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Correct Answer: C Section: (none)

Explanation:

Reactive arthritis consists of a triad of nonspecific urethritis, conjunctivitis, and asymmetric arthritis, usually involving the large joints of the lower extremities. Genitourinary causes of reactive arthritis include Chlamydia or Ureaplasma. GI infections due to Salmonella, Shigella, Yersinia, Klebsiella, and Campylobacter can also cause reactive arthritis. Gout attacks are typically monoarticular and begin abruptly with the affected joint being exquisitely painful, warm, red, and swollen. These attacks often spontaneously resolve in 310 days. While the symptoms from pseudogout may mimic those of gout, they tend to be less painful and take longer to reach peak intensity. Gonococcal arthritis is seen more often in females, is associated with migratory arthralgia, tends to favor the upper limbs and knees and may be associated with cutaneous lesions (pustules). The absence of attacks and joint distribution makes gout and pseudogout less likely. The history of conjunctivitis and association with diarrhea makes the diagnosis of reactive arthritis more likely than resistant gonococcal arthritis. His clinical symptoms do not suggest ankylosing spondylitis, although if he was HLA-B27 positive he would be at increased risk of developing spondylitis. This patient has the classic symptoms and exposure risk (GI infection) to suggest reactive arthritis. For the articular symptoms, reduction of inflammation and restoration of function can be achieved with nonsteroidal antiinflammatories alone. A sufficient number of patients with reactive arthritis will not be HLA-B27 positive, thus rendering this test useless as a screening test. However, it may be useful when the clinical picture is incomplete (such as absence of antecedent infection or lack of extraarticular features).

Once an antecedent infection has triggered reactive arthritis, it is unlikely that antibiotics will affect the course of the illness (except in the case of chlamydiaassociated urogenital disease where a trial of prolonged antibiotic therapy may be reasonable).

Systemic corticosteroids are usually ineffective in reactive arthritis, but may be tried for resistant disease or conditions such as AIDS in which cytotoxic therapy is contraindicated. Given the absence of skin lesions, penile discharge, or urogenital symptoms, one would be hard-pressed to challenge the patient's statement that he has not engaged in unprotected sex at the risk of jeopardizing the physicianpatient relationship. Reactive arthritis may be the first manifestation of HIV infection. Therefore, HIV antibody status should be determined when the appropriate risk factors and/or clinical features are present. As mentioned previously, systemic steroids are usually ineffective for reactive arthritis and, with the possibility of joint infection, would necessitate ruling out infection by arthrocentesis of the affected joints. Joint infection cannot be ruled out based on his presentation, and joint sepsis must be excluded prior to corticosteroid injection. The clinical presentation is classic for reactive arthritis, and the absence of systemic symptoms makes the likelihood of disseminated bacterial infection low. Indomethacin, at a dose of 150200 mg/day, is the prototypic NSAID medication for treatment of reactive arthritis. Doses higher than this are associated with significant GI complications and do not improve efficacy in a patient resistant to the standard dose. In the event that the patient does not respond to 200 mg of indomethacin or alternative NSAIDs, disease-modifying antirheumatic drugs (DMARD) such as methotrexate, azathioprine, or sulfasalazine may be used, provided that HIV test results are negative, as these immunosuppressants have been reported to precipitate the onset of AIDS in HIV-positive patients.

Correct Answer: E Section: (none)

Explanation:

This patient has sickle cell anemia. This is evident from sickle cells forms on the peripheral blood smear in Figure 1-13. Pain medication is an important initial concern. It is often difficult to determine whether a patient in sickle cell crisis has an ongoing infection. Infections can precipitate sickle cell crisis. With respect to community-acquired pneumonia, the diagnosis is difficult. A patient with sickle cell crisis can have fever as a result of the sickle crisis. They can have an increased respiratory rate, physical examination, and CXR findings which suggest pneumonia as a result of pulmonary infarctions. A white blood count can be elevated due to marrow stimulation. In the presence of the acute chest syndrome, characterized by chest pain, hypoxia, and CXR infiltrates, antibiotics would be indicated. Without further information, it is hard to decide to empirically start broad-spectrum antibiotics for community-acquired pneumonia. Transfusions should generally be avoided in patients with sickle cell anemia who are not symptomatic due to the anemia. Since patients in sickle cell crisis have intravascular hemolysis, their reticulocyte counts are usually high and they can replace their blood quickly. Repeated small transfusions will lead to autoantibodies that will make further transfusions difficult. Arterial blood gas determination should not be the first step, given the above information. A CT scan of the abdomen is not indicated given the nonspecific nature of the patient's abdominal findings. Parvovirus B19 can cause aplastic crisis in patients with hemoglobinopathies, including sickle cell disease. A tip to this diagnosis is the decreased reticulocyte count in a patient who normally would have a high reticulocyte count. Given the information listed above, there is no indication for broad-spectrum antibiotics. Splenectomy is not a reasonable alternative at this point. Patients with sickle cell disease have autosplenectomy by the time they are adults. A bone marrow biopsy maybe indicated because of the low platelet count, but not initially. GnCSF is not indicated because the patient does not have neutropenia. Patients with sickle cell disease typically have isosthenuria.

This is due to repeated infarction of the renal papilli. This causes destruction and interference with the counter current mechanism that causes urine concentration. As a result, patients with sickle cell anemia have the inability to concentrate their urine. This results in fluid and electrolyte abnormalities. Patients in sickle cell crisis are usually fluid depleted. This and the sickled blood cells cause hyperviscosity and microinfarctions. There is no evidence that the patient has diabetes insipidus, which usually has a urine specific gravity less than 1.005. Patients with UTIs do not have isosthenuria due to RBCs and WBCs that increase the urine specific gravity. Sickle cell patients may have zinc deficiency, but this is not a cause of isosthenuria.

Correct Answer: E Section: (none)

Explanation:

Although this is the first time that your patient has been noted to have an elevated blood pressure reading, given his family history and obesity, it is important to consider the coexistence of other cardiovascular risk factors. His evaluation should include, among other things, screening for DM and dyslipidemia along with an ECG. It is reasonable to ask the patient to submit himself to a strict diet (low in fat and salt) and to increase his exercise and activity, since these lifestyle modifications will likely result in weight loss, decreased blood pressure, and improve his risk profile for cardiovascular disease. Nonetheless, it is rarely enough to normalize blood pressure in all but the earliest stages of hypertension. Provided that no other comorbidities exist, the patient should return to clinic in no more than 2 months for a repeat blood pressure check. There is no need to consider secondary causes of hypertension, given his age and presentation.

You should not start antihypertensive medications until further evaluation is completed, and a second elevated reading confirms your diagnosis of hypertension. In the initial evaluation of hypertension (as per the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure [JNC-7], 2003), it is important to evaluate the patient for end-organ damage. This should include the heart, kidneys, eyes, and nervous system. It is recommended to obtain a urinalysis to assess for proteinuria, glucosuria, or hematuria; to obtain an ECG to evaluate the heart for potential hypertrophy or early signs of cardiovascular disease; to obtain a fasting lipid profile, particularly after the age of 35, to assess the cardiovascular risk profile; and to check the patient's renal function to assess for damage or dysfunction. Thyroid function tests are only indicated in the workup of secondary causes of hypertension. According to the JNC-7, this patient's blood pressure falls into the stage 2 hypertension classification in which either systolic blood pressure (SBP) is at least 160 mmHg or diastolic blood pressure (DBP) is at least 100 mmHg.

Stage 1 hypertension is characterized by a SBP of 140159 mmHg and a DBP of 9099 mmHg. Prehypertension is characterized by a SBP of 120139 mmHg and a DBP of 8089 mmHg. Normal blood pressure is characterized by a SBP of less than 120 mmHg and a DBP of less than 80 mmHg. In classifying a patient's blood pressure and determining appropriate therapy, the higher of the two categories corresponding to the SBP and DBP is the one that is used. Per JNC-7 guidelines, treatment of stage 2 hypertension should involve the consideration of a two-drug regimen initially. The goal blood pressure in patients with diabetes is a SBP less than 130 mmHg and a DBP less than 80 mmHg. An ACE inhibitor should be used as the drug class has been shown to slow the progression of diabetic nephropathy and reduce albuminuria. Thiazide diuretics, betablockers, and calcium channel blockers are appropriate choices to consider in this patient in addition to an ACE inhibitor.