Colorectal Ca Flashcards

1
Q

what is CRC? define

A

colorectal cancer

adenocarcinoma is most common
- other subtypes of adenocarcinoma exist

other non-adenocarcinoma cancers include:
- carcinoid tumours
- Gastrointestinal stromal tumours
- NHL
- sarcomas

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2
Q

what is a colorectal polyp?

A

it’s a protuberance into the lumen of a normally flat colonic mucosa (inwards)

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3
Q

explain non-neoplastic vs neoplastic examples of colorectal polyps

A

non-neoplastic ➔ usually a hyperplastic situation (most common
- mucosal polyps and hamartomas are also potential histological findings

neoplastic polyps are things like adenomas ➔ they are premalignant and can invade into the submucosa
- histological cell type informs the invasiveness of the polyp (villous is most vs tubular is less)
- tubular polyps are more common vs villous

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4
Q

epi of crc?

A

3rd most common cancer (lung > breast > colon)

in general the incidence of CRC is decreasing however the age at dx is getting younger

more common in Caucasians

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5
Q

RF for CRC

A
  • fhx of CRC, breast cancer, or hereditary cancer syndromes (familial adenomatous polyposis and lynch syndrome)
  • personal hx of cancer
  • inflammatory bowel diseases
  • celiac
  • increased age (>50Y)
  • abdo/pelvic radiation
  • comorbidities: DM< uncontrolled acromegaly disease, LT immunosuppresants, and obesity
  • diet: processed meat and food and low-fiber diet
  • smoking and alcohol
  • androgen deprivation therapy (prostate ca tx)
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6
Q

common sites of CRC mets?

A

liver, lung, bone, brain

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7
Q

general patho of how colorectal

A
  1. collection of cell line mutation (can be somatic or germline via the hereditary cancer syndromes)
  2. may result in precancerous polyps (adenomatous polyp)
  3. over time (10-15Y) more mutations accumulate which can result in dyplastic changes
  4. can evolve into an invasive carcinoma
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8
Q

what are 2 of the 3 major molecular pathways that result in CRC?

A
  1. chromosomal instability
  2. damaged mismatch repair mechanisms
  3. hypermethyaltion of tumour suppressor genes
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9
Q

common genes involved in CRC

A
  1. RAS
  2. APC
  3. TP53
  4. MMR genes
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10
Q

what are red flags for crc?

A
  1. iron deficiency anemia in older males or postmenopausal females
  2. pencil stools
  3. melena
  4. bright red blood per rectum
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11
Q

what are some general s/s of CRC?

A
  1. hematochezia
  2. melena
  3. abdo pain
  4. changes in BM
  5. tenesmus
  6. constitutional s/s: fatigue, wt loss
  7. s/s of obstruction

P/E: physical mass on DRE or RLQ w/ a R colon mass

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12
Q

walk me through screening recommendations for CRC

A

average risk: start at 50Y-74Y, fecal immunochemical test every 2 yearsor sigmoidoscopy

high risk: first degree relative ➔ start at 50Y or 10Y before the age of dx; colonoscopy every 5Y (if relative was <60Y) or 10Y (if relative was >60Y)

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13
Q

how would you dx a colon cancer?

A

colonosocpy w/biopsy

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14
Q

how do you work up a dx colorectal cancer

A
  1. CBC with diff
  2. ferritin
  3. electrolytes and extended
  4. creatinine and urea
  5. liver: ALT/ALP bilirubin
  6. CEA - tumour marker – baseline for tx response
  7. coagulation - PT/INR and aPPT re potential bleeding

imaging
- baseline CT CAP w/ contrast to look for mets

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15
Q

how do you tx crc?

A
  1. refer to surg onc and med onc

early disease: resection w/ LN and mesentery

consider neoadjuvant therapy if tumour is large ➔ chemoradiation (alkylating agent +/- antimetabolite)

adjuvant therapy of chemo: alklylating agent +/- antimetabolite

with stage 4 – palliative
- procedures to help with s/s management ➔ obstruction (ostomy), bleeding/pain (radiation)

organize follow-up surveillance with CT CAP and CEA and colonoscopy every 1, 3, and 5Y

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