Self-assessment Module (SAM) for RPS Satellite Meeting, USCAP
Transcription
Self-assessment Module (SAM) for RPS Satellite Meeting, USCAP
Self-assessment Module (SAM) for RPS Satellite Meeting, USCAP, Seattle, March 13th, 2016 Instructions: 1. This activity qualifies for two and a half (2.5) SAM credits for the American Board of Pathology (ABP) Maintenance of Certification, part II. 2. First, obtain CME credit from the College of American Pathology (CAP), as follows: a. On the sign-in sheet at the meeting, provide your name and email address (in block capitals please). Approximately four to six weeks after the event ends, you will receive an e-mail from the CAP with instructions on claiming your credit(s)/hour(s) and printing your online certificate. You will click on the link supplied in the e-mail and login using your CAP User ID and password. (If you do not have a CAP User ID, you will be able to create an ID using a link on that page. A CAP User ID will be sent to you via e-mail within 24 hours.) You must claim your CME/CE credit(s)/hour(s) within six months of the date the learning activity was completed. If you have not claimed after six months, the credits for this activity will remain as unclaimed on your CAP Transcript and you will not be able to claim credits. If you misplace your e-mail or do not receive one, you can claim your CME/CE credit(s)/hour(s) and print your certificate from the CAP Web site: 1. 2. 3. 4. 5. Go to www.cap.org and log in using your user ID and Password. Click Learning from the top menu bar. Click Learning Transcript from the top menu bar. Click the Activity Name On the Claim Credit tab, click the Claim button and follow the instructions. If you have any questions regarding logging into www.cap.org please contact customer service at 800/323-4040 1#. If you have questions regarding the claiming process, please contact CAP Education at [email protected] or at 800/323-4040 and request CAP Education. Please note that the RPS has up to three weeks after the activity concludes to submit attendee participation information to the CAP for processing continuing education credits. Please check with the sponsoring organization if you do not receive the email from the CAP within four to six weeks of the activity to ensure they have submitted your information to us. 3. Complete the 20 multiple choice questions and send your answers to: Jan Becker MD Chair, RPS Education Committee [email protected] Sixteen questions (i.e., 80%) must be answered correctly, and you will have three (3) attempts to successfully complete the test 4. After successfully completing the SAM, you will receive a confirmation letter from Dr. Becker, with an explanation of the answers. Later in the year, you will receive a certificate of SAM completion from the RPS Secretary. 5. Keep a copy of the CAP CME certificate and RPS SAM confirmation letter in your files, as these may be requested by the ABP when you submit a request for SAM credit. 6. The deadline for completion of this SAM is November 30th, 2016. RPS Satellite SAM Questions 1. The Mayo clinic/RPS classification is primarily based on: A. B. C. D. Pattern of injury Etiology/pathophysiology Clinical modifiers Electron microscopy findings 2. Which one of the following categories of glomerulonephritis does not relate to a specific pathogenetic mechanism? A. B. C. D. Anti-GBM nephritis Lupus nephritis C3 glomerulopathy Pauci-immune GN 3. Which is the correct order of the primary diagnosis in the biopsy report: A. B. C. D. primary disease/pathogenic type, pattern of injury, score/grade, additional findings pattern of injury, primary disease/pathogenic type, score/grade, additional findings primary disease/pathogenic type, additional findings pattern of injury, score/grade primary disease/pathogenic type, pattern of injury, additional findings, score/grade 4. Which of the following should be included in the primary diagnosis? A. B. C. D. Laboratory values Clinical modifiers where appropriate References Differential diagnosis 5. In retrospective clinicopathological studies of IgA nephropathy, the strongest pathological predictor of progression to end-stage renal disease is: A. B. C. D. Presence of cellular/fibrocellular crescents Extent of mesangial hypercellularity % tubular atrophy/interstitial fibrosis Presence of endocapillary hypercellularity 6. The VALIGA study demonstrated that in patients with IgA nephropathy and low level proteinuria at presentation, a histological lesion that is associated with progression to proteinuria >1g/day during follow-up is: A. B. C. D. Segmental glomerulosclerosis % tubular atrophy/interstitial fibrosis Arteriosclerosis Endocapillary hypercellularity Figure 1 (Q7) 7. This image (Figure 1) of a glomerulus from a biopsy of IgA nephropathy with focal segmental glomerulosclerosis demonstrates: A. B. C. D. Collapsing glomerulopathy Endocapillary hypercellularity Podocyte hypertrophy Perihilar segmental sclerosis 8. In retrospective clinicopathological studies of IgA nephropathy, steroid/ immunosuppressive therapy is associated with an improved renal outcome in patients whose biopsies show: A. B. C. D. >50% tubular atrophy/interstitial fibrosis Presence of endocapillary hypercellularity Focal (<50% of glomeruli) mesangial hypercellularity Presence of fibrous crescents Figure 2 (Q9) 9. According to the ISN/RPS classification for lupus nephritis, the findings in Figure 2 are best classified as: A. Class IV-S (A) B. Class II C. Class IV-G (A) D. Class III >50% Figure 3 (Q10). Figure 4 (Q10). 10. The patient whose biopsy is shown in Figures 3 and 4 has well-documented SLE, normal renal function, and proteinuria of 9 grams per 24 hours. The EM in Figure 4 is representative, although other EMs showed several tubulo-reticular inclusions. According to the ISN/RPS classification, the biopsy in Figures 3 and 4 is best classified as: A. Class I B. Class II C. Class V D. The lesion shown is probably related to SLE but is not included in the ISN/RPS classification 11. The ISN/RPS classification of lupus nephritis: A. Is an evidence-based classification, similar to the Oxford/MEST classification for IgA nephropathy B. Includes glomerular, tubulo-interstitial, and vascular lesions C. Showed better inter-observer agreement than the WHO (1995) classification in a UK-wide study D. Is poorly reproducible because unlike the WHO (1982) classification it does not include strictly defined cutoffs for focal versus diffuse glomerular lesions 12. Renal survival rates in ISN/RPS Class IV lupus nephritis: A. Have generally been shown to be similar to those in Class III lupus nephritis B. Have in most studies been shown to be significantly worse in IV-S than IV-G lesions C. Have in most studies been shown to be significantly worse in IV-G than IV-S lesions D. Are strongly influenced by whether or not the patient attains a remission in response to therapy following the biopsy 13. TMA involving the arterial vasculature: A. B. C. D. Distinguishes malignant hypertension from other forms of TMA Invariably is a consequence of thrombosis May be the result of calcineurin inhibitor exposure Is a consequence of pre-existing arteriosclerosis 14. Structural alterations in glomeruli characteristic of TMA can be used to: A. Distinguish hemolytic-uremic syndrome (HUS) from thrombotic thrombocytopenic purpura (TTP) B. Identify an anti-phospholipid antibody mediated injury C. Distinguish transplant glomerulopathy from recurrent HUS in a transplanted kidney D. Establish the diagnosis of scleroderma 15. Thrombotic microangiopathy is: A. A morphologic diagnosis in which the severity of the structural changes can be used to direct patient treatment B. A clinico-pathologic entity with multiple etiologies C. A diagnosis requiring the demonstration of thrombosis in tissues D. An irreversible vascular injury 16. The diagnosis of TMA: A. Requires a renal biopsy B. Is established by a clinical history of exposure to calcineurin inhibitors such as cyclosporine C. Requires clinical evidence of hemolysis D. May lead to identification of hereditary disorders involving the complement or coagulation systems 17. The major risk factor for the de novo development of Donor Specific Antibody (DSA) is? A. Concomitant liver transplantation B. Non-compliance C. Transplant glomerulopathy D. Proteinuria 18. The detection of Donor Specific Antibody (DSA): A. Is necessary to diagnose Antibody-mediated rejection (ABMR) in renal allografts B. Is only observed in the setting of active ABMR C. Is rare in non-compliant patients D. Is frequently associated with recurrent glomerulonephritis 19. According to the 2013 Banff classification, a Banff v-lesion/ endothelialitis: A. Is specific for hyperacute (vascular) rejection B. Is only observed in T cell mediated rejection C. Is only observed in antibody-mediated rejection D. May be observed in T cell mediated, antibody-mediated, or mixed rejection 20. As per 2013 Banff consensus, molecular quantification as correlate of the interaction between antibody and the vascular endothelium in the graft should be? A. Ignored B. Considered equivalent to C4d positivity C. Studied in every allograft biopsy D. Not reported to the clinician