"Steroid" is the name given to a chemical compound with a specific structure. In everyday speech, the term steroid is applied to several medications that share this structure; however, these medications have very different uses. Anabolic steroids are a class of drug that mimic the effects of male sex hormones called androgens which stimulate muscle growth and secondary male sex characteristics. They are often abused by bodybuilders and other athletes to build muscle mass and so should be used with caution. When prescribed, oral steroids should be taken as directed. If you come across extra pills that haven't been taken, and are unsure if they are steroids, you can identify the pill based on its physical appearance, information on the bottle, or by consulting a professional.
Continuing with the acute bronchitis case, this patient would usually be given a short term steroid “burst” of high dose prednisone. Those high daily dose is usually tapered off over the course of a few days to avoid adrenal exhaustion and withdrawal effects. You see, when you introduce prednisone (which the body recognizes as cortisol) to the body, the adrenals stop making their own supply. The theory behind tapering off of steroids like prednisone is that by slowly removing the external steroid source, the body can adapt and begin making its own again with less stress placed on the system. The practice of tapering in short term therapy, even in higher doses is debated by many clinicians. Some doctors and clinicians claim that not only is a taper not necessary in short term therapy (14 days or less) but it is better to stop this therapy earlier, the adrenals and body adjust just fine. Using a taper just introduces more of the artificial source for a longer period of time, which is best to be avoided to minimize side effects and more quickly restore natural body hormone levels.
Glucocorticoids are potent anti-inflammatories, regardless of the inflammation's cause; their primary anti-inflammatory mechanism is lipocortin-1 (annexin-1) synthesis. Lipocortin-1 both suppresses phospholipase A2 , thereby blocking eicosanoid production, and inhibits various leukocyte inflammatory events ( epithelial adhesion , emigration , chemotaxis , phagocytosis , respiratory burst , etc.). In other words, glucocorticoids not only suppress immune response, but also inhibit the two main products of inflammation, prostaglandins and leukotrienes . They inhibit prostaglandin synthesis at the level of phospholipase A2 as well as at the level of cyclooxygenase /PGE isomerase (COX-1 and COX-2),  the latter effect being much like that of NSAIDs , potentiating the anti-inflammatory effect.