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211 Cards in this Set

  • Front
  • Back
Esophageal cc, 2 major types. Localization for each type. Prevalance for each.
SCC : 75%, all over the esophagus, mainly middle
Adenocc : 25%, on the rise, ONLY LOWER 1/3.
Esophageal SCC : 3 major risk factors, what does it look like grossly
Risk factors : Esophageal disorders (achalasia, esophagitis), Life style/diet, Tylosis. Small white plaques resembling leukoplakia
Esophageal SCC : 3 morphological types
1. Polypoid fungating
2. Necrotizing ulcerations
3. Diffuse infiltrative
Esophageal Adenocc : 3 main features
Arise from Barret's espohagus, May invade gastric mucosa, Start as plaques which develop into large ulcerative/infiltrative nodules
Give 3 types of gastrc polyps. Which one is a ture neoplasm that can advance to adenomacc ?
Hyperplastic polyps (NOT neoplasms), fundic gland polyps, adenomatous polyps ==> true neoplasm, may advance into Adenocc
Gastric cc : 2 types, which one is decreasing in frequency, which one arises from chronic gastritis?
Gastric cc :
Intestinal type, Diffuse (Signet ring cell) type.
Intestinal type has decreased in freq., also intestinal type arises from metaplasia due to chronic gastritis (h. pylori)
Gastric cc : give 3 Signette ring cell type cc features (arises from, age of onset, pathogenesis)
Arises from mucous cells, at an early age, pathogeneis is largely unknown. Maybe due to E-cadherin mutations
Gastsric cc : give 3 Intestinal type risk factors. Also what is the typical location for it ?
Chronic gastritis with Pylori, AI gastritis, diet (nitrites). Location is mostly in the lesser curvature of the antral region
Gastric cc : give 4 growth patterns
1. Exophytic
2. Flat depressed
3. Excavated --> ulcerative, looks like peptic ulcer but ELEAVTED margins
4. Linitis plastica (desmoplasia)
Gastric cc : histology of intestinal type and diffuse (signette ring) type. Also give 2 possible metastases for this cc
Intestinal : neoplastic glands, resembling colonic adenocc
Diffuse : invidivudal or small clusters of signette ring cells (PAS+). Metastases - to Virchow node, Krukenberg (ovaries)
Breast cc : Hereditary form-which genes. Also, give 4 risk factors, give prevalant locations
Hereditary - BRCA1, chr 17, BRCA2, hr 13. Further risk factors - c-ERB2 protooncogene, oral contraceptives, nulliparty, smoking, obesity. Locations - mostly LEFT breast, mostly outer-upper quadrant
non-invasive DCIS : arise from, name of famous high-grade type, what may it show on mammography,
DCIS : arise from terminal duct, Comedo subtype, May show calcifications due to necrosis and cell debris
Invasic ductal cc of the breast : another name + origin for name, common/uncommon, consistency, histology
Schirrous cc due to abundunt fibrous stroma. Most common, associated with DCIS. Connsistency is very hard. Histology - dense stroma with nests of round cells with small/dark nuclei
Paget disease of the breas : arises from, age of onset, starts where and extends to where. Also, histology of cells
Arises from DCIS at a slightly older age than usual, starts from the terminal duct and grows into skin/areola.Pleomorphic nuclei, surrouned by a halo of MPS (either clusters or single)
Fibroadenoma of the breast : common/uncommon, develops due to, gross appearance, two histological types. Malignant potential.
Most common <35years, develops due to estrogen excess. Well-circumscribed, rubbery, with glandular areas. Two histological types - Pericanalicular (open spaces), Intracanaliuclar (star shaped spaceS). Almost never becomes malignant.
Phyllodes tumor (Breast) : malignancy, origin of name, size. Chance for distant metastatses upon malignancy
Benign with malignant potential. Looks like a leaf (cysts, clefts) in section, usually large, >4cm. Low chance (15%) of distant metastases even if becomes malignant
Intrductal cc of breast : histology. Outer layers of papillae
Mutiple papilla, surrouned by CT and covered by epithelium. Cover is double layered, outer layer is myoepithel
Two patterns of intraductal papilloma of breast
Central papilloma, solitary
--> benign
Peripheral papilloma, multiple, in several ducts
--> malignant
Sex cord tumors of the ovary : 3 types, freq. Also, describe Theca fibroma (cells, gross, hormones, malignancy)
Granulosa Theca, Theca-fibroma, Sertoli-leydig. 10% of all ovarian tumors.
Theca fibroma : Fibrous and Theca cells, grossly solid yellow, hormonally inactive, rarely malignant. causes HYDROTHORAX
Describe Granulosa theca-cell tumor (cells, gross, malignancy, hromones, special histology). Also describe Sertoli-leydig cell tumor (gross, histology, malignancy, hormonal)
Granulosa-theca tumor : Cuboidal granulosa cells + sheets of spindeled theca cells. grayish-yellow cystic mass, rarely malignant, feminization effect. Creates follicles called Call-Exner bodies.
Sertoli-leydig cells : small, solid brown. Histology - seminephrous tubules + pink sertoli cells, rarely malignant. Causes masculization and feminization (produces androgens)
Germ-cell tumors of the ovary : Arise from, 3 types, freq.
Arise from totipotent cells, 20% of all ovarian tumors, Types : Teratoma, Dysgerminoma, Choriocarcinoma
Teratoma : 3 subtypes, malignancy, age
Bening mature cystic teratoma, malignant immature teratoma, Struma ovarii (thyroid). Usually benign, however malignant if in early age. usually <20years
Dysgerminoma : female counterpart of, risk factor, histology, malignancy
Female counterpart of testicular seminoma. Sheets of large clear cells, with fibrous stroma + granulomas. Malignant, but not aggressive. Risk factor - Turner syndrome
Choriocarcinoma : malignancy, age, gross, cell types
Malignant, peak at 30years, small hemorrhagic focus, cytoytrophoblasts/syncytiotrophoblasts
Origin of follicle and luteal cysts ? Filled with ?
Ruptured or unruptured graafian follicle. Filled with serous fluid
Polycystic ovaries : another name, Produces what ? , histology, consequneces
Stein-Leventhal syndrome. PRoduces androgens and estrogens. Cysts are lined by granulosa cells with hypertrophic/hyperplastic theca interna. Consequences are oligomenorrhea, hirsutism, infertility
Tumors derived from coelomic epithelium : frequency, derived from, two types - two subtypes each
Most common ovarian tumor, 90%, derived from multipotential coverin (Coelomic epi). Types :
Epithelial tumors - serous, mucinous
Stroma tumors - cystadenofibroma, Brenner tumor
Tumors derived from coelomic epithelium - Serous tumors : Cystadenoma (gross, histology, speial). Cystadenocc (gross, histology)
Cystadenoma : large, upto 30cm, multiple cysts, papillary projections smooth&glistening, single layer of columnar ciliated cells. Special -psamomma bodies.
Cystadenocc -nodular surface, cavity contains a large bulky mass. Histology - multilayers, anaplasia
Tumors derived from coelomic epithelium - Mucinous:
Differences from serous tumors, 2 types
Differences : contain mucin, less papillaries, no psamomma bodies. Less malignant. Two types : intestinal - resembles colonic epi, Mullerian - endocervix like
Tumors derived from coelomic epithelium - Stromal :
Cystadenofibroma (variant of, malignancy)
Brenner (histology, gross)
Cystadenofibroma - variant of serosal cystadenoma, rarely malignant.
Brenner - stroma with nests of transitional epi. Gross - encapsulated, large
Tumors of endometrium and myometrium are ?
Endometrial polyps, endometrial cc, leiomyoma, leiomyosarcoma
Endometrial polyps (gross, coverage, neoplastic component, common when)
Sessile, round small lesions, projection into uterine cavity, covered by columnar cells. Neoplastic component is the stroma, they are common at menopause
Leiomyoma (another name, frequency, risk factors, gross, 3 types, malignancy)
"Fibroid", most common benign tumor of women, risk factors are estrogen exposure, genetic causes (blacks), grossly firm, white, multiple. 3 Types - intramural, submucosa, subserosal. Rarely transforms to malignant
Leiomyosarcoma (arises from, gross, name for borderline malignancy, criteria for dx)
Arises from mesenchymal cells of myometrium, NOT leiomyomas. Borderline malignancy - leiomyoblastoma. Criteria - cellular atypia, mitosis. Gross - solitary, bulky, polypoid lesion
Endometrial cc (frequency, , usually arises from, risk factors, clinical, stages)
most frequent tumor of women genital tract, Usually arises from endometrial hyperplasia. Risk factors is excess estrogen (in all its forms, nullipara, dm, anovulation, contraceptives..). Clinical : leucurrhea, uterine enlargment fixation. Stages - I - corpus, II - Cervix also, III - beyond uterus
Types of endometrial cc (give prognosis)
Adenocc - most freq.
Adenoachantoma - w/squamos metaplasia, good prog.
Adenosquamous cc - very malignant, bad prog.
Fallopian tube pathology (freq, causative agents, clinical signs, consequnces, cancer)
Rare organ for primary disease, Gonorrhea, chlamydia, Strep, Staph, Clinically fever, lower abd. pain. Consequences - ectopic preg, sterility. Cancer- Adenocc.
Tumors of the cervix - talk about ?
Endocervical polyp, CIN, Cervical cc
Endocervical polyp (Origin,surface epi, histology, complications)
Origin is probably inflammatory, surface epi is columnar. Cystically dilated spaces filled w/mucous. Complications - Superimposed inflammation and sq. metaplasia. Bleeding.
CIN (frequency, age grading, risk factors)
Freq. is increasing, risk factors are smoking, multiple preg, STDs, HPV 16/18. Grading is from CIN I (mild atypia) to CIN III (CIS). Peak at 30 years.
CIN : main features of CIN I/II/III
CIN I : mild dsyplasia, koilocytosis
cIN II : Moderate dysplasia affecting most layers, mitosis over basal layer
CIN III : severe dysplasia, CIS, mitosis in whole thickness. NO koilocytosis
Cervical cc (screening, precursor types, age, types)
Screening - pap smear,
Precursor - CIN, always
types - Fungating, ulcerating, infiltrative
Age - peak at 45
Special feature of cervical cc - Barrel cervix
Barrel cervix - the tumor encircles the pelvis penetrating the underlying stroma. Palpable.
Pathology of the vagina, what to mention
Congenital malformation, Vaginitis, Vaginal adenosis, Clear cell adenocc, SCC
Vaginal adenosis / Clear cell adenocc. What is the relation, what is the risk factor, what is the appearance of vaginal adenosis
Vaginal adenosis is the precursor of Clear cell adenocc. Risk factor is intra-uterine exposure to dielthylstrilbestrol. Vaginal adenosis - glandular or microcystic inclusions that appear red on the surface, lined by mucous columnar cells.
SCC of the vagina (risk factor, association)
HPV 16,18. Over 60 years old, associated with cervical cc.
Cervicitis (what is erosions, cause of acute specific, acute non=specific, chronic)
Erosions - exposed columnar epi in the exocervix zone.
Acute specific - gonorrhea, acute non-specific - strep, staph, chlamydia. Chronic- HSV2, HPV, Chlamydia
Appearance of cervicitis. Complication ?
Cervical epithelium shows hyperplasia and atypia (not dysplasia). Glycogen depletion. Leukorrhea with shedding epi cells. Complication - sterility by obstruction of external os
What are Vulvar dystrophies and what do you mention there ? what are the tumors of vulva ?
Valvular dystrophies - non-neoplastic epi disorders. Lichen Sclerosus, Lichen simplex chronicus. Tumors of vulva - Condyoloma, cc of vulva, Paget's disease of vulva, melanoma of vulva
Lichen sclerosus (gross, histology, pathogenesis)
Lichen simplex (gross, histology)
Lichen sclerosus - Atrophy of epi, superficial hyperkeratosis, dermal fibrosis, mac infil. White plaque, whole vulva, constricted orifice of labia. Pathogenesis probably autoimmune (T cells). Lichen simplex - hyperplasia of epi, hyperkeratosis, increased mitotic activity. leukocytes.
CC of vulva (types, most common relation, precursors, risk factors)
90% are SCC, most commonly HPV16 related, usually co-exist with cervical cc. Precursors are usually VINs. Risk factors are HPV and smoking. Note some cc have no relation to HPV but to lichens
CC of vulva (early morphology, late morphology, HPV relation)
Early - leukoplakia, epi thickening, pigmentation. Late - exophytic, endophytic=ulcerative
HPV + --> multifocal, poorly diff
HPV - --> Solitary, keratinizing, well dif.
CC of prostate (lethality,risk factors, localization in prostate, staging
2nd most deadly in males >50years. Risk factors - hormonal (increased estrogne, DHT), genetics, environmental. In peripheral zones. Staging - TNM, T1 non palpalbe, T2 - palpable, T3-local expansion
Prostate CC - morphology, histology
Adenocc. Poorly demarcated, pale, invasive, variable diff.
Well-dif : back-to-back small glands, invading thru CT stroma in haphazard fashion. No basal layer (no CK staining).
Prostate CC - grading, precursor lesion, metastases
PRecuros - PIN, foci of cellular atypia. Low grade to high grade.
Grading - Gleason 1-5
Metastases : Early- LN
Late - bones (mostly osteolytic), urinary bladder, recturm, lungs, liver
Testicular neoplasms (age, risk factors, types)
Young age, ~25, Risk factors - cryptorchism, testicular femimization, Kleinfelter. Types - Germ cell (95%), non-germ cell (leydig, sertoli, granulosa)
Testicular neoplasms - Germ cells (subtypes)
Germ cell - seminoma
Totipotent cells - embryonal cc. Embryonic tissues - Teratoma. Extraembryonic tissues - Yolk sac cc, Choriocarcinoma
Seminoma (gross, histology, markers). Embryonal cc (gross, histology, markers)
Seminoma - soft, large, well demarcated. Confined by tunica albuginea, not malignant. Small lobules seperated by septa. Lymph inf. Marker - hCG
Embryonal cc - rare, small, invasive, hemorrhage, necrosis. Large cells with large nuclei/nucleoli, basophilic. hCG+AFP
Yolk sac tumor (gross, histology, markers). Choriocarcinoma (gross, histology, markers)
Yolk sac - endodermal sinus tumor - most common in children. Large, well demarcated. Mimics yolk sac with cysts lined by epi. AFP.
Choriocarcinoma - well dif. extraembryonic lines, either cytoytrophoblast (small cuboidal) or syncytiotrophoblasts (large many nuclei)
What is special about yolk sac tumor ?
tumors has spaces lined by epi cells which look like glomeruli with capillaries inside --> Schiller-duval bodies
Leyding cell tumor (malignancy, hormonal effects). Sertoloy cell tumor (same), Granulosa cell tumor (same)
Leyding - mostly benign, androgens+estrogens -->gynicomastia
Sertoly - rare, either malignant/benign, estrogen --> feminization
Granulosa - young-benign, adults-malignant
Penis CC (settings, freq., gross, precursor)
Rare, in uncircumscribed 40years, HPV16/18, due to smegma irritation
Gray, crusty, papular lesion in glans or prepuce. Precursor - Bowen's CIS of the penis
Gallbladder cc (freq, survival, stones association, two forms)
5th most common in GI, in old women, 5 year survival 1% !. Gallstones present in 60-90% (not in asia). Exophytic or infiltrating (more common, thickening)
Causes of gallbladder cc, types (with markers)
Recurrent trauma or infection, gallstones. Most are Adenocc (CK7) (infiltrative or exophytic). Others are SCC (CK14) or carcinoids
Tumors of the liver, what do you mention ?
Most common are metastases from lung, breast, colon.
TLL's : FNH, Nodular regenerative hyperplasia, Peliosis hepatis, Cysts
Benign : Cavernous hemagniomas, Liver adenoma
Malignant : Hepatocellular cc
Fibrolamellar cc, Cholangiosarcoma, Hepatoblastoma, Angiosarcoma
FNH (gross, causes). Regenerative nodular hyperplasia (gross, causes)
FNH - 1 (!!) focus, large, center has stellate scar, well demarcated but poor capsule. Spontaneous. Regeneratve nodular HP - more than 1 focus (!!), small, no scar, usualy with portal HT and in transplants. Response to local vascular injury.
Type of cysts in liver
Simple - fluid filled, cuboidal epi
Polycystic - biliary epi, associated with ADPKD
Caroli's disease - bile duct hematomas - dilations under glissons' capsule
Benign hepatic neoplasms : Cavernous hemangiomas (freq, gross, histo). Liver adenoma (common in, gross, histo)
Cavernous hemangioma - most common benign lesion. Well circumscribed, large venous spaces lined by endothel with intervening stroma. Liver adenoma - Common in females taking oral contraceptives. Yellow-tan, well demarcated, subcapsular. Sheets/cords that resemble hepatocytes, NO portal tracts --> however arteries and veins distributed in the substance
Hepatocellular cc (epidemiology, pathology, 3 types)
HBV is major epidemilogical risk. If HBV is uncommon --> cirrhosis. Pathology - HBV, Hepatocarcinogens (aflatoxin), chronic liver disease and cirrhosis, hemochromatosis. 3 types - unifocal, multifocal, diffuse infiltrative
Hepatocellular cc (morphology, invasion, histo)
Soft. Little stroma.
Unifocal - massive tumor, hemorrhage, necrosis, bile stain. Multifocal - widely distributed nodules with varying sizes. Diffusely infiltrative - involves entire liver. Invasion of vascular channels either to portal vein or IVC. Histo - from well dif. cords/nests to poorly diff. large anaplastic cells.
Malignant neoplasms of liver - Fibrolamellar cc (prog, risk factors, gross, histo)
Very good prognosis, no association with cirrhosis. Single hard fibrous tumor. Well differentiated nests/cords with dense collagen septa
Cholangiocarcinoma (causes, arises in, morphology, metastases)
Causes - primary sclerosing cholangitis, exposure to throtrast. Arises in intra-hepatic bile ducts. Morph - well diff. adenocc with desmoplasia. Metastases to lung, vertebra, brain, LN
Carcinoind tumors of the GI - what do you talk about ?
definition, localization, gross, hormones-clinical, markers
Carcinoid tumors of GI (definition, localization, aggressivenes, gross)
Neoplasms of neuroendocrine cells, from epithelial stem cells. Found in gut, GI, liver. Least aggressive in the rectum/appendix (rarely metastasize). Grossly they are solid yellow-tan
Carcinoid tumors of GI (hormones, markers, clinical)
Secrete various hormones, amy be gastrinomas, somatostatinomas, or insulinomas. Markers are Chromogramin A, NSE, Synaptophysin. Clinical - Zollinger-Ellison, Cushing, Carcinoid syndrome(note - only when liver dysfunction is also present), etc. Very good survival rate.
Colorectal cc (definition, precursor lesion, 3 risk factors)
Malignant epithelial tumor of the colon/rectum, that has penetrated the muscularis mucosa (otherwise not malignant). Arise from Adenomas (adenomatous polyps). Risk factors - diet, NSAIDs, IBDs (UC,CD)
Colorectal cc (Localization, morphology, Statging systems used)
Mostly in sigmoid colon and rectum. However tumors of the MSI pathway more in the proximal colon. Morph - mostly appear singly, Proximal colon - polypoid fungating, Distal colon - annular encircling (napkin ring). Staging - old system (Duke's), today - TNM
Colorectal cc (subtypes, detection, clinical)
subtypes - mucinous adenocc, Signet ring cell, Adenosquamous. Detection - PR, occult blood loss, colonoscopy, marker - CEA (sensitive, non-specific). Clinical - Melena, bowel habits change, iron-def. anemia
Familial polyposis syndromes (hereditary pattern, what to mention)
AD, mention FAP, Gardner syndrome, Turcot syn., Peutz Jeghers polyp, Cowden syndrome
FAP (definition, gene, risk for cc, minimum for diagnosis)
Carpet of 500-2500 colonic adenomas covering the mucosal surface, mostly tubular. Risk for cc is 100%. Minimum for diagnosis is 100 adenomas. APC gene of Chr 5.
Familial polyposis syndromes - what are Gardner syndrome, Turcot syndrome
Gardner - same genetic defect as FAP but with osteomas and fibromatosis.
Turcot - same as FAP, but with colonic adenomas and Gliomas.
Adenoma-carcinoma sequences : what are 3 features of it, and what are the 2 pathways involved.
3 features : Adenomas show up before cc, Invasive cc is surrouned by adenomas, risk for cc is directly related to number of adenomas. 2 pathways - APC Beta cathenin, MSI (HNPCC)
What is the morphology and the molecular features of the APC beta Cathenin pathway of the adenoma-cc sequence ?
Morph - localized epithelial proliferations --> small adenomas --> enlarge --> become more dysplastic --> invasive cc. Molecular : Loss of APC --> K-RAS --> DCC --> TP53
MSI - HNPCC (DNA mismatch repair) pathway of the Adenoma-cc sequence (genes, consequence, special)
No morphological sequence, Genes - MSH2/6, MLH1, PMS1/2. MLH1 most common. Causes microsatellite instability in cell growth genes. Some hyperplastic polyps have been shown to have MSI !
Non-neoplastic polyps in the colon - what do you mention ?
Definition, Hyperplastic polyps, Juvenile polyps, Peutz-Jeghers, Inflammatory polyps
Definition of non-neoplastic polyps. What are hyperplastic polyps, what are juvenile polyps ?
Definition -found in many old people, are NOT precursors of colorectal cc. Hyperplastic polyps are the most common, mostly in rectosigmoid, lined by goblet/absorptive cells. Juvenile polyps occur in the rectum, and are hamartomatous proliferations of the lamina propria with dilated glands.
What are Peutz-jeghers polyps
Peutz Jeghers polyps are hamartomatous, have a central smooth muscle core with tree like branching. Also, melanocytic pigmentation of skin and increased risk for breast/lung cc.
Adenomas (intestine) : definition, arise from, precursor of, subtypes,
Neoplastic polyps with intraepithelial neoplasia. All arise from epithelial proliferation and dysplasia. Are precursors of colorectal cc. Subtypes - Tubular (most common), Villous (most dangerous), Tubulovillous, Serrated
Adenomas (intestine) : morphology (of tubular, of villous), Histology (of tubular, villous). Special about villous.
Morphology - Tubular : mostly in rectosigmoid, upto 2.5cm with a tubular gland shape, with a thin stalk. Histo - Tubular : stalk is covered with normal colonic mucosa but head shows neoplastic epi forming branching glands. Villous - Morphology : Larger, rectosigmoid, velvety projectings 1-3 above surface. Histo : leaf-like extensions covered by dysplastic columnar epi.
Special - villous adenomas harbor invasive cc in upto 40% of the cases.
Gastric polyps - what do you mention ? Which one can progress to cc ?
Hyperplastic polyps, fundic gland polyps, adenomatous polyps --> these show dysplasia and may progress to adenocc.
Salivary glands tumors (most affected, 2 benign types, 2 malignant types)
Mostly affected is the parotid, although submaxillary tumors are more dangerous. Benign - Pleomorphic adenoma, Warthin's tumor.
Malignant - Malignant Pleomorphic adenoma, Mucoepidermoid cc
Benign salivary gland tumors - Pleomorphic adenoma (Gross, histology, origin of cells, removal of tumor may damage)
Gross - Encapsulated, 6cm max. Histo - epithelial component, myxoid (Stroma) component. Epithelial shows glands, tubules etc, Myxoid shows stroma with mucoid and cartilage. Origin of all cells is Myoepithelial. Removal may damage CN7.
Salivary gland benign tumor - Warthin's tumor (another name, gross, histo)
Papillary Cystadenoma Lymphomatosum, gross - small well encapsulate round lesion in the parotid. Histo - mucin containing cysts or clefts + heavy reactive lymphocytic proliferation.
Malignant salivary glands tumor - Mucoepidermoid cc (components)
Has a SCC like component and also mucous producing lightly staind cells. Very malignant.
Precancerous lesions and cancers of the oral cavity - what do you mention ?
Squamous cell papilloma, Condyloma Accuminatum, Verrucae vulgaris, Focal epitheloid hyperplasia, Inflammatory papillary hyperplasia, Leukoplakia, Erythroplasia, SCC
Lesions of the oral cavity - Leukoplakia (malignancy, gross, localization, histo, risks)
It is a precancerous lesion, grossly white well defined plaque. Localized to the tongue, lower lip, vermillion border mostly. Histo - varies from simple hyperkeratosis to severe dysplasia bordering CIS. Risk factors are tobacco, HPV, alcohol, age
Lesions of oral cavity - erythroplasia/plakia (malignancy, gross, histo, transformation rate, color due to)
Precancerous lesion, red granular elevated plaque. Histo - epithelial dysplasia. Transformation rate is more than 50%, color is due to dilated vessels.
Oral cavity lesions - what are the benign tumors, and what is the difference between Squamous cell papilloma and Condyoloma accuminatum ?
Benign - Squamous cell papilloma, Condyoloma accuminatum, Inveretd papilloma, Verruca vulgaris, Focal epithelial hyperplasia. Difference between SC Papilloma and condyolma is that condyoloma shows Achantosis, Parakeratosis, and Koilocytosis while SC Pailooma shows only hyperkeratosis
What are the HPV strands mostly involved in benign oral cavity lesions ?
SC papilloma / Condyloma - HPV6,11
Verruca vulgaris - HPV2,4
Focal epithelial hyperplasia - HPV13,32
SCC of oral cavity (risk factors, subtypes, localization, morphology, special)
Risk factors - HPV11,16,18, tobacco, leukoplakia, erythroplasia, sunlight. Subtypes - Spindle cell (very aggressive), Baseloid form, Verrucous. Localization - mostly lower lip, floor of mouth. Morphology - forms keratin pearls --> exopyhtic --> endophytic/ulcer
CC of larynx (age, risk factors, subtypes)
Occurs after 40years, risk factors are smoking, alcohol, asbestos. Subtypes are SCC (95%) and Adenocc
CC of larynx (localization)
Glotic - on vocal cords - early detection, good prog
Supraglottic - above the cords, rich in lymphatics, may metastasize quickly. Subglottic - may remain clinically silent for long periods and therefore dangerous.
CC of larynx (gross, histo, symptoms)
Gross - begins as a small CIS with gray plaques on mucosa and advances into an ulcerating lesion. Histo - anaplasia, giant cells. Symptoms - hoarseness, pain, dysphagia, hemoptysis
Nasopharyngeal cc (epidemiology, pathology, variants)
Rare, high frequency in Chinese. Viral - EBV related. EBV found in all nasopharyngeal cc. It replicates in epithelium and then infects tonsiallar lymphocytes. Variants - Keratinzing SCC, Nonkeratinizng SCC, Undifferentiated cc (most common)
Nasopharyngeal cc - what is a special feature ? Also what is the histology of the tumor ?
Lymphoepithelioma --> influx of mature (non neoplastic) lymphocytes due to EBV. Histo - large epi cells with syncitial growth, and prominent eosinophilic nuclei.
Malignant mesothelioma (difference from benign, freq, risk factors, markers)
Difference from benign - benign tumors are solitary, single nodules and do not ensheeth the lung as malignant ones do. This is a rare tumor, risk factors are moslty amphibole asbestos. Markers are CD34 (endothelial markers, from fibroblasts), CK+, Vimentin+, E-Cadherin+
Malignant mesotheliooma (relation to asbestos, smoking, morphology and precursor lesions)
Amphibole asbestos is direct cause - long, 30 years of exposure are needed. Smoking has no effect. Morphology - preceeded by pleural fibrosis and pleural plaqus and finally evolve into pleural ensheething of the lung by a yellowish gelationous layer that obliterates the pleural space.
Malignant mesothelioma (histology, patterns)
Histo - mesothelial cells are biphasic and give both the lining cells and fibrous tissue. So 3 patterns : Epithelial (cuboidal), sarcomatoid (spindle), biphasic
Morphology of the bronchial cc - which ones should you mention ?
SCC, Adenocc, Bronchioalveolar cc, Large cell cc, Small cell cc, Combined
Morphology of bronchial cc - SCC (Risk factor, Differentiation levels, arise in, symptoms when, metastases early/late, growth patterns, Paraneoplastic)
Risk factor - Smoking. Differentiation levels - Well diff. - CK14, Moderately - CK14 + CK7 (ADENO!), Poorly - CK7 (ADENO). Arise in a major bronchus. Symptoms when obstrucs a broncus, Metastasizes later than others, Growth patterns - exophytic, sessile, polypoid. Paraneoplastic- PTHrP
Morphology of bronchial cc - Adenocc (Age, Marker, localization, Association with smoking, metastasize early/late, Precursors, special morphology)
Under 40years, CK7, Localized to the periphery, LEAST associated with smoking, metastasizes early. Precursors : Atypical Adenomatous Hyperplasia AHH --> Bronchoalveolar cc --> Adenocc (just like CIS --> Adenoma --> Carcinoma). Special morphology - shows scars, probably due to desmoplasia
Bronchoalveolar cc (precursor of, localization, structure, invasivness, growth pattern)
Precursor of Adenocc, Localized to periphery, preserved alveolar architecture, non-invasive, Lepidic growth pattern
Small cell cc of the lung (another name, origin, cell size, morphology, markers, metastasize early/late, response to chemo, cell shape). Also - give prognosis for Large cell cc of the lung
"Oat cell" cancer, origin is from neuroendocrine cells of the lung. Morphology - gray central mass with extension into parenchyma and LN. Markers - NSE, Synaptophysin, Chromogramin. Metastasizes the earliest, but responsds well to chemo.Cells are either spindle or fusiform. Large cell cc - Bad prognosis, eary metastases.
Bronchogenic cc (etiology, pathogenesis)
Bronchogenic cc is a general term - 90% are cc, 5% carcinoids. Main killer cancer. Pathogenesis - Cigarettes, asbestos (combined risk x50), hyper active p450 system. Pathogenesis : Smoking --> epi changes and cilia destruction --> sqamous metaplasia --> dysplasia --> CIS --> cc
Bronchogenic cc (genetics, subtypes, extrabronchial involvement)
Oncogenes involved - myc, RAS, EDGFR. TSG involved are p53 and RB. Subtypes - SCC, Adenocc, SCLC, LCLC, mixed. Extrabronchial - pleural effusions, SVC syndrome, Pancoast syndrome, metastases to brain/bone/liver/adrenals, Paraneoplastic syndromes
Bronchogenic cc (most common types, clinical categories with main differences (markers, cell type, chemo response). Lastly - PN syndromes of SCLCs
There's a shift from SCC to Adeno --> from central location to peripheral. Clinical categories are SCLS and Non-SCLC. SCLC cells have no nucleoli, and scant cytoplasm, while NSCLCs have nucleoli and abundant cytoplasm. SCLSs arE NSE+, Chromgramin+. SCLCs respond to chemo, NSCLS dont. PN of SCLCs --> Cushing, SIADH
Renal cc (derived from, localization, gross, special growth, subtypes)
Derived from tubular epi, localized to the cortex. Gross - Yellow-gray firm mass. May be hemorrhagic, necrotic. Special growth into renal vein and IVC. Subtypes - Clear cell cc, Papillary cc, Chromophobe
Renal cell cc - Clear cell variant (freq, gross, genetics, histology)
Most common renal cell cc. Grossly large, yellow lesion with cystic softening. Genetics - Associated with VHL, chr. 3 defects (also with hemangioblastomas in cerebellum and retina). Histo - Cells with lipids and glycogen, thus look clear. May grow in cords, little stroma.
Renal cell cc - Papillary cc (unilateral/bilateral, genetics, gross, histo)
Bilateral, associated with 7+ (or 16, 17 MET tK). Multiple hemorrhagic and cystc lesions, less lipid content than clear cell cc. Histo - papillary formation with fibrovascular cores.
Chromophobe renal cell cc (arises from, genetics, gross, prognosis, cells contains...)
Arises from cortical collecting ducts, multiple losses of chromosomes. Best prognosis. Cells contain many mitochondria and stain darker.
Urinary tract tumors - what do you mention
Most common are bladder transitional cell cc. Proliferative lesions - Cystitis Cystica, metplastic lesions, benign - transitional cell papilloma, Malignant - transitional cell cc. SCC of the trigone.
Urinary tract tumors : what is cystitis cystica, Transitional cell cc (freq, histo grading, malignancy criteria)
Cystitis cystica - Nests of transitional epi (Brunn nests) grow into the lamina propria and undergo transformation to cystic spaces - interstitial metaplasia. Transitional cell cc - Very common, proliferation of transitional cells. G1 - normal layering, G2 - Irregular layering, G3 - no layering. Malignancy is when there are at least 7 layers of cells.
Urinary tract tumors - SCC (morphology, arises from, aggressiveness, freq)
Causes extreme wall thickening, usually arises from the trigone. Much more aggresive. Rare.
Thyroid tumors in general (when are they more likely to be malignant ?)
Solitary, cold nodules, young patients, males --> all higher tendency towards malignancy
Thyroid adenomas (morphology, pathogenesis)
Morphology - solitary, enacpsulated, well-damarcated with a fibrous capsule. May be accompanied by hemorrhages, fibrosis. Patho - somatic mutations in TSH-r signaling
Thyroid adenomas (histology, variants, difference from cc, functionality, progression to cc)
Histo - Close nests and trabecules to well developed follicles with colloid. Variants - hurtle cell adenoma. Difference from cc is that adenomas do not invade capsule and do not penetrate veins. They are rarely functional ("cold"). Rarely progress to cc.
Follicular tyhroid cc (risk factors, morphology, histo)
Risk factors - Increased prevalance in areas of dietary I def. (so goiter may predispose). Morphology - ranges from well demaracated to invasive. Histo - most have microfollicular patterns with colloid, no nuclear features of papillary cc, some have hurtle cells.
Cc of thyroid in general (freq, types, pathogenesis)
Uncommon, mainly in adults. Tyes - papillary, follicular, medullary, anaplastic. Pathogenesis - Ionizing radiation, nodular goiter and Hashimoto, RET protoncogene (MEN2), P53,
Papillary cc of thyroid (freq, gross, histo, functional)
Most common thyroid cc, in women. Varies from infiltrative to well-circumscribed, may show calcfication and fibrosis. Histo - 1. Empyti nucle ("Orphan annie eyes") with nuclear grooves. 2. Eosinophilic inclusions. 3. Psammoma bodies (calcifications). Non-functional
Medullary cc of the thyroid (origin, genetics, gross, histo, effects on calcium)
Origin - neuroendocrine C cells of the thyroid (calcitonin). Genetics : solitary- RET protooncogene, Familial - MEN IIa/b. Gross - solitary if sporadic, multiple if familial. May contain hemorrhagic/necrotic areas. Histo - spindle cells, forming nests or follicles. Amyloid deposits from calcitonin may be present. NO hypocalcemia though.
Anaplastic cc of thyroid (gross, predisposition, histo-variants, prognosis)
Gross - bulky mass that grows rapidly beyond the capsule. Predisposition is an endemic goiter. Histo - highly anaplastic cells with these patterns : 1. Large pleomorphic giant cells, 2. Spindle cells, 3. Small anaplastic cells. Very bad prognosis, do not respond to therapy, death in 1 year.
Pheochromocytoma (origin,may arise where, genetics)
Origin is chromaffin cells, may arise in the adrenal medulla (85%) or in the extraadrenal para-ganglion system (Paragangliomas). Genetics- Associated with MENIIa/b, NF1, VHL
Pheochromocytoma (gross, histo, clinical, diagnostics, criteria for malignancy)
Gross - Large, gray/brown, can be with hemorrhages, necrosis, cysts. Histo - polyogonal spindle cells in small nests (Zellballen). Clinical - HT, tachychardia, sweating, tremors. Diagnositcs - Zanker stain for oxidation of NE, VMA/Metanephrins in urine. Only criteria for malignancy is metastasis. Benign ones also invade bv
Neuroblastoma (definition, occurs in, genetics, common locations)
Neoplasm of sympathetic nervous system neurons. Occurs in young kids (MOST common solid tissue tumor of kids). Genetics - Chr1, increase in myc. Most common locations are the adrenal medulla and the retroperitoneal sympathetic ganglions
Neuroblastoma (gross, histo, clinical)
Gross - ranges from microscopic lesions to large abdomen filling tumors, with areas of hemmorhage, necrosis, calcifications. Histo - poorly diff. neural crest cells in rosette formations. Clinical - Hepatomegaly, ascites, bone pain. NO hypertension.
Fibrous dysplasia of bone (Definition, types, genetics, gross)
TLL, bone trabecule is replaced by fibrous tissue & islands of malformed bone. Types - Monostotic, polystotic, polystotic +endocrine. Genetics- FOS protooncogene. Gross - circumscribed bone lesions surrounded by a rim of sclerotic bone.
Fibrous dysplasia of bone (histo, Monostotic type, Polystotic type)
Histo - proliferation of fibroblasts and collagen, surrounding islands of woven bone. Monostotic - most common, single bone, stops when growth stops, ribs, femur, tibia, jaw. Polystotic - multiple bones, persists in adulthood, mostly craniofacial
Fibrous dysplasia of bone - Polystotic + endocrine type (gross, histo, Albright syndrome)
Mostly females, gross & histo same as monostotic. Albright - Associated with NF1 --> unilateral bone lesions + unilateral cafe-au-lait spots (same side) + precocious puberty
Bone forming tumors - common ?, Osteoma (definition, locations, gross, histo)
Bone forming tumors are LESS common than metastatic lesions. Osteoma - benign outgrowth of membranous bones -- may be reactive. Mostly in skull/face. Gross - solitary, hard exophytic lesions. Histo - may be "ivory" - made of mature bone with no haversian canals or fibrous CT. "Trabecular" - made of trabecular bone with marrow
Bone forming tumors - osteoid osteoma (locations, gross, histo, clinical)
<2 cm. Location - proximal femur, tibia (esp in diaphysis or metaphysis). Gross - Brownish red lesion. Histo - Combination of osteoid and woven bone surrouned by osteoblasts and sclerotic bone. Clinical - dull pain at night, sweating.
Osteoblastoma - locations, gross ,histo
>2 cm. Locations- mostly vertebrae, gross - red-brown with hemorrhages. Histo is like osteoid osteoma.
Osteosarcoma : types, conventional osteosarcoma (locations, freq, histo)
Types : Conventional, Telangiectactic, Low grade, Small cell, Surface (Parosteal, Periosteal). Conventional osteosarcoma - Mainly distal femur or prox tibia. 2nd most common malignant bone tumor, histo - high grade, islands of primitive trabecule rimmed by malignant osteoblasts. Spindle shaped cells. (may be osteoblastic, chondroblastic, or fibroblastic)
Osteosarcoma - surface variants
Parosteal - metaphysis of long bones, low grade, encircles the bone. Periosteal - diaphysis, large cartilage component -- looks like chondroblastic osteosarcoma
Osteochondroma (freq, clinical, genetics, gross)
Most common skeletal neoplasm. Mostly kids. Either sporadic or as part of "multiple hereditary exostoses". Stops growing when growth stops. Gross - irregular bony mass with a hyaline cartilage cap. >2cm malignancy.
Chondroma (Gross, Maffuci syn.)
Gross - bluish gray mature hyaline cartilage within medullary cavity of bones. Maffuci syn- Multiple chondromas + angiomas
Chondrosarcoma (definition, localization, gross, histo, variants)
Definition - Malignant tumor producing cartilage matrix. Most common in pelvis,ribs. Gross - grayish lobulated, glistening, erodes the cortex. Histo - High grade, low grade. Variants - Mesenchymal, Clear cell, Dedifferentiated
Giant cell tumor of bone (2nd name, freq, localization, malignancy)
Osteoclastoma, very common, mainy in the long bones epiphysis. Benign, can progress to malignancy.
Giant cell tumor of bone (gross, histo, clinical)
Gross - brown, firm, with necrosis and cysts. Histo - 2 cell populations - multinucleated giant cells (like osteoclasts), mononuclear - neoplastic component. Clinical - local pain in joints
Ewing sarcoma (definition, freq, localization, genetics)
Malignant, primitve neoplasm of bones and soft tissue. Very common in children. Genetics - Associated with t(11;22) PNET.
Ewing sarcoma (gross, histo, clinical, markers)
Gross - gray-white, poorly demarcated, soft with necrosis and hemorrhage. Histo - Pseudorosettes of small blue cells (onion skin pattern). Clinical - pain, swelling, eryhthema --> may be mistaken for osteomyelitis. Markers - PAS+, CD99+
Astrocytomas (freq, gross, subtypes)
Most common primary CNS tumor. from circumscribed to highly-malignant. It's a glioma. subtypes : fibrillary (well-diff, anaplastic, glioblastoma multiforme), Pilocytic
Fibrillary astrocytomas : general, main features of each type
Infiltrating diffuse tumor, mostly in the hemispheres.
Well-diff astrocytoma : poorly demarcated, gray-white border, microcysts. Anaplastic - same + abnormal blood vessels (contrast enhancing). Gliobasltoma multiforme - Aggressive, infiltrating, hemorrhage. Causes shift of brain to other side.
Pilocytic astrocytoma : gross, prog, histo
In cerebellum, well-defined, cystic. Histo - astrocytes have elongated processes, eosinophilic fibers- Rosenthal fibers. Better prognosis.
Oligodendrogliomas : location, gross, histo, genetics
Mostly cerebral hemispheres, soft, better-circumscribed than astrocytomas. Histo - cells cluster around neurons (Satellitosis), anaplastic, mitotic. Genetics - loss of heterozygosity in chr 19, 1
Ependymoma (location, gross)
Mostly in ventricles, central canal of spinal cord. Adults = spinal, young = ventricles. Gross = well-circumscribed lesion on ventricular wall, projecting into.
Ependymoma (histo, clinical)
histo - radiating processes around bv (pseudorosettes) or surrounding the lumen (rosettes). Clinical - obstruction of CSF flow --> hydrocephalus, IICP
PNET (definition, groups, types)
Neoplasms composed of primitive embryonal small BLUE cells, varying from undiff to neuronal, glial or mesenchymal diff. Groups = CNS PNET, Non-CNS PNET. Types --> CNS PNET - medulloblastoma, Neuroblastoma, pineoblastoma, ependymoblastoma. Non-CNS : Ewing sarcoma
PNET --> Medulloblastoma (localization, gross, histo)
In cerebellum, obliterates cerebellar vermis/hemispheres and projects into ventricles. Histo - small blue cells, Homer-wright rosettes
PNET --> Neuroblastoma (localization, histo, special)
Usually in adrenal medulla (origin is CNS though). Histo- Homer-wright rosettes. Special - if mature cells present --> Ganglioneuroma
Meningeal neoplasms (what do you mention ?).
Meningiomas, meningioblastomas, Hemangiopericytomas, Meningeal sarcoma
Meningiomas (definition, genetics, gross)
Tumors of meningothelial cells lining the arachnoid. Usually outside brain parenchyma. Genetics - Progesterone R usually present, also NF2 or other Merlin (chr 22) mutations. Gross - Firm lobulated lesion, attached to dura mater and pushing brain parenchyma
Meningiomas (histo and variants)
Syncytial - tight clusters. Fibroblastic - collagen deposition. Transitional - mixed, Psamomatous - psammoma bodies.
Metastatic neoplasms of brain (age, most common origins, gross)
Mainly elders, mainly from Lung, breast, melanoma. Gross - usually well-demarcated, multiple spherical. Surrounded by edema. May also metastasize to leptomeninges.
What is sinus histiocytosis ? when does it occur ?
Chronic lymphadenitis with distension of sinusoids due to HT of endothelial cells + infiltration with histiocytes. Usually occur due to cancer, in LN draining tumor products
What is dermatopatchi lymphadenopathy ? What does the skin show ?
Widespread lymphadenopathy due to skin disorders. Shows exfoliative skin lesions and histiocytes may contain melanin
Langerhans cell histiocytosis (second name, general info, markers, special histo, subtypes)
Histiocytosis X. Clonal proliferation of Langerhans cells. Markers : CD1+. Histo - Birbeck granules (HX bodies) with a tennis racket appearance in EM. Also shows reactive infilatration of PC, Mac's, Eos'. Subtypes - Unifocal, Multifocal, Acute disseminated
Langerhans cell histiocytosis - Unifocal (second name, general info
EOSINOPHILIC GRANULOMA. Erosive accumulation of langerhans cells in skeletal system. May cause fractures.
Langerhans cell histiocytosis - Multifocal (second name, general info, triad)
Hand-Schiller-Christian. In children, fever, diffuse, may involve posterior pituitary to produce the triad : Diabetes insipidus + bone defects + exophthalmus
Langerhans cell histiocytosis - Acute disseminated type (Second name, age, general info, clinical)
Letterer-Siwe. <2 years. Aggressive, systemic, langerhans cells invade skin, spleen, liver, lung, bm. Anemia + destructive bone lesions
Lymphoblastic lymphomas and leukemias - what do you mention ?
Lymphoblastic lymphoma, ALL (B-ALL --> Early Precursor B-ALL, Pre-B ALL Mature B-ALL. T-ALL)
Lymphoblastic lymphoma (grade, markers, morphology, resembles what ?)
High grade, TdT, CD3, CD7, Acid-phosphatase. Large size, large nucleus. Resembles T-ALL.
ALL (grade, genetics, T/B?, Age)
High-grade, may show Ph chr (9;22) or (8;14). 80% B-cell origin, Affects children 2-10y.
B-ALL : Differences between different stages
Early precursor - small lymphocytes, Some CD19+, some CD19/10+, TdT+. Pre-B : Larger, TdT+, CD19/10+, Cytoplasmic Miu chains. Mature-B : Large cells, Poor prognosis, Surface Ig, TdT-, CD19/10+ (such as Burkitt lymphoma)
Follicle center cell lymphomas (what do you mention ?)
Burkitt lymphoma, Centro-blastic lymphoma, CB-CC, Centrocytic lymphoma
Burkitt lymphoma (grade, cells, markers, genetics, two forms, special)
High grade, Cells are between lymphoblasts and centroblasts. IgM+, CD19/10+. t(8;14) myc to Heavy chain. Endemic (EBV), Non-endemic. Special -starry sky pattern.
Centroblastic lymphoma (cells, markers, prog). Centrocytic lymphoma (cells)
Centroblastic - Centroblasts mixed with immunoblasts. Ig-, CD10+. Fatal. Centrocytic lypmhoma - Centrocytes or mantle zone B cells.
CB-CC lymphoma (genetics, special (3 things)
t(14;18) Bcl-2 to heavy chain. Special - only lymphoma with IgG=IgM, Light chain restriction, no immunocomplexes on FDC's.
Perifollicular B-cell zones and their leukemias and lymphomas - what do you mention ?
Perifollicular cells, Mantle zone : CLL, SLL, IDL/MZL (both are Centrocytic lymphoma types). Marginal zone : MBCL, HCL
Perifollicular lymphomas/leukemias --> CLL/SLL (derive from, zone, markers, special component, age)
Derive from recirculating B-cells that home back to Mantle zone. IgM/IgD/CD5+. Prolymphocytic component --> medium size cells with leptochromatic nucleus. Usually old age.
Perifollicular lymphomas/leukemias --> IDL/MZL (zone, equivalent to, markers, lack what, age, which one is low, grades)
Mantle zone, Equivalent to Centrocytic lymphoma, IgD/IgM/CD5+, lack a Prolymphocytic component, usually middle/old age. IDL - intermediate grade, MZL - low grade
Perifollicular lymphomas/leukemias --> MBCL (zone, markers, grade, common features with ?)
Marginal zone, IgD/CD5-, CD11c+ (!!), Low grade - bad, common features with Low-grade MALT lymphoma
Perifollicular lymphomas/leukemias --> HCL (zone, similar to, marker)
Marignal zone, TRAP+, Similar to MBCL
Plasma cell reaction, plasmacytoid, plasmacytic neoplasms - which cancers do you mention ?
Immunocytoma (IC), Polymorphic Immunocytoma (PIC), B-cell immunoblastic lymphoma (B-IB), MM, Extramedullary Plasmacytomas, Solitary skeletal myelomas
Immunocytoma (cells, markers, infiltration of ?). Polymorphic Immunocytoma ?
Surface Ig+ B cells + Cytoplasmic Ig+ Lymphoplasmacytoid cells, Markers : Some CD5+, some negative. Infiltrate spleen, BM. PIC --> Plasmacytoids + various centroblasts/cytes/immunoblasts/PCs
B-cell immunoblastic lymphoma (two types, special)
Types : Follicle-center cell reaction (nodular, with centroblasts), Plasma-cell reaction. Special is B-IB transformation from B-CLL called Richetr's syndrome
Extramedullary Plasmacytomas (EMP) (where ? disseminate ?)
Local proliferations in the upper resp. tract. Rarely disseminate.
Peripheral T-cell lymphomas - what do you mention ? what is the mnemonic ?
Lymphoepitheloid lymphoma (Lennert's), Angioimmunoblastic Lymphadenopathy-like T lymphoma, T-zone lymphoma, Pleomorphic T-cell lymphoma, Large-cell anaplastic lymphoma. Mnemonic : Laughing And Talking Pleases Ladies
Peripheral T-cell lymphomas (grade, what does it mean 'peripheral'), also Lymphoepitheloid Lymphoma (general, resemblence to what ?)
Peripheral T-cell lymphomas : Similarties with Hodgkin, High-grade, . Peripheral means outside the thymus.
Lennert's lymphoma : Epitheloid cells and some blasts. Resembles Lymphocyte Predominant hodgkin but no RS cells.
Angioimmunoblastic Lymphadenopathy-like T lymphoma (cells, resemblance to what, Special feature, special marker)
Small/medium/large immunoblastic cells. Resembles Mixed Cellularity Hodgkin. Special - prolferation of HEVs and Reticular Dendritic cells without GCs. These dendritic cells are CD23+ (!!!)
T-zone lymphoma (say something...)
T-cell areas of lymph nodes, follicular hyperplasis of CD4 Th cells
Large cell anaplastic lymphoma (special cells, resembles two things, where is it found, marker)
Has giant cells, therefore resembles Lymphocyte depletion Hodgkin. Also resembles malignant histiocytosis. Found within sinuses of lymph nodes, Marker : CD30+ (Activation !)
Lymphomas of GI tract (which ones ?)
Low-grade B-cell MALT lymphoma, Lymphomatous Polyposis of GI tract.
Low-grade B-cell MALT lymphoma (similar to what, cells from which zone in the follicular center, what lesions are formed, prognosis, dissemination)
Similar to Peyer patches. Marginal zone cells. Forms lymphoepitheloid lesions in the mucosa. Prognosis is good (even though this is LOW grade !!) as these tumors remain localized and respond well to therapy. Are not tumorigenic if disseminate.
Lymphomatous Polyposis of GI (cells, zone, presentation)
Centrocytes of Mantle zone. Usually present as a systemic malignancy.
Cutaneous lymphomas (general, which lymphomas do you mention, what is the mnemonic)
Arise from SALT, May remain local for years, 80% are T(!) cells. Mention Mycosis Fungoides, Sezary syndrome, Large cell Anaplastic lymphoma, Primary cutaneous B-cell lymphoma, Monoblastic lymphoma (histiocytic). Mnemonic : My Sex Life Pleases Me
Mycosis fungoides (definition, cells, infiltration, phases)
SLL with epidermotropism. Peripheral CD4 cells. Infiltrate epidermis. Mycosis cells --> immunoblasts. Phases : Pre-mycotic --> Plaque --> Tumor --> dissemination
Sezary syndrome (defintion, special)
SLL with epidermotropism, erythroderma with sezary cells (found also in plaque/tumor of Mycosis fungoides)
Primary cutaneous B-cell lymphoma (freq, two types, markers, localization)
Uncommon, Follicular and Lymphoplasmocytic types, Markers are usual B-cell markers. Found on skin of back and scalp (!)
Monoblastic lymphoma (histiocytic) --> freq, manifestation, prog
Rare, skin tumor with systemic manifestation and leukemia. Poor prognosis
Lymphomas of respiratory tract and mediastinum (what do you mention, mnemonic)
Low-grade B-cell lymphoma of MALT origin, Angiocentric T-cell lymphoma, Lethal midline granuloma, Lymphomatoid granulomatosis, Mediastinal Large Cell Lymphoma with Sclerosis. Mnemonic : Lev And Liron Love Maria
Angiocentric T-cell lymphoma (3 features)
1.Mostly resp tract, but may be systemic.
2. Vasculitis of CNS/Skin
3. Infarctive necrosis of involved tissue
Lethal midline granuloma (second name, grade, 2 features)
Granuloma Gangrenescene. Low-grade variant of Angiocentric T-cell lymphoma. Features : to sinonasal region. 2. Pleomorphic T-cell lymphoma with angiocentric growth
Lymphomatoid Granulomatosis (second name, 3 features)
Leibow's disease. Features : 1.Angiocentricity. 2. Affects lower resp tract and CNS/Skin. 3. Requires intense chemotherapy
Mediastinal large cell lymphoma with sclerosis (4 features)
1. B-cell lymphoma affecting anterior mediastinum and SVC.
2. Young females.
3. Sclerosis compartmantalizes cells
4. Aggressive
Differences of Hodgkin's from NHL (4)
1. Presence of RS cells
2. Localized to single axial group of LN
3. No waldeyer ring involvement
4. CD15/CD30+
Morphology of RS cells, Morphology of Hodgkin cells :
RS cells - Origin is B cells, Secrete IL-5, Large 15-45mM, Binucleated or multinucleated. Owl-eye appearence of nuclei.
Hodgkin cells : Mononuclear cells with vesicular nucleus
What are the morphological subtypes of Hodgkin's ?
Lymphocyte predominance, Mixed cellularity, Lymphocyte depletion, Nodular sclerosis
Hodgkin's disease - Lymphocyte predominance (freq, RS cells, Special, prognosis)
Uncommon - 4%, RS cells almost absent(therefore also few eos, neut, PC), Popcorn cells present. Excellent prognosis
Hodgkin's Disease - Mixed Cellularity (freq, RS cells, cellualr infiltrate, prognosis)
25% - most common >50. Many RS cells -- therefore heterogenous infiltrate, good prognosis
Hodgkin's - Lymphocyte depletion (freq, age, two forms, prognosis)
Least common, 1%. Older patients. Diffuse fibrosis (hypocellular) or Reticular Variant (vvery cellular, few typical RS cells though). Aggressive, bad prognosis
Nodular sclerosis (freq, sex, two special features, prognosis)
Most common, 70%. Women. Special : 1.Lacunar cells (hyperlobulated, same as RS cells but no B/T specific antigens) 2. Collagen bands.
Excellent prognosis