GI Cancers

Question 1

What are the 3 histological types of oral cancers?

Answer 1

Pleiomorphic Adenoma, Mucoepidermoid carcinoma, Warthin tumor.

Question 2

Which salivary gland has the worst cancer prognosis?

Answer 2

Sublingual gland is 75% malignant tumors vs only 25% of the Parotid and 50% of Submandibular.

Question 3

What percentage of Warthin tumors are malignant?

Answer 3

Only 10%.

Question 4

Which nerve runs through the Parotid gland?

Answer 4

CN VII - Facial nerve.

Question 5

If not resected entirely, what often occurs with a Pleiomorphic Adenoma?

Answer 5

It will often just regenerate from the tissue not resected entirely.

Question 6

What are the two main types of Esophageal cancer?

Answer 6

Upper 2/3rds and larynx are Squamous Cell Carcinoma. Lower third is Adenocarcinoma, like most of the GIT.

Question 7

What are Risk Factors for Esophageal cancer?

Answer 7

Achalasia is for both. Alcohol, Smoking, Hot liquids are RFs for SCCa. GERD is naturally the RF for Adenocarcinoma after the metaplasia to glandular mucosal and columnar cells has taken place.

Question 8

What are the two types of Gastric Adenocarcinoma?

Answer 8

Intestinal is localized and appears as an ulcer with raised margins, usually found at the Lesser curvature of the stomach.

Question 9

What are the RFs for Gastric Adenocarcinoma?

Answer 9

Nitrosamine ingestion from smoked foods (Scandinavia, Japan, Russia). Group A Blood type (that’s me!), Chronic gastritis with H. Pylori (though not in the diffuse linitis plastica type), and cigarette smoking. Also salty preserved foods diet.

Low socioeconomic status. And males have it at a ratio of 2:1 because they boars who eat anything except my Jeremy. jk.

Question 10

Describe the Diffuse type of gastric Adenocarcinoma.

Answer 10

Presents with a diffuse leathery bottle thickened rigidity of the stomach. Has mucus-filled signet ring cells in which the nucleus has been pushed to the edge. It is highly aggressive and highly malignant. Not associated with H. Pylori. Most cases due to E-cadherin mutation.

Question 11

Gastric Adenocarcinoma is 90% of stomach cancers. Which other types are in the 10% minority?

Answer 11

Lymphoma, GI stromal tumor, Carcinoid (especially rare).

Question 12

Describe the Intestinal type of gastric adenocarcinoma.

Answer 12

Appears like an ulcer but with raised margins. Commonly on the lesser curvature of the stomach and highly associated with H. Pylori and smoked foods.

Question 13

Name the 4 metastases of gastric cancer.

Answer 13

Virchow’s node is left supraclavicular lymph node from stomach. Umbilicus of Sister Mary Joseph is subcutaneous periumbilical metastasis. Krukenberg tumor is BILATERAL ovaries with abundant mucin secreting signet ring cells.

Then we have Bookshelf - oops, i mean Blumer shelf - a palpable mass on DRE suggesting metastasis to the rectouterine pouch of Douglas.

Question 14

How does gastric cancer present?

Answer 14

Unfortunately late, like esophageal and pancreatic. Weight loss, abdominal pain, early satiety and in half of patients with acanthosis nigricans or Leser Trelat sign.

Question 15

Describe Acanthosis Nigricans and what other times will you see it present.

MCC?

Answer 15

Simply hyperpigmented patches on the skin and thickened velvety body creases - under breasts, arms, groin, back and sides of neck.. More common to those of African, Hispanic, and Native American descent, oddly enough.

Discoloration can be light brown to deep gray or black (cow patch colors!). Usually a symmetrical distribution.

Seen in diabetics, hypothyroidism, PCOS, some pituitary disorders, and stomach cancer.

Corticosteroids ad Aripiprazole can cause it by affecting insulin. As can OCPs.

Too much insulin in the body is the MCC.

Not contagious, not harmful.

https://www.youtube.com/watch?v=T-8O1KcRx_k

Question 16

What is the Leser-Trelat sign?

How are they removed?

Answer 16

Seborrheic Keratosis. Waxy, rough benign growths usually on the head, arm or trunk of the body. Looks stuck on as if you could pull it off.

Cryotherapy with liquid nitrogen is removal technique.

Question 17

RET proto-oncogene encodes which receptor? Which chromosome is it on?

Which diseases is it implicated in with loss of function? What occurs with gain of function?

Answer 17

Tyrosine Kinase. Chromosome 10.

RET loss of function mutations are associated with the development of Hirschsprung’s disease.

While gain of function mutations are associated with the development of various cancer, including medullary thyroid carcinoma, MEN type 2A and 2B, pheochromocytoma and parathyroid hyperplasia.

Question 18

What is the third most common cancer to both men and women?

Answer 18

Colon cancer.

Question 19

What are the 3 shapes of colon polyps?

Answer 19

Pedunculated, Sessile (having no stalk), and Flat.

Question 20

Mucosal and Submucosal polyps are generally what…

Answer 20

Benign. No threat.

Question 21

Hamartomatous polyps are shaped how and made up of what?

What two conditions is it associated with?

Answer 21

Benign, pedunculated, disorganized mature cells. Not developmentally abnormal as in the case of cancer.

Peutz-Jeghers and Juvenile Polyposis. Despite the hamartomas being benign, these two do predispose the pt to colorectal cancer.

Question 22

Inflammatory pseudopolyps are made up of what and associated with which disease?

Answer 22

Scar tissue and edema. IBD - esp UC.

Question 23

Hyperplastic polyp vs Serrated polyp?

Answer 23

Low to moderate risk of cancer. Serrated polyp is definitely precancerous. Unfortunately both look like sawtooth crypts.

Hyperplastic tend to be tiny and under 5mm and found in the rectosigmoid region. They very rarely are on the right side but these have premalignant potential.

Question 24

Pedunculated with cellular atypia is high risk and known as what type of polyp?

Answer 24

Adenomatous polyp with the villous type being the most malignant and tubular the third most malignant.

Question 25

Which two types of polyps are incredibly high risk for cancer? Which is pedunculated?

Answer 25

Serrated and adenomatous. Adenomatous is pedunculated.

Question 26

What is the cancer pathway for Adenomatous polyps?

Answer 26

APC-Kras mutations with chromosomal instability.

Question 27

Pathway for serrated polyp cancer?

Answer 27

BRAF mutations - CpG hypermethylation pathway with microsatellite instability.

Question 28

Name the Polyposis Syndromes.

Answer 28

All autosomal dominant heritance. All cause colon polyps. All predispose to colorectal cancer.

FAP is loss of function of APC tsg disinhibiting mitosis. FAP has thousands of polyps and begins in rectum.

Question 29

Familial Adenomatous Polyposis requires what intervention?

Answer 29

These pts are 100% going to get colorectal adenocarcinoma. Prophylactic Colectomy required by early 20’s.

Question 30

What are the 2 types of FAP?

Answer 30

Gardner Syndrome is FAP with bone and soft tissue tumors. What fun.

Turcot Syndrome is FAP with CNS tumors. Lovely.

Question 31

Which two polyposis syndromes have benign hamartomatous polyps along with increased risk of colorectal cancer?

Answer 31

Peutz-Jeghers and Juvenile Polyposis (under age 5).

PJS is characterized by hyperpigmentation of lips, hands, mouth, genitalia.

Question 32

Lynch Syndrome has what percentage of occurance vs FAP?

Answer 32

Lynch has 80% prevalence whereas FAP is 100%. Like everything else colorectal, it is AD heritance.

Question 33

Which area of the colon is affected by Lynch Syndrome?

Answer 33

Always involves Ascending colon whereas FAP always involves Rectum.

Question 34

Lynch Syndrome is caused by loss of function of what type of gene?

Answer 34

DNA repair genes - so it can lead to also skin, ovarian, endometrial cancer.