Drug Identification - NCLEX-PN

Adalimumab is a tumor necrosis factor alpha (TNF-alpha) inhibitor. This class of drugs suppresses response to TNF-alpha, a potent pro-inflammatory cytokine. Inhibition of folic acid metabolism is the method of action of methotrexate. Reversible inhibition of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) is the mechanism of non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen. Rheumatoid arthritis drugs such as rituximab, and almost all drugs that end in -mab, including adalimumab function as monoclonal antibodies.

The correct answer is "insomnia," as steroids are known to increase patients' vigilance and energy levels, thereby frequently making it difficult for patients to fall asleep and/or stay asleep while taking their steroid medication. The other choices are incorrect. Decreased appetite is not a side effect of taking steroid medications. Patients on steroids often have increased appetite. Hyponatremia and hyperkalemia both are not side effects of taking steroid medications. Hypernatremia and hypokalemia are more common side effects of steroids. Hypertension, rather than hypotension is a known side effect of steroid use.

Misoprostol is used for the prevention of non steroidal anti inflammatory drug (NSAID) induced gastric ulcers. Taking this drug will prevent gastric ulcers and relieve epigastric pain.

A direct bilirubin level of 2mg/dL or greater indicates acetaminophen toxicity.

Fentanyl citrate comes in solid form on a stick (often referred to as a "fentanyl lollipop"). This form is 80-100 times more potent than morphine and intended for use by cancer patients and patients that have become tolerant to opioids.

Naloxone antidotes opioid overdose by competitively binding to μ-opioid receptors. Flumazenil is an antidote to benzodiazepines. Glucagon is an antidote for beta blocker overdose. N-acetylcysteine is an antidote for acetaminophen.

Acetaminophen in doses over 3000mg per day can result in significant liver damage or liver failure. From 1998 to 2003, acetaminophen was the leading cause of acute liver failure in the United States. According to a population-based report in 2007 there are an estimated 1600 cases of acute liver failure in the United States every year, with acetaminophen being the most common etiology.

Celecoxib is a nonsteroidal anti-inflammatory drug (NSAID). These drugs work by inhibiting cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), which reduces the synthesis of pro-inflammatory prostaglandins and thromboxane.

The correct answer is "NSAIDs." This is the correct answer because NSAIDs are known to be irritants of the gastrointestinal tract, and prolonged and/or extensive use of NSAIDs can increase the risk of developing gastrointestinal ulcers, as well as consequent gastrointestinal bleeds in the setting of ulcers. Given this patient's medical history, which already contains multiple gastrointestinal bleeds and peptic ulcer disease, NSAIDs should be used very, very carefully, if at all, in this patient.

The other choices are incorrect. Acetaminophen is not known to increase the risk of gastrointestinal bleeding or peptic ulcer formation. Morphine, oxycodone, and hydromorphone are all opioid analgesics and are not known to increase the risk of gastrointestinal bleeding or peptic ulcer formation.

Amoxicillin inhibits bacterial cell wall synthesis by interfering with the formation of cross-links between peptidoglycan polymer chains.

Macrolides, streptogramins, and clindamycin all work by inhibition of the 50S subunit of bacterial ribosomes. Tetracyclines have a similar mechanism of action, but instead affect the 30S unit of bacterial ribosomes.

Polymyxin antibiotics function by interfering with phospholipid function in bacterial cell membranes. After binding to lipopolysaccharide (LPS) in the outer membrane, polymyxins' hydrophobic tail causes damage to both the inner and outer membranes of Gram-negative bacteria.

Rifampin inhibits bacterial RNA synthesis by inhibiting RNA polymerase. This prevents the transcription of proteins within the bacterial cell, leading to cell death.

Hepatotoxicity and potential liver failure are the most serious potential adverse effects of rifampin use. Patients on this medication must establish baseline liver function tests and be monitored for liver damage. None of the other conditions listed are associated with rifampin use.

Aminoglycoside antibiotics are used to treat Gram negative bacteria. They have not been shown to be effective against Gram positive bacteria and are not antifungal. Recall the major difference between the Gram negative and positive bacteria are their cell wall composition; Gram negative have a small proportion of peptidoglycan and a high proportion of lipopolysaccharide, while Gram negative bacteria have a large proportion of peptidoglycan.

The only aminoglycoside antibiotic among those listed is streptomycin. Other examples of aminoglycosides include tobramycin and gentamicin. All aminoglycosides either end in -mycin or -micin. However, this suffix is not exclusive to aminoglycosides. It is also seen in the macrolides: erythromycin and azithromycin and both macrolides, and in lincosamides such as clindamycin.

Aminoglycoside antibiotics such as streptomycin and gentamicin have been associated with vestibular toxicity and hearing loss. Aminoglycosides remain in inner ear fluids longer than serum and can have a latent ototoxic effect, causing hearing loss even after the antibiotic has been discontinued. None of the other antibiotics listed are associated with ototoxicity.

The correct answer is "inhibition of topoisomerase II," as this is the mechanism of action of fluoroquinolone antibiotics, such as levofloxacin.

The other choices are incorrect for the following reasons:

Blockage of tRNA-ribosome-mRNA complex binding is the mechanism of action of tetracycline antibiotics.

Disruption of mycolic acid synthesis is the mechanism of action of various anti-fungal agents.

Disruption of peptidoglycan cross-linkage is the mechanism of action of vancomycin.

Inhibition of peptidoglycan synthesis is the mechanism of action of beta-lactam antibiotics.

Vancomycin is the correct answer. Antibiotics that inhibit bacterial cell wall synthesis include the beta-lactam antibiotics (penicillins and cephalosporins), vancomycin, and bacitracin. Synthesis of the bacterial cell wall takes place in 4 steps: 1) Precursors of the cell wall are synthesized within the bacterial cytoplasm. 2) The precursors are transported across the cell membrane. 3) Outside the cell membrane, the precursors are linked together to form chains called peptidoglycans. 4) The peptidoglycan chains are cross-linked to form a rigid, stable cell wall.

• Beta-lactam antibiotics act by inhibiting step 4, the cross-linking of peptidoglycans. They also activate hydrolytic enzymes, which degrade already-existing cell walls. This usually results in lysis and death of the bacteria. (Mutant bacterial strains, which lack the hydrolytic enzyme, are not killed by beta-lactams, but their growth is arrested)
• Vancomycin inhibits step 3, the elongation of the peptidoglycan chains
• Bacitracin interferes with step 2, the transport of precursors across the cell membrane

Aminoglycosides, tetracyclines, macrolides (erythromycin and its relatives), clindamycin, and chloramphenicol are inhibitors of bacterial protein synthesis. They act by binding to ribosomal subunits.

• Aminoglycosides bind to several sites on the bacterial ribosome. They interfere with the movement of ribosomes along the strand of mRNA. They also induce misreading of the mRNA so that incorrect amino acids are incorporated into the elongating peptide chain
• Tetracyclines bind to the 30S ribosomal subunit. Macrolides, clindamycin, and chloramphenicol bind to the 50S subunit. These antibiotics interfere with the attachment of tRNA to the ribosome, thus preventing the addition of amino acids to the peptide chain

Sulfonamides and trimethoprim act by inhibiting the synthesis of folic acid. Certain bacteria synthesize folic acid from precursors by a series of enzyme-catalyzed reactions. Sulfonamides and trimethoprim block different steps in this synthetic pathway by binding competitively to different enzymes. When used together, their actions are synergistic (mammals do not synthesize folic acid, but require it as a vitamin; therefore, these drugs do not interfere with metabolism in mammalian cells).

Quinolones (e.g. norfloxacin and ciprofloxacin) inhibit bacterial nucleic acid synthesis by interfering with DNA gyrase, a bacterial enzyme that catalyzes supercoiling of DNA.

Polymyxins have a detergent action that disrupts bacterial cell membranes. They can also have the same toxic effect on mammalian cells; for this reason, they are seldom used except in topical preparations.