Compilation of AP Board Remembrances ( page references are for Robbins 5th edition

unless otherwise specified)

[Note: this is as received from Sara; I modified it and added to it a bit in the
document called “Board summary-AP.Modified”; take your pick, they’re roughly
the same-Mike]

*BASIC PATH – ROBBINS

1. Choristoma – (Robbin’s Chp 7, p.243) an ectopic (heterotopic) rest of normal
tissue, eg: a rest of adrenal cells under the kidney capsule or pancreatic rest in
small intestinal mucosa

2. Fat in an EtOH fatty liver is composed of

a. Triglycerides (Robbins page 25)
3. Irreversible cell injury includes (chart Robbins page 7)
a. Cell membrane defects
b. Nucleus pyknosis, karyolysis, or karyorrhexis
c. Rupture of lysosomes and autolysis
d. Lysis of ER
e. Myelin figures (submembrane)
f. Large mitochondrial densities
4. Increased permeability in inflammation occurs where? (This question may be
more complicated than it seems. If they asked about a specific stage or type of
inflammation, it could be one choice, but in general if all stages and forms of
injury are considered, the answer is all three – meaning the microcirculation.
Panvascular is wrong. READ Robbins page 54-56)
a. Venules **The most common mechanism of vascular leakage classically
affects only venules 20-60um in diameter and leaves the arterioles and
capillaries unaffected.
b. Arterioles
c. Capillaries
5. Complement C5a chemotactic effect activated by (Robbins page 66)
a. Ag-Ab complex
b. Microbial surfaces
c. Endotoxins
d. Aggregated IgA
e. Complex polysaccharides
f. Neutrophil lysosomal enzymes
g. Plasmin
h. Cobra venom
6. Cell mediated immunity decreased in
a. From Robbins, could be AIDS, Severe combined immunodeficiency,
Digeorge’s syndrome (thymic hypoplasia), and Common Variable
Immunodeficiency
b. ?prob not myeloma
7. CD4 and MHCII interaction
 a. CD4 Tcells recognize antigen when it is presented associated with MHCII
molecule on antigen presenting cell (CD8 recognizes Ag with MHC I)
8. Acetyl cholinesterase is positive in (k type)
a. ?mast cell, polys
9. p53 - Single most common target for genetic alteration in human tumors
(Robbins chp 8)
10. Eosinophils have which type of Leukocyte-endothelial adhsion molecule (table
Robbins p58)
a. Receptor VLA-4 (a beta-1integrin) on eos binds to endothelial cell
molecule VCAM-1 (an immunoglobulin)
b. All leukocytes including eos use the LFA-1 and Mac-1 receptors to bind
to ICAM-1
11. Structure of amyloid
a. Protein made up of 95% fibrillary B-pleated sheet and 5% P substance
glycoprotein (Robb p 231-32)
12. Which is not true about amyloid
a. ?Not branching fibrils (person thought this was answer)
13. GVHD – which cell is responsible
a. Donor T lymphocytes (p194, Robb)
14. Neutrophils can do what?
a. Could be a lot of things, but probably answer is somewhere in pp59-65 in
Robbins
15. Learn the allergic response (don’t know question)
a. Type I hypersensitivity, Robb p179 table
16. Which reaction is type II hypersensitivity reaction
a. Antibody mediated reactions (pp182-184)
b. Examples
i. Transfusion reactions
ii. Erythroblastosis fetalis
iii. Autoimmune hemolytic anemia, agranulocytosis, or
thrombocytopenia
iv. Myasthenia gravis
17. Which is not produced by macrophages
a. Bradykinin (source is plasma substrate, p73, table)
b. Note: the following are produced by macrophages :Eicosinoids (another
name for arachidonic acid metabolites – prostagandins and leukotrienes)
,pdgf, and fgf . (p77, fig 3-28)

ADRENAL
18. Non-chromaffin reactive pheochromocytoma
a. ?
19. Atrophic adrenal sparing glomerulosa and medulla. What is cause?
a. Secondary adrenocortical insufficiency – anything that has reduced ACTH
i. Exogenous steroid tx (reduces ACTH by feed back)
ii. Hypothalamic disfunction
iii. Pituitary disfunction
 iv. These diseases relatively spare glomerulosa, meaning aldosterone
synthesis is relatively normal
v. Review of adrenal structure
1. Cortex
a. Glomerulosa – thin outer most layer. Produces
mineralocorticoids, mainly aldosterone
b. Fasciculata – thick middle layer (75% of cortex)
c. Reticularis – thin inner most layer next to medulla
The Fasciculata an reticularis act as a functional unit to
produce glucocorticoids (cortisol) and sex steroid
(testosterone)
2. Medulla – neuroendocrine tissue which is source of
catecholemines
a. Epinephrine, neuroepinephrine, and dopamine

BLADDER

BONE/JOINTS
20. Which does not cause secondary malignant changes? Choices: bone infarct,
fibrous dysplasia, osteoma.
a. Note: I think they mean which does not undergo malignant transformation
i. Answer
1. Bone infarcts can. This is rare and occurs with medullary
infarcts. (p1229)
2. Fibrous dysplasia can. This is rare and is usually with
polyostotic involvement (p1243)
3. Osteoma does not undergo malignant transformation
(p1233)
4. Other things associated with increased incidence of bone
neoplasia: (p1232)
a. Chronic osteomyelitis
b. Pagets
c. Radiation
d. Metal prostheses

21. Osteoblastic and clastic activity are seen in what disease besides Paget’s?
Choices: Osteoporosis, osteomalacia, osteitis fibrosa
a. An INCREASE in both osteoblastic and osteoclastic activity is found in
Paget’s and Osteitis fibrosa cystica (hyperparathyroidism related –
p1226). The others don’t have increased activity. They all have at least
minimal activity of both, but the question probably means increased
activity.
22. Low complement in synovial fluid in what ds? Choices: Gonorrhea, rheumatoid,
others
 a. answer – I think gonorrhea. Gonococcal arthritis is assoc with genetic
deficiency of C5,C6, and C7 (p1254, 2nd column)
23. Enlarged osteoid seams in renal dialysis pt (enlarged osteoid seams correspond to
the osteomalacia component of renal osteodystrophy) due to? Choices: Low Ca,
hypophosphate, aluminum
a. Answer: Low Ca and aluminum of the choices in part A because (This is
painful) (p1227)
i. Renal failure causes hyperphosphatemia
ii. Hyperphosphate causes hypocalcemia, which causes secondary
hyper PTH
iii. HyperPTH causes bone resorption to try to maintain serum
calcium
iv. Renal failure also makes the kidney unable to activate Vit D to
(1,25 (OH)2 -D3). Without the active form, less Ca2+ is absorbed
in the intestine, which contributes to the hypocalcemia
v. Aluminum deposition at the site of mineralization, iron deposition,
and metabolic acidosis of renal failure also play a role in renal
osteodystrophy

BREAST
24. What gives 4-5x increased risk for invasive breast CA
a. Atypical duct hyperplasia
b. (not papilloma or FCC)
25. Why do you grade DCIS? Choices: no clinical signif., dictates management,
dictates node dissection
a. Recurrence/invasion occurs in 40% of people with high grade DCIS and
lumpectomy alone and <10% of those with low or intermediate grade
(non-palpable) – ?dictates management
26. Medullary breast CA
a. Peritumor lymphoid infiltrate
b. High nuclear grade
c. Minimal DCIS
27. Soft lesions of the breast include all except? Choices: Lobular CA vs medullary
CA vs lipoma
a. Of these, lobular CA is not soft. Is usually accompanied by a fibrous
stroma.
28. Metaplastic carcinoma of breast looks most like? Choices: myofibroblastoma,
fibromatosis, others
a. Probable myofibroblastoma (more common in male breast, spindle cell
lesion)

CARDIOVASCULAR
29. Monkeberg’s medial calcific sclerosis Robb p484
a. Ring-like calcification of media of small to medium-sized muscular
arteries in people over 50
 b. No inflammation and do not narrow lumen
c. May coexist with atherosclerosis
d. Most common affected arteries are
i. Femoral
ii. Tibial
iii. Radial
iv. Ulnar
v. Genital tract arteries
30. Findings in syphilitic aortitis (Robb p501)
a. Aneurysmal dilatation confined to thoracic aorta
b. Starts with inflammation and occlusion of adventitial vasa vasorum
c. Ischemia, inflammation, scarring, and revascularization of media due to
occlusion of vasa vasorum
d. Dissection unusual
e. Tree barking – wrinkling of intima
f. Involvement of aortic root with atherosclerosis (not a site for usual
atherosclerosis)
g. Involvment of aortic valve with dilatation and aortic insufficiency
h. Cor bovinum secondary to aortic insufficiency
i. ?Orig stated valve adhesion to wall, ?endocardial pocket
31. Chronic rejection in heart transplant bx associated with
a. ? (don’t know choices)
32. Which arteritis is not associated with giant cells
a. Giant cell arteritis, Takayuso’s arteritis, Wegener’s vasculitis, and
Buerger’s ds (Thromboangiitis obliterans) all have granulomatous
inflammation. Don’t know what the choices were (pp492-498)
33. Cardiac amyloid, is it primary or secondary amyloidosis (p233)
a. Depends on type. Primary amyloidosis is when it is associated with
plasma cell dyscrasia (AL type). Secondary is secondary to
inflammatory conditions (AA type). Primary amyloidosis involves the
heart more often than the secondary type.
b. Senile cardiac amyloidosis in old people is not classified in Robbins as
either primary or secondary. It is either transthyretin or atrial natriuretic
peptide.
34. Causes of angiosarcoma (don’t know choices)
a. Radiation
b. Arsenic
c. Thorotrast
d. Polyvinyl chlorid
(angiosarcs assoc with b-d are primarily in liver or spleen)
35. Death in pt with floppy mitral valve due to
a. Sudden death is due to arrythmias (p546-47)
b. Can get stroke from leaflet thromboemboli
36. Which valve ds is unlikely to be post infectious? Choices: AS,AI,MS,MI
a. If post-infectious means rheumatic, then the most common in decreasing
order are
 i. Mitral stenosis
ii. Aortic stenosis
iii. Tricuspid stenosis
iv. Rare pulmonic involvement
b. Don’t know if you get secondary insufficiencies with these stenoses too.
37. Cystic medial necrosis occurs in (p502)
a. Frequently occurs in Marfans
b. However, occurs in other non-specific aortic dissecting aneurysms and is
found at autopsy occasionally in older or hypertensive patients

CYTOLOGY
38. Use of cytology in colon
a. ?Good for evaluation of stricture
39. PAP cytology, nucleolus useful in distinguishing
a. Reg/repair of endocervix vs squamous dysplasia
40. PAP with atypical degenerated squames in elderly
a. ?trial of estrogen
41. What makes a PAP unsatisfactory?
a. ?
42. Cytology of cirrhosis shows all except (don’t know choices)
a. ?nucleoli
43. What determines adequate sputum
a. ?carbon containing macrophages

EM
44. EM intranuclear and cytoplasmic inclusions? Choices: PML, EBV, herpes
a. Thought all were intranuclear only, can find only mention of intranuclear
inclusions

ENDOCRINE
45. Which pituitary adenoma is associated with calcification
a. Prolactinoma (Robbins says 10-15% calcify)
46. What is the most common functioning endocrine tumor?
a. ?Islet cell tumor of pancreas
47. Islet cell tumors of pancreas (Robbins pp922-24)
a. May rarely produce more than one hormone when active
b. Most common type is insulinoma (beta cell)
48. Do beta cell tumors occur outside the pancreas?
a. Yes, but these occur in ectopic pancreatic tissue (p923, pink part)
b. Also, 5% are malignant and metastasize to other organs.
49. Neuroendocrine microtumors of the fundus
 a. Assoc with ZE syndrome (hypergastrinemia secondary to duodenal or
pancreatic gastrinoma which then causes fundic enterochromaffin cell
hyperplasia, microcarcinoids, or carcinoids of the stomach)
50. “pseudo ZE syndrome” – primary G cell hyperplasia of antrum which causes
increased gastrin without gastrinoma and symptoms like ZE. Can have nodules of
hyperplastic G cells in stomach
51. Dx of parathyroid adenoma – requires at least one other normal parathyroid
52. MEN syndromes
a. MEN I (Wermer’s syndrome) –
i. Chromosome 11q13
ii. Parathyroid ds – PTH hyperplasia or adenoma
iii. Pacreatic islet cell tumors of any kind
1. Insulinomas present with hypoglycemia
2. Gastrinomas present with ZE syndrome
iv. Pituitary adenomas – Prolactinoma most common
v. May also have carcinoids, thyroid adenomas, adrenal cortical
adenomas, lipomas
b. MEN II (2a), (Sipple’s sydrome)
i. RET protooncogene mutation of receptor tyrosine kinase which
binds glial neurotroophic factor and normally transmits growth
signals. The mutation causes an upregulation or gain in function,
which is an unusual mech of tumorogenesis – normally get loss of
tumor suppressor gene function instead of gain of growth signal fx.
ii. Parathyroid ds as above
iii. Pheochromocytoma
iv. Thyroid medullary CA – commonly multifocal and may be
associated with C cell hyperplasia also. May be aggressive and
secrete calcitonin
c. MEN III (2b)
i. Different RET protooncogene mutation – single amino acid
mutation of tyrosine kinase catalytic core
ii. Pheochromocytoma
iii. Thyroid medullary CA
iv. Mucocutaneous neuromas and ganglioneuromas
v. Marfanoid habitus
vi. May have parathyroid hyperplasia (less common than in MEN I
and II)
53. Parathyroid - which cells make hormone?
a. Chief cells are major source of PTH
b. Oxyphil cells contain lots of mitochondria
54. Cushing’s with thymic carcinoid (don’t know question)
a. 1/3 of thymic carcinoids are associated with cushing’s (Ackerman surgical
pathology, p 458.) Some of these are associated with MEN I or Iia
syndrome. Many of them simply produce ACTH on their own.

ENT
55. Salivary acinic cell CA differs from renal cell CA (?fat, glycogen)
a. RCC clear cells contain both fat and glycogen
b. Acinic cell CA
i. Basophilic granular cells contain zymogen granules (PAS-D +) and
occasional mucin.
ii. The clear or vacuolated cells contain glycogen but not fat or
mucin
56. Most common site of cannalicular adenoma of salivary gland
a. Upper lip
57. Oral hairy leukoplakia caused by
a. EBV
b. May be associated with HPV
58. Laryngeal papilloma
a. HPV 6,11 most common
b. (original copy said “laryngeal polyp”, but these are AKA singers nodules,
are not virus associated, but are trauma associated)
59. Warthin’s tumor association
a. Males 50-70 yrs
b. 10% multifocal, 10% bilateral
c. Benign (James says no malignant change but there are sporadic reports of
malignant change)
60. Endolymphatic sac tumor of the ear (don’t know question or choices) Ackerman
surgical pathology p2515
a. Called “aggressive papillary middle ear tumor (APMET) or “low-grade
adenocarcinoma of probable enolymphatic sac origin” – thought to be the
same entitiy
b. Papillary structures with vascular stroma lined by uniform cuboidal cells
c. May have cystic dilatation resembling thyroid follicular tumor or
cytoplasmic clearing resembling renal cell CA
d. Associated with Von Hipple Lindau
e. Locally invasive, bony invasion
61. Most common tumor of the submandibular gland (don’t know choices)
a. Adenoid cystic is the most common malignant tumor. Margie’s book
doesn’t even say the most common tumor overall
b. Robbins p752 says adenoid cystic is “the most common neoplasm in the
other salivary glands” excluding the parotid
62. Necrotizing sialometaplasia (don’t know question)
a. Benign, necrotizing ulcerative inflammatory condition
b. Most common in minor salivary glands of palate, also other salivary
glands
c. Commonly associated with hx of trauma and vascular compromise of area,
(eg – compression from endotracheal intubation)
d. Lobular necrosis and sialadenitis with squamous met of ducts
e. May have pseudoepitheliomatous hyperplasia of overlying epithelium
f. May be confused with squamous cell CA or mucoepi CA
 g. Heals spontaneously, but occasionally arises in association with a
malignant tumor
63. Prognosis of adenoid cystic CA (don’t know question)
a. Related to histologic grade (I-III – grade III is >30% solid pattern and is
poor prognosis)
b. Also dependent on Stage
c. Dependent on location, from best to worst prognosis:
i. Palate (best)
ii. Parotid
iii. Submandibular gland (worst)
d. High rate of local recurrence
64. HIV with bilateral cystic parotid lesions
a. Called “AIDS related parotid cysts”, or “cystic benign lymphoepithelial
lesion of AIDS” (Margie’s head and neck pathology, p334)
b. Squamous lined cysts with hyperplastic lymphoid tissue surrounding
c. Has similar histologic appearance to regular BLEL, but usually less cystic
65. What is in cytoplasm of Warthin’s tumor
a. Oncocytic cells in the epithelial lining – so answer is mitochondria if it’s a
choice.

FORENSICS
66. How can cocaine cause MI? (k type)? Choices:+/-pre-existing CAD, arrythmia
a. (p395) can cause vasoconstriction with or without pre-existing CAD
b. can cause arrythmias
c. Can cause direct catecholamine injury to myocytes
67. What information can be obtained from the vitreous humor of an embalmed pt?
Choices: multiple electrolytes, k type
a. Hyperglycemia
b. Increased urea nitrogen
c. Drugs: - barbiturates, meprobamate, propoxyphene, pentazocine,
ampetamines, digoxin
d. Not alcohol.

GENETIC DISORDERS
68. Chronic granulomatous disease (Robbins page 63)
a. Inherited defect in genes encoding components of NADPH oxidase, which
in the neutorphil converts NADPH to NADP and superoxide.
Superoxide then forms peroxide, which is converted to HOCL by
myeloperoxidase and kills bacteria (This process is call OXIDATIVE
BURST)
b. Causes recurrent bacterial infection
c. Can be x-linked or autosomal recessive
69. Neurofibromatosis associated with
a. NF-1 (von Recklinghausen) (p149)
i. Half are autosomal dominant inheritance, half are new mutations
ii. Chromosome 17q11.2 mutation
 1. codes for neurofibromin protein which down regulates p21
ras oncoprotein, a tumor suppressor gene
iii. Multiple neural tumors anywhere on body – neurofibromas
including plexiform type
1. These neurofibromas can undergo malignant
transformation, especially the ones attached to large central
nerve trunks
iv. Pigmented lesions including Café au lait spots
v. Lisch nodules – pigmented iris hamartomas
vi. Can have unilateral acoustic neuromas (bilateral are in type 2)
vii. Associated lesions
1. Skeletal
a. Erosive defects
b. Scoliosis
c. Intraosseous and subperiosteal cysts
d. Psseudarthrosis of the tibia
2. Other tumors
a. Meningiomas
b. Optic gliomas
c. Pheochromocytoma
b. NF-2
i. Less frequent than type 1
ii. Bilateral acoustic neuromas
iii. May or may not have skin neurofibromas
iv. Café au lait spots are present
v. No lisch nodules
vi. Chromosome 22 mutation of a tumor suppressor gene

70. Peutz Jeghers syndrome associated with which tumor

a. Sex-cord tumor with annular tubules
b. See GI section for review of Peutz Jeghers

71. Testicular feminization (aka complete androgen insensitivity syndrome) Robb

pp162. (eg Jamie Lee Curtis)
a. Normal male genotype (46XY)
b. Female phenotype or ambiguous external genitalia due to mutation in the
gene for the androgen receptor located on Xq11-Xq12
c. Inherited as x-linked recessive
d. Is the most common form of male pseudohermaphroditism
72. Klinefelter’s syndrome p159-160)
a. Most are 47, XXY
i. Rarer genotypes include mosaic 46XY/47XXY,
47XXY/48XXXY, etc
b. Male phenotype
c. Atrophic testis
d. Long eunichoid body habitus
 e. Infertility
f. Slightly lower IQ, but not usually retarded
g. Elevated FSH

73. Sickle cell trait assoc with which renal tumor

a. Renal medullary CA – a variant of renal cell CA which is centered in the
medulla and shows a reticular, yolk sac-like, or adenoid cystic appearance
on histology which can be focally poorly diff and associated with
desmoplastic stroma with neutophillic infiltrates and surrounding
lymphocytes. (Ackerman p1150). The book says it’s assoc with SS
disease.
b. Review of Sickle Cell ds
i. Autosomal recessive
ii. Point mutation – substitutes Valine for glutamic acid at 6th position
of beta-globin chain
iii. 8% of black Americans are carriers (heterozygous)
iv. Heterozygotes have about 40% HbS, remaining is Hb A
v. When present along with HbC, is less serious because the Hb C
prevents polymerization of the HbS, which causes the sickling
74. Why not do Polycystic Kid ds 1 mutation analysis on RT-PCR
a. ?
75. Father is mosaic for an autosomal dominant ds with one son already affected.
What is the highest % that the second offspring will be affected?
a. ? 50%
76. Adrenoleukodystrophy (p1281, table 28-3)
a. Long chain fatty acids collect because of defect in fatty acyl-CoA ligase
b. X-linked
c. Neurologic symptoms and adrenal insufficiency
77. Von Hipple Lindau (don’t know question) p268 and p1163, tables
a. Chromosome 3p25-26
b. Autosomal dominant
c. Renal cell carcinomas
d. Pheochromocytoma
e. Retinal and cerebellar hemangioblastoma
f. Renal, hepatic, pancreatic, and epididymal cysts
g. Angiomatosis
78. Adrenal hypoplasia with anencephaly
a. ?
79. Monosomy 21 in XY pt. What is disease
a. ?Down’s, Marfan’s , female, others
b. Could be the Robertsonian translocation in a parent of Down’s syndrome,
depending how the question is worded. If it is a karyotype with
monosomy at 21 and an extra piece on chromosome 22 or 14, this is the
Robertsonian translocation in a parent which leads to Down’s if the
offspring gets the extra piece and non-viable if the offspring actually
has monosomy 21. (p155, Robb). 4% of Down’s syndrome arise from
 parents with this Robertsonian translocation. The other 96% are from
non-disjunction during meiosis, which is maternal age related.
80. Which is not usual in NF1
a. Bilateral acoustic Schwannoma/neuroma (found in type 2)
b. Can get unilateral in type 1
81. Description of Marfan’s pt, what is protein involved
a. Fibrillin (p131, table)
82. Which ds not caused by point mutation – learn same table, p131 Robb.
a. Thalassemia was one of choices, is not point mutation,
b. Sickle cell is point mutation

GI
83. Mucinous cystic tumor of the pancreas (Ackerman)
a. Most located in body/tail,
b. Usually multilocular but may be unilocular,
c. Have cellular or ovarian type stroma
d. ?communicates with pancreatic duct (don’t know yet, know that
intraductal papillary mucinous tumor does communicate with the main
pancreatic duct)
84. Most common pediatric polyp
a. Retention polyp – sometimes simply called juvenile polyp
i. Located in recto-sigmoid
ii. Autoamputation is common
iii. Surface ulceration and granulation tissue
iv. Underlying cystically dilated glands with mucus
v. Inflamed, edematous stroma
vi. May have hyperplastic mucosal changes. Only rare cases have
shown dysplasia
vii. 1/3 of cases occur in adults
85. Pattern of UC involvement (maybe this question showed a picture)
a. Rectum and a continuous segment of colon involved. No skip lesions as
seen in Crohn’s, however may have cecal patch. May have small bowel
involvement in the form of backwash ileitis, but otherwise small bowel
not involved.
b. Muscularis is spared, no mural thickening
c. Many pseudopolyps
d. Toxic megacolon is complication (can rarely occur in Crohn’s too)
86. Review of Crohn’s
a. Skip lesions
b. Fistulas, creeping fat
c. Transmural involvement with non-caseating granulomas
d. Aphtous ulcers which coalesce to form linear ulcers with cobblestoning
of intervening normal
e. Strictures may lead to “string sign” on barium study
87. Celiac ds injury
a. Diffuse small intestinal enteritis, more severe proximally
 b. Loss of villi
c. Intraepithelial lymphocytosis, increase inflammation of lamina propria
d. Caused by immune response to the gliadin protein in gluten – wheat, rye,
oats, etc (pts have antigliadin antibodies)
88. Polyposis syndromes – review
a. Peutz-jeghers (p811)
i. Autosomal dominant
ii. Multiple hamartomatous polyps, no malignant potential in these
polyps. distribution
1. stomach 25%
2. colon 30%
3. small bowel 100%
iii. Melanotic pigmentation of lips, face,oral genital
iv. Increased risk of extra intestestinal malignancies in pancreas,
breast, lung, ovary, and uterus
v. Assoc with sex cord tumor with annular tubules of ovary and
adenoma malignum of cervix
b. Familial adenomatous polyposis FAP (p814)
i. Autosomal dominant
ii. Gene 5q21
iii. Multiple TA’s of colon
iv. At least 100 tubular adenomas to make dx, usually >500
v. 100% progress to cancer within 10-15 years of dx
c. Gardner’s syndrome
i. Variant of FAP, same gene 5q21
ii. Autosomal dominant with variable penetrance
iii. Multiple TA’s, multiple osteomas of bone, epidermal cysts,
fibromatosis, dental abnormalities, duodenal and thyroid CA
d. Turcot’s syndrome
i. Variant of FAP
ii. Multiple TA’s, CNS tumors (gliomas)
89. Which is not GI tract hamartomatous polyposis?
a. Answer – Familial polyposis (is adenomatous)
90. Most common gastric polyp
a. Hyperplastic (p779, Robb)
91. Small intestine obstruction due to enlarged lymphoid nodules ( choices Giardia vs
Salmonella/Shigella)
a. Lymphoid inflammation/peyers patch hyperplasia is seen in infection with
Salmonella or Yersinia enterocolitica (p793, table, and 794, Robb)
92. Necrotizing enterocolitis associated with (don’t know question)
a. Perforation, bacterial overgrowth, enteral feeding of premature infants
93. Which has worst prognosis in anus/rectum? Choices: Melanoma, squamous cell,
mucinous adenoCA
a. Melanoma
94. Prognosis of colon CA most related to? Choices:LN mets, inflammation, depth,
necrosis
 a. Single most important prognostic indicator is extent of tumor, AKA stage
of tumor (p817, Robb) – I think this means lymph node mets would be the
answer, although depth of invasion is also included in extent. If k-type,
both would be good choices.
95. First genetic defect in colon CA (p814 Robb)
a. First mutation is in APC (adenomatous polyposis coli tumor suppressor
gene)
b. Sequence in the multi-hit theory of colon cancer is:
i. APC deletion
ii. DNA loss of methylation
iii. Oncogene activation - ras (most common), myc, myb, trk, hst
iv. 18q allelic loss (called “DCC” for deleted in colon cancer)
v. loss at 17p (site of p53suppressor gene)
vi. microsatellite DNA stability on chromosome 2

GYN
96. What determines if a teratoma is immature /how is teratoma graded? (this is for
ovary)
a. Grades 1-3 based on the histologic proportion of the tumor which contains
immature neuroepithelial elements
i. Grade I – Abundat mature tissues intermixed with loose
mesenchymal tissue with occasional mitoses, immature cartilage,
tooth anlage
ii. Grade II – Fewer mature tissues; rare foci of neuroepithelium with
common mitoses, not exceeding 3 low power(x40) fields on any
one slide
iii. Grade III – Few or no mature tissues; numerous neuroepithelial
elements merging with a cellular stroma occupying 4 or more low
power fields
97. IH pattern of multinucleated stellate cell of vaginal polyp
a. If the dx is fibroepithelial polyp, here is a review of fibroepithelial polyp
i. Adult women (esp pregnant) or neonates
ii. Not neoplasm, but hormone induced hyperplasia
iii. Central fibrovascular core covered by normal squamous epithelium
iv. May have edematous or cellular stroma
v. Stromal cells may be highly atypical and stellate shape and stain
with
1. vimentin, desmin , and steroid receptors
2. not usually actin
vi. May be mistaken for botryoid rhabdomyosarc in babies because
of desmin positivity and atypia, but do not have a cambium layer,
epithelial invasion, or cross striations
98. Small cell ovarian CA associated with hypercalcemia
99. Cytogenetics in partial vs complete mole (p1082-1083)
a. Complete
i. >90% are 46,XX
 ii. rare 46, XY
b. Partial
i. Most are triploid (69,XXY)
ii. Rare tetraploid (92,XXXY)
100.Karyotype XO from abortus, which is least likely
a. Mole is not likely, but don’t know other choices.
101.Polycystic ovary associated with
a. Endometrial hyperplasia (p1057, 1064, 1065) and also increased risk
of endometrial CA (Essentials of OBGYN)– This is because of
unapposed estrogen stimulation due to persistant anovulation. These
patients also have increased androgens which are converted to estrone
also)
b. Polycystic ovary with oligomenorrhea = Stein Leventhal syndrome
i. Hirsuitism, obesity, masculinization, infertility
102.Difference between borderline and malignant tumors
a. Destructive infiltrative growth is not seen in borderline
103.Metastatic colon CA to ovary most commonly mimics
a. ?endometrioid adenoCA
104.Fibroepithelial polyp of vagina, cells stain for
a. See above – Desmin, vimentin, steroid receptors.

INFECTIOUS DS
105.Histoplasmosis found geographically
a. Ohio River valley
b. Mississippi River valley
c. Caribbean
106.Changes which occur with transition from HIV infection to AIDS – don’t know
choices (Robb pp227-228)
a. Increased viral replication (increased viral titer in blood)
b. CD4 count less than 200 cells/ul
c. Opportunistic infections/AIDS defining illnesses (table 6-10,p228)
i. Cryptosporidium or isosporidium enteritis
ii. PCP
iii. Toxoplasma pneumonia or CNS infection
iv. Candidiasis – esophageal, tracheal, pulmonary
v. Cryptococcal CNS infec
vi. Disseminated coccidiodomycosis
vii. Disseminated histoplasmosis
viii. Tuberculosis – pulmonary or extrapulmonary
ix. MAI – disseminated or extrapulmonary
x. Nocardia - pneumonia, meningitis or disseminated
xi. Disseminated salmonella
xii. CMV – pulmonary, intestinal, retinits, CNS
xiii. Localized or disseminated HSV
xiv. Varicella Zoster
xv. Progressive mulitfocal leukoencephalopathy (JC virus
 xvi. Neoplasms – KS, lymphoma, primary CNS lymphoma, invasive
cervical cancer
107.Which is not due to Chlamydia species (don’t know choices).
a. The following are due to Chlamydia (Lev and Jaw, p150)
i. C. psittaci –psittscosis pneumonia from birds
ii. C. trachomatis
1. urethritis
2. genital tract infections (associated with Reiter’s syndrome)
3. conjunctivitis (neonatal)
4. lymphogranuloma venereum
5. Trachoma (endemic chronic conjunctivitis)
iii. C. pneumoniae – atypical pneumonia
108.Mucosporidiosis associated with
a. ?gelfoam
109.EBV associated diseases include (p287)
a. Infectious mono
b. Burkitt lymphoma (African form)
c. Other B cell lymphoma (especially in immunosuppressed/HIV)
d. Nasopharyngeal CA
e. Oral hairy leukoplakia
f. Association with Hodgkin’s
110.Which is not a protozoa – don’t know exact choices here.
a. ?Rhinosporidium vs cryptococcus. Crytptococcus is a yeast.
Cryptosporidium is a protozoa.
b. ?Babesia, microsporidium, isospora, rhinosporidium – Babesia,
microsporidium, and isospora are protozoa.
111.Ornithosis (don’t know question)
a. Chlamydia psittici pneumonia caused by aspirated particles from bird
excrement.
112.Not a feature of aspergillus – don’t know choices
a. These are features of aspergillus (Robb p355)
i. 3 toxins
1. Aflatoxin – carcinogen which may lead to African liver CA
2. Restrictocin – degrades host mRNA
3. Mitogillin - degrades host mRNA. Induces IgE involved in
allergy and aspergillus
ii. Causes allergies through types III and IV hypersensitivity reactions
iii. Allergic bronchopulmonary aspergillosis – common in asthmatics.
Hypersensitivity due to bronchial colonization with Aspergillus
and may lead to COPD
iv. Aspergilloma – colonization within pre-existing cavity. No
invasion.
v. Invasive aspergillosis
1. Usually immunocompromised
2. Starts in lung. May involve heart valves, brain, kidneys
 3. Target lesions – gross foci of necrotizing pneumonia with
hemorrhagic border
4. Blood vessel invasion
vi. Morphology
1. Septate hyphae 5-10um thick
2. Acute angle (40 degree) branching
3. May see fruiting body

KIDNEY
113.Learn kidney chp pictures and tables Robbins chp 20

114.Angiomyolipoma (don’t know question, here is review)

a. Tumor of fat, blood vessles, and smooth muscle
b. May grossly resemble RCC
c. Commonly multiple or bilateral (15-30%)
d. Blood vessles lack elastic lamina
e. Mature fat
f. Smooth muscle may show hypercellularity and atypical forms
i. Type of bizarre, epithelioid cell in some cases which may be
multinucleated and is thought to be of smooth muscle origin but
has other properties
1. cytoplasm may contain glycogen
2. Stains with actin, but also HMB-45
3. Cytoplasmic crystalloids
4. premelanosome-like organelles
5. May resemble oncocytes or RCC cells
g. 1/3 of pts with renal angiomyolipoma have tuberous sclerosis –
i. tuberous sclerosis –
1. CNS hamartomas (cortical tubers, subependymal
hamartomas),
2. Seizures and mental retardation
3. retinal glial hamartomas,
4. pulmonary and cardiac myomas
5. cysts of liver, kidney, pancreas
6. Cutaneous lesions – angiofibromas, shagreen patches
(leathery thickenings), ash-leaf patches (hypopigmented),
subungual fibromas
7. 2 different loci on chromo 9 and 16 (16 codes for tuberin
protein similar to GTPase acitivating protein)
8. Autosomal dominant with variable penetrance
h. Angiomyolipoma also assoc with lymphangioleiomyomatosis
i. Also occur in retroperitoneal space unconnected to kidney, liver, and other
sites
115.Cystic renal dysplasia, is it bilateral or inherited? (pp934-35)
a. Not inherited (sporadic disorder)
b. Can be unilateral or bilateral
c. Congenital defect with persistence of islands of undifferentiated
mesenchymal elements in the kidney with cystification and abnormal
lobar organization
d. Assoc with other urinary tract deformities (atresia, etc)
e. Other cystic renal ds, review (p934-37, Robb)
i. Autosomal dominant (adult) polycystic kidney ds
1. 90% on chromosome 16, remaining unknown
2. Almost 100% penetrance by age 70-80
3. Always bilateral
4. Initially cysts involve only portion of nephron, so function
usually retained until 5th or 6th decade of life
a. Cysts eventually involve whole nephron
5. Also cysts in liver, spleen, pancreas, lungs
6. Berry aneurysms in 10-30%, is cause of death in 10% of pts
ii. Autosomal recessive (childhood) polycystic kidney ds
1. Usually have severe symptoms in neonatal period, can
present later in childhood
2. Always bilateral
3. Smaller cysts than AD polycystic kidney with elongated
channels present at right angles to cortical surface
a. Cysts involve cortex and medulla
4. May develop congenital hepatic fibrosis if they survive
infancy
iii. Medullary cystic ds
1. Medullary sponge kidney –
a. Cysts of medulla collecting ducts
b. Adults
c. Unknown pathogenesis
d. Usually normal function
e. Secondary complications include calcification,
infection, hematuria, and calculi
2. Nephronophthisis-Uremic medullary cystic disease
complex (AKA hereditary tubulointerstitial nephritis)
a. Usually childhood onset. Responsible for >20% of
childhood renal failure
b. Cysts in medulla
c. Cortical tubular atrophy and interstitial fibrosis
which is the cause of renal insufficiency
d. 4 types
i. Sporadic nonfamilial (20%)
ii. Familial juvenile nephroonophthisis (50%) –
recessive inheritance.
iii. Renal-retinal dysplasia (15%) – assoc with
retinitis pigmentosa. Recessive inheritance
iv. Adult onset medullary cystic ds (15%) –
dominant inheritance
116.Pediatric renal tumors – prognosis (don’t know question, here is review)
a. In order from best prognosis to worst (compiled from Ackerman pp1135-
1144)
i. Multicystic nephroma/multilocular cyst – benign cystic lesion
with areas that have appearance of a fully differentiated Wilm’s
tumor (tubules, etc)
ii. Mesoblastic nephroma – AKA fetal mesenchymal hamartoma,
congenital, benign but may recur
1. Spindle cell tumor with fibroblasts, myofibroblast, or
smooth muscle differentiation
2. No epithelial component, but surrounds epithelial cells
iii. Wilm’s tumor (nephroblastoma) – 80-90% cure rate overall with
surgery +/- chemo. Prognostic indicators include
1. Stage (most important) – based on tumor extent -
capsular/vascular invasion, renal sinus invasion, mets,
bilaterality
2. Age of pt - <2 years is good
3. Tumor size – larger is worse in stage I tumors
4. Presence of anaplasia = unfavorable histology
5. Review of Wilms (p463-464)
a. Most common renal primary tumor of childhood,
usually <6 years
b. Mutation on chromosome
i. 11p13 – (a transcription factor protein) –
WT-1
ii. 11p15.5 (function unknown) - WT-2
c. Blastemal, stromal, and renal epithelial elements on
histology
d. May have heterologous elements (eg cartilage)
e. 5% contain anaplasia
f. Express insulin-like growth factor
g. Syndromes associated with Wilms
i. WAGR - Wilms, aniridia, genital
anomalies, mental retardation – WT-1
ii. Denys-Drash – gonadal dysgenesis (male
pseudohermaphroditism) and nephropathy
WT - 1
iii. Beckwith-Wiedemann – organomegaly,
hemihypertrophy, adrenal cytomegaly, may
have hepatoblastoma, adrenocortical tumors,
rhabdomyosarc, pancreatic tumors. WT-2
iv. Clear cell sarcoma (AKA bone metastasizing renal tumor) – was
previously considered variant of Wilms. Rare. Small blue round
cell histology, not necessarily clear cells. Near 70% mortality
(May be improving with new chemo)
 1. Expresses insulin-like growth factor but not WT-1
transcripts
v. Rhabdoid tumor – Blue round cell tumor of usually infants (may
have spindle features)
1. Cytoplasmic eosinophilic hyaline globule made of
intermediate filaments which displaces nucleus giving a
plasmacytoid appearance
a. Positive for Vimentin and CK, not usually muscle
or neural markers
b. High mortality (>75%)
c. Occur in other sites besides kidney
i. Soft tissue , pelvis, bladder, thymus
117.Glomerulonephritis in pt with SLE. Where are immune deposits
a. Depends on what type of lesion, but if question is k-type, in Lupus in
general, depositis can be seen in the following areas (p204-205 – pink
text)
i. Mesangial
ii. Intramembranous
iii. Subepithelial
iv. Subendothelial
118.Renal papillary necrosis occurs in (Ackerman p1123)
a. Pyelonephritis
b. Diabetes mellitus (Robbins says pyelonephritis assoc with DM)
c. Infection associated with obstruction
d. Alcoholism
e. Vascular thrombosis
f. Sickle cell ds
g. Analgesic abuse
h. Long term Rifampin therapy for TB
i. Hemodialysis
119.Which will recur in renal transplant
a. ?Dense deposit, IgA, post infx GN
120.Which glomerular diseases recur after transplant
a. ?
121.Features of renal oncocytoma (don’t know question, here is review)
a. Circumscribed
b. May be multiple or bilateral
c. Mahogany brown with a central fibrous scar
d. Oncocytes with uniform nuclei, abundant granular cytoplasm
(mitochondria), nested or tubular pattern
e. No prominent papillary formations, clear cells, or necrosis
f. Usually benign regardless of size
g. Immuno
i. Keratin positive
ii. Dot-like positivity for Keratin 8 and 18
iii. Negative Vimentin (usually)
LIVER
122.Mallory hyaline bodies are seen in
a. EtOH
b. PBC
c. Wilson’s
d. Chronic cholestatic syndromes
e. Wilson’s disease
(question may specify in the portal tract, need to look up if one is specifically
in portal tract)
123.Significance of cholestatic sclerosing cholangitis in posttransplantation
a. ?Harvesting injury
124.Kayser-Fleischer rings (original said “Kleinfeisher ring”) Robb pp864
a. Green-brown depostis of copper in Descemet’s membrane of the cornea
b. Seen in Wilson’s ds. , but may be seen in other forms of chronic
cholestasis (don’t know if they contain copper in other forms)
125.Primary biliary cirrhosis assoc with
a. Anti mitochondrial antibodies (M2 antibodies to mitochondrial pyruvate
dehydrogenase) (p868, Robb)
126.Drug and toxin induced liver disease
a. See chart on page 857 Robbins – there are at least 2 questions. One had to
do with thorotrast and vinyl chloride associated with HCC and
angiosarcoma. The other was an unspecified question about drugs and
liver injury – LEARN THE CHART!
127.Description of HCV histology (k type, don’t know choices. Here is review)
a. Lymphoid aggregates in portal tracts with accompanying mixed
inflammatory infiltrate
b. Fatty change more so than Hep B
c. No ground glass hepatocytes as seen in Hep B
d. Bile duct damage
e. Piecemeal necrosis
f. Bridging necrosis, fibrosis ,eventual cirrhosis
128.Histology of alcoholic hepatitis (p858)
a. Hepatocyte ballooning necrosis – centrilobular
b. Mallory bodies (cytokeratin and other filaments – eosinophillic
cytoplasmic inclusion, not specific to alcohol, see above)
c. Neutrophillic infiltrate in lobule
d. Fibrosis – sinusoidal and perivenular
e. Fatty change may or may not be present
129.Alcoholic fatty change
a. Completely reversible. Fibrosis is not reversible.
130.Hemachromatosis defect
a. Hemachromatosis gene located on chromosome 6, but the functional
defect is unknown still (as of Robbin 5th edition)
131.Anti Actin Ab seen in ? choices:Hep A, B, C, autoimmune hep
a. Anti smooth muscle AB definitely seen in autoimmune. (p853 Robb)
 b. ? Hep A, B, C
132.What stain gives a cannalicular pattern in hepatoma/hepatocytes? Choices:
CK20, EMA, CEA, s100
a. Answer (ackerman p 909) Alk phos, CEA (biliary glycoprotein
component of it), low molecular weight cytokeratin

LYMPHOID
133.Pattern of lymph node involvement by Langerhans histiocytosis and what is
immuno staining of the langerhans histiocytes?
a. Sinusoidal infiltrates of Langerhans cells and eos
b. Review – disease with Langerhans histiocytosis include
i. Eosoinophilic granuloma – localized
ii. Hand-Schuller-Christian – multifocal
iii. Letter-Siwe – systemic
iv. 2-chlorodeoxyadenosine activity in adults
v. Langerhans cells – large mononuclear cells with folded or grooved
nuclei and abundant pale cytoplasm. Imuno is same as normal
Langerhans cells
1. s-100
2. cd68
3. PNA (peanut agglutinin)
4. cd1a, cd4, cd11c, and cd14 in frozen tissue (cd1a is also
available on paraffin)
5. adenosine triphosphate
6. alpha-D-mannosidase
vi. Have birbeck granules on EM
134.Most common site of lymph nodes with benign mesothelial inclusions? Choices
: Retroperitoneal or mesenteric or pleural
a. Looks like mediastinal and abdominal lymph nodes are the most common
according to Strauchen .
b. Other benign lymph node inclusions
i. Mullerian
ii. Salivary
iii. Thyroid
iv. Mammary
v. Pancreatic heterotopia
vi. Renal tubular inclusions with Tamm-Horsfall protein in children
with Wilms
vii. Nevus cells – usually in superficial lymph nodes – axillary,
inguinal , cervical
135.PTLD – know features and associations
a. Heart or lung transplant is higher risk than other organs
b. Therapy with cyclosporine A or OKT3 is high risk
c. Assoc with EBV
d. Spectrum of appearance
i. Plasmacytic hyperplasia (low grade PTLD)
 1. Tonsil/Waldeyer’s ring/ and LN involvement
2. Polyclonal
3. Multiple forms of EBV
4. Preservation of architecture with interfollicular zone
expansion by infiltrates of plasmacytoid lymphocytes and
plasma cells
ii. Polymorphic B-cell hyperplasia/Polymorphic B cell lymphoma –
Intermediate grade PTLD)
1. Nodal or extranodal
2. Single form of EBV
3. Majority are monoclonal
4. Effacement of architecture by polymorphous proliferation
of lymphocytes and immunoblasts with varying degrees of
plasmacytoid differentiation. Lympohoma version has
more atypia and necrosis
iii. Immunoblastic lymphoma/ Multiple myeloma (high grade PTLD)
1. Nodal or extranodal
2. Monoclonal
3. contains 1 or more oncogene or tumor suppressor
mutations
a. N-RAS
b. p53
c. C-MYC
4. Single form of EBV
5. Effacement of architecture by monomorphic proliferation
of plasma cells and immunoblasts
e. Therapy in all cases is based on withdrawal of immunosuppresion. Higher
grades may also need chemo/radiation
136.Ki-1 lymphoma markers
a. Ki-1 = CD30
b. Positive in Reed-Sternberg cells in Hodgkin’s
c. Positive in anaplastic large cell lymphoma
d. May also be positive in nasopharyngeal carcinoma, embryonal carcinoma,
melanoma (faint) and rarely in other carcinomas (faint)
137.Follicular dendritic cells
a. MHC II antigen presenting cells – present antigen to B-cells in follicular
center
b. Immuno
i. CD21 (complement C3d receptor)
ii. CD35 (complement C3b receptor)
c. Other dendritic cells of the lymph nodes include
i. Interdigitating reticulum cells
1. In paracortex
2. Present antigen to T-cells
3. S-100 positive (neg for CD21 and 35)
ii. Langerhans cells
 1. In paracortex
2. Present antigen to T-cells
3. S-100 and CD1a positive
138.Toxoplasma lymphadenitis vs Kikuchi’s ds vs SLE histo
a. Toxoplasma lymphadenitis
i. Heterphile-negative mononucleosis syndrome
ii. Lymphadenitis of Piringer-Kuchinka
1. Follicular lymphoid hyperplasia
2. Clusters of epitheliod histiocytes within and between
follicular centers
3. Monocytoid B-cells in sinuses
4. Combination of above 1,2,3 together is fairly specific for
toxo.
5. May rarely see toxo cysts in lymph nodes
b. Lupus lymphadenitis
i. Follicular lymphoid hyperplasia
ii. Paracortical foci of necrosis
iii. +/- Hematoxylin bodies – Masses of altered DNA – Feulgen
positive
iv. Neutrophils are absent
v. Immunoblasts and plasma cells may be prominent
c. Kikuchi’s disease
i. Classic – young women with cervical adenopathy and viral
prodrome
ii. Circumscribed paracortical foci of necrosis with karyorrhectic
debris, which are surrounded by zone of immunblasts and
macrophages
iii. Crescentic histiocytes (macs with c-shaped nuclei) are prominent
iv. Scant polys and plasma cells
v. Xanthoma cells may be prominent
vi. 3 histologic patterns
1. Proliferative
2. necrotizing
3. xanthomatous
vii. CD 8 t-cells and macrophages in necrotic zones
d. Kawasaki’s ds (mucocutaneous lymph node syndrome)
i. Febrile illness of childhood (less than 6 years of age)
ii. Skin rash – desquamation of palms and soles, erythema of
conjunctiva, lips, and oral mucosa; cervical adenopathy, systemic
vasculitis assoc with coronary artery involvement and coronary
artery aneurysm
iii. Lymph node histo ( not common to get LN bx, dx based on
clinical)
1. Fibrin thrombi in small vessles
2. Irregular foci of necrosis in paracortex and follicles
 iv. Abnormal macrophage and t-cell activation of unknown cause
(possible postinfectious)
v. Treated with IV immunoglobulin
e. Kimura’s ds
i. Angiolymphoid proliferation of head and neck involving males
from the Far East – unknown etiology
ii. Peripheral eosinophilia and increased serum IgE
iii. Histo
1. follicular lymphoid hyperplasia
2. Interfollicular eosinophils
3. Eosinophillic folliculolysis
4. proliferation of thin-walled vessles
5. May have Warthin Finkeldy giant cells, hyalinization of
follicles, and Charcot-Leyden crystals
6. Preponderance of B-cells
7. IgE in follicular centers
iv. Confused with angiolymphoid hyperplasia with eosinophilia,
which is in western women in the head and neck and considered to
be a form of hemangioma with epitheliod appearance and
eosinophils
1. No peripheral IgE or eosinophilia
139.Hodgkin’s ds staging (k-type question in which all were correct. Don’t know
choices, but here is a review of Hodgkin’s staging)
a. Ann-Arbor staging I-IV
i. Stage I – single LN region (I)or single extralymphatic organ or site
(Ig)
ii. Stage II – 2 or more LN regions on same side of the diagphragm
(II) or localized involvement of extralymphatic organ or site (IIg)
iii. LN regions on both sides of diaphragm (III) or localized
involvement of an extralymphatic organ or site (IIIg) or spleen
(IIIg) or both (IIIse)
iv. Stage IV – Diffuse or disseminated involvement of one or more
extralymphtic organs +/- LN involvement. – A=asymptomatic and
B=with symptoms (fever, wt loss, etc)
b. Early peak in adolescence is usually nodular sclerosis of Stage I or II
c. Later peak in older age is usually mixed cellularity or lymphocyte
depletion and presents with Stage III or IV
140.Hodgkin’s ds –B cell malignancy most likely confused with which type of
lymphoma (don’t know choices)
a. Possibilities include peripheral T-cell, anaplastic large cell, and t-cell rich
B-large cell.
b. Most likely to be confused is anaplastic large cell.
c. Don’t forget infectious mono can be confused with Hodgkin’s
i. RS-like cells in mono are CD15 negative, CD30 positive, CD45
negative.
141.PCR of cat scratch disease shows what organism
 a. Bartonella henselae most common
b. Rare – Afipia felis
142.HIV lymphoma (don’t know question but here is review)
a. Non-Hodgkins lymphoma (can commonly C-MYC rearrangements and
EBV)
i. Commonly associated with HIV – aggressive B-cell neoplasia
1. Diffuse large cell, B-cell
2. Burkitt’s like
ii. More rare associated with HIV
1. Primary effusion lymphoma assoc with HHV-8 (like
Kaposi’s sarcoma)
2. CD 30 positive anaplastic large cell lymphoma
3. Peripheral T cell lymphoma
4. Immunoblastic T cell lymphoma
b. Hodgkin’s
i. Distinct clinical presentation – associated with b-symptoms and
50% bone marrow involvement
ii. RS cells contain EBV
iii. CD4:CD8 ratio of lympocytes is reversed compared
immunocompetant Hodgkin’s
iv. Usually mixed cellularity type
143.MDS, what affects prognosis? Choices: Age, 5qdeletion, % blasts
a. (WHO classification of heme, p67) Age <60 is better prognosis
b. Increase percentage of blasts is worse prognosis
c. Genetics:
i. Normal karyotype, 5q del, 20qdel, and –Y are in the Good
prognosis category
ii. >3 genetic abnormalities or chromosome 7 mutation = Poor
iii. Any other = Intermediate
144.Characteristics of Sinus histiocytosis with massive lymphadenopathy
a. AKA Rosai Dorfman
b. Usually cervical adenopathy in young people, can occur anywhere
c. Fever, elevated sed rate, hypergammaglobulin
d. Unknown etiology
e. Histology
i. Dilated sinuses with large histiocytes with prominent nucleoli and
finely vacuolated cytoplasm
1. Histiocytes S-100, CD68, CD11c, CD14, CD33,
antichmotrypsin, lysozyme positive
ii. Emperipolesis – histiocytes engulf other hematologic elements
iii. Thickened capsule
iv. Plasma cells in intersinusoidal tissue
f. Can have extranodal involvement
g. Benign, self limiting condition
145.Immuno of L&H cells in Hodgkin’s
 a. L & H cells occur in nodular lymphocyte predominance Hodgkin’s
disease, not in classical Hodgkin’s.
b. L&H cells stain with a typical B-cell phenotype
i. CD20, CD79a, CD45, EMA positive
ii. Usually CD15 and CD30negative
iii. May express CD30 weakly
iv. Usually surface immunoglobulin negative
146. Which are chloroacetate positive cells
a. ?

MEDIASTINUM
147.Most common mass of posterior mediastinum in children (don’t know choices)
a. ?Probably neuroblastoma (para vertebral region of posterior mediastinum
is 2nd most common site of neuroblastoma after adrenal medulla) (p459
Robbins)
148.Most likely dx of anteorsuperior mediastinal mass, 20 yo? Choices: Lymphoma
vs seminoma etc
a. Nodular sclerosis Hodgkin’s probably most common in this age
b. Thymoma occurs in ant-superior mediastinum, but usually in patients
older than 40years.
c. Thymoma makes up only approx 25% of ant-sup mediastinal tumors
because this is a common location for Hodgkin’s and non-hodgkins
lymphoma.

MOLECULAR
149.RFLP – be able to interpret (p 168, Robbins, diagram)
150.Genome of a retrovirus (p221, Robb, diagram)
a. Gag gene codes for core proteins
b. Pol gene codes for reverse transcriptase
c. Env codes for envelope glycoproteins
151.C-myc overexpression occurs in Burkitt’s lymphoma
a. Normal myc gene on chromo 8
b. Get translocation b/t 8q24 and chromo 14 so that myc gene is under
control of immunoglobulin gene enhancer and get overexpression
152.Identify these chromosomal abnormalities (karyotypes with arrow at affected
chromo)
a. Burkitt’s – t(8;14)
b. Ewing’s – t(11;22)
c. Follicular lymphoma – t(14;18) - BCL-2
153.Know DNA ploidy grams (hyperdiploid, hypo, etc)
154.BRCA 1 and 2 are
a. ?tumor suppressor genes

NEURO
155.Morton’s neuroma – don’t know question. Choices:?3/4 metatarsal, ?grossly
nodular tumor of nerve, fibrous thickening of nerve
 a. Morton’s neuroma, review
i. Traumatic neuroma
ii. Classic location is metatarsal area, esp. interdigital nerve b/t 3rd and
4th toe
iii. More common in adult female
iv. Extensive perineurial fibrosis, often concentric
v. Thickened arterioles which may have thrombi
156.Ependymoma with best prognosis – don’t know choices
a. Myxopapillary type
i. Restricted to conus medullaris and filum terminale. >90% curable
by surgery, though rare examples have spread
b. Subependymoma has a better prognosis than any ependymoma including
myxopapillary. Don’t know if it was choice
i. Subependymoma
1. Derived from subependymal neuroglial cells around
ventricles
2. Most commonly in 4th ventricle in older men, asymptomatic
and found at autopsy
3. Solid, dense white tissue with calcification
4. Usually non-invasive, well defined.
5. May be secondary to irritation of ventricles
6. Fibrillar meshwork with groups of small tumor cells
huddled together throughout. Microcystic changes in
fibrillar background
7. May have nuclear atypia, but behave benign

157.Craniopharygioma
a. Derived from Rathke’s pouch remnants
b. Most commonly suprasellar, may be sellar
c. Cystic, multiloculated, some solid
d. AKA ameloblastoma or adamantioma because recapitulates tooth enamel
organ
e. Calcification and metaplastic bone formation common
f. Benign, rare malignant behavior
g. Crank case oil/machinery oil grossly in cystically degenerated tumors
which contains cholesterol crystals
h. Kids, young adults, but may be any age
i. Question: Which is most likely to present as pituitary tumor? – don’t know
other choices, answer was thought to be craniopharyngioma
158.Most common tumor of the pineal gland
a. Germinoma (replicates either seminoma or dysgerminoma)
159.Brain with necrosis of globus pallidus, what is cause
a. ?
160.Which has more aggressive course? Choices: Hemangioblastoma vs
Gemistocytic astrocytoma
a. Of these 2, gemistocytic astrocytoma is the more aggressive.
 b. Hemangioblastoma
i. Young adults, cerebellar.
ii. May be extracranial – spinal, optic nerves, etc
iii. Von Hippel Lindau
iv. May produce EPO and cause erythrocytosis
v. Histogenesis uncertain, thought to be stromal cell with
neuroendocrine diff (s-100 positive)
vi. Vascular tumor with bland stromal cells containing clear or
vacuolated fat-containing cytoplasm
vii. Benign, curable by resection
c. Gemistocytic astrocytoma
i. Predominance of gemistocytes and perivascular lymphoid cuffing
ii. May transform into more aggressive tumor (GBM)
161.What changes can be seen in Antoni B areas
a. Antoni B area of Schwannoma are the looser, less cellular myxoid
edematous regions that undergo cystification
b. Antoni A – cellular areas with palisading/ Verocay bodies
162.Which of these tumors has hemangiopericytoma like areas (no pics, don’t know
choices)
a. Solitary fibrous tumor has frequent hemangiopericytoma-like areas
b. Others?
163.Chordoma immuno
a. CK and EMA positive

PROSTATE
164.Most common cause of caseating granulomatous inflammation in prostate in U.S.
a. ?BCG infusion vs tuberculosis
165.High molecular weight cytokeratin can be used to distinguish PIN from prostate
CA
166.High vs low grade PIN (don’t know question)
a. Based on
i. cell crowding and stratification,
ii. nuclear enlargement, pleomorphism and chromatin
iii. nucleolar appearance
b. Low grade PIN includes grades 1-2
c. High grade PIN includes grade 3 and has cytologic appearance of prostatic
carcinoma.
167.What is the basis of the Gleason grading system
a. 2 most prevalent grades are added to get Gleason score (combined grade)

RESPIRATORY (Most of the non-neoplastic information came from Katzenstein and

Askin Surgical Path of Non-neoplastic Lung Disease)
168.Vasculitis and granulomatous inflammation (don’t know question).
Choices:Wegenner’s, TB, ?other infections, ? Langerhan’s histiocytosis
a. Wegener’s, TB, and other infections (blasto, histo, other fungal) definitely
have both granulomatous inflammation and vasculitis. (Vasculitis is
 common in mycobacterial and fungal infections, but is usually not
necrotizing as in Wegener’s) –
b. Langerhans histiocytosis (eosinophillic granuloma) has infiltration of the
vessles with inflammatory cells which has been called vasculitis by many
authors, but Katzenstein thinks that term is wrong because it is not a true
vasculitis. It is just invasion of the vessel by the eosinophillic granuloma.
169.Coccidioidomyocosis does not have which type of inflammation? Choices:
granulomatous, polys, eosinophilic, LIP
a. Coccidio shows a necrotizing granulomatous inflammation with purulent
(neutrophillic) zones and prominent eosinophils
b. Does not show LIP
170.Giant cell CA of the lung is derived from squamous or adeno
a. No definitive origin, but mucin positivity in some tumors suggests adeno
171.Lung abscess formation
a. Usually associated with aspiration of oral contents, usually anaerobe
172.Bronchioloalveolar CA prognostic factors
a. Localized lesion better prognosis than multiple/diffuse
b. Non-mucinous better than mucinous
173.IVBAT – intravascular bronchoalveolar tumor
a. is considered a form of epithelioid hemangioendothelioma
174.Allergic bronchocentric granulomatosis – don’t know question.
a. Name of disease is Bronchocentric granulomatosis
i. It is associated with asthma and allergic bronchopulmonary
aspergillosis in about half of the patients
ii. Combination of angiitis and granulomatous ds which centers
around bronchioles. Get bronchiolar destruction by granulomatous
inflammation
175.Pulmonary alveolar proteinosis associated with(don’t know choices)
a. AKA lipoproteinosis or phospholipoproteinosis
b. Alveoli filled with pink material, PAS positive
c. Interstitial architecture not significantly altered
d. May be isolated or associated with
i. Occupational exposure to silica, aluminum, and other dusts
ii. Immunosuppresion,
iii. Hematolymphoid malignancy
iv. Nocardia infection is encountered with increased frequency
v. Infection with mycobacteria and various fungi have also been
associated
176.Difference in diffuse alveoalar damage in adults vs kids (p677)
a. Infants – mechanism is pulmonary surfactant deficiency with hyaline
formation
b. Adults – mechanism is damage to alveolar capillary walls, increased
capillary permeability, alveolar edema and fibrin with hyaline formation
177.Causes hypoglycemia
a. Solitary fibrous tumor of pleura
 i. Spindle cell lesion with fibroblast-like cells, abundant focally
dense collagen, and hemangiopericytoma-like areas
ii. CD34, vimentin positive. (Occasional desmin)
iii. Majority benign (>90% cure with surgery)
178.Lung cancer producing CRH
a. ?
b. Small cell CA of lung produces ACTH, ACTH-like substance, and ADH.
Can get related paraneoplastic syndromes. (Don’t know about CRH) –
See table 7-9. p296, Robbins
179.Etiology of UIP (don’t know question or choices)
a. Associated with collagen vascular ds, esp RA and scleroderma
b. Auto antibodies esp RF and ANA are frequent
c. Circulating immune complexes frequent
d. Progressive downhill course
e. Older pts – avg age 60
f. Interstitial chronic inflammation, fibrosis and honeycomb change with
intervening normal – temporal heterogeneity
180.Morphology of diffuse alveolar damage/ARDS
a. Early stage (less than 1 week)
i. Interstitial and alveolar edema
ii. Hemorrhage and fibrin deposition
iii. Hyalin membrane 1 or more days after injury
iv. Sloughing of alveolar lining cells
v. Sparse interstitial inflammatory infiltrate – lymphs, plasma cells,
macs
vi. Fibrin thrombi in capillaries
b. Late stage
i. Alveolar lining hyperplasia (begins 3-7days after injury)
ii. Organization – fibroblastic foci in interstitium and air spaces
iii. Increased interstitial inflammation
iv. Hyalin membranes and edema not prominent
v. Arterial changes – medial hypertrophy and intimal fibrosis
vi. Bronchiolar squamous met
c. The stages overlap somewhat

181.Bleomycin induced lung ds, which are not seen? Choices: organizing
pneumonia, DAD, alveolar hemorrhage, fibrosis
a. The Following are seen (p82, Katzenstein and Askin, table 4-2)
i. DAD
ii. Pleural fibrosis
iii. Eosinophilic pneumonia
iv. BOOP
v. Pulmonary veno occlusive ds
vi. Alveolar hemorrhage can be associated with the DAD (p86,
Katzenstein), so answer must be a different choice
SKIN
182.Nevus sebaceous most commonly associated tumor
a. ?BCC/syringocystadenoma papilliforum
183.Warty dyskeratoma
a. Assoc with acantholysis, not virus
184.Most common site of cellular blue nevus
a. ?Buttock
185.Most commonly associated with pseudoepitheliomatous hyperplasia
a. ?Granular cell tumor
186.Hydropic degeneration of skin occurs in which K type
a. ?SLE
187.What is helpful in differentiating Spitz nevus from melanoma
a. ?age ?morphologic atypia, ?mitoses
188.Neurothekoma
a. Cutaneous nerve sheath myxoma
b. Benign
c. Cellular and myxoid variant
d. Cellular can be confused with melanoma
e. S-100 +, HMB-45 neg
f. Not assoc with NF or other syndromes
189.Microscopic features of intradermal nevus (don’t know choices)
a. You know this
190.Melanoma vs intradermal nevus
a. IDN has discrete, regular round borders and regular pigmentation.
191.Prognosis of melanoma related to
a. ?depth vs thickness
192.Trichilemomma location
a. Facial skin predominantly
b. (Cowden’s ds – multiple trichilemomma, multi hamatomas of brst,
thyroid, GI, multi acral keratosis, hyperkeratotic papillomas,
INCREASED BRST CA RISK)
193.Melanocytes (or melanin) are seen in which of the following lesions (don’t know
choices)
a. ?
194.Langerhans cells in skin (don’t know question)
a. Dendritic histiocytic antigen presenting cells
195.Eccrine poroma
a. ?Positive EMA
196.Basaloid squamous cell, which does not fit
a. ?location, LN mets, distant mets, etc
197.DFSP immuno
a. CD34
198.Mucin deposition in skin
a. Granuloma annulare
199.Mixed tumor of skin is AKA
a. Chondroid syringoma
SOFT TISSUE
200.Rhabdomyosarcoma ID’d by immuno – what is translocation
a. t(2;13) (seen in alveolar rhabdo but not consistent in other types)
b. Immuno for Rhabdomyosarc
i. Myoglobin, Desmin, myosin, tropomyosin alpha-actinin, titn, Z
protein, Actin, Vimentin, MyoD1, ILGF II, muscle enzymes
201.Synovial sarcoma
a. t(X;18)
202.Giant cells associated with dead skeletal muscle (don’t know question) Choices:
Infarct, gun shot wound, polymyositis
a. Probably the giant cells are myofiber bags (atrophic muscle cells)
b. Would see atrophic muscle cells in:
i. ?
203.Most frequent location for myxoid liposarcoma
a. Lower extremities, esp thigh
b. Is the most common type of liposarc
204.Spindle cell tumor most likely to metastasize? Choices:DFSP vs liposarc vs
myxoid liposarc (hopefully there is another more obvious choice)
a. Myxoid and well diff liposarc seldom metastasize
b. DFSP also has very low rate of mets
c. Pleomorphic and round cell liposarc metastasize often
205.Translocation of myxoid liposarc
a. t(12;16) – creates TLS/CHOP fusion (p1263)
206.Genetic abnormality in desmoplastic small round cell tumor
a. t(11;22) (p13;q24) – involves EWS in 22q24and WT1 in 11p13

SPLEEN
207.Splenic blood lakes
a. ?
208.Fibrosis around splenic vessles caused by
a. Lupus – causes onion-skin lesions of central penicilliary arteries (p207)
209.Histologic findings of ITP (p619)
a. Sinusiodal congestion
b. Hyperplastic enlargement of follicles with germinal centers – White pulp
hyperplasia
c. Increased macrophages in sinusoids
210.What infiltrates red pulp (don’t know choices)
a. ?
211.Spleen in TTP(don’t know choices)
a. Thrombi in arteries and arterioles without inflammation
b. PAS + hyaline subendothelial deposits
c. Hyperplasia of germinal centers, periarteriolar concentric fibrosis,
hemosiderin macs, hemophagocytosis, extramedullary hematopoiesis

TESTIS
 212.Positivity for what is seen in embryonal CA but not most other germ cell tumors
a. CD30 is positive in >80% embryonal but not in other germ cell tumors
(very rare)
b. Cytokeratins (pancytokeratin AE1/AE3, Cam 5.2) are positive in
embryonal also.
c. PLAP positive in >85%
d. EMA is negative
e. Good panel for embryonal: CK +, PLAP +, CD30 +, EMA -
213.Which germ cell tumor is most likely to metastasize?
a. Choriocarcinoma is correct if it is a choice, then the other non-
seminomatous germ cell tumors, then seminoma
214.What is associated with a worse prognosis in seminoma?
a. The presence of other non-seminomatous elements (embryonal, etc)
b. Not isolated syncitiotrophoblasts
215.Enlarged testis in 70 year old, most likely dx
a. Lymphoma

THYMUS
216.Thymic carcinoid and ACTH
a. See #54 above– Cushing’s and thymic carcinoid

THYROID
217.Black thyroid associated with
a. Minocyclin
218.Hurthle cells are not seen in –
a. ? James thought that it was either Graves or colloid goiter, but you can see
Hurthle cells in both of these. He said the other choices were straight
forward, but obviously not.
219.Papillary thyroid CA oncogene
a. RET is the protooncogene, PTC is the name of the new oncogene or
abnormal form (forms a RET/PTC hybrid)
220.Definition of micropapillary thyroid CA
a. Papillary microcarcinoma (Ackerman p 520) is defined as a papillary CA
measuring 1cm or less in diameter
221.De Quervain subacute granulomatous thyroiditis, although the cause is uncertain,
is associated with (p1127)
a. Viral infection (history of previous mumps, measles, flu, adenovirus,
coxsackie, echo)

MISCELLANEOUS
222.Acute rejection shows (don’t know what organ the question specified)
a. Infiltration of mixed population of inflammatory cells
b. Cellular injury/necrosis
c. Endothelialitis
d. May see regenerative changes (eg bile ducts in liver)
223.HLA matched hyperacute rejection shows (don’t know what organ specified)
 a. Arthus type reaction with neutrophils in arterioles, glomeruli, and
peritubular capillaries, endothelial injury, platelet thrombi, eventual
vascular occlusion and infarct (p192, robb)
224.Most common location for angiosarc (don’t know choices)
a. Skin, then soft tissue, then breast , then liver (Robb page 510)
225.Congophilic angiopathy associated with lobar hemorrhage occurs in
a. Alz ds. (Amyloid angiopathy ) ? not systemic amyoidosis (don’t know
about this lobar hemorrhage, which lobes? In lung or brain somewhere? I
found this thing about HCHWA-Dutch – familial ds form of Alzheimers –
hereditary cerebral hemorrhage with amyloidosis, get hemorrhage and
amyloid angiopathy
b. Features of Alzheimer’s (pp1329-31, Robb)
i. Cortical atrophy with wide sulci
ii. Neurofibrillary tangles ( not specific to Alz ds, found in other ds)
1. Contain tau protein, ubiquitin, amyloid beta, MAP2
iii. Neuritic plaques (not specific to Alz ds, but increased numbers of
plaques is suspicious)
1. Spherical collection of dystrophic neurites around an
amyloid core
iv. Plaques and tangles relatively spare motor and sensory cortex but
occur in other cortex areas
v. Amyloid angiopathy
1. Amyloid beta protein in vessel walls(APP is precursor
protein)
vi. Granulovacuolar degeneration
1. Intraneuronal cytoplasmic vacule containing argyrophillic
granule
2. In hippocampal pyramidal cells
vii. Hirano bodies (non-specific)
1. Elongated, eosinophillic bodies containing actic
2. In hippocampal pyramidal cells

226.Fibrinous changes occur in

a. Gastric ulcer, rheumatoid arthritis, Polyarteritis nodosa
b. Not medial cystic degeneration ( occurs in aortic dissection in Marfan’s
p502-503
227.Adenomatoid tumor immuno
a. ?CK +
228.Mesothelial hyperplasia
a. ?Does not go into bowel wall or form gross nodules
229.Problem with insurance/billing
a. ?Look up CPT code
230.Fibrosclerosing diseases include:
a. Riedel’s thyroiditis
b. Retroperitoneal fibrosis
c. Peyronie’s disease
 d. ?PBC or PSC
e. ?Mesenteric retraction
231.Most common site for papillary mesothelioma
a. ?Pleura vs peritoneum (probably pleura)
232.Benign papillary mesothelioma associated with
a. ?Young females, psammoma bodies, etc
233.CD 34 is positive in which of the following tumors
a. DFSP, solitary fibrous tumor
b. ?others
234.S-100 is positive in which of the following
a. ?
235.Retrolental fibroplasia
a. Retinopathy of prematurity caused by excessive arterial oxygen tensions
used to treat respiratory insufficiency in premature newborns
b. Get fibrovascular proliferation in retina, causing blindness (Stevie
Wonder)
236.Rhabdoid tumor (don’t know question)
a. ?
237.EW-1/FT-1 associated with? (Don’t know choices)
a. Think this is a typo and they meant EW-1/WT-1 (for ewings sarcoma and
wilms tumor (see #206)
b. Answ is desmoplastic small round cell tumor
238.Peutz jehger syndrome and sex cord tumor with annular tubules and
adenocarcinoma of the cervix. (don’t know question)
a. Yes, they are associated. The adenoCA of cervix is a well diff adeno
called adenoma malignum
239.Which is least likely to exhibit stromal fatty infiltration
a. Heart, liver, pancreas, lymph nodes
b. Answer is liver (fat is intracellular, not stromal)
240.Wegener’s, what is most specific
a. Positive anca vs blue granular necrosis
241.Wegener’s granulomatosis is associated with
a. C-ANCA
242.Wegener’s question: if all occur at same time
a. Sinus, renal, lung – I think they do (p496, Robb)
243.Which of the following does not have giant cells
a. ?Giant cell reparative granuloma, brown tumor of bone, cherubism,
fibrous dysplasia
244.Least likely to metastasize to CNS in male
a. ? Prostate, GI, renal, liver, melanoma
245.Features of the neonatal alcohol syndrome
a. ?Small head
246.Pt with angiomyolipoma and facial fibroma likely to have
a. ?TSC
247.Ghost cells are seen in the following except
 a. ?Pilomatrixoma, craniopharyngioma, chordoma, calcifying odontogenic
fibroma
248.Cause of myospherulosis
a. Gelfoam
249.Placenta in monozygotic twins
a. ?
250.What is invariably present in TOF
?