- Author: John C Li, MD; Chief Editor: Arlen D Meyers, MD, MBA more...
Use antibiotics in treating various types of infections (eg, tonsillitis, pharyngitis, sinusitis). Use antivirals if the causative agent is suspected to be viral such as in cases associated with herpes zoster or shingles. Antifungals are indicated if the source is caused by a fungus (eg, oral thrush/candidiasis). Antiulcer/antacid medications can be used for esophagitis or gastroesophageal reflux disease. Use NSAIDs when myalgias and neuralgias are suspected. Reexamine the patient after a 2-week trial of NSAIDs.
Perform a detailed search for the underlying diagnosis before initiating treatment. Starting analgesics before reaching a diagnosis increases the difficulty of determining the cause and may possibly obscure a life-threatening condition such as an occult cancer.
Any of the previously mentioned treatments can be implemented when the exact cause of referred otalgia is suspected. If the problem persists after a 2- to 3-week trial, a more advanced algorithm is indicated.
Therapy must be comprehensive and cover all likely pathogens in the context of this clinical setting. Resort to empiric antimicrobial therapy only after an exhaustive search for a source of pain has failed.
Treats bacteria resistant to beta-lactam antibiotics.
Interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria.
Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes causing cessation of RNA-dependent protein synthesis.
Fluoroquinolone with activity against pseudomonads, streptococci, MRSA, Staphylococcus epidermidis, and most gram-negative organisms, but no activity against anaerobes. Inhibits bacterial DNA synthesis, and consequently, growth.
Nucleoside analogs are initially phosphorylated by viral thymidine kinase to eventually form a nucleoside triphosphate.
Has demonstrated inhibitory activity against both HSV-1 and HSV-2. Selectively incorporated into infected cells.
Prodrug that when biotransformed into active metabolite, penciclovir, may inhibit viral DNA synthesis/replication.
Prodrug rapidly converted to the active drug acyclovir. More expensive but has a more convenient dosing regimen than acyclovir.
Mechanism of action may involve an alteration of RNA and DNA metabolism or an intracellular accumulation of peroxide that is toxic to the fungal cell.
Synthetic PO antifungal (broad-spectrum bistriazole) that selectively inhibits fungal cytochrome P-450 and sterol C-14 alpha-demethylation.
Fungicidal and fungistatic antibiotic obtained from Streptomyces noursei. Effective against various yeasts and yeastlike fungi. Changes permeability of fungal cell membrane after binding to cell membrane sterols, causing cellular contents to leak.
These agents can be used for esophagitis or gastroesophageal reflux disease.
Competitively inhibits histamine at H2 receptor of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and reduced hydrogen concentrations.
Inhibits histamine stimulation of the H2 receptor in gastric parietal cells, which reduces gastric acid secretion, gastric volume, and hydrogen concentrations.
Inhibits gastric acid secretion.
Inhibit gastric acid secretion by inhibiting H+/K+ ATPase enzyme system at secretory surface of gastric parietal cells.
S-isomer of omeprazole. Inhibits gastric acid secretion by inhibiting H+/K+ -ATPase enzyme system at secretory surface of gastric parietal cells.
Used in severe cases of and patients not responding to H2 antagonist therapy.
Used for up to 4 wk to treat and relieve symptoms of active duodenal ulcers; may be used up to 8 wk to treat all grades of erosive esophagitis.
Pain control is essential to quality patient care.
DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
Drug combinations indicated for moderate to severe pain.
Drug combination indicated for the relief of moderate to severe pain.
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