NMS Q&A Family Medicine

84 NMS Q&A Family Medicinemacrolides may be better choices than penicillin.Cefadroxil is classified as a first-generation cephalosporinbut is generally more effective against the gram-negativespectrum and usually considered in “below the waist”infections.15. The answer is C. M. pneumonia has been named oneof the atypical pneumonias, based on x-ray findings out ofproportion to clinical findings. Headache is a hallmark ofmycoplasmal respiratory infection. The course is slow andsymptoms fairly mild, although mycoplasmal infectionsmay be associated with a multitude of extrapulmonaryinvolvements, such as the Raynaud phenomenon, relatedto cold agglutinins present during the acute infection andcardiac involvement in dysrhythmias, CHF, and EKGabnormalities. Streptococcal (pneumococcal) pneumoniais classically the opposite of the picture presented here(i.e., rapidly developing course, discrete or lobar x-rayfindings, significant leukocytosis and fever). Pneumoniafrom K . pneumoniae is uncommon, being a gram-negativeinfection that produces lobar pneumonia in its classicform, and found as an opportunist in people who areimmunologically defenseless such as diabetics, alcoholics,and COPD patients. S . aureus is also found as a pathogenin the lungs only as an opportunist. Gram-negative sepsisis, of course, a systemic critical condition in which pneumoniais not particularly a prominent finding.16. The answer is D, Legionella. The case illustrates severalpoints: Bradycardia is common and headache andstupor not uncommon in Legionella disease; early laboratoryfindings are nonspecific. However, diagnosis is ultimatelymade by the 3- to 5-day growing culture in bufferedcharcoal yeast extract agar or less often by acute and convalescentantibody titers in a fourfold rise to 1:128, requiring4 to 12 weeks for the change, earlier for immuneglobulin M (IgM) and later for immune globulin G (IgG)types; hyponatremia reflects a phase of syndrome of inappropriateanti-diuretic hormone (SIADH), associatedoften with lung disease but is often out of proportion tothe clinical severity of the disease, and V. pneumonia ischaracterized by one of the most severe nonproductivecoughs encountered in primary care medicine. The otherchoices have been discussed elsewhere.17. The answer is B. The stroke patient with bulbar signsand symptoms is at risk of aspiration pneumonia. Aspirationpneumonia is usually produced by aspirated oralanaerobes. Neurologic deficits that are associated withdysphagia, level of consciousness, seizures, drug overdose,alcoholism, and recent dental procedures may all causeaspiration. Influenza pneumonic complications are mostlikely to be pneumococcal or staphylococcus. The SouthwestU.S. traveler must be considered to have coccidioidomycosis.AIDs patients may have any of thepneumonitides discussed, depending on their clinical status,but their specific susceptibility is to Pneumocystiscarinii .18. The answer is C, a 32-year-old with mild shortness ofbreath with heavy exertion for 1 year and with a distantsmoking history of 1 pack-year. The question emphasizesthat not all COPD is caused by smoking. When COPDpresents in the absence of a severe smoking history or significantother environmental air pollution history, alpha 1protease inhibitor deficiency must be considered as anetiology. If present, the enzyme can be given exogenously.19. The answer is E. Inhaled tiotropium (Spiriva) ananticholinergic agent, is the first-line drug therapy forCOPD. Tiotropium has some incremental advantagesover ipratropium, such as once-daily dosing and a marginaltherapeutic edge as measured by the amount of supplementalbeta 2 agonists and Transitional Dyspnea Indexscores. Otherwise ipratropium is equally effective. All thelisted agents are sometimes used in COPD patients(although inhaled corticosteroids have been shown tohave little effect), but inhaled anticholinergics such as discussedshould be the starting agent because of its bettertherapeutic profile.ReferencesHolmes RL , Fadden CT . Evaluation of the patient with chroniccough . Am Fam Physician . 2004 ; 69 : 2159 – 2166 , 2169 .Karnani NG , Reisfield GM , Wilson GR . Evaluation of chronicdyspnea . Am Fam Physician . 2005 ; 71 : 1529 – 1537 , 1538 .Lipsky MS , Sternbach M . Pneumonias, bronchitides and chroniclung disease . In: Rudy DR , Kurowski K , eds. Family Medicine:House Officer Series . Baltimore, MD : Williams & Wilkins ;1997 : 185 – 200 .Mintz M . Asthma update: Part I. Diagnosis, monitoring andprevention of disease progression . Am Fam Physician . 2004 ;70 : 893 – 898 .National Asthma Education and Prevention Program . ExpertPanel Number 2 . Washington, DC : National Institutes ofHealth/National Heart, Lung, and Blood Institute ; 1997 (NIHpublication 97–4951) .Rakel RE, Bope EP, eds. Conn’s Current Therapy . Philadelphia,PA: Saunders; 2009.