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The patient’s fasting gastrin level is 500 pg/ml (normal value generic 20mg erectafil otc, < 100 pg/ml) discount 20mg erectafil amex. For this patient, which of the following statements is true? An upper GI series that is diagnostic of a bulbar duodenal ulcer will preclude endoscopy B. Treatment failure with clarithromycin-based regimens occurs in approximately 30% of cases of H. A positive serum antibody test (sensitivity and specificity > 90%) would indicate persistent infection and require retreatment with metronidazole, tetracycline, and bismuth, as well as continuation of a proton pump inhibitor D. Ulcers refractory to pharmacotherapy are seen in acid hypersecretory states; this patient’s fasting gastrin level is diagnostic of the Zollinger- Ellison syndrome Key Concept/Objective: To understand the diagnostic modalities used in peptic ulcer disease Despite having a lower sensitivity and specificity than endoscopy, an upper GI series using barium and air (double contrast) may be favored by primary care physicians and patients over referral for endoscopy for suspected uncomplicated ulcer. An upper GI series offers lower cost, wider availability, and fewer complications. However, for troublesome and undiagnosed dyspepsia, an upper GI series may be superfluous, because a normal result will often necessitate endoscopy (endoscopy is more sensitive than radiography) and because an upper GI series showing a gastric ulcer will also necessitate endoscopy and biopsy to exclude gastric malignancy. In many patients, only a finding of a duodenal bul- 4 BOARD REVIEW bar ulcer on an upper GI series will preclude endoscopy. A 2-week course of a three-drug regimen that includes a proton pump inhibitor, clarithromycin, and amoxicillin has a success rate approaching 90%. The major causes of treatment failure are poor compliance with the reg- imen and clarithromycin resistance; the latter occurs in around 10% of current strains and is increasing with increased macrolide use in the population. Breath testing is more useful than serology in diagnosing failure of eradication of H. A fasting serum gastrin concentration can be used to screen for an acid hypersecretory state resulting from Zollinger-Ellison syndrome. Antisecretory drugs (especially proton pump inhibitors) can also raise serum gastrin levels modestly (to 150 to 600 pg/ml). Definitive documentation of an acid hypersecretory state requires quantitative gastric acid measurement (gastric analysis). A 54-year-old man with a history of COPD and tobacco abuse presents for evaluation of burning epi- gastric pain and melena. The epigastric pain has persisted for several weeks; the melena began several hours ago. His current medical regimen includes albuterol and ipratropium bromide nebulizers, long- term oral steroids, and theophylline. He also reports that he recently used an NSAID for joint pain. On physical examination, the patient’s heart rate is 115 beats/min and his blood pressure is 98/45 mm Hg. Abdominal examination does not demonstrate tenderness, rebound, or rigidity. A complete blood count is significant for a hematocrit of 39%; serum electrolytes are within nor- mal limits. EGD is performed, and the patient is found to have a gastric ulcer with a visible vessel. For this patient, which of the following statements is true? Corticosteroids not only are ulcerogenic but also impair healing of pre- existing ulcers B. The patient’s hemoglobin concentration makes a significant GI bleed unlikely C. To exclude a diagnosis of ulcerated gastric cancer, gastric ulcers should be followed endoscopically until they are completely healed D. Corticosteroids, which block cyclooxygenase-2 (COX-2) but not COX-1, are not ulcerogenic when used alone, though they impair healing of preexisting ulcers. However, when corticosteroids are used in combination with NSAIDs, the risk of ulcer formation is much greater than when NSAIDs are used alone. In the first several hours after an episode of acute ulcer bleeding, the hemoglobin concentration will not completely reflect the severity of the blood loss until compensatory hemodilution occurs or until intravenous fluids such as isotonic saline are administered. Thus, the pulse rate and blood pressure in the supine and upright posi- tions are better initial indicators of the extent of blood loss than are red cell counts. Because they are larger than duodenal ulcers, gastric ulcers take longer to heal. Thus, after antibiotic administra- tion, the patient should be treated with an acid antisecretory agent for an additional 4 to 8 weeks. A 43-year-old woman presents to establish primary care. Her medical history is significant for an uncom- plicated duodenal ulcer, which she experienced 18 months ago. At the time of diagnosis, she was treat- 4 GASTROENTEROLOGY 5 ed with a clarithromycin-based regimen for H. For this patient, which of the following statements is true? Patients who experience recurrence of ulcer symptoms during the first 2 years after therapy should be assessed by EGD, a urea breath test, or fecal antigen test D. The sensitivity of the urea breath test is unaffected by use of a proton pump inhibitor Key Concept/Objective: To understand the mechanism and diagnosis of treatment failure for eradication of H.
Specific antiviral therapy has been attempted with intravenous ribavirin order erectafil 20 mg on line, but its value for patients with HCPS is uncertain discount 20mg erectafil with amex; a controlled trial is in progress. There is currently no clinically available vaccine to prevent hantavirus infections. His medical history is significant for type 2 diabetes, for which he takes glyburide. For this patient, which of the following statements is true? Antigenic drift is the major change that causes annual variation in this infectious agent 84 BOARD REVIEW B. Definitive diagnosis will have little impact on the treatment of this patient C. Vaccination in this patient rules out influenza as an etiologic agent D. Chemoprophylaxis is effective for one type of this infectious agent Key Concept/Objective: To know and understand influenza virus infections Two major types of antigenic change can occur: drift and shift. Antigenic drift refers to relatively minor changes in hemagglutinin and less often with neuraminidase that occur frequently (usually every few years) and sequentially in the setting of selective immunologic pressure in the population. Drift results from point mutations of the cor- responding RNA segment. The surface glycoproteins induce host humoral and cellular immune responses and are responsible for the changing antigenicity of influenza virus- es. Antigenic shift occurs only in influenza A viruses and results from acquisition of a new gene segment for hemagglutinin with or without one for neuraminidase. Several rapid assays are commercially available in the United States to detect influenza A and B occurring together; one of these assays is able to rapidly differentiate between influen- za A and influenza B. Making a definitive diagnosis can have a significant impact on medical management. The efficacy of the influenza vaccine is 70% to 90% in young adults, especially when the vaccine antigen and the circulating strain are closely matched. Although vaccination is less effective in elderly and immunocompromised patients, vaccination provides partial protection against pneumonia and death. Amantadine and rimantadine are active against influenza A only. A new class of com- pounds, the neuraminidase inhibitors, is active against influenza A and B viruses. The neuraminidase inhibitors are also effective for prophylaxis of influenza A and B infec- tions. A 22-year-old female college student presents to your office as a new walk-in patient. She has no med- ical history and takes no medications. She states that she had unprotected sex with a new partner about 1 week ago. Four days ago, she developed fever and chills, severe fatigue, painful groin swellings, and "blisters" on her labia. She states that she has had a total of five sexual partners. On physical examination, the patient is afebrile, has tender superficial inguinal lymphadenopathy measuring 2 cm bilaterally, and has several clustered vesicular lesions on her labia majora. Which of the following statements regarding herpes simplex virus (HSV) infections is false? Direct contact with infected secretions is the principal mode of transmission of HSV B. Herpes simplex virus type 2 (HSV-2) is transmitted more efficiently from males to females than from females to males C. HSV-2 is a local infection that is confined to the genitourinary system D. Among the general public, herpetic whitlow is typically caused by HSV-2 Key Concept/Objective: To understand the important clinical features of HSV-2 infection Direct contact with infected secretions is the principal mode of HSV transmission. HSV- 1 is usually transmitted by an oral route and HSV-2 by a genital route. Transmission of HSV occurs frequently, even in the absence of lesions. HSV-2 is transmitted more effi- ciently from males to females than from females to males. Autoinoculation to other skin sites also occurs, more often with HSV-2 than with HSV-1. Extragenital lesions 7 INFECTIOUS DISEASE 85 develop during the course of primary infection in 10% to 18% of patients. Aseptic meningitis is not uncommon with primary genital herpes, particularly in women; in rare instances, herpetic sacral radiculomyelitis occurs. Primary finger infections, or whitlows, usually involve one digit and are characterized by intense itching or pain fol- lowed by the formation of deep vesicles that may coalesce. Among the general public, whitlows are most often caused by HSV-2, whereas among medical and dental person- nel, HSV-1 is the principal culprit. A 70-year-old male patient who has diabetes and hypertension presents with a complaint of severe flank pain.
He does not smoke discount erectafil 20mg with amex, drinks alcohol only occasionally purchase 20 mg erectafil free shipping, and has been monogamous with his wife over the 5 years they have been married. He has had no fever, chills, eye symptoms, anorexia, nausea, diarrhea, bloody stool, abdominal pain, penile sores or discharge, dysuria, or joint pains. On examination, the patient is afebrile, with multiple sharply demarcated scaly papules 3 to 10 mm in diam- eter distributed symmetrically on his trunk, arms, palms, and penis. There are no target lesions or oral lesions, and no lymphadenopathy is found. What is the most likely cause of this patient’s rash? Drug reaction Key Concept/Objective: To be able to recognize guttate psoriasis This is a classic presentation of guttate psoriasis, with onset after a recent streptococcal infection; a symmetrical distribution involving trunk, extremities, palms, and penis; and 8 BOARD REVIEW well-demarcated, small, scaly, erythematous papules. In contrast, the rash of primary HIV infection is a maculopapular, diffuse eruption, with poorly defined borders and no scal- ing, usually accompanied by low-grade fever, malaise, lymphadenopathy, and other flu- like symptoms. Secondary syphilis can cause a scaly rash that may include the palms and soles, but the rash is not itchy and is usually accompanied by lymphadenopathy and/or oral lesions. Secondary syphilis is also accompanied by a positive rapid plasma reagin test. Reiter syndrome usually presents as a tetrad of arthritis, urethritis, conjunctivitis/uveitis, and mucocutaneous lesions. The skin and nail lesions of Reiter syndrome can be difficult to distinguish clinically from psoriasis. For example, the balanitis of Reiter syndrome can look scaly or pustular as in psoriasis; the keratoderma blennorrhagicum can cause a scaly or pustular rash on the palms or soles that can be indistinguishable from psoriasis; and Reiter syndrome nail changes (ridging, pitting, onycholysis) can mimic psoriasis. Though this patient does have penile lesions that could be confused with balanitis, he does not have the rest of the tetrad of symptoms. Most patients with Reiter syndrome also describe a preceding diarrheal illness or sexually transmitted infection, which this patient did not report. Drug reactions usually occur sooner after use of antibiotics than was seen in this patient, who took penicillin several weeks before his rash developed. Additionally, though drug reactions are often symmetrical, they are usually more diffuse, maculopapular erup- tions and are worse on the trunk than on the extremities. If scaly at all, a drug reaction is then usually diffuse, involving the entire skin surface with an erythroderma or exfoliative dermatitis rather than with the small, discrete papules seen in this patient. A 62-year-old man wishes to continue oral therapy begun by another physician for onychomycosis. He reports disfigured nails over the past year, and he began daily oral ketoconazole 2 months ago without much change in the appearance of his nails. His past medical history includes hyperuricemia, chronic neck and back pain, sciatica, and excessive alcohol ingestion. On review of systems, he also reports fin- ger stiffness and pain, especially in the distal interphalangeal (DIP) joints of multiple fingers. On exam- ination, the patient’s fingers are red, tender, and slightly swollen, appearing somewhat sausage-shaped, without obvious synovitis. Multiple fingernails show deep longitudinal ridging with some pitting, thick- ening, yellowish discoloration, and onycholysis. The distal ends of multiple fingers are encased in heaped-up scale, debridement of which reveals necrotic tissue underneath. No lymphadenopathy is found in the neck, axillae, or epitrochlear areas. Laboratory testing shows mild anemia with a normal white blood cell count; negative rheumatoid factor, rapid plasma reagin, and antinuclear antibody tests; and a mildly elevated uric acid and ESR. Hand x-rays show erosions in some DIP joints without hyper- ostosis or bone-cyst formation. Which of the following is the most likely diagnosis for this patient? Systemic lupus erythematosus (SLE) Key Concept/Objective: To be able to recognize psoriatic arthritis Arthritis involving DIP joints and associated with characteristic psoriatic fingernail changes, including pitting, yellow discoloration, onycholysis, ridging, and subungual hyperkeratosis, is most likely to be psoriatic arthritis. Elevated uric acid and mild iron deficiency anemia can also accompany psoriasis because of high skin turnover. Careful examination of this patient’s scalp, umbilicus, gluteal fold, and groin may reveal more characteristic scaly plaques. Chronic gouty arthritis can occur with chronic elevations of uric acid, but it is usually accompanied by tophi, seen on examination as gross deformi- ties in or near the affected joints, and punched-out erosions with overhanging cortical bone (also called “rat-bite” lesions) adjacent to tophaceous deposits, seen on x-ray: find- ings that are not present in this patient. Additionally, gouty arthritis would not explain the skin findings. Osteoarthritis, like psoriatic arthritis, can affect DIP joints; but unlike psoriatic arthritis, osteoarthritis will cause Heberden nodes at the DIP joints and will dis- 2 DERMATOLOGY 9 play x-ray findings of hyperostosis and sometimes bone-cyst formation. Rheumatoid arthritis usually spares the DIP joints and causes a spongy swelling of synovial tissue at the metacarpophalangeal and/or wrist joints. Unlike the rash of psoriasis, that of SLE characteristically appears on the face or other sun- exposed areas and produces localized red plaques, follicular plugging, atrophy, and telang- iectasias: quite unlike the isolated periungual scaling seen in this patient. The arthropathy of SLE does not cause bony erosions. A 23-year-old man presents with worsening pain and swelling in his right ankle, which he has had for the past month. He is otherwise healthy, though he admits to an unhealthy lifestyle, including night- shift work, heavy alcohol use on the weekends, and occasional unprotected sex with men, though he has had none in the past 12 months. He denies any history of sexually transmitted disease or intra- venous drug use, diarrheal illness, fever, chills, weight loss, dysuria, penile discharge, or other joint pains. Removal of his baseball cap reveals a 6 × 15 cm patch of a sharply demarcated, erythematous, scaly rash on his anterior scalp and forehead.
It is associated with distal leg and proximal weakness order erectafil 20 mg mastercard, fatigue and myalgia cheap erectafil 20mg amex, exercise intolerance, respiratory failure, milder cardiomyopathy, hepatic dysfunction. Patients may develop axonal neuropathy due to glycogen storage in endoneurial cells and axons. GSD IV GSD IV (brancher deficiency) is associated with myopathy, cardiomyopathy, and liver disease. In addition brain and spinal cord can be affected resulting in progressive involvement of the upper and lower motor neurons, sensory loss, sphincter problems, and dementia. GSD IV can be associated with adult poly- glucosan body disease and is seen especially in Ashkenazi Jews. GSD V GSD V (McArdle’s disease) usually starts in the early teens and is more common in males. It is characterized by exercise intolerance, and severe cramping that may last several hours, myoglobinuria, proximal muscle involvement, and a “second wind” phenomenon in which the patient’s symptoms may temporarily resolve. In the infantile form severe weakness and respiratory failure may be seen, and late onset GSD IV may be associated with only mild fatigue. GSD VII GSD VII (Tarui’s disease) occurs predominantly in males of Ashkenazi Jewish or Italian ancestry. Clinical features are similar to McArdle’s although the “second wind“ is less common than in McArdle’s. High carbohydrate meals exacerbate exercise intolerance, because the patient cannot metabolize glucose and ends up depleting free fatty acids and ketones – the “out of wind“ phenomenon. Occasionally in children there may be a severe myopathy, respiratory failure, cardiomyopathy, arthro- gryposis, seizures, and corneal opacification. GSD VII is also associated with accumulation of polyglucosan bodies over time and may result in a further deterioration in strength later in life that resembles IBM. GSD VIII–XIII are characterized by intolerance to intense exercise, cramps and/ GSD VIII–XIII or myoglobinuria. GSD X occurs almost exclusively in blacks and heterozy- gotes may also have exercise intolerance. GSD are a group of predominantly autosomal recessive disorders. GSD I is Pathogenesis caused by deficiencies in the activity of G6Pase system consisting of two membrane proteins that work in concert to maintain glucose homeostasis, G6PT (11q23) and G6Pase (17q21). G6PT translocates glucose-6-phosphate (G6P) from cytoplasm to the lumen of the endoplasmic reticulum and G6Pase catalyzes the hydrolysis of G6P to produce glucose and phosphate. Deficien- cies in G6Pase and G6PT cause GSD Ia and GSD Ib, respectively. GSD II is an autosomal recessive disorder due to deficiency of l acid α-1,4- glucosidase coded by a gene on chromosome 17q23. GSD III results from nonsense mutations, small deletions or insertions, or splice site changes on chromosome 1p21. There is a deficiency of amylo-1,6-glucosidase (AGL) that catalyzes both a transferase and a hydrolysis reaction. In GSD V several mis- sense, stop, start codon or frameshift mutations of 11q13 have been described. There is a deficiency of muscle phosphorylase resulting in impaired ATP generation from aerobic and anaerobic glycolysis and reduced production of pyruvate. GSD VII is due to a deficiency of 6-Phosphofructokinase (PFK – 1cen- q32). Other listed enzyme deficiencies resulting in defects of glycogen storage include: GSD XII – Aldolase A: 16q22, GSD XIII – β-Enolase: 17pter, GSD XI- Lactate dehydrogenase: 11p15, GSD IX – Phosphoglycerate Kinase: Xq13, X – Phosphoglycerate Mutase: 7p12, and GSD VIII – Phosphorylase β kinase: Xq12. Laboratory: Diagnosis The serum CK is usually very high. The ischemic forearm test shows an insufficient rise in venous lactate, but is non-specific for the GSD, relies on patient compliance, and may have complications such as myoglobinuria. Other changes include hyperuricemia, hyperbilirubinemia, and a high potassium with exercise. GSD VII is associated with a compensated hemolytic anemia. Electrophysiology: Nerve conduction studies are usually normal, however in GSD III there is often evidence of an axonal neuropathy. During contractures, the muscle is electri- cally silent in GSD. EMG shows an increase in insertional activity in distal muscles, along with short duration motor unit action potentials typical of myopathy. Myotonic discharges may be observed, and in GSD II there may be a mixture of myotonic and complex repetitive discharges observed especially in paraspinal muscles. In GSD VII repetitive nerve stimulation at 20 Hz results in a decrement in the motor response. Electron microscopy shows glycogen in cytoplasm with membrane- bound, autophagic vacuoles. In GSD III, V, and VII there are subsarcolemmal and intermyofibrillar vacuoles (Fig. In GSD VII, partial reductions in PFK to 20% of normal may be artifactual due to the lability of the enzyme in incorrect- ly handled fresh frozen muscle.
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