Oncology CE 2.0 Past Paper PDF

Charlotte Eikaas 2023/24 ESOPHAGEAL CANCER EPIDEMIOLOGY DIAGNOSIS Rare- 1% of all cancers: western world = AC; whole Gastroscopy with biopsy world = SCC...

Charlotte Eikaas 2023/24 ESOPHAGEAL CANCER EPIDEMIOLOGY DIAGNOSIS Rare- 1% of all cancers: western world = AC; whole Gastroscopy with biopsy world = SCC EUS- endoscopic USG M >F CT AA: 45+ for SCC, 70 for AC Liver parameters DISTINGUISING SUBTYPES TREATMENT: Squamous cell carcinoma: Surgery = usually best option; +/- pre-op RT/chemo Risk factors: alcohol + smoking (MC), low socioeconomic Inoperable → radical chemoradiotherapy standard, poor diet, hot beverages, nitrosamines in diet, Intracavital brachytherapy irradiation, HPV, achalasia, Plummer-Vinson syndrome, Metastatic → symptomatic treatment chemical injury Location: usually in middle third PROGRESSION & PROGNOSIS Adenocarcinoma: also processed meat. No Poor prognostic factors: tumor >5cm, weight loss >10%, Risk factors: Barrett’s esophagus ( GERD), obesity, tobacco, esophageal obstruction, high grade tumor radiation; protective factors = healthy diet, H.Pylori Metastasis: lymphatic spread to lungs, liver or adrenal Location: usually in distal third glands Generally not great prognosis PRESENTATION Dysphagia Odynophagia Weight loss: if >10% = poor prognostic factor Vomiting Cough Hoarseness- recurrent laryngeal n. paralysis Dyspnea 15  Charlotte Eikaas 2023/24 COLON CANCER EPIDEMIOLOGY DIAGNOSIS: based on colonoscopy with biopsy 3rd MC cancer- most common cancer of GIT After biopsy results: CT abdomen + chest- search for Responsible for 10% of cancer deaths- 3rd MC metastasis Peak incidence 60-70 y/old; M=F Molecular testing: KRAS, NRAS, BRAF, MSI, HER2, FAP; if positive for Lynch/FAP → checkup on family members RISK FACTORS & ETIOLOGY Staging: DUKES, ASTLER-COLLER or AJCC/TNM Genetic: only 5% of cases; FAP, Lynch syndrome, juvenile polyposis, Peutz-Jeghers TREATMENT- SURGERY +/- other options IBD- UC (>) Crohn’s Stage I + II: resection is the best option Poor diet- refined carbs, no fiber, rich in fat Stage III: surgery +/- post-op chemo Blood group O = higher risk Stage IV: chemo + surgery- removing tumor + mets Chemo (FOLFOX) + Panitumumab (anti-EGFR) if positive SUBTYPES for KRAS/BRAF mutation; note severe skin toxicity- Vast majority are adenocarcinomas without inherited actually good predictive sign genetic mutations; most develop from adenomas- NO RADIOTHERAPY higher risk if large, dysplastic/metaplastic, sessile or flat, villous architecture, multiple polyps PROGRESSION & PROGNOSIS FAP- familial adenomatous polyposis (AD; APC mutation): results in extreme polyp formation in 20-25% are diagnosed at metastatic stage- MC = liver adolescence; 100% risk of colon cancer at 55 y/old- Prognostic factors: grade + lymphatic invasion + >4 lymph colon must be surgically removed. ↑risk of many nodes involved + presurgical CEA >5 other cancers- gastric, thyroid, hepatoblastoma 50% of patients after surgery will relapse; 80% of relapses HNPCC/ Lynch syndrome (AD, MSI); also high risk of within 3y after surgery other malignancies- endometrial, gastric, ovarian, renal and intestinal cancer; NOT sensitive to 5-FU; OTHERWISE NOTEWORTHY right-sided cancer MC Screening: annual DRE from 40; fecal occult blood test from 50; if positive → colonoscopy; if higher risk patients PRESENTATION → colonoscopy every 10y from 50; reduce risk by 30% CEA: marker for several cancers, also colon cancer; cannot Iron deficiency anemia + blood in stool- tumor bleed be used for screening, but good for monitoring treatment Altered bowel habits- diarrhea, constipation Locations of cancer within large intestine: left colon + Hematochezia sigmoid (36%) > right colon + cecum (27%) > rectum > Abdominal pain transverse colon > anus > other Ileus- risk of obstruction Suggesting right-sided cancer: anemia Suggesting left-sided cancer: obstruction, pencil-shaped stool 16  Charlotte Eikaas 2023/24 RECTAL CANCER EPIDEMIOLOGY DIAGNOSIS Less prevalent than colon cancer Colonoscopy with biopsy 16% of colorectal cancers CT/MRI to assess for metastasis RISK FACTORS & ETIOLOGY: essentially the same as colon TREATMENT: cancer Stage I + II → surgery- TME- total mesorectal excision Stage III → pre-op RT + surgery +/- post-op chemo SUBTYPES: Stage IV → surgery + chemo/RT Adenocarcinoma- vast majority SCC PROGRESSION & PROGNOSIS Neuroendocrine tumors 5YS DUKES: A=80-90%, B= 70-80%, C= 30-50% PRESENTATION Bleeding from anus- more typical for rectal cancer than colon cancer Constipation and/or diarrhea Abdominal pain- often crampy 17  Charlotte Eikaas 2023/24 ANAL CANCER EPIDEMIOLOGY DIAGNOSIS: biopsy M >F (4x) Peak incidence in 50s RISK FACTORS & ETIOLOGY: TREATMENT: HPV (16,18)- genital warts; 30x risk Should be conservative- preserve anal sphincter: chemo Immunodeficiency- HIV, immunosuppression + RT = curable in 80-90% Anal intercourse- 33x If F, AA 60 y/old RISK FACTORS & ETIOLOGY: many RFs depend on subtype; others include… TREATMENT Adenomatous gastric polyps Surgery = only radical treatment- either total or partial Partial gastrectomy gastrectomy + lymphadenectomy Family history, blood group A Radical resection of stage IB or higher → combine with chemo Herceptin: used in around 20%- for specific mutation SUBTYPES 95% are adenocarcinomas; two subtypes exist (Lauren classification) 1. Intestinal AC Decreasing incidence; MC in Japan PROGRESSION & PROGNOSIS M>F, average age 55 Very poor prognosis- T1 = 50% 5YS, stage IV = 3% Related to chronic gastritis (H.Pylori), Spread: direct to GIT, or hematogenous- to liver or to nitrosamines, FAP and HNPCC ovaries- Bilateral mucinous AC- Krukenberg tumor 2. Diffuse AC Stable incidence Uniform across countries, M=F OTHERWISE NOTEWORTHY May be related to EBV- better prognosis Related to CDH1 mutation (Cadherin loss) Specific lymph nodes associated: Virchow’s node (= Troisier sign-metastasis to left supraclavicular from PRESENTATION abdominal cancer), left axillary nodes, Sister Mary Joseph’s node (periumbilical) Epigastric pain; sometimes also in back if advanced Vomiting; sometimes hematemesis Anorexia, weight loss Dysphagia Iron-deficiency anemia Hepatomegaly Lymphadenopathy Epigastric mass Paraneoplastic syndromes: Acanthosis Nigricans, Leser-Trelat syndrome 20  Charlotte Eikaas 2023/24 LIVER CANCER EPIDEMIOLOGY DIAGNOSIS 5th MC cancer worldwide USG, CT, MRI MC in Asia and Africa- higher prevalence of viral AFP level- increased in HCC; not diagnostic, not used for hepatitis screening RISK FACTORS & ETIOLOGY (hepatocellular carcinoma) Chronic hepatitis: HCV > HBV; HBC can cause HCC TREATMENT: without cirrhosis Surgery may be curative in some cases Cirrhosis- only 15-20% in non-cirrhotic livers; usually Inoperable → Sorafenib related to alcoholism and poor lifestyle M>F Aflatoxins (Aspergillus toxin in food) PROGRESSION & PROGNOSIS PBC- primary biliary cholangitis Generally poor prognosis- hidden by cirrhosis; death due Genetic: beta-catenin, TP53, TERT to liver failure or complications of portal HTN Alpha1-antitrypsin deficiency Tendency to invade portal vein Intrahepatic metastasis = MC SUBTYPES: Hepatocellular carcinoma: MC primary subtype Fibrolamellar carcinoma: 85% biopsy; Rare in women - HER2+ → Trastuzumab- receptor antagonist + CHEMO histochemistry confirm by central scar (2+) FSH Chemo: in triple neg, metastasis, or if unresponsive to High breast density (more glands) on mammography hormonal therapy Contralateral breast cancer, endometrial cancer Bisphosphonates: taken for 5y if N+, or after chemo Preventative: Oophorectomy (↓75%), Tamoxifen therapy, Aromatase inhibitors, exercise, pregnancy, breastfeeding- accumulative effect PROGRESSION & PROGNOSIS Originate from DCIS (higher risk, MC precursor) or LCIS Strongly depends on subtype; Luminal A has great prognosis, Triple neg very poor SUBTYPES Most important prognostic factors: tumor size, lymph node Luminal A: MC; highly + for ER and PR- responsive to status, ER-status and HER2 status hormonal therapy- best prognosis Mortality: has decreased in the last decades in Western Luminal B: ER+, PR +/-, may respond to hormonal therapy Europe + USA - due to adjuvant therapy and use of HER2+: ER and PR-, worse prognosis, but we may use mammography targeted therapy; negative prognostic, positive predictive F Metastatic BC is uncurable- goal is prolonging life; MC sites Triple negative: worst prognosis; ER-, PR- HER2- are bone, lung, liver and brain CNs pleura umph nodes , , Prognosis of metastatic BC: good = skin, soft tissue, bone, and Each molecular subtype can be of different histological subtypes; single lung lesions; bad = viscera I liver brain peritonium SC) , , , , Luminal A = usually invasive ductal carcinoma NST; HER2 = apocrine or micropapillary; TN = medullary, metaplastic or secretory carcinoma OTHERWISE NOTEWORTHY > - kist-proliferation HER2 positivity: checked by immunohistochemistry (+1) = PRESENTATION negative; (+2) → do FISH to confirm; (+3) = positive Painless palpable mass = MC Prevention- screening: mammography every 3y from 50-70 Skin changes: retraction, Peau d’orange (dimpling), nipple y/old- ↓mortality in women >50 y/old; self-examination is inversion, satellite nodules NOT recommended Lymphadenopathy- usually axillary nodes > - may edema cause ar m Spiculated mass on MG = highly suggestive of cancer Inflammation- must be diff. from mastitis Breast cancer = #1 origin of metastatic bone cancer- most. common cause of pathologic fractures 22  Charlotte Eikaas 2023/24 MESENCHYMAL CANCER- SARCOMAS EPIDEMIOLOGY DIAGNOSIS 1% in adults, 10% in children MRI: best choice for STS Benign tumors of mesenchyme are more common CT: to exclude bone involvement and metastases AA depends on type of cancer; 60 y/old for STS and Biopsy: usually core needle biopsy GIST, 16 y/old for osteosarcoma and Ewing sarcoma, Staging: focused on histologic grade, size of primary and presence 5 y/old for rhabdomyosarcoma of metastases RISK FACTORS & ETIOLOGY TREATMENT 95% = unknown etiology Surgery is the cornerstone of treatment, but is often combined Hereditary (rare): Li-Fraumeni, Gorlin-Goltz, Gardner, with chemo and RT Werner, Recklinghausen (NF1) Low grade, superficial, small, good location → surgery Acquired mutations: cKIT in GIT stromal tumor straight away Environmental: ionizing radiation, vinyl chloride, High grade, deep location, advanced, recurrent → arsenic, thorotrast consider induction chemo + post-op RT SUBTYPES Pre-op RT: lower risk of secondary cancer, higher risk of healing May arise from different tissues: adipose tissue, bone, complications (reversible) cartilage, smooth and skeletal muscle Post-op RT: higher risk of secondary cancer, semi-frequent STS- soft tissue sarcoma = 75% irreversible complications- edema, fibrosis, stiffness Liposarcoma Specific regimens Leiomyosarcoma Osteosarcoma: RT-resistant → chemo + surgery Rhabdomyosarcoma- usually in H&N or GUT Chondrosarcoma: chemo + RT resistant Kaposi sarcoma Ewing sarcoma: RT + chemo-sensitive; induction chemo GIST- gastrointestinal stromal tumor = 15% → surgery + RT → maintenance chemo (1 year) Disseminated disease → chemo BTS- bone tissue sarcoma Osteosarcoma PROGRESSION & PROGNOSIS Chondrosarcoma Low grade sarcomas: metastases in 15% Ewing sarcoma High grade sarcomas: metastases in 50%; if on extremities then usually to lungs, if visceral then liver PRESENTATION Increased risk of recurrence: age> 50, positive surgical margins, Location: lower extremities (45%), upper extremities (15%), fibrosarcoma, MPNST, previous recurrence corpus (15%), retroperitoneal (15%), visceral (10%), H&N (8%) Increased risk of metastasis: size >5cm, high grade, deep location, Codman’s triangle on X-ray: in Ewing sarcoma, osteosarcoma, recurrent disease, leiomyosarcoma but also subperiosteal abscess 33