial glucose metabolism (Tamez-Perez, Proskauer-Pena, Hernrndez-Coria, & Garber, 2013). The patient was started on an insulin drip to achieve an immediate reduction in glucose concentrations (550mmol/dL) to normal levels. The exogenous insulin therapy was also meant to minimize the effects of glucose toxicity and ketoacidosis by preventing ketosis. Rapid-acting insulin analogues can also be used in place of insulin drips.

Early-stage T2DM can be controlled through diet to achieve appropriate BMI levels. The treatment plan for the patient includes diet and weight management plan targeting the modifiable risk factors. The plan will involve working with the patient to help him achieve healthy eating, quit drinking, and start exercising/resistance training.

The pharmacological management of T2DM involves various anti-diabetic drugs. Sulfonylureas are second-line anti-hyperglycemic agents that could be given to the patient if he cannot respond to metformin or biguanine (Tamez-Perez et al., 2013). The sulfonylureas induce insulin secretion through pancreatic β cell stimulation (Cullmann et al., 2012). However, this class of drugs is not recommended for obese/overweight patients.

The first-line drugs that will be prescribed to the patient will be biguanide (metformin, 100mg twice daily). The drug reduces glucose production by the liver by inhibiting gluconeogenesis and glycogenolysis (Handelsman, 2013). It also stimulates glucose metabolism in skeletal muscle cells. The rationale for giving metformin at the early stage of T2DM is to improve treatment success rates. Metformin combination therapy with GLP-1 RAs (sulfonylureas) would lead to effective glycemic control without causing hypoglycemia (Handelsman, 2013). GLP-1 RAs induce feelings of satiation through slow gastric emptying, resulting in steady weight loss (Handelsman, 2013).

Conclusions

T2DM is a severe metabolic disorder with systemic disruption of glycemic control. In the introduction, T2DM was associated with chronic co-morbidities, such as hypertension, stroke, and nephrosis. Comparable clinical manifestations of T2DM seen in the case study imply hyperglycemia that has remained undetected in the patient; hence the severe abdominal pain. The T2DM progression has followed the typical path described in literature. In the patient, a family history and morbid obesity occasioned a progressive development of the pathophysiological features of T2DM, i.e., impaired insulin production and resistance, leading to disease onset. The two factors are the likely etiologies of T2DM. The associated clinical manifestations included elevated blood pressure, signs of nephropathy, polydipsia, and polyurea.

References

Cullmann, M., Hilding, A., & Ostenson, C. (2012). Alcohol consumption and risk of pre-diabetes and type 2 diabetes development in a Swedish population. Diabetic Medicine Journal, 29(4), 441–452.

Handelsman, Y. (2013). Diabetes and hypertension: A comprehensive report on management and the prevention of cardiovascular and renal complications. The Journal of Clinical Hypertension, 13(4), 221-223.

Kahn, S., Cooper, M., & Prato, S. (2014). Pathophysiology and treatment of type 2 diabetes: Perspectives on the past, present, and future. The Lancet, 383(9922), 1068-1083.

O’Keefe, J., Abuannadi, M., Levie, C., & Bell, D. (2012). Strategies for optimizing glycemic control and cardiovascular prognosis in patients with type 2 diabetes mellitus. Mayo Clinic Proceedings, 86(2), 128-138.

Pulgaron, E., & Delamater, A. (2015). Obesity and type 2 diabetes in children: Epidemiology and treatment. Current Diabetes Reports, 14(8), 508-515.

Puttanna, A., & Padinjakara, R. (2014). Diabetic ketoacidosis in type 2 diabetes mellitus. Practical Diabetes, 31(4), 155-158.

Sanghera, D., & Blackett, P. (2013). Type 2 diabetes genetics: Beyond GWAS. Journal of Diabetes and Metabolism, 3(1), 198-205.

Tamez-Perez, H., Proskauer-Pena, S., Hernrndez-Coria, M., & Garber, A. (2013). AACE comprehensive diabetes management algorithm 2013 endocrine practice. Endocrine Practice, 19(4), 736-737.

Wu, Y., Ding, Y., Tanaka, Y., & Zhang, W. (2014). Risk factors contributing to type 2 diabetes and recent advances in the treatment and prevention. International Journal of Medical Sciences, 11(11), 1185-1199.

Zhang, J., Yang, Z., Xiao, J., Xing, X., Lu, J., Weng, J.,…Yang, W. (2016). Association between family history categories and prevalence of diabetes in Chinese population. Plos One, 10(2), 1-8.

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