Prednisone, a glucocorticoid, exerts its primary mechanism of action in systemic lupus erythematosus (SLE) by inhibiting the synthesis of inflammatory mediators and suppressing the activation and proliferation of immune cells.

The other options are incorrect because:

A. It inhibits the synthesis of inflammatory mediators and suppresses the activation and proliferation of immune cells: Glucocorticoids like prednisone have potent anti-inflammatory and immunosuppressive effects. They work by suppressing the production of various pro-inflammatory mediators, such as cytokines and prostaglandins. Additionally, glucocorticoids can inhibit the activation and proliferation of immune cells, including T cells and B cells, which play a role in the pathogenesis of SLE.

B. It blocks the activation of T cells by inhibiting the enzyme calcineurin, which is required for the transcription of interleukin-2: This mechanism of action describes the action of calcineurin inhibitors like cyclosporine, not prednisone. Prednisone does not directly inhibit calcineurin or interfere with the transcription of interleukin-2.

C. It interferes with the synthesis of nucleic acids, which are essential for the replication and function of immune cells: This statement is not accurate. Prednisone primarily acts by modulating immune cell function and reducing inflammation rather than interfering with nucleic acid synthesis.

D. It binds to specific antigens or receptors on the surface of immune cells and either neutralizes them or induces their destruction: This statement does not accurately describe the mechanism of action of prednisone. Prednisone acts through intracellular receptors rather than binding to antigens or surface receptors on immune cells.

Fludrocortisone, a mineralocorticoid, is used in the treatment of Addison's disease, a condition characterized by adrenal insufficiency. The primary pharmacologic effects of fludrocortisone in this condition are related to its mineralocorticoid activity. It promotes sodium reabsorption and potassium excretion in the kidney, increasing blood volume and blood pressure: Fludrocortisone acts on the kidneys to enhance the reabsorption of sodium and increase the excretion of potassium. This action helps to regulate electrolyte balance and fluid volume, which can contribute to an increase in blood volume and blood pressure.

The other options are incorrect because:

B. It reduces inflammation, pain, fever, and allergic reactions by inhibiting the synthesis of prostaglandins and leukotrienes: This statement describes the pharmacologic effects of glucocorticoids, not mineralocorticoids like fludrocortisone. While fludrocortisone may have some mild anti-inflammatory effects, its primary role is related to electrolyte and fluid balance rather than inflammation modulation.

C. It regulates the secretion of adrenocorticotropic hormone (ACTH) from the anterior pituitary gland, maintaining the feedback loop of cortisol production: This statement describes the role of cortisol, not fludrocortisone. Fludrocortisone primarily acts as a synthetic mineralocorticoid and does not directly regulate ACTH secretion or cortisol production.

D. It influences the carbohydrate, protein, and fat metabolism in various tissues, increasing blood glucose and suppressing immune response: This statement describes the pharmacologic effects of glucocorticoids like cortisol, not mineralocorticoids. Fludrocortisone has minimal impact on carbohydrate, protein, and fat metabolism and does not exert significant immunosuppressive effects.

These adverse effects are more commonly observed with inhaled corticosteroids like fluticasone. Inhaled corticosteroids can cause local side effects in the mouth and throat, such as oral candidiasis (thrush), a fungal infection. Hoarseness, cough, and dysphonia (voice changes) may also occur due to local irritation of the throat.

The other options are incorrect because:

A. Hyperglycemia, osteoporosis, glaucoma, and cataracts: These adverse effects are associated with systemic corticosteroid use, particularly when administered orally or by injection. When using inhaled corticosteroids like fluticasone, the systemic absorption is minimal, and the risk of these adverse effects is significantly lower compared to systemic administration.

B. Hypoglycemia, osteomalacia, myopia, and dry eyes: Hypoglycemia is not a commonly observed adverse effect of inhaled corticosteroids like fluticasone. Osteomalacia (softening of bones) is more commonly associated with long-term systemic corticosteroid use. Myopia (nearsightedness) and dry eyes are not typically seen as adverse effects of inhaled corticosteroids.

D. Oral ulcers, dysphagia, wheeze, and dyspnea: Oral ulcers, dysphagia (difficulty swallowing), wheeze, and dyspnea (difficulty breathing) are not commonly associated with inhaled corticosteroids and are not typical adverse effects of fluticasone.

Decreased frequency and severity of diarrhea, abdominal pain, and rectal bleeding . These are the main symptoms of ulcerative colitis, a chronic inflammatory condition of the colon and rectum that causes ulcers, bleeding, and mucus production in the lining of the bowel. Infliximab is a monoclonal antibody that works by blocking the action of tumor necrosis factor-alpha (TNF-alpha), a cytokine that mediates inflammation and tissue damage in ulcerative colitis. Infliximab can reduce the inflammation and ulceration of the bowel and improve the clinical symptoms of ulcerative colitis .

- Improved endoscopic findings and mucosal healing . Endoscopy is a procedure that uses a flexible tube with a camera and light to examine the inside of the digestive tract. Mucosal healing is the restoration of the normal structure and function of the bowel lining. Infliximab can improve the endoscopic appearance and mucosal healing of the colon and rectum in patients with ulcerative colitis . This may reduce the risk of complications such as strictures, fistulas, abscesses, or cancer .

- Decreased levels of inflammatory markers such as C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) . CRP and ESR are blood tests that measure the level of inflammation in the body. CRP is a protein produced by the liver in response to inflammation, and ESR is a measure of how fast red blood cells settle in a tube of blood. Both tests are elevated in patients with ulcerative colitis due to the chronic inflammation of the bowel. Infliximab can lower the levels of CRP and ESR by reducing the inflammation and tissue damage in ulcerative colitis . This may reflect the improvement in disease activity and prognosis .

- Resolution of extraintestinal manifestations associated with ulcerative colitis (e.g., joint pain, skin lesions) . Extraintestinal manifestations are symptoms or conditions that affect other organs or systems outside the digestive tract. They occur in about 25% of patients with ulcerative colitis and may include arthritis (joint inflammation), uveitis (eye inflammation), erythema nodosum (skin nodules), pyoderma gangrenosum (skin ulcers), primary sclerosing cholangitis (liver inflammation), or ankylosing spondylitis (spine inflammation) . Infliximab can resolve or improve some of these extraintestinal manifestations by blocking TNF-alpha, which is involved in their pathogenesis .