I lomon^TTimu hkninofpu wrlh. Stanilir Spjrmp

FIGURE I-94

I-95. The answer is E. (Chap. 28) The differential diagnosis of a red, painful eye is broad and includes corneal abrasion, subconjunctival hemorrhage, infective or allergic conjunctivitis (the most common cause of red, painful eye), keratoconjunctivitis sicca (medications, Sjogren’s syndrome, sarcoidosis), keratitis (contact lens injury, trachoma, vitamin A deficiency), herpes infection, episcleritis (autoimmune, idiopathic), scleritis (autoimmune), uveitis, endophthalmitis, or acute angle-closure glaucoma. Uveitis requires slit-lamp examination for diagnosis. Anterior uveitis involving the iris is usually idiopathic but may be associated with sarcoidosis, ankylosing spondylitis, juvenile rheumatoid arthritis, inflammatory bowel disease, psoriasis, inflammatory arthritis, Behçet’s disease, and a variety of infections. Posterior uveitis in the vitreous, retina, or choroid is more likely to be associated with a systemic disease or infection than anterior uveitis. Acute angle-closure glaucoma, although rare, is often misdiagnosed unless intraocular pressure is measured. Many physicians avoid dilating patients’ pupils for fear of provoking acute angle-closure glaucoma. The risk is remote and rarely causes permanent vision loss. The value of a complete funduscopic examination outweighs the risk of this rare event. Transient ischemic attack (TIA) caused by temporary interruption of blood flow to the retina for more than a few seconds causes transient visual abnormality (amaurosis fugax). TIA is usually associated with atherosclerosis. If flow is restored quickly vision returns to normal.

I-96. The answer is A. (Chap. 28) Age-related macular degeneration is a major cause of painless, gradual bilateral central visual loss. It occurs as nonexudative (dry) or exudative (wet) forms. Recent genetic data have shown an association with the alternative complement pathway gene for complement factor H. The mechanism link for that association is unknown. The nonexudative form is associated with retinal drusen that leads to retinal atrophy. Treatment with vitamin C, vitamin E, beta-carotene, and zinc may retard the visual loss. Exudative macular degeneration, which is less common, is caused by neovascular proliferation and leakage of choroidal blood vessels. Acute visual loss may occur because of bleeding. Exudative macular degeneration may be treated with intraocular injection of a vascular endothelial growth factor antagonist (bevacizumab or ranibizumab). Blepharitis is inflammation of the eyelids usually related to acne rosacea, seborrheic dermatitis, or staphylococcal infection. Diabetic retinopathy, now a leading cause of blindness in the United States, causes gradual bilateral visual loss in patients with longstanding diabetes. Retinal detachment is usually unilateral and causes visual loss and an afferent pupillary defect.

I-97. The answer is B. (Chap. 29) A history of severe respiratory infection, including the common cold, influenza, pneumonia, or HIV, is the most common cause of long-lasting loss of smell. The mechanism, along with cases of chronic rhinosinusitis (another common cause) is likely related to permanent damage to the olfactory epithelium. Head trauma, causing shearing and scarring of olfactory fila at the cribiform plate, may cause anosmia. Fewer than 10% of patients with posttraumatic anosmia regain normal function. The severity of disease is associated with the likelihood of olfactory abnormality in trauma and chronic rhinosinusitis. Significant decrements in smell are present in more than 50% of people older than 65 years old. This finding may explain the common finding of loss of food flavor and nutritional deficiencies in elderly adults. Confirming popular wisdom studies have shown that at any age, women have a better ability to identify odorants than men (Figure I-97).

FIGURE I-97

I-98. The answer is E. (Chap. 30) Hearing loss is a common complaint, particularly in older individuals. In this age group, 33% have hearing loss to a degree that requires hearing aids. When evaluating hearing loss, the physician should attempt to determine whether the cause is conductive, sensorineural, or mixed. Sensorineural hearing loss results from injury of the cochlear apparatus or disruption of the neural pathways from the inner ear to the brain. The primary site of damage is the hair cells of the inner ear. Common causes of hair cell injury include prolonged exposure to loud noises, viral infections, ototoxic drugs, cochlear otosclerosis, Meniere’s disease, and aging. In contrast, conductive hearing loss results from impairment of the external ear and auditory canal to transmit and amplify sound through the middle ear to the cochlea. Causes of conductive hearing loss include cerumen impaction, perforations of the tympanic membrane, otosclerosis, cholesteatomas, large middle ear effusions, and tumors of the external auditory canal or middle ear among others. The initial physical examination can often differentiate between conductive or sensorineural hearing loss. Examination of the external auditory canal can identify cerumen or foreign body impaction. On otoscopic examination, it is more important to assess the topography of the tympanic membrane than to look for the presence of a light reflex. Of particular attention is the area in the upper third of the tympanic membrane known as the pars flaccida. This area can develop chronic retraction pockets that are indicative of Eustachian tube dysfunction or a cholesteatoma, a benign tumor composed of keratinized squamous epithelium. Bedside tests with a tuning fork also are useful for differentiating conductive from sensorineural hearing loss. In the Rinne’s test, air conduction is compared with bony conduction of sound. A tuning fork is placed over the mastoid process and then in front of the external ear. In conductive hearing loss, the intensity of sound is louder when placed on the bone, but in sensorineural hearing loss, the intensity is greatest at the external ear. In the Weber test, the tuning fork is placed in the midline of the head. In unilateral conductive hearing loss, the intensity of sound is loudest in the affected ear, but in unilateral sensorineural hearing loss, the intensity of sound is loudest in the unaffected ear. This patient reports left greater than right hearing loss that is suspected to be sensorineural in nature. Thus, the sound is expected to be greatest in the right ear on the Weber test. A more formal evaluation of hearing loss would include pure tone audiometry that plots hearing threshold versus frequency. Pure tone audiometry

establishes the severity, type, and laterality of hearing loss. In this patient, high-frequency hearing loss would be expected based on his complaints of inability to hear the alarm tone of his digital watch.

I-99. The answer is E. (Chap. 31) Acute sinusitis is a common complication of upper respiratory tract infections and is defined as sinusitis lasting less than 4 weeks’ duration. Acute sinusitis typically presents with nasal drainage and congestion, facial pain or pressure, and headache that is worse with lying down or bending forward. The presence of purulent drainage does not differentiate bacterial from viral causes of sinusitis. The vast majority of cases of acute sinusitis are caused by viral infection. However, when patients with acute sinusitis present to a medical professional, antibiotics are prescribed more than 85% of the time. Indeed, this should not be the preferred treatment because most cases improve without antibiotic therapy. Rather, the initial approach to a patient with acute sinusitis should be symptomatic treatment with nasal decongestants and nasal saline lavage. If a patient has a history of allergic rhinitis or chronic sinusitis, nasal glucocorticoids can be prescribed as well. Antibiotic therapy is recommended in adults for symptom duration longer than 7–10 days and in children longer than 10–14 days. In addition, any patient with concerning features such as unilateral or focal facial pain or swelling should be treated with antibiotics. The initial antibiotic of choice for acute sinusitis is amoxicillin 500 mg orally three times daily or 875 mg twice daily. If a patient has had exposure to antibiotics within the past 30 days or treatment failure, a respiratory fluoroquinolone can be give. Ten percent of individuals do not respond to initial antibiotic therapy. In these cases, one can consider referral to otolaryngology for sinus aspiration and culture. Radiologic imaging of the sinuses is not recommended for evaluation of acute disease unless the sinusitis is nosocomially acquired because the procedures (CT or radiography) do not differentiate between bacterial or viral causes.

I-100. The answer is B. (Chap. 31) Approximately 5–15% of all cases of acute pharyngitis in adults are caused by Streptococcus pyogenes. Appropriate identification and treatment of S. pyogenes infection is needed because antibiotic therapy is recommended to decrease the small risk of acute rheumatic fever. In addition, treatment with antibiotics within 48 hours of onset of symptoms decreases symptom duration and, importantly, decreases transmission of streptococcal pharyngitis. In adults, the recommended diagnostic procedure by the Centers for Disease Control and Prevention and the Infectious Disease Society of America is a rapid antigen detection test for group A streptococci only. In children, however, the recommendation is to perform a throat culture for confirmation if the rapid screen result is negative to limit spread of disease and minimize potential complications. Throat culture generally is regarded as the most appropriate diagnostic method but cannot discriminate between colonization and infection. In addition, it takes 24–48 hours to get a result. Because most cases of pharyngitis at all ages are viral in origin, empiric antibiotic therapy is not recommended.

I-101. The answer is D. (Chap. 33) Shortness of breath, or dyspnea, is a common presenting complaint in primary care. However, dyspnea is a complex symptom and is defined as the subjective experience of breathing discomfort that includes components of physical as well as psychosocial factors. A significant body of research has been developed regarding the language by which a patient describes dyspnea with certain factors being more common in specific diseases. Individuals with airways diseases (asthma, chronic obstructive pulmonary disease [COPD]) often describe air hunger, increased work of breathing, and the sensation of being unable to get a deep breath because of hyperinflation. In addition, individuals with asthma often complain of a tightness in the chest. Individuals with cardiac causes of dyspnea also describe chest tightness and air hunger but do not have the same sensation of

being unable to draw a deep breath or have increased work of breathing. A careful history will also lead to further clues regarding the cause of dyspnea. Nocturnal dyspnea is seen in congestive heart failure or asthma, and orthopnea is reported in heart failure, diaphragmatic weakness, and asthma that is triggered by esophageal reflux. When discussing exertional dyspnea, it is important to assess if the dyspnea is chronic and progressive or episodic. Whereas episodic dyspnea is more common in myocardial ischemia and asthma, COPD and interstitial lung diseases present with a persistent dyspnea. Platypnea is a rare presentation of dyspnea in which a patient is dyspneic in the upright position and feels improved with lying flat. On physical examination of a patient with dyspnea, the physician should observe the patient’s ability to speak and the use of accessory muscle or preference of the tripod position. As part of vital signs, a pulsus paradoxus may be measured with a value of greater than 10 mmHg common in asthma and COPD. Pulsus paradoxus greater than 10 mmHg may also occur in pericardial tamponade. Lung examination may demonstrate decreased diaphragmatic excursion, crackles, or wheezes that allow one to determine the cause of dyspnea. Further workup may include pulmonary function testing, chest radiography, chest CT, electrocardiography, echocardiography, or exercise testing, among others, to ascertain the cause of dyspnea.

I-102. The answer is B. (Chap. 34) Chronic cough should not be diagnosed until consistently present for over 2 months. The duration of cough is a clue to its etiology. Acute cough (<3 weeks) is most commonly due to a respiratory tract infection, aspiration event, or inhalation of noxious chemicals or smoke. Subacute cough (3–8 weeks duration) is frequently the residuum from a tracheobronchitis, such as in pertussis or “post-viral tussive syndrome.” Chronic cough (>8 weeks) may be caused by a wide variety of cardiopulmonary diseases, including those of inflammatory, infectious, neoplastic, and cardiovascular etiologies. In virtually all instances, evaluation of chronic cough merits a chest radiograph. The list of diseases that can cause persistent coughing without other symptoms and without detectable abnormality on physical examination is long. It includes serious illnesses such as Hodgkin’s disease in young adults and lung cancer in an older population. An abnormal chest film leads to evaluation of the radiographic abnormality to explain the symptom of cough. A normal chest image provides valuable reassurance to the patient and the patient’s family, who may have imagined the direst explanation for the cough. Chest PET-CT is often helpful in evaluation of solitary pulmonary nodules or suspected malignancy. Sinus CT should not be utilized in the initial evaluation of chronic cough without strong historical or physical examination of sinus disease or infection. While ACE-inhibitor medications are a common cause of chronic cough, measurement of ACE levels is not helpful clinically. Measurement of serum IgE may be a component of the comprehensive evaluation of patients with refractory asthma or suspected allergic bronchopulmonary aspergillosis. It is not helpful in the initial evaluation of cough in a patient without allergic history.

I-103. The answer is D. (Chap. 34) It is commonly held that medications (most notably ACE-inhibitors); post-nasal drainage; gastroesophageal reflux; and asthma, alone or in combination, account for more than 90% of patients who have chronic cough and a normal or noncontributory chest radiograph. However, clinical experience does not support this contention, and strict adherence to this concept discourages the search for alternative explanations by both clinicians and researchers. Serious pulmonary diseases, including inflammatory lung diseases, chronic infections, and neoplasms, may remain occult on plain chest imaging and require additional testing for detection. Any patient with chronic unexplained cough who is taking an ACE inhibitor should be given a trial period off the medication, regardless of the timing of the onset of cough relative to the initiation of ACE inhibitor

therapy. In most instances, a safe alternative is available; angiotensin-receptor blockers do not cause cough. Post-nasal drainage of any etiology can cause cough as a response to stimulation of sensory receptors of the cough-reflex pathway in the hypopharynx or aspiration of draining secretions into the trachea. Many patients with symptomatic post-nasal drip do not develop chronic cough. Linking gastroesophageal reflux to chronic cough poses similar challenges. It is thought that reflux of gastric contents into the lower esophagus may trigger cough via reflex pathways initiated in the esophageal mucosa. Reflux to the level of the pharynx with consequent aspiration of gastric contents causes a chemical bronchitis and possible pneumonitis that can elicit cough for days after the aspiration event. Reflux may also elicit no or minimal symptoms. Assigning the cause of cough to gastroesophageal reflux must be weighed against the observation that many people with chronic reflux (such as frequently occurs during pregnancy) do not experience chronic cough. Cough due to asthma in the absence of wheezing, shortness of breath, and chest tightness is referred to as “cough-variant asthma”, and is more common in children than adults. Chronic eosinophilic bronchitis causes chronic cough with a normal chest radiograph. This condition is characterized by sputum eosinophilia in excess of 3% without airflow obstruction or bronchial hyperresponsiveness and is successfully treated with inhaled glucocorticoids. Treatment of chronic cough in a patient with a normal chest radiograph is often empiric and is targeted at the most likely cause or causes of cough as determined by history, physical examination, and possibly pulmonary-function testing. Therapy for post-nasal drainage depends on the presumed etiology (infection, allergy, or vasomotor rhinitis) and may include systemic antihistamines; antibiotics; nasal saline irrigation; and nasal pump sprays with corticosteroids, antihistamines, or anticholinergics. Antacids, histamine type-2 (H2) receptor antagonists, and proton-pump inhibitors are used to neutralize or decrease production of gastric acid in gastroesophageal reflux disease; dietary changes, elevation of the head and torso during sleep, and medications to improve gastric emptying are additional therapies. Cough-variant asthma typically responds well to inhaled glucocorticoids and intermittent use of inhaled beta-agonist bronchodilators. In this patient, the symptoms of heartburn and the timing of the cough with meals merits an empiric therapeutic trial directed toward reducing acid reflux. Empiric therapy for H. pylori eradication is not indicated at this time.

I-104. The answer is D. (Chap. 35) When a patient presents for evaluation of hypoxia, it is important to consider the underlying mechanism of hypoxia in order to determine the etiology. The primary causes of hypoxia are related to respiratory disease and include ventilation/perfusion (V/Q) mismatch, hypoventilation, and intrapulmonary right-to-left shunting. Causes of hypoxia outside of the respiratory system include intracardiac right-to-left shunting, high-altitude hypoxia, anemic hypoxia, circulatory hypoxia, and carbon monoxide poisoning. In this patient, the mechanism of hypoxia can be narrowed to two possibilities—intracardiac versus intrapulmonary right-to-left shunting—quite easily because the patient failed to correct his hypoxia in response to 100% oxygen. The history of platypnea and orthodeoxia is suggestive that the likely cause is intrapulmonary rather than intracardiac shunting. The finding of a possible lung nodule on chest radiographs in the lower lung fields also is supportive of a pulmonary cause of shunting through an arteriovenous malformation, which can appear as a lung nodule on chest x-ray. An intracardiac right-to-left shunt is caused by congenital cardiac malformations and Eisenmenger syndrome. If there was an intracardiac cause of shunt, the cardiac examination would be expected to demonstrate a murmur and/or evidence of pulmonary hypertension. V/Q mismatch is the most common cause of hypoxia and results from perfusion of areas of the lung that receive limited ventilation. Examples of V/Q mismatch include asthma, chronic obstructive pulmonary disease, and pulmonary embolus. Hypoxia caused by V/Q mismatch can be corrected with supplemental

oxygen. Hypoventilation can be caused by multiple causes, including acute respiratory depression or chronic respiratory failure with elevations in PaCO₂. Hypoxia caused by hypoventilation is also

correctable with oxygen but frequently has a normal alveolar–arterial oxygen gradient. Causes of hypoxia outside the respiratory system are less common. High-altitude hypoxia becomes apparent when individuals travel to elevations greater than 3000 m. Anemic hypoxia is not associated with a decrease in PaO₂, but a decrease in hemoglobin does cause decreased oxygen-carrying capacity

in the blood and relative tissue hypoxia if severe. Circulatory hypoxia refers to tissue hypoxia that occurs because of a decrease cardiac output that leads to greater tissue extraction of oxygen. As a result, the venous partial pressure of oxygen is reduced, and there is an increased arterial-mixed venous oxygen gradient.

I-105. The answer is C. (Chap. 35) In the evaluation of cyanosis, the first step is to differentiate central from peripheral cyanosis. In central cyanosis, because the etiology is either reduced oxygen saturation or abnormal hemoglobin, the physical findings include bluish discoloration of both mucous membranes and skin. In contrast, peripheral cyanosis is associated with normal oxygen saturation but slowing of blood flow and an increased fraction of oxygen extraction from blood; subsequently, the physical findings are present only in the skin and extremities. Mucous membranes are spared. Peripheral cyanosis is commonly caused by cold exposure with vasoconstriction in the digits. Similar physiology is found in Raynaud’s phenomenon. Peripheral vascular disease and deep venous thrombosis result in slowed blood flow and increased oxygen extraction with subsequent cyanosis. Methemoglobinemia causes abnormal hemoglobin that circulates systemically. Consequently, the cyanosis associated with this disorder is systemic. Other common causes of central cyanosis include severe lung disease with hypoxemia, right-to-left intracardiac shunting, and pulmonary arteriovenous malformations.

I-106. The answer is C. (Chap. e13) Mitral valve prolapse is characterized by a midsystolic nonejection sound (click) followed by a late systolic murmur that crescendos and terminates with S2. A decrease in venous return induced by standing will move the click closer to S1 and increase the duration of the murmur. Squatting will increase venous return and shorten the duration of the murmur. The murmur of hypertrophic cardiomyopathy behaves in a similar fashion, but there would be no nonejection click, and left ventricular hypertrophy would be expected on electrocardiography (ECG). Aortic stenosis is best heard at the right second intercostal space radiating to the carotid and is crescendo–decrescendo in character. Congenital pulmonic stenosis is crescendo–decrescendo in character and is heard best in the second to third left intercostal space. If severe, there is a parasternal lift right ventricular overload on ECG. Tricuspid regurgitation causes a holosystolic, not midsystolic, murmur that increases with inspiration.

I-107. The answer is C. (Chap. e13) Tricuspid regurgitation and mitral regurgitation (along with ventricular septal defect) cause holosystolic murmurs. These murmurs have their onset with S1 and terminate at or with S2. Whereas tricuspid regurgitation is heard best over the left sternal border, mitral regurgitation is heard best at the apex with radiation to the base or axilla. The onset of a murmur after S1 with a nonejection sound (click) is characteristic of mitral valve prolapse. Amyl nitrate decreases the intensity of mitral regurgitation and ventricular septal defect murmurs. Tricuspid regurgitation increases with inspiration. Wide splitting of S2 is characteristic of ventricular septal defects. Inaudible A2 at the ventricular apex is characteristic of mitral regurgitation. Because of the incompetent tricuspid valve, the murmur of tricuspid regurgitation is associated with prominent c-v waves and a sharp y-

descent in the jugular venous pulse.

I-108. The answer is A. (Chap. e13) Evaluating the splitting of the aortic (A2) and pulmonic (P2) components of the second heart sound (S2) during auscultation can be diagnostically useful. In normal conditions, P2 follows A2, and the splitting increases during inspiration. Reversed (or paradoxical) splitting of S2, when P2 precedes A2 during expiration (and they come closer together during inspiration), is attributable to a delay in A2 and is characteristic of severe aortic stenosis, hypertrophic obstructive cardiomyopathy, left bundle branch block, right ventricular pacing, or acute myocardial ischemia. Wide splitting of S2 is an accentuation of the physiologic pattern usually caused by delayed pulmonic valve closing (right bundle branch block, pulmonary stenosis, pulmonary hypertension) or early aortic valve closure (severe mitral regurgitation). Fixed splitting (no respiratory variation) with the murmur described is characteristic of an atrial septal defect. This is an important finding because it may be asymptomatic until the third or fourth decade of life and, if undiagnosed, may lead to severe pulmonary hypertension and Eisenmenger syndrome.

I-109. The answer is B. (Chap. 53) This patient presents with complaints of diffuse hair loss that has been associated with increased stress as well as hormonal changes after pregnancy and delivery. On physical examination, there is diffuse shedding of normal hairs without scalp lesions or scarring consistent with a diagnosis of telogen effluvium. Telogen effluvium occurs when a stressor causes the typical asynchronous hair growth pattern to become synchronous. This can occur from physical or mental stress (high fever, severe infection) or hormonal changes. When the hair growth becomes more synchronous, more hairs enter the telogen (dying) phase at the same time. The patient may present with complaints of significant hair loss, but hair density to the examiner may appear normal. Broken hairs are not observed, and gentle pulling of the hair results in more than four hairs falling out. Telogen effluvium is reversible without treatment, and this patient has identifiable stressors that are related to the cause. Reassurance and observation are all that are recommended. Some medications can cause telogen effluvium. If identified, these should be discontinued. In addition, both hyper- and hypothyroidism can lead to the condition. One should consider evaluation for these and other metabolic disorders if the condition does not reverse or the patient has additional symptoms. Other causes of nonscarring alopecia include androgenic alopecia, alopecia areata, tinea capitis, and traumatic alopecia. Androgenic alopecia is the cause of male and female pattern baldness. It does not typically result from androgen excess. Rather, it is associated with an increased sensitivity of the affected hairs to the effects of androgens. Androgenic alopecia can be treated with minoxidil, finasteride, or hair transplants. Alopecia areata is a condition of focal hair loss measuring about 2–5 cm in diameter. The surrounding tissue demonstrates increased T lymphocytes, and the treatment includes intralesional glucocorticoids or topical anthralin or tazarotene. Tinea capitis is also usually a focal area of hair loss related to an underlying superficial fungal infection. However, in severe cases, large plaques and pustules can develop. Treatment with oral griseofulvin or terbinafine with topical selenium sulfide or ketoconazole is usually effective in treating the disease. Traumatic alopecia presents with multiple broken hairs at sites of increased stress related to the use of hair care products, including rubber bands, curlers, or chemicals. It can also result from trichotillomania. Discontinuation of any offending practice or agent is all that is required to return the hair to normal. Counseling is typically required for those with trichotillomania.

I-110. The answer is D. (Chap. 55) Immediate drug reactions rely on the release of mediators from mast

cells or basophils, which can occur directly or through immunoglobulin E (IgE)–dependent activation of these cells. Anaphylactoid reactions that are the result of the direct mast cell degranulation do not require prior exposure to the drug or agent to cause the reaction as in this case. The major causes of anaphylactoid reactions are nonsteroidal anti-inflammatory drugs and radiocontrast media. IgE-dependent drug reactions require prior exposure to the drugs to generate the appropriate antibodies, which are expressed on the surfaces of the sensitized cells. Upon reexposure to the drug, drug protein conjugates cross-link these IgE molecules to cause activation of the cells and release of inflammatory mediators. The major drugs classes that cause IgE-dependent reactions are penicillins and muscle relaxants. The symptoms of immediate drug reactions are similar regardless of whether they are caused by direct mast cell activation or IgE mechanisms and begin within minutes of drug exposure. The symptoms include pruritus, urticaria, nausea, vomiting, diarrhea, abdominal cramping, bronchospasm, laryngeal edema, and cardiovascular collapse.

Other causes of drug reactions include deposition of immune complexes and delayed hypersensitivity T-cell reactions. Both of these types of drug reactions cause delayed reactions. The clinical scenario associated with immune complex deposition is serum sickness, which typically occurs 6 days or more after exposure to the drug. However, if the patient has had a prior exposure to the drug, the symptoms could occur at an earlier time frame. Symptoms of serum sickness include fever arthritis, nephritis, neuritis, edema, and an urticarial rash. Delayed hypersensitivity reactions are the most common causes of allergic drug eruptions and include the mild morbilliform eruptions as well as toxic epidermal necrolysis and Stevens-Johnson syndrome. Drug-cell specific T cells have been demonstrated in these reactions directed against the native drug rather than its metabolites. Hepatic metabolism into toxic intermediate compounds may occur with some drug toxicity; the prototype for this phenomenon is acetaminophen toxicity and hepatic failure.

I-111. The answer is A. (Chap. 55) Hypersensitivity syndromes can occur with many drugs, including phenytoin, carbamazepine, barbiturates, lamotrigine, minocycline, dapsone, allopurinol, and sulfonamides. This syndrome is also known as DRESS (drug reaction with eosinophilia and systemic symptoms) and presents with a diffuse purpuric and lichenoid rash associated with fever, facial and periorbital edema, generalized lymphadenopathy, leukocytosis, hepatitis, and occasionally nephritis or pneumonitis. Eosinophilia and atypical lymphocytosis can be seen. The reaction typically begins within 2–8 weeks after starting the drug but may persist for several weeks after cessation of the drug, especially if there is associated hepatitis. Mortality rates can be as high as 10% with DRESS, and it is important to recognize this as a drug reaction as immediate cessation of the offending agent is required. Mortality is highest in those with acute hepatitis. In addition to stopping the drug, treatment with systemic corticosteroids at prednisone doses of 1.5–2 mg/kg daily is recommended with a slow taper over 8–12 weeks. Topical steroids may also be helpful. Patients should be closely followed for resolution of symptoms, and the patient should be observed carefully for the late development of autoimmune thyroiditis, which can occur as long as 6 months after the initial presentation of the syndrome. Although it is important to treat the patients underlying seizure disorder, cross-reactions with other aromatic anticonvulsants can occur, and these compounds, including carbamazepine and barbiturates, can also lead to the syndrome.

I-112. The answer is E. (Chap. 56) The photosensitivity reactions of phototoxicity or photoallergy can be related to both topical or systemic administration of drugs and require the absorption of energy by the drug to create a photosensitizer that can generate reactive oxygen species. Phototoxicity is a

nonimmunologic reaction that leads to erythema resembling a sunburn. Photoallergy is a less common immunologic reaction that leads to a hypersensitivity syndrome characterized severe pruritus with eczematous dermatitis. This can progress to lichenification in sun-exposed areas. Drugs that can cause both photoallergy and phototoxicity are fluoroquinolones, sulfonamides, and sulfonylureas.

I-113. The answer is B. (Chap. 57) The first step in diagnosing polycythemia vera is to document an elevated red blood cell (RBC) mass. A normal red blood cell (RBC) mass suggests spurious polycythemia. Next, serum erythropoietin (EPO) levels should be measured. If EPO levels are low, the diagnosis is polycythemia vera. Confirmatory tests include Janus kinase (JAK) 2 mutation analysis, leukocytosis, and thrombocytosis. Elevated EPO levels are seen in the normal physiologic response to hypoxia as well as in autonomous production of EPO. Further steps in the workup include evaluation for hypoxia with an arterial blood gas, consideration of smoker’s polycythemia (elevated carboxyhemoglobin levels), and disorders of increased hemoglobin affinity for oxygen. Low serum EPO levels with low oxygen saturation suggest inadequate renal production (renal failure). High RBC mass and high EPO levels with normal oxygen saturation may be seen with autonomous EPO production, such as in renal cell carcinoma.

I-114. The answer is E. (Chap. 58) von Willebrand disease (VWD) is an inherited disorder of platelet adhesion that has several types. The most common type is inherited in an auto-somal dominant fashion and is associated with low levels of qualitatively normal von Willebrand factor. As a disorder primary hemostasis associated with the development of a platelet plug, VWD is primarily associated with mucosal bleeding. General bleeding symptoms that are more common in VWD include prolonged bleeding after surgery or dental procedures, menorrhagia, postpartum hemorrhage, and large bruises. However, easy bruising and menorrhagia are common complaints and are not specific for VWD in isolation. Factors that raise concern for VWD in women with menstrual symptoms include iron-deficiency anemia, need for blood transfusion, passage of clots more than 1 inch in diameter, and need to change a pad or tampon more than hourly. Epistaxis is also a very common occurrence in the general population, but it is the most common complaint of males with VWD. Concerning features of epistaxis that may be more likely to indicate an underlying bleeding diathesis are lack of seasonal variation and bleeding that requires medical attention. Although most gastrointestinal bleeding in individuals with VWD is unrelated to the bleeding diathesis, VWD types 2 and 3 are associated with angiodysplasia of the bowel and gastrointestinal bleeding. Spontaneous hemarthroses or deep muscle hematomas are seen in clotting factor deficiencies and not seen VWD except severe VWD with associated decreased factor VIII levels less than 5%.

I-115. The answer is B. (Chap. 58) The activated partial thromboplastin time (aPTT) measures the integrity of the intrinsic and common coagulation pathways, and as such, is affected by all of the coagulation factors, except factor VII. The aPTT reagent contains phospholipids derived from animal or vegetable sources and includes an activator of the intrinsic coagulation system, such as nonparticulate ellagic acid or kaolin. The phospholipid reagent frequently varies from laboratory to laboratory. Thus, an aPTT measured in one hospital may differ from another. Isolated elevations in the aPTT can be related to factor deficiencies, heparin or direct thrombin inhibitors, lupus anticoagulant, or the presence of a specific factor inhibitor. To differentiate between the presence of factor deficiencies and inhibitors, mixing studies should be performed. Mixing studies are performed by mixing normal plasma and the patient’s plasma in a 1:1 ratio. The aPTT and prothrombin time (PT) are incubated at 37°C, and

levels are measured immediately and serially thereafter for about 2 hours. If the cause is an isolated factor deficiency, the aPTT should correct to normal values and remain normal throughout the incubation period. In the presence of an acquired inhibitor, the aPTT may or may not correct immediately, but upon incubation, the inhibitor becomes more active, and the aPTT will progressively prolong. In contrast, the aPTT does not correct immediately or with incubation in the presence of lupus anticoagulants. The presence of serious bleeding in the presence of mixing studies suggesting an inhibitor should further rule out lupus anticoagulant as a cause because the lupus anticoagulant typically presents with no symptoms or as a thrombotic disorder. The mixing studies do not, however, eliminate the presence of heparin as a cause of the prolonged aPTT. If heparin were present, the thrombin time, but not the reptilase time, would be prolonged. In this scenario, both values were normal, ruling out the presence of heparin or a direct thrombin inhibitor. Likewise, disseminated intravascular coagulation can be ruled out in the presence of normal fibrinogen levels. In serious vitamin K deficiency, both the PT and aPTT should be prolonged.

I-116. The answer is E. (Chap. 59) Lymphadenopathy has many causes, including infections, immunologic diseases, and malignancy among others. In the vast majority of cases, the cause of enlarged lymph nodes is a benign process. In the primary care practice, fewer than 1% of individuals will have malignancy, and in individuals referred for lymphadenopathy, this number rises only to 16%. Some features on history and physical examination lead to an increased likelihood that the cause of lymphadenopathy is malignant in origin. Malignancy is more common in individuals older than 50 years. Fevers and chills are more commonly present in benign respiratory illness but can be present in malignancy. Thus, fever is a nonspecific symptom. Likewise, generalized versus focal lymphadenopathy is also not specific. The site of lymph node enlargement can be important and raise the risk of malignancy. The presence of supraclavicular lymphadenopathy is never normal. These lymph nodes drain the thoracic cavity and retroperitoneal space and are most commonly enlarged in malignancy. However, infectious etiologies can also cause supraclavicular lymphadenopathy. The size and texture of the lymph nodes also provide important information. Nodes less than 1.0 cm × 1.0 cm are almost always benign, but lymph nodes greater than 2.0 cm in maximum diameter or with an area of 2.25 cm² (1.5 × 1.5 cm) are more likely to be malignant. Nodes containing metastatic cancer tend to be described as hard, fixed, and nontender. In lymphoma, however, the nodes can be tender because of rapid enlargement of the node with subsequent stretching of the capsule of the lymph nodes. Lymphomatous nodes are also frequently described as firm, rubbery, and mobile.

I-117. The answer is F. (Chap. 59) This patient’s lymphadenopathy is benign. Inguinal nodes smaller than 2 cm are common in the population at large and need no further workup provided that there is no other evidence of disseminated infection or tumor and that the nodes have qualities that do not suggest tumor (not hard or matted). A practical approach would be to measure the nodes or even photograph them if visible and follow them serially over time. Occasionally, inguinal lymph nodes can be associated with sexually transmitted diseases. However, these are usually ipsilateral and tender, and evaluation includes bimanual examination and appropriate cultures, not necessarily pelvic ultrasonography. A total-body CT scan would be indicated if other pathologic nodes suggestive of lymphoma or granulomatous disease are present in other anatomic locations. Bone marrow biopsy would be indicated only if a diagnosis of lymphoma is made first.

I-118. The answer is C. (Chap. 59) Portal hypertension causes splenomegaly via passive congestion of

the spleen. It generally causes only mild enlargement of the spleen because expanded varices provide some decompression for elevated portal pressures. Myelofibrosis necessitates extramedullary hematopoiesis in the spleen, liver, and even other sites such as the peritoneum, leading to massive splenomegaly caused by myeloid hyperproduction. Autoimmune hemolytic anemia requires the spleen to dispose of massive amounts of damaged red blood cells, leading to reticuloendothelial hyperplasia and frequently an extremely large spleen. Chronic myelogenous leukemia and other leukemias and lymphomas can lead to massive splenomegaly caused by infiltration with an abnormal clone of cells. Marginal zone lymphoma typically presents with splenomegaly. If a patient with cirrhosis or right heart failure has massive splenomegaly, a cause other than passive congestion should be considered.

I-119. The answer is A. (Chap. 59) The presence of Howell-Jolly bodies (nuclear remnants), Heinz bodies (denatured hemoglobin), basophilic stippling, and nucleated red blood cells (RBCs) in the peripheral blood implies that the spleen is not properly clearing senescent or damaged RBCs from the circulation. This usually occurs because of surgical splenectomy but is also possible when there is diffuse infiltration of the spleen with malignant cells. Hemolytic anemia can have various peripheral smear findings depending on the etiology of the hemolysis. Spherocytes and bite cells are an example of damaged RBCs that might appear because of autoimmune hemolytic anemia and oxidative damage, respectively. Disseminated intravascular coagulation is characterized by schistocytes and thrombocytopenia on smear with an elevated international normalized ratio and activated partial thromboplastin time as well. However, in these conditions, damaged RBCs are still cleared effectively by the spleen. Transformation to acute leukemia does not lead to splenic damage.

I-120. The answer is A. (Chap. 59) Splenectomy leads to an increased risk of overwhelming postsplenectomy sepsis, an infection that carries an extremely high mortality rate. The most commonly implicated organisms are encapsulated. Streptococcus pneumoniae, Haemophilus influenzae, and sometime gram-negative enteric organisms are most frequently isolated. There is no known increased risk for any viral infections. Vaccination for S. pneumoniae, H. influenzae, and Neisseria meningitidis is indicated for any patient who may undergo splenectomy. The vaccines should be given at least 2 weeks before surgery. The highest risk of sepsis occurs in patients younger than 20 years of age because the spleen is responsible for first-pass immunity and younger patients are more likely to have primary exposure to implicated organisms. The risk is highest during the first 3 years after splenectomy and persists at a lower rate until death.

I-121. The answer is E. (Chap. 60) Chronic granulomatous disease (CGD) is an inherited disorder of abnormal phagocyte function. Seventy percent of cases are inherited in an X-linked fashion with the other 30% being autosomal recessive. Affected individuals are susceptible to infectious with catalase-positive organisms, especially Staphylococcus aureus. Other organisms that can be seen include Burkholderia cepacia, Aspergillus spp., and Chromobacterium violaceum. Most individuals present in childhood, and infections commonly affect the skin, ears, lungs, liver, and bone. Excessive inflammatory reaction can lead to suppuration of lymph nodes, and granulomatous inflammation can be seen on lymph node biopsy and found in the gastrointestinal and genitourinary tracts. Aphthous ulcers and eczematous skin rash can also be seen. The underlying genetic defect in CGD is the inability of neutrophils and monocytes to generate the appropriate oxidative burst in response to infectious organisms. Several mutations can lead to the disease, and these affect one of the five subunits of the NADPH (nicotinamide adenine dinucleotide phosphate) oxidase enzyme. The test of choice to diagnose

chronic granulomatous disease is the nitroblue tetrazolium dye test, which demonstrates lack of superoxide and hydrogen peroxide production in the face of an appropriate stimulus.

I-122. The answer is A. (Chap. 60) Under normal or nonstress conditions, roughly 90% of the neutrophil pool is in the bone marrow, 2–3% in the circulation, and the remainder in the tissues. The circulating pool includes the freely flowing cells in the bloodstream and the others are marginated in close proximity to the endothelium. Most of the marginated pool is in the lung, which has a vascular endothelium surface area. Margination in the postcapillary venules is mediated by selectins that cause a low-affinity neutrophil–endothelial cell interaction that mediates “rolling” of the neutrophils along the endothelium. A variety of signals, including interleukin 1, tumor necrosis factor α, and other chemokines, can cause leukocytes to proliferate and leave the bone marrow and enter the circulation. Neutrophil integrins mediate the stickiness of neutrophils to endothelium and are important for chemokine-induced cell activation. Infection causes a marked increase in bone marrow production of neutrophils that marginate and enter tissue. Acute glucocorticoids increase neutrophil count by mobilizing cells from the bone marrow and marginated pool.

I-123. The answer is E. (Chap. 60) Many drugs can lead to neutropenia, most commonly via retarding neutrophil production in the bone marrow. Of the list in the answer choices, trimethoprimsulfamethoxazole is the most likely culprit. Other common causes of drug-induced neutropenia include alkylating agents such as cyclophosphamide or busulfan, antimetabolites including methotrexate and 5-flucytosine, penicillin and sulfonamide antibiotics, antithyroid drugs, antipsychotics, and anti-inflammatory agents. Prednisone, when used systemically, often causes an increase in the circulating neutrophil count because it leads to demargination of neutrophils and bone marrow stimulation. Ranitidine, an H₂ blocker, is a well-described cause of thrombocytopenia but has not been

implicated in neutropenia. Efavirenz is a nonnucleoside reverse transcriptase inhibitor whose main side effects include a morbilliform rash and central nervous system effects, including strange dreams and confusion. The presence of these symptoms does not require drug cessation. Darunavir is a new protease inhibitor that is well tolerated. Common side effects include a maculopapular rash and lipodystrophy, a class effect for all protease inhibitors.

I-124. The answer is E. (Chap. e49) Mercury is one of the metals that is a significant cause of health concern because of low-level exposure in environmental and occupational exposures. The toxicity of low level organic mercury exposure (as manifested by neurobehavioral performance) is of increasing concern based on studies of the offspring of mothers who ingested mercury-contaminated fish. With respect to whether the consumption of fish by women during pregnancy is good or bad for offspring neurodevelopment, balancing the trade-offs of the beneficial effects of the omega-3-fatty acids (FAs) in fish versus the adverse effects of mercury contamination in fish has led to some confusion and inconsistency in public health recommendations. Overall, it appears that it is best for pregnant women to either limit fish consumption to species known to be low in mercury contamination but high in omega-3-FAs (e.g., sardines or mackerel) or to avoid fish and obtain omega-3-FAs through supplements or other dietary sources. Current evidence has not supported the recent contention that ethyl mercury, used as a preservative in multiuse vaccines administered in early childhood, has played a significant role in causing neurodevelopmental problems such as autism. Dimethylmercury, a compound only found in research labs, is “supertoxic”—a few drops of exposure via skin absorption or inhaled vapor can cause severe cerebellar degeneration and death. Acute mercury exposure can be

assessed with serum levels, but chronic exposure is best assessed by assaying hair samples.

I-125. The answer is C. (Chap. 396) This patient has the typical manifestations of ciguatera poisoning from ingested snapper, grouper, or barracuda. Ciguatera poisoning is the most common nonbacterial food poisoning associated with fish in the United States; most U.S. cases occur in Florida and Hawaii. The poisoning almost exclusively involves tropical and semitropical marine coral reef fish common in the Indian Ocean, the South Pacific, and the Caribbean Sea. Among reported cases, 75% (except in Hawaii) involve the barracuda, snapper, jack, or grouper. Most, if not all, ciguatoxins are unaffected by freeze drying, heat, cold, and gastric acid. None of the toxins affects the odor, color, or taste of fish. The onset of symptoms may come within 15–30 minutes of ingestion and typically takes place within 2– 6 hours. Symptoms increase in severity over the ensuing 4–6 hours. Most victims develop symptoms within 12 hours of ingestion, and virtually all are afflicted within 24 hours. More than 150 symptoms have been reported, including abdominal pain, nausea, vomiting, diarrhea, chills, paresthesias, pruritus, tongue and throat numbness or burning, odontalgia or dental dysesthesias, and an extensive variety of neurologic findings. Bradycardia, hypotension, central respiratory failure, and coma may occur. Death is rare. Symptoms may persist for 48 hours and then generally resolve. A pathognomonic symptom is the reversal of hot and cold tactile perception, which develops in some persons after 3–5 days and may last for months. More severe reactions tend to occur in persons previously stricken with the disease. Therapy is supportive and symptom directed. Consumption of fish in ciguatera-endemic regions should be avoided. All oversized fish of any predacious reef species should be suspected of harboring ciguatoxin. Neither moray eels nor the viscera of tropical marine fish should ever be eaten.

I-126. The answer is B. (Chap. e50) More than 5 million poison exposures occur in the United States each year. Most are acute, accidental (unintentional), involve a single agent, occur in the home, result in minor or no toxicity, and involve children younger than 6 years of age. Pharmaceuticals are involved in 47% of exposures and 84% of serious or fatal poisonings. Unintentional exposures can result from the improper use of chemicals at work or play; label misreading; product mislabeling; mistaken identification of unlabeled chemicals; uninformed self-medication; and dosing errors by nurses, pharmacists, physicians, parents, and elderly adults. Excluding the recreational use of ethanol, attempted suicide (deliberate self-harm) is the most common reported reason for intentional poisoning. Recreational use of prescribed and over-the-counter drugs for psychotropic or euphoric effects (abuse) or excessive self-dosing (misuse) are increasingly common and may also result in unintentional self-poisoning. About 20–25% of exposures require bedside health professional evaluation, and 5% of all exposures require hospitalization. Poisonings account for 5–10% of all ambulance transports, emergency department visits, and intensive care unit admissions. Up to 30% of psychiatric admissions are prompted by attempted suicide via overdosage. Overall, the mortality rate is low: fewer than 1% of all exposures. It is much higher (1–2%) in hospitalized patients with intentional (suicidal) overdose, who account for the majority of serious poisonings. Acetaminophen is the pharmaceutical agent most often implicated in fatal poisoning. Overall, carbon monoxide is the leading cause of death from poisoning, but this is not reflected in hospital or poison center statistics because patients with such poisoning are typically dead when discovered and are referred directly to medical examiners.

I-127. The answer is D. (Chap. e50) Sympathetic toxidromes share many features, including increased pulse, blood pressure, neuromuscular activity, tremulousness, delirium, and agitation. In many cases, these syndromes can be subclassified according to other features or relative strengths of the above

symptoms. Sympathomimetics such as cocaine and amphetamines cause extreme elevations in vital signs and organ damage caused by peripheral vasoconstriction, usually in the absence of hallucinations. Benzodiazepine and alcohol withdrawal syndromes present similarly, but hallucinations and often seizures are common in these conditions. Hot, dry, flushed skin; urinary retention; and absent bowel sounds characterize anticholinergic syndromes associated with antihistamines, antipsychotics, antiparkinsonian agents, muscle relaxants, and cyclic antidepressants. Nystagmus is a unique feature of ketamine and phencyclidine overdose.

I-128. The answer is A. (Chap. e50) Lithium interferes with cell membrane ion transport, leading to nephrogenic diabetes insipidus and falsely elevated chloride. This can cause the appearance of low anion gap metabolic acidosis. Sequelae include nausea, vomiting, ataxia, encephalopathy, coma, seizures, arrhythmia, hyperthermia, permanent movement disorder, and encephalopathy. Severe cases are treated with bowel irrigation, endoscopic removal of long-acting formulations, hydration, and sometimes hemodialysis. Care should be taken because toxicity occurs at lower levels in chronic toxicity compared with acute toxicity. Salicylate toxicity leads to a normal osmolal gap as well as an elevated anion gap metabolic acidosis, respiratory alkalosis, and sometimes normal anion gap metabolic acidosis. Methanol toxicity is associated with blindness and is characterized by an increased anion gap metabolic acidosis, normal lactate and ketones, and a high osmolal gap. Propylene glycol toxicity causes an increased anion gap metabolic acidosis with elevated lactate and a high osmolal gap. The only electrolyte abnormalities associated with opiate overdose are compensatory to a primary respiratory acidosis.

I-129. The answer is B. (Chap. e50) The clinical implications of understanding the difference between therapeutic drug dosing and overdosage are critical. Drug effects begin earlier, peak later, and last longer in the context of overdose compared with commonly referenced values. Therefore, if a patient has a known ingestion of a toxic dose of a dangerous substance and symptoms have not yet begun, then aggressive gut decontamination should ensue because symptoms are apt to ensue rapidly. The late peak and longer duration of action are important as well. A common error in practice is for patients to be released or watched less carefully after reversal of toxicity associated with an opiate agonist or benzodiazepine. However, the duration of activity of the offending toxic agent often exceeds the half-life of the antagonists, naloxone or flumazenil, requiring the administration of subsequent doses several hours later to prevent further central nervous system or physiologic depression.

I-130. The answer is E. (Chap. e50) Gastric decontamination is controversial because few data are available to support or refute its use more than an hour after ingestion. It remains a very common practice in most hospitals. Syrup of ipecac is no longer endorsed for inhospital use and is controversial even for home use, although its safety profile is well documented and therefore it likely poses little harm for ingestions when the history is clear and the indication strong. Activated charcoal is generally the decontamination method of choice because it is the least aversive and least invasive option available. It is effective in decreasing systemic absorption if given within 1 hour of poison ingestion. It may be effective even later after ingestion for drugs with significant anticholinergic effect (e.g., tricyclic antidepressants). Considerations are poor visibility of the gastrointestinal tract on endoscopy after charcoal ingestion and perhaps decreased absorption of oral drugs. Gastric lavage is the most invasive option and is effective, but it is occasionally associated with tracheal intubation and bowel wall perforation. It is also the least comfortable option for the patient. Moreover, aspiration risk is

highest in those undergoing gastric lavage. All three of the most common options for decontamination carry at least a 1% risk of an aspiration event, which warrants special consideration in the patient with mental status change.

I-131. The answer is E. (Chap. e51) Whereas acute mountain sickness (AMS) is the benign form of altitude illness, high-altitude cerebral edema (HACE) and high-altitude pulmonary edema (HAPE) are life threatening. Altitude illness is likely to occur above 2500 m but has been documented even at 1500-2500 m The acclimation to altitude includes hyper-ventilation in response to the reduced inspired PO₂ initially followed by increased erythropoietin and 2,3-bisphosphoglycerate. AMS is

characterized by nonspecific symptoms (headache, nausea, fatigue, and dizziness) with a paucity of physical findings developing 6-12 hours after ascent to a high altitude. AMS must be distinguished from exhaustion, dehydration, hypothermia, alcoholic hangover, and hyponatremia. The most important risk factors for the development of altitude illness are the rate of ascent and a history of high-altitude illness. Exertion is a risk factor, but lack of physical fitness is not. One protective factor in AMS is high-altitude exposure during the preceding 2 months. Children and adults seem to be equally affected, but people greater than 50 years of age may be less likely to develop AMS than younger people. Most studies reveal no gender difference in AMS incidence. Sleep desaturation—a common phenomenon at high altitude—is associated with AMS. Gradual ascent is the best approach to prevent AMS. Acetazolamide or dexamethasone beginning 1 day before ascent and continuing for 2-3 days is effective if rapid ascent is necessary. A double-blind placebo-controlled trial demonstrated no benefit on AMS from gingko biloba. Mild cases of AMS can be treated with rest; more serious cases are treated with acetazolamide and oxygen. Descent is therapeutic in all serious cases, including HACE and HAPE. Patients who have recovered from mild cases of AMS may reascend carefully after recovery; patients with HACE should not.

I-132. The answer is D. (Chap. e51) High-altitude pulmonary edema (HAPE) is related to an enhanced or atypical pulmonary vascular response to hypoxia. It is not necessarily preceded by acute mountain sickness. HAPE develops within 2-4 days after arrival at high altitude; it rarely occurs after more than 4 or 5 days at the same altitude. A rapid rate of ascent, exercise, a history of HAPE, respiratory tract infections, and cold environmental temperatures are risk factors. Men are more susceptible than women. People with abnormalities of the cardiopulmonary circulation leading to pulmonary hypertension (e.g., patent foramen ovale, mitral stenosis, primary pulmonary hypertension, unilateral absence of the pulmonary artery) are at increased risk of HAPE even at moderate altitudes. Echocardiography is recommended when HAPE develops at relatively low altitudes (<3000 m) and whenever cardiopulmonary abnormalities predisposing to HAPE are suspected. The initial manifestation of HAPE may be a reduction in exercise tolerance greater than that expected at the given altitude. A dry, persistent cough may presage HAPE and may be followed by the production of blood-tinged sputum Tachypnea and tachycardia, even at rest, are important markers as illness progresses. Crackles may be heard on auscultation but are not diagnostic. Fever and leukocytosis may occur. Descent and oxygen (to raise ^Sa°2 >⁹⁰%) are the mainstays of therapy for HAPE. Nifedipine can be used as adjunctive therapy. Inhaled beta-agonists, which are safe and convenient to carry, are useful in the prevention of HAPE and may be effective in its treatment, although no trials have yet been carried out. Inhaled nitric oxide and expiratory positive airway pressure may also be useful therapeutic measures but may not be available in high-altitude settings. No studies have investigated phosphodiesterase-5 inhibitors in the treatment of HAPE, but reports have described their use in

clinical practice. Patients with HAPE who have recovered may be able to reascend. In high-altitude cerebral edema, reascent after a few days is not advisable.

1-133. The answer is E.(Chap. e52) Untreated pneumothorax has the risk of rapidly expanding and potentially causing tension upon decompression. Patients with extensive bullae should be considered carefully because they may have a similar risk. The effect of hyperbaric oxygen in patients with chronic C0₂ retention has not been studied. The other commonly quoted contraindication to hyperbaric oxygen

therapy is a history of receiving bleomycin chemotherapy. Bleomycin is associated with a dose-dependent risk of pneumonitis, and this risk may be enhanced with hyperbaric oxygen exposure. There are reports of patients developing pneumonitis with high FI0₂ or hyperbaric therapy even years after

receiving bleomycin. Radiation proctitis and carbon monoxide poisoning are clinical conditions in which hyperbaric oxygen therapy may be warranted. The indications for hyperbaric oxygen therapy are evolving with some advocating therapy for delayed radiation injury, wound therapy, myonecrosis, thermal injuries, and other conditions in which local hypoxia may occur or impaired oxygen delivery may be present.

1-134. The answer is D.(Chap. e52) Because for every 10.1-m increase in depth of seawater, the ambient pressure (P_amb) increases by 1 standard atmosphere, at 20-m depth, a person is exposed to a

P_amb of approximately 3 atmospheres absolute. Decompression sickness (DCS) is caused by the formation of bubbles from dissolved inert gas (usually nitrogen) during or after ascent (decompression) from a compressed gas dive. Deeper and longer dives increase the amount of dissolved inert gas, and more rapid ascent increases the potential for bubbles to form and affect end organs. Although variable, DCS usually does not occur unless the dive depth exceeds 7 m (1.7 arm absolute). DCS usually develops within 8-12 hours of ascent. The majority of patients present with mild symptoms, including musculoskeletal pain; fatigue; and minor neurologic manifestations, such as patchy paresthesias. A feared complication is cerebral arterial gas embolism (CAGE). To lessen the chance of gas bubbles entering the cerebral circulation, patients with DCS should remain in a horizontal posture. Initial first aid should include 100% oxygen to accelerate inert gas washout and resolution of bubbles. For patients with symptoms beyond mild DCS, recompression and hyperbaric oxygen therapy are generally recommended. If evacuated by air, the patient should be transported at low altitude by helicopter. After full recovery, diving can be restarted after at least 1 month.

1-135. The answer is B.(Chap. 268) ALI and ARDS are both characterized by diffuse lung injury, bilateral radiographic infiltrates, and hypoxemia in the absence of left atrial hypertension. ALI is considered a less severe form of diffuse lung injury that may evolve to ARDS or warrant intensive therapy to forestall the progression. The distinction between ALI and ARDS is made by the magnitude of the Pa0₂/FI0₂ ratio with ARDS defined as a ratio of 200 mmHg or below and ALI 300 mmHg or

below. Many medical and surgical illnesses are associated with the development of ALI and ARDS, but most cases (>80%) are caused by a relatively small number of clinical disorders, namely, severe sepsis syndrome and bacterial pneumonia (40-50%), trauma, multiple transfusions, aspiration of gastric contents, and drug overdose. Among patients with trauma, pulmonary contusion, multiple bone fractures, and chest wall trauma or flail chest are the most frequently reported surgical conditions in ARDS, but head trauma, near drowning, toxic inhalation, and burns are rare causes. The risks of developing ARDS are increased in patients with more than one predisposing medical or surgical condition (e.g., the risk for ARDS increases from 25% in patien

Date: 2016-04-22; view: 565