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This option is wrong because it describes the mechanism of action of calcineurin inhibitors, not glucocorticoids. Calcineurin inhibitors are a type of immunosuppressant that target T cells specifically, while glucocorticoids have a broader effect on various immune cells and inflammatory mediators.

This option is wrong because it describes the mechanism of action of antimetabolites, not glucocorticoids. Antimetabolites are a type of immunosuppressant that interfere with the synthesis of nucleic acids, which are the building blocks of DNA and RNA. This affects the replication and function of immune cells, as well as other rapidly dividing cells such as cancer cells.

This option is wrong because it describes the mechanism of action of monoclonal antibodies, not glucocorticoids. Monoclonal antibodies are a type of immunosuppressant that bind to specific antigens or receptors on the surface of immune cells and either neutralize them or induce their destruction. This can prevent the activation or function of immune cells that are involved in transplant rejection or autoimmune diseases.

This is incorrect because ibuprofen also blocks the production of prostaglandins that regulate platelet aggregation. Therefore, ibuprofen can increase the risk of bleeding by inhibiting platelet function².

This is incorrect because ibuprofen also blocks the production of prostaglandins that maintain renal function. Therefore, ibuprofen can cause sodium and water retention by impairing renal perfusion and glomerular filtration².

This is incorrect because ibuprofen also blocks the production of prostaglandins that mediate bronchodilation. Therefore, ibuprofen can cause bronchoconstriction by shifting the balance between prostanoids and leukotrienes in favor of leukotrienes².

This is incorrect because azathioprine is not known to cause nephrotoxicity or damage to the kidneys². However, some other drugs that are used to treat IBD, such as mesalazine or sulfasalazine, may have this effect³. Therefore, you should have your kidney function checked before starting these drugs and periodically during treatment³.

This is incorrect because azathioprine is not known to cause neurotoxicity or damage to the nervous system². However, some other drugs that are used to treat IBD, such as metronidazole or ciprofloxacin, may have this effect³. Therefore, you should report any signs of neurological problems (such as numbness, tingling, weakness, vision changes, confusion) to your doctor³.

This is incorrect because azathioprine is not known to cause hepatotoxicity or damage to the liver². However, some other drugs that are used to treat IBD, such as methotrexate or 6-mercaptopurine, may have this effect³. Therefore, you should have your liver function checked before starting these drugs and periodically during treatment³.

This is incorrect because these are systemic side effects of corticosteroids that are more likely to occur with oral or injectable forms of the drug². Fluticasone inhalation has a low systemic absorption and a high first-pass metabolism, which means that only a small amount of the drug reaches the bloodstream and most of it is broken down in the liver before it can cause systemic effects¹. Therefore, these side effects are rare with fluticasone inhalation².

This is incorrect because these are not known side effects of fluticasone inhalation or corticosteroids in general². Hypoglycemia (low blood sugar) is more likely to occur with drugs that lower blood glucose levels, such as insulin or oral antidiabetic agents⁴. Osteomalacia (softening of the bones) is more likely to occur with drugs that affect vitamin D metabolism, such as anticonvulsants or antiretrovirals⁵. Myopia (nearsightedness) and dry eyes are more likely to occur with drugs that affect the eye muscles or tear production, such as antihistamines or anticholinergics⁶.

This is incorrect because these are not common side effects of fluticasone inhalation or corticosteroids in general². Oral ulcers (sores in the mouth) are more likely to occur with drugs that irritate the mucous membranes, such as nonsteroidal anti-inflammatory drugs (NSAIDs) or chemotherapy agents. Dysphagia (difficulty swallowing) is more likely to occur with drugs that affect the esophageal motility or sphincter function, such as calcium channel blockers or antipsychotics. Wheeze (a high-pitched sound when breathing) and dyspnea (shortness of breath) are more likely to occur with drugs that cause bronchoconstriction or respiratory depression, such as beta blockers or opioids.

These are the main symptoms of ulcerative colitis that affect the quality of life of patients. Infliximab can reduce these symptoms by healing the inflammation and ulcers in the colon and rectum. Several studies have shown that infliximab can induce and maintain clinical remission, response, and mucosal healing in patients with moderate to severe ulcerative colitis who are refractory to conventional therapies²³⁴.

These are the secondary outcomes of ulcerative colitis that reflect the nutritional status and well-being of patients. Infliximab can improve these outcomes by reducing the systemic effects of inflammation, such as malabsorption, anemia, fatigue, and fever. Several studies have shown that infliximab can improve the health-related quality of life, nutritional status, and functional status of patients with moderate to severe ulcerative colitis²³⁴.

These are the laboratory tests that indicate the severity and complications of ulcerative colitis. Infliximab can normalize these tests by reducing the bacterial translocation, blood loss, dehydration, and liver involvement that may occur in ulcerative colitis. Several studies have shown that infliximab can improve the stool culture, hemoglobin, albumin, C-reactive protein, and liver enzymes of patients with moderate to severe ulcerative colitis²³⁴.