section epub:type=”chapter” id=”c0240″ role=”doc-chapter”> This chapter presents select chronic disorders to educate the perianesthesia nurse. In an effort to reduce the incidence of postoperative complications in surgical patients with chronic disorders, this chapter provides information about the different disease processes to facilitate appropriate evidence-based nursing interventions that will lead to a positive outcome for the patient. COPD; diabetes mellitus; multiple sclerosis; myasthenia gravis; rheumatoid arthritis; sickle cell disease A chronic disorder is a health condition or disease persistent in its effects that lasts more than 3 months. Many times, chronic disorders may cause physiologic changes that require surgical intervention; however, no matter the reason for undergoing surgery, patients with chronic disorders are at greater risk of developing postoperative complications. If the patient’s health can be enhanced before surgery, the patient’s ability to have a positive perioperative experience will increase. In this chapter, selected chronic disorders will be presented to educate perianesthesia care clinicians. For example, patients with chronic obstructive pulmonary disease can have significant preoperative respiratory dysfunction, of which some improvement can be accomplished with intense and knowledgeable nursing care. Patients diagnosed with one or more chronic disorders described in this chapter present a significant challenge to the perianesthesia nurse. In an effort to reduce the incidence of postoperative complications in patients with chronic disorders, this chapter provides information about the different disease processes to facilitate appropriate evidence-based nursing interventions that will lead to a positive outcome for the patient. Definitions A1C Blood test measuring the amount of red blood cells glycosylated over the course of the past 2 to 3 months, helping to assess diabetes control in that time period. Asplenia Absence of normal spleen functions and associated with serious infection risks. Axial Muscles Muscles of the head and trunk. Bulbar Muscles Muscles of the mouth and throat responsible for speech and swallowing. Cor Pulmonale Right heart failure as a result of primary lung disease. Diplopia Double vision. Hemolyze Breakdown of red blood cells that causes a release of hemoglobin. Hypercarbia Abnormally high levels of carbon dioxide in the blood. Insulin Resistance The body’s inability to metabolize glucose despite the presence of insulin. Immunosuppressants Agents that significantly interfere with the ability of the immune system to respond to antigenic stimulation with inhibiting cellular and humoral immunity. Microangiopathy A disease of the small blood vessels. Miosis Contraction of the sphincter muscle of the iris that causes the pupil to become smaller. Myasthenic Facies The common facial expression in myasthenia gravis, consisting of drooping of the eyelids and corners of the mouth with weakness of the facial muscles. Plasmapheresis Removal of plasma from previously withdrawn blood via centrifugation, reconstitution of the cellular elements in an isotonic solution, and reinfusion of this solution into the donor or another person who needs red blood cells rather than whole blood. Ptosis Abnormal condition in which the upper eyelids droop because of muscle weakness. The term chronic obstructive pulmonary disease (COPD) describes an inflammatory disease characterized by progressive development of obstructed airflow that is not fully reversible. This chronic inflammation causes structural changes in small airways, destroys the lung parenchyma, disrupts the usual repair and defense mechanisms of the lungs, and affects pulmonary vasculature. Previous definitions of COPD have emphasized emphysema and chronic bronchitis as the primary defining types of COPD. However, evidence shows COPD to be more than the alveoli destruction of emphysema and the productive cough of chronic bronchitis. The characteristic pathologic changes found in COPD are due to chronic inflammatory response and structural changes from repeated injury and repair. It is increasingly recognized that patients with COPD have systemic features that may initiate or worsen comorbidities such as cardiovascular disease, normocytic anemia, diabetes, and depression.1,2 Recognized as the third leading cause of morbidity and mortality worldwide, COPD is the fourth leading cause of death in the United States.1,3 COPD prevalence and the social burden of COPD are projected to increase in the near future due to the changing age structure of the world’s population and continued exposure to COPD risk factors, such as smoking. The economic impact of COPD on health care systems is considerable. In the United States, a 20-year projection shows that the direct medical costs attributed to COPD are estimated to be $800.90 billion, with a range of 565.29 billion to 1081.29 billion by 2038 when associated with current patterns of smoking and treatments.4 COPD exacerbations explain the greatest proportion of the total burden on health care systems with a direct relationship between COPD severity and cost of care. Active smoking remains the main risk factor for COPD, with lifetime smokers having up to a 50% chance of developing COPD; however, other factors may influence its development, such as air pollution; occupational exposure to chemicals, gases, and dusts; genetic factors (alpha-1 antitrypsin deficiency); and chronic respiratory infections.1,4 There is increasing evidence that women have a higher predisposition to developing COPD because of an increased susceptibility to cigarette smoke. Women have smaller airways than men, and this could lead to a greater dose effect from each cigarette. Female smokers also have differences in metabolism of cigarette smoke as well as reduced estrogen compared with male smokers.1,5 COPD prevalence also increases with age and is approximately six times higher in at-risk persons 70 and older compared with those 40 to 49 years old.1,3 The pathogenesis of COPD appears to be a modified inflammatory response of the airways to chronic irritants such as cigarette smoke. The multiple mechanisms of this amplified inflammation are not fully understood. However, they include a definite pattern of inflammation involving increased cytotoxic lymphocytes (CD8+) present only in smokers who develop COPD.1,5 These cells release inflammatory mediators and enzymes that further amplify the inflammatory process and interact with the structural cells of the airways, lung parenchyma, and pulmonary vasculature, thereby stimulating fibrosis of the bronchia wall, hypertrophy of submucosal glands, mucus hypersecretion, and loss of elasticity throughout lung fibers and alveolar tissues. The disease process in COPD leads to characteristic physiologic abnormalities and symptoms. For example, the surface area for gas exchange within the lungs is decreased when destruction of alveolar tissue occurs. As the alveolar septa are destroyed, insufficient alveolar ventilation ensues, eventually leading to hypercarbia. With disease progression, carbon dioxide cannot be expelled from the lungs and is retained there. The patient usually increases minute ventilation to try to compensate for the hypercarbia. Respiratory acidosis develops slowly as the various acid-base buffer systems try to neutralize the accumulated acid. In this compensated state, the patient usually has a near-normal pH, high plasma bicarbonate, low chloride concentration, and high total carbon dioxide levels. Elastic lung fibers, which normally provide traction and hold open the airways, lose function when damaged and lead to impaired expiratory flow, increased air trapping, and predisposition to airway collapse. The extent of inflammation damage in small airways is correlated with the reduction in the forced expiratory volume in the first second (FEV1) and the ratio between FEV1 and the forced vital capacity (FVC) of exhalation. A diagnosis of COPD is confirmed when airflow obstruction is a post-bronchodilator FEV1 to FVC ratio less than 0.70.1,5 Exacerbation of symptoms and comorbidities may add to the severity of COPD in individual patients. During respiratory exacerbations, there are usually increased hyperinflation, gas trapping with reduced expiratory airflow, and increased dyspnea. There is also a worsening of ventilation-to-perfusion (VA/Q) abnormalities and resultant hypoxemia. Manifestations of COPD range from dyspnea, poor exercise tolerance, chronic cough with or without sputum production, and wheezing to cor pulmonale or respiratory failure.2 When subjected to surgery, the patient with COPD has a higher incidence of pulmonary risk for postoperative complications. These patients must be given meticulous preoperative care so that they are in the best possible health when they enter surgery. Preoperative medical treatment usually includes hydration, nutrition, chest physiotherapy, bronchodilators, and prophylactic antibiotics if an infection is present. Serial pulmonary function tests and arterial blood gas determinations are used to monitor the progression of the preoperative treatment.1 When the patient’s pulmonary function tests and arterial blood gas results no longer show continued improvement, surgery is considered because the patient has reached optimal pulmonary status. Cigarette smoking affects the manner in which a patient recovers from an anesthetic and has been shown to be an independent risk factor of poor early perioperative outcomes after a variety of surgical procedures.6 Specifically, higher rates of cardiopulmonary events and surgical site infections (SSIs) have been reported in current smokers.2 Research shows that preoperative smoking cessation decreases the risk of perioperative morbidity when compared with those who continue smoking. After approximately 2 weeks of abstinence, airways may be less reactive. Sputum continues to accumulate until cilia are able to recover, which may take around 8 weeks.7 The perianesthesia nurse should be aware of the diverse reactions that smoking can have on the patient emerging from an inhalation anesthetic. The characteristic pulmonary function alterations in smokers usually include a reduction in vital capacity, an increase in residual volume to total lung capacity, an uneven distribution of inspired gas, a decrease in dynamic compliance, and an increase in nonelastic resistance. With the prevalence of COPD, it is likely that a perianesthesia nurse will care for patients with a diagnosis of COPD or for patients undergoing a surgery related to COPD treatment such as a lung volume reduction surgery. As noted earlier, patients with COPD have significant risks when undergoing anesthesia and surgery. The Centers for Medicare and Medicaid Services (CMS) reports that health care organizations may receive penalties for readmission of patients with COPD who have undergone surgery and experienced postoperative complications considered a result of the surgery.8 The modified stir-up regimen should be used by the postanesthesia care unit (PACU) nurse when caring for patients with COPD. The modified stir-up regimen includes frequent cascade coughing, sustained maximal inspirations (SMIs), and repositioning of the patient (see Chapters 12 and 28). An appropriately implemented modified stir-up regimen is of great importance, especially in patients recovering from upper abdominal or thoracic operations. Surgery at these sites can cause decreased ventilatory effort and a complete absence of sighs by the patient. Given that the patient already has compromised respiratory function, the possibility of retained secretions and atelectasis is magnified. As a result, these patients may represent a significant challenge to the perianesthesia nurse. Opioids and other respiratory depressant drugs should be given in low doses, or they should be avoided completely if the patient has severe COPD. Repositioning of the patient and splinting of the incision site reduces the need for opioids and the anxiety usually seen in these patients. Other ways to maximize analgesia are intercostal nerve blocks and the use of patient-controlled analgesia. When the patient is completely reactive from anesthesia, the use of the incentive spirometer may be helpful in reducing the incidence of atelectasis. Consequently, the perianesthesia nurse responsible for supportive measures should assist and encourage the patient in using the SMI with or without the incentive spirometer. The perianesthesia nurse should also encourage and monitor the patient’s performance of the cascade cough to facilitate early secretion clearance. Patients with COPD have some component of reactive airway disease. Consequently, the airway becomes compliant and can become compressed during a forced expiratory maneuver. This dynamic compression of the airways is a function of the equal pressure point theory as discussed in Chapter 12. To reduce the amount of dynamic compression of the airway during exhalation, the patient should be encouraged to use pursed-lip breathing. Breathing through pursed lips during exhalation can be the same as adding 5 to 10 cm H2O of positive end-expiratory pressure. Increasing the pressure inside the airway during exhalation reduces the amount of dynamic compression of the airways and decreases the amount of air trapping that commonly occurs in patients with COPD. Arterial blood gases may be ordered and capnography may be used to monitor end-tidal CO2 levels. Hypoventilation occurs in patients with severe COPD as they may be unable to maintain a level of alveolar ventilation sufficient to eliminate CO2 and keep arterial oxygen levels within normal range. The overall goal of oxygen therapy is to maintain an oxygen saturation of at least 90% in a patient with COPD. However, close monitoring of these patients is important because increasing arterial Po2 above 60 mm Hg tends to depress the hypoxic stimulus for ventilation and often leads to hypercapnia and thus hypoventilation. Hypoventilation affects arterial blood gases in two important ways. First, there is usually an increase in Pco2 directly related to the level of ventilation (reduction of ventilation by one-half causes Pco2 to double), and second, hypoventilation may cause hypoxemia (arterial Po2 < 55 mm Hg). Hypoxemia accompanied by increased respiratory drive and increased sympathetic response can be readily eliminated by supplemental oxygen administration. Administration of continuous low-flow (1 to 2 L/min) oxygen to maintain Po2 levels between 55 and 65 mm Hg decreases dyspnea and pulmonary hypertension. Many adverse consequences of hypoventilation and hypercapnia are due to respiratory acidosis and include depression of cardiac contractility, decreased respiratory muscle contractility, and arterial vasodilation. Therefore, the patient with COPD should also be under constant surveillance for signs of cardiopulmonary decompensation, including rapid gasping respirations, severe dyspnea, substernal retraction, and disorientation. Blood pressure may be elevated or low, but the patient usually has tachycardia. Perianesthesia care focuses on prevention of complications. Because variations among patients with COPD exist, the perianesthesia nurse should consult with the physician about any further specific nursing care to be administered to the patient with COPD. Diabetes mellitus (DM) affects approximately 34.2 million people in the United States, or 10.5% of the population, including the 7.3 million people undiagnosed. The percentage of older Americans, age 65 and up, remains high at 26.8% or 14.3 million seniors (diagnosed and undiagnosed persons). DM is the seventh leading cause of death, and it is believed that DM as a comorbidity or the actual cause of death is underreported due to the lack of documentation on the death certificate.9 However, it is what transpires between the diabetes diagnosis and death that determines the level of health, the health care needed, and the number of surgical interventions required. The type of diabetes and the level of DM control over the lifetime of the person with diabetes have a direct impact on the incidence of acute or long-term complications and the need for hospitalization and surgery. The two main forms of diabetes are type 1 and type 2. Type 1 has an onset usually before the age of 40; however, it can develop at any age. Nearly 1.6 million Americans have type 1 diabetes, including about 187,000 children.9 Although type 1 is still the most prevalent category among children, the rise in obesity forewarns that childhood type 2 will become the most common by 2030. Additionally, much evidence shows a faster progression of type 2 in pediatric patients contrasted with type 1 or adult-onset type 2 DM.10 Treatment for type 1 DM centers on meal planning, exercise, and dependence on insulin administration. Type 2 diabetes affects about 90% of those diagnosed and most are older than 40 years, have a family history of diabetes, and are obese. Here, the focus is on meal planning, exercise, and weight loss with the possible inclusion of oral hypoglycemics, injectable noninsulin products, and treatment with insulin. As the U.S. population ages, becomes more obese, and is less active, a continued rise in the number of persons with diabetes is expected (Table 48.1).9 From Centers for Disease Control and Prevention. National Diabetes Statistics Report, 2020. Atlanta, GA: Centers for Disease Control and Prevention, U.S. Dept of Health and Human Services; 2020. The diagnosis of DM is determined by multiple methods. A fasting blood glucose (FBG) level equal to or greater than 126 mg/dL (7 mmol/L) indicates DM. An oral glucose tolerance test (OGTT) with a 75-g sugar load may also be used with a resultant blood glucose (BG) of greater than 200 mg/dL (11.1 mmol/L) indicating DM. A random or casual BG >200 mg/dL (11.1 mmol/L) in the presence of the classic signs of DM or a hyperglycemic crisis also meets the diagnostic criteria. The A1C level is a laboratory-based standardized reference assay used to measure a patient’s 3-month average BG level and is a strong diagnostic test. An A1C greater than 6.5% indicates DM (Table 48.2). However, when an A1C is used for diagnosing DM, remember that it is an indirect measure of averaged glucose levels and it is important to consider other patient data that may impact A1C values such as hemodialysis status, pregnancy, HIV, age, ethnicity, and anemias.11 FPG, Fasting plasma glucose; OGTT, oral glucose tolerance test. From American Diabetes Association. Diabetes Care 2021;44(Suppl. 1):S6. Hyperglycemia is most often cited as the primary problem with diabetes. However, it is usually the resultant long-term physiologic changes from chronic hyperglycemia that cause the person with diabetes to require surgery. Chronic hyperglycemia stimulates numerous pathological pathways that results in oxidative stress. Research shows that diabetes-induced oxidative stress is associated with the complications of chronic hyperglycemia such as macrovascular complications, including immune system dysfunction, pulmonary disorders, cardiovascular disease, and microvascular complications, including retinopathy, nephropathy, and neuropathy.12 Perioperative goals for the person with diabetes obviously include the universal positive outcomes sought for all surgical patients. For patients with DM and those with hyperglycemia but not diagnosed with DM, glycemic control is paramount, avoiding both hyperglycemia and hypoglycemia. The American Diabetes Association defines hyperglycemia for all hospitalized patients as a BG level >140 mg/dL (7.8 mmol/L) regardless of a diagnosis of DM. Hypoglycemia is defined as a BG level <70 mg/dL (3.9 mmol/L) with or without symptoms.13 The balancing act of avoiding hyperglycemia while not triggering hypoglycemia proves to be difficult. Yet, both have been shown to carry consequences if not controlled. Varied combinations of medications prescribed make it difficult to find a standardized preoperative plan that works for all people with type 1 or type 2 DM. In fact, it is important to remember that type 1 and type 2 DM are distinctly different diseases. The incidences of perioperative hyperglycemia and hypoglycemia occur significantly more frequent in patients with type 1 DM than in patients with type 2 DM.14 This warrants DM type-specific plans for perioperative treatment of patients with diabetes. The nature and duration of the surgical procedure affects the glucose level and the insulin interventions needed. Doses and frequency may be determined by hospital or surgical center protocols. The relative insulin deficiency (type 2) and the absolute deficiency (type 1) require supplemental insulin IV or subcutaneous basal or bolus injections dependent on where the person is in the perioperative process. Insulin resistance rises during surgery but then rapidly decreases in the postoperative period, increasing the risk of hypoglycemia.15 It is important to recognize that stress-induced hyperglycemia (BG >140 mg/dL) is regularly seen in both diabetic and nondiabetic patients undergoing surgery. Hyperglycemia is estimated to occur in 20%–40% of noncardiac surgery patients, 35% of vascular surgery patients, and 80% of cardiac surgery patients.12,15 Evidence suggests that controlled BG levels in diabetic and nondiabetic surgical patients improve postoperative outcomes versus those surgical patients who do not have controlled BG levels during the perioperative period.13,16 A large retrospective study on diabetic and nondiabetic patients undergoing noncardiac surgery showed that length of stay (LOS) and postoperative complications were linked to poor perioperative glycemic management. Interestingly, researchers found that hyperglycemia and glycemic variability were associated with outcomes differently in the diabetic patient versus the nondiabetic patient during surgery and the immediate postoperative phase of care (first 24 hours postoperative). Higher glycemic variability in the diabetic surgical patient was associated with an increased LOS, increased complications, and higher risk for mortality, whereas in the nondiabetic surgical patients, both glycemic variability and higher mean glucose values were associated with increased LOS and more risk of postoperative complications.17 This evidence suggests that diabetic and nondiabetic patients may experience surgical stress-induced hyperglycemia in different ways and may require different glycemic management approaches for positive surgical outcomes. Determination of any long-term complications and the level of BG control should be made in the preoperative period, hopefully weeks before the scheduled surgery through assessment, medical diligence, and intervention from the primary care physician (PCP) and/or the diabetes specialist. Additionally, people living with DM have associated comorbidities such as cardiovascular and cerebrovascular diseases, renal disease, and neuropathies that increase the risk for perioperative complications.11 Input from medical records can also provide a more thorough assessment for the emergent surgical patient with diabetes. An A1C should be performed preoperatively in all patients with diagnosed DM and any patients with BG >140 mg/dL (7.8 mmol/L) if not done 3 months prior. However, it is important to remember that the A1C value is used to determine long-term management of DM to reduce the risk of heart disease, peripheral vascular disease, and stroke. Research has shown that increasing A1C values may lead to adverse postoperative outcomes as seen in a recent prospective, an observational study including 7655 surgical patients, age 54 and older, who demonstrated that increased A1C values were independently associated with postoperative complications, intensive care unit (ICU) admissions, and longer hospitalizations.18 However, a large retrospective study on the effect of A1C and glucose on postoperative mortality in more than 13,000 noncardiac and cardiac surgeries showed that higher preoperative A1C results may not be associated with 30-day mortality when glucose, age, sex, and age are statistically controlled.19 Preoperative guidelines for medications depend on the person’s home regimen and should be discussed with the person’s PCP and diabetes specialist before the surgical intervention. If possible, those with DM should be scheduled for an early morning surgery to reduce the time without oral intake and medications.20 Surgery involving children or adolescents should take place at a facility designated for that age group.11 In general, persons on oral medications or noninsulin injectables should be advised to hold those medications the evening before or the day of surgery primarily for prevention of hypoglycemia. In addition, metformin is withheld to prevent the possibility of lactic acidosis (Table 48.3). Persons with type 1 DM may be advised to reduce the bedtime insulin to prevent hypoglycemia while NPO before surgery. However, some form of maintenance insulin must be continued to prevent hyperglycemia from the lack of basal insulin. Basal insulin is the amount of exogenous insulin per unit of time necessary to prevent hepatic gluconeogenesis and ketogenesis. From 2020 List of Insulin Products. Available at http://diabeticincontrol.com. Accessed February 2021. Those with type 1 are usually maintained on a basal dose of 1 or 2 injections of long-acting insulin, multiple injections of short or rapid insulin, or continuous subcutaneous insulin infusion (i.e., insulin pump with a rapid-acting analog). Refer to individual hospital policies for details on use of an insulin pump in that facility. In general, the pump may be put into “suspend” mode for minor or short-duration surgeries. Longer procedures in which the person will have a longer period of sedation necessitates removal of the pump and implementation of an IV insulin drip. The bagged and labeled pump and equipment should be sent with the family and that action documented. Persons with type 2 DM who require insulin may also be instructed to reduce the bedtime insulin, but it is equally important that insulin be used to prevent hyperglycemia before surgery (Table 48.4). From American Diabetes Association. Diabetes Care 2021;44(Suppl. 1): S111–S124.
48: Care of the Patient with Chronic Disorders
Abstract
Keywords
Chronic obstructive pulmonary disease
Surgical Considerations
Care of the Patient with COPD
Diabetes mellitus
Group
Number and Percentage
Age < 20 years
210,000 or 0.25% of all people in this age group
Age 18–44 years
4.9 million or 4.2% of all people in this age group
Age 45–64 years
14.8 million or 17.5% of all people in this age group
Age > 65 years
14.3 million or 26.8% of all people in this age group
Men
17.9 million or 14.0% of all men aged 18 or older
Women
16.2 million or 12.0% of all women aged 18 or older
Diagnosis
Plasma Glucose Values
FPG
OGTT
A1C
Normal
< 100 mg/dL (5.6 mmol/L)
< 140 mg/dL (7.8 mmol/L)
< 5.7%
Prediabetes
100–125 mg/dL (6.9 mmol/L)
140–199 mg/dL (11 mol/L)
5.7%–6.4%
Diabetes
≥ 126 mg/dL (7 mmol/L)
> 200 mg/dL (11.1 mmol/L)
≥ 6.5%
Surgical Considerations
Care of the Patient with Diabetes Mellitus
Type of Insulin
Compounds
Onset
Peak
Duration
Rapid-acting analogs
Lispro
15–30 minutes
30–90 minutes
3–5 hours
Lispro-aabc
12–18 minutes
2–3 hours
4.5–7.5 hours
Aspart
12–18 minutes
30–90 minutes
3–5 hours
Glulisine
12–30 minutes
30–90 minutes
3–5 hours
Afrezza
inhaled insulin
12–30 minutes
30–60 minutes
1.5–2.5 hours
Short-acting
Regular
30–60 minutes
2–4 hours
5–8 hours
Regular U 200
30–60 minutes
2–4 hours
5–8 hours
Regular U 500
30 minutes
4–8 hours
Up to 24 hours
Intermediate-acting
NPH
1–2 hours
4–12 hours
14–24 hours
Basal analogs
Glargine
1–2 hours
Peakless
20–26 hours
Glargine U 300
1–2 hours
Peakless
Up to 36 hours
Degludec
30–90 minutes
Peakless
> 42 hours
Detemir
1–2 hours
4–6 hours
Up to 24 hours
Mixed insulin: 70% intermediate and 30% short-acting regular
10–30 minutes
1–6 hours
Up to 24 hours
Mixed insulin: 75% intermediate and 25% rapid-acting insulin
10–30 minutes
1–4 hours
12–24 hours
Mixed insulin: 50% intermediate and 50% rapid-acting insulin
15–30 minutes
1–4 hours
12–24 hours
Chemical Class
Compounds
Action
Biguanides
Metformin
↓ endogenous hepatic glucose production,
↑peripheral glucose uptake
Sulfonylureas
Glipizide
Glyburide
Glimiperide
↑ secretion of insulin from beta cells
Meglitinides
Repaglinide
Nateglinide
↑ secretion of insulin from beta cells
Thiazolidinediones
Pioglitazone
Rosiglitazone
Improves insulin action in the periphery and the liver
α-Glycosidase inhibitors
Acarbose
Miglitol
Inhibits intestinal α-glucosidase, delaying glucose absorption
GLP-1 receptor agonist–injectable
Exenatide
Liraglutide
Albiglutide
Dulaglutide
Stimulates insulin secretion, facilitates homeostasis following food ingestion
Amylinomimetic-injectable
Pramlintide
Regulates glucose concentration post meal (PP), ↑ satiety, slows gastric emptying, ↓ glucagon secretion
DPP-4 inhibitors
Sitagliptin
Saxagliptin
Linagliptin
Alogliptin
↓ endogenous hepatic glucose production,
↑secretion of insulin from beta cells
Bile acid sequestrants
Colesevelam
Poss. ↓ endogenous hepatic glucose production, ↑ incretin levels
Dopamine-2 agonist
Bromocriptine
Hypothalamic regulation–metabolism,
↑insulin sensitivity
SGLT2 inhibitors
Canagliflozin
Dapagliflozin
Emapgliflozin
Blocks glucose reabsorption in the kidneys, increasing glucosuria
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