What are corticosteroids?
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Overview of corticosteroids, their anti-inflammatory mechanisms, common agents, and clinical indications.
By mastering this deck, you will understand the pharmacological basis of corticosteroid therapy, identify key drugs and their mechanisms, and apply this knowledge to optimize clinical management of inflammatory conditions while minimizing adverse effects.
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| # | Front | Back | Hint |
|---|---|---|---|
| 1 | What are corticosteroids? | Corticosteroids are steroid hormones produced by the adrenal cortex or synthetic analogs that have potent anti-inflammatory, immunosuppressive, and metabolic effects. | Think of the adrenal cortex as the body's natural steroid factory. |
| 2 | Name the main classes of corticosteroids used therapeutically. | Glucocorticoids (e.g., cortisol, prednisone, dexamethasone) and mineralocorticoids (e.g., aldosterone). Therapeutic focus is mainly on glucocorticoids. | Glucocorticoids control inflammation; mineralocorticoids regulate salt and water balance. |
| 3 | What is the primary mechanism of anti-inflammatory action of glucocorticoids? | They suppress the expression of inflammatory genes by inhibiting transcription factors such as NF-ÎșB and AP-1, leading to decreased production of cytokines, prostaglandins, and leukotrienes. | Think of glucocorticoids as gene expression silencers for inflammation mediators. |
| 4 | How do glucocorticoids affect phospholipase A2 activity? | They induce the synthesis of lipocortin (annexin-1), which inhibits phospholipase A2, reducing arachidonic acid release and subsequent prostaglandin and leukotriene synthesis. | Lipocortin acts as a brake on inflammatory eicosanoid production. |
| 5 | Name three commonly used glucocorticoids and their relative potencies. | Hydrocortisone (least potent), Prednisone (intermediate potency), Dexamethasone (high potency). | Potency increases from hydrocortisone to dexamethasone. |
| 6 | Which glucocorticoid is often used for its minimal mineralocorticoid activity? | Dexamethasone; it has negligible mineralocorticoid effects, making it suitable for anti-inflammatory purposes without causing fluid retention. | Dexamethasone is preferred when mineralocorticoid effects are undesirable. |
| 7 | What are the main clinical indications for glucocorticoid therapy? | Inflammatory and autoimmune diseases (e.g., rheumatoid arthritis, lupus), allergic reactions, asthma exacerbations, adrenal insufficiency, and organ transplantation. | Think of conditions involving overactive immune or inflammatory responses. |
| 8 | What is the mechanism behind the immunosuppressive effects of glucocorticoids? | They induce apoptosis of lymphocytes, inhibit cytokine production, and suppress macrophage and T-cell function. | Glucocorticoids dampen immune activity at multiple levels. |
| 9 | Describe the metabolic effects of glucocorticoids. | They increase gluconeogenesis, promote lipolysis, cause insulin resistance, and lead to hyperglycemia. | Think of glucocorticoids as stress hormones that raise blood sugar. |
| 10 | What are common side effects of long-term glucocorticoid therapy? | Osteoporosis, hyperglycemia/diabetes, hypertension, muscle wasting, skin thinning, Cushingoid features (moon face, central obesity), and increased infection risk. | Chronic use mimics features of Cushing's syndrome. |
| 11 | How do glucocorticoids cause osteoporosis? | They decrease osteoblast activity, increase osteoclast activity, and reduce calcium absorption, leading to decreased bone density. | Think of glucocorticoids as bone resorption accelerators. |
| 12 | What is the effect of glucocorticoids on the hypothalamic-pituitary-adrenal (HPA) axis? | They suppress the HPA axis via negative feedback, reducing endogenous cortisol production. | Long-term therapy can lead to adrenal suppression. |
| 13 | Why is tapering necessary when discontinuing long-term glucocorticoid therapy? | To allow the HPA axis to recover and prevent adrenal insufficiency. | Gradual dose reduction prevents withdrawal symptoms. |
| 14 | What is 'Cushingoid' appearance, and which drugs can cause it? | Features include central obesity, moon face, buffalo hump, striae; caused by excess glucocorticoids. | Named after Cushing's syndrome, a condition of cortisol excess. |
| 15 | How can glucocorticoid-induced hyperglycemia be managed? | Monitor blood sugars, adjust diabetic medications, and consider using the lowest effective dose of steroids. | Control blood glucose as you would in diabetes management. |
| 16 | Name a mineralocorticoid with potent salt-retaining effects. | Aldosterone. | A key hormone in electrolyte and blood pressure regulation. |
| 17 | What is the significance of selective glucocorticoid receptor agonists/antagonists? | They aim to maximize anti-inflammatory effects while minimizing side effects like metabolic disturbances. | Think of targeted therapies for safer steroid use. |
| 18 | Give an example of a synthetic glucocorticoid with long half-life used for chronic therapy. | Dexamethasone or Betamethasone. | Long-acting steroids reduce dosing frequency. |
| 19 | What are the contraindications for glucocorticoid therapy? | Systemic fungal infections, live vaccines, and caution in osteoporosis, diabetes, and hypertension. | Use carefully in infections and metabolic conditions. |
| 20 | How do glucocorticoids influence wound healing? | They impair wound healing by suppressing inflammation and collagen synthesis. | Steroids can delay tissue repair. |
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