cme examination

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Cl\1E examination Identification No. 894-101 Instructions for CME credit appear in the front advertising section. See last page of Contents for page number. Questions 1-33, Schwartz RA. J AM ACAD DERMATOL 1994;30:1-19. Directions for questions J -29: Give single best response. 1. The Ferguson Smith type of multiple keratoacan- thomas shows (a) a. female predominance of 3:1 b. male predominance of 3:1 c. female predominance of 10:I d. male predominance of 10:1 e. no predominance for either sex 2. The Grzybowski type of multiple eruptive KAs shows (a) a. female predominance of 3:1 b. male predominance of 3:1 c. female predominance of 10:1 d. male predominance of 10:I e. no predominance for either sex 3. When literally thousands of 2 to 3 mm KAs develop in a patient, the most likely diagnosisis a. multiple KAs of Ferguson Smith b. multiple eruptive KAs of Grzybowski c. Torre syndrome d. xeroderma pigmentosum e. nevus sebaceus of J adassohn 4. KA occurs mainly on the a. legs of men b. sun-exposed areas of elderly persons c. soles d. scalp e. genitalia 5. The Ferguson Smith type of multiple KAs are prob- ably inherited in a manner best characterized as a. autosomal recessive b. x-linked recessive c. autosomal dominant d. x-linked dominant e. autosomal corecessive 6. The Torre syndrome is probably inherited in a man- ner best characterized as a. autosomal recessive b. x-linked recessive c. autosomal dominant d. x-linked dominant e. autosomal corecessive 7. The likelihood of a KA developing within a nevus se- baceus is probably about a.O% b.lO% 20 c.75% d.95% e. 100% B The likelihood of the p53 oncogene being demon- strated in a human KA employing the presentlyuti- lized monoclonal antibody technologyis probably a.O% b. 99.9% c. 100% d. less common than an actived H-ras oncogene e. more commonlythan an actived H-ras oncogene 9. The presenceof which of the following can be reliably used to distinguish KA from squamous cell carci- noma (SeC)? a. .B2-Microglobulin b. Filaggrin c. p53 Oncogene expression d. Peanut agglutinin lectin staining e. None of the above 10. The presence of wh ich of the following histologic features can reliablybe used to distinguish KA from SCC? a. Atypical eccrine duct hyperplasia b. Abnormal keratinocyte nuclear morphology on ultrastructural sections c. Increased content of epidermal intracytoplasmic glycogen d. The presenceof actinicallydamaged elastic fibers e. None of the above 11. KA has been induced in a. mice b. ducks c. hedgehogs d. hamsters e. all of the above 12. If a patient has three small KAs and one sebaceous adenoma, he should be evaluated for a. gastrointestinal cancer b. urogenital Cancer c. family members with a gastrointestinal or uro- genital cancer d. all of the above e. none of the above 13. KA at a subungualsite a. appears as a persistent,painful,locallydestructive tumor b. affects men more commonly than women

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Page 1: CME examination

Cl\1E examination Identification No. 894-101

Instructions for CME credit appear in the front advertising section. See last page of Contents for page number.

Questions 1-33, Schwartz RA. J AM ACAD DERMATOL 1994;30:1-19.

Directions for questions J-29: Give single bestresponse.

1. The Ferguson Smith type of multiple keratoacan­thomas shows (a)a. female predominance of 3:1b. male predominance of 3:1c. female predominance of 10:Id. male predominance of 10:1e. no predominance for either sex

2. The Grzybowski type of multiple eruptive KAsshows (a)a. female predominance of 3:1b. male predominance of 3:1c. female predominance of 10:1d. male predominance of 10:Ie. no predominance for either sex

3. When literally thousands of 2 to 3 mm KAs developin a patient, the most likely diagnosis isa. multiple KAs of Ferguson Smithb. multiple eruptive KAs of Grzybowskic. Torre syndromed. xeroderma pigmentosume. nevus sebaceus of Jadassohn

4. KA occurs mainly on thea. legs of menb. sun-exposed areas of elderly personsc. solesd. scalpe. genitalia

5. The Ferguson Smith type of multiple KAs are prob­ably inherited in a manner best characterized asa. autosomal recessiveb. x-linked recessivec. autosomal dominantd. x-linked dominante. autosomal corecessive

6. The Torre syndrome is probably inherited in a man­ner best characterized asa. autosomal recessiveb. x-linked recessivec. autosomal dominantd. x-linked dominante. autosomal corecessive

7. The likelihood of a KA developing withina nevus se­baceus is probably abouta.O%b.lO%

20

c.75%d.95%e. 100%

B The likelihood of the p53 oncogene being demon­strated in a human KA employing the presentlyuti­lized monoclonal antibody technologyis probablya.O%b. 99.9%c. 100%d. lesscommon than an actived H-ras oncogenee. more commonlythan an actived H-ras oncogene

9. The presenceof which of the following can bereliablyused to distinguish KA from squamous cell carci­noma (SeC)?a. .B2-Microglobulinb. Filaggrinc. p53 Oncogene expressiond. Peanut agglutinin lectin staininge. None of the above

10. The presence of which of the following histologicfeatures can reliablybe used to distinguish KA fromSCC?a. Atypical eccrine duct hyperplasiab. Abnormal keratinocyte nuclear morphology on

ultrastructural sectionsc. Increased content of epidermal intracytoplasmic

glycogend. The presenceof actinicallydamaged elasticfiberse. None of the above

11. KA has been induced ina. miceb. ducksc. hedgehogsd. hamsterse. all of the above

12. If a patient has three small KAs and one sebaceousadenoma, he should be evaluated fora. gastrointestinal cancerb. urogenital Cancerc. family members with a gastrointestinal or uro­

genital cancerd. all of the abovee. none of the above

13. KA at a subungual sitea. appears as a persistent,painful,locallydestructive

tumorb. affects men more commonly than women

Page 2: CME examination

Journal of the American Academy of DermatologyVolume 30, Number I

c. has a greater malignant potential than KA else­where on the body

d. a and b are correcte. all of the above are correct

14. The peak incidence of KA is betweena. 12 and 19 years of ageb. 20 and 30 years of agec. 30 and 49 years of aged. 50 and 69 years of agee. 70 and 89 years of age

15. The Ferguson Smith type of multiple KA most oftenhas its onset betweena. 12 and 19 years of ageb. 20 and 30 years of agec. 30 and 49 years of aged. 50 and 69 years of agee. 70 and 89 years of age

16. KA probably derives from thea. sebaceous glandb. sebaceous ductc. hair follicled. eccrine glande. eccrine duct

17. A KA exhibiting peripheral growth up to 20 emin diameter with concurrent central healing iscalleda. keratoacanthoma centrifugumb. Ferguson Smith type of KAc. Grzybowski type of KAd. a KA typical of the Torre syndromee. none of the above

18. Multiple KAs, up to hundreds in number, that sud­denly appear, grow to 2 to 3 ern in diameter, slowlyinvolute and periodically reappear for many years,are seen with (the)a. keratoacanthoma centrifugumb. Ferguson Smith type of KAc. Grzybowski type of KAd. xeroderma pigmentosume. none of the above

19. A KA developing at the site of a venipuncture sug­gests the possibility ofa. keratoacanthoma centrifugumb. Ferguson Smith type of KAc. nevus sebaceusd. xeroderma pigmentosume. none of the above

20. A KA in a child should prompt consideration ofa. keratoacanthoma centrifugumb. Ferguson Smith type of KAc. Grzybowski type of KAd. xeroderma pigmentosume. both band d

CME examination 21

21. The association of KA with human papillomavirus(HPV) infection shows (that)a. HPV type 25 is causativeb. HPV type 25 DNA has been detected in some

KAsc. HPV type 25 is linked only with the Grzybowski

type ofKAd. HPV type 33 is causativee. none of the above

22. There has been a significantly increased incidencereported of KA ina. pathologistsb. veterinariansc. medicalstudentsd. tar and pitch workerse. both band d

23. TheKAa. is often a rapidly growing tumorb. displays a histologic pattern resembling that of an

seec. is relatively commond. has been viewed as a pseudomalignancye. all of the above

24. The disease most frequently considered in the clini­cal differential diagnosis of a KA isa. Kaposi's sarcomab. secc. Merkel ceIl tumord. melanomae. none of the above

25. A KA typically heals asa. clinically normal-appearing skinb. a puckered, depressed, hypopigmented scarc. a hypertrophic hyperpigmented scard. a keloidal scare. none of the above

26. Histologically, a KA in its early proliferative stageoften, or at least occasionally. containsa. pronounced keratinization with pale-staining cy-

toplasmb. mitotic figuresc. eosinophilsd. neutrophilse. all of the above

27. The histologic diagnosis of a KA is usually basedona. its cytologic featuresb. the presence of a dermal fibroblastic reactionc. the presence of a dermallymphohistiocytic reac­

tiond. its architecturee. none of the above

28. The best therapeutic option for a solitary rapidly

Page 3: CME examination

CME examination

growing tumor of the dorsum of the hand suspectedof being a KAa. punch biopsyb. excisional biopsyc. intralesional 5-fluorouracild. curettage and electrodesiccatione. all of the above

29. The best biopsy procedure for a large KA isa. a fusiform incision through the entire KA to

include its center, both sides (including normal­appearing skin), and normal subcutaneous fat

b. a punch biopsy through the centerc. a fusiform incision focusing on a border

Answers to CME examination*

Journal of the American Academy of DermatologyJanuary 1994

d. a punch biopsy through a border regione. a fusiform incision through the entire KA to

include its center and both sides

Directionsfor questions 30-33: For each numbereditem, choose the appropriate lettered item.

a. More commonly associated with KA than secb. More commonly associated with sec than KA

30. Homogeneous staining pattern for involucrin31. Actinically damaged elastic fibers32. An increased content of intracytoplasmic glycogen33. Atypical eccrine duct hyperplasia

Identification No. 893-112

December 1993 issueof the JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY

Questions 1-33, Summers BK, Siegle RJ. JAM ACAD DERMATOL 1993;29:917-41.

1. c (p 917, C 2, pa 2-p 918, c 1, pa 1)2.d (p918,cl,pal)3. e (p 919, C 1, pa 2)4. d (p 919, C 2, pa 2; p 920, c 2, pa 3-p 922, c 2,

pa 2)5. d (p 923, c I, pa 4)6. e (p 923, C 1, pa 2; p 924, c 2, pa 3-pa 4)7. C (p 922, e2, pa 3;p923, C 1,pa 4-c2, pa l;p 925,

c 1, pa 3-p 926, c 1, pa 3)8. C (p 926, C 1, pa 4-c 2, pa 2)9. C (p927,cl,pa3)

10. d (p 927, C 2, pa 2)11. d (p 928, C 2, pa 1; p 929, c I, pa 2)12. c (p 930, C 1, pa 4)13. C (p930,cl,pa4)14. d (p 930, c 2 pa 2)15. a (p 932, C 1 pa 2; p 932, c 2, pa 1)16. e (p 934, C 2, pa I-p 935, c 1, pa 2)

"p: page; c: column; pa: paragraph.

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17. e (p 935, C 2, pa 2)18. b (p 936, C 1, pa 3-c 2, pa 1)19. e (p 936, c 2, pa 5-p 937, c 1, pa 1)20. e (p 936, c 2, pa 4; p 937, C 1, pa 2)21. e (p 937, C 2, pa 2)22. b (p 923, C 2, pa 2)23. a (p 923, C 2, pa 1)24. d (p 923, C 1, pa 4; p 923, c 2, pa 2-p 924, C 1,

pa 1)25. a (p 923, C 1, pa 4-p 924, C 1, pa 1)26. C (p 930, C 1, pa 4-c 2, pa 2)27. d (p 930, C 1, pa 4-c 2, pa 2)28. c (p 930, c 1, pa 4-c 2, pa 2)29. c (p 930, c 1, pa 4-c 2, pa 2)30. b (p 932, c 1, pa 3-c 2, pa 1)31. d (p 932, C 1, pa 1; p 917, C 2, pa 1)32. b (p 932, C 2,p 2-p 933, c 1, p 1)33. C (p 919, C 1, pa 1; p 932, c 1, pa 2)